Care of People with Diabetes

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Diabetes mellitus is a metabolic disorder in which the body’s capacity to utilise glucose,fat and protein is disturbed due to insulin deficiency or insulin resistance. Both states lead to hyperglycaemia and glycosuria.


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Fourth Edition Care of People with Diabetes A M A nu A l o F n ursing Pr A ctic E T risha Dunning

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Care of People with Diabetes To Cure Diabetes Click Here

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This book is dedicated to all people with diabetes who taught me so much of what I know about life with diabetes people with diabetes who need health care and to all the health professionals who care for them.

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Care of People with Diabetes A Manual of Nursing Practice Fourth Edition To Cure Diabetes Naturally Click Here Professor Trisha Dunning AM RN MEd PhD CDE FACN DLF Inaugural Chair in Nursing and Director Centre for Nursing and Allied Health Research Deakin University and Barwon Health Geelong Victoria Australia

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This edition first published 2014 © 2014 by John Wiley Sons Ltd. Third edition first published 2009 © Trisha Dunning Second edition first published 2003 © Blackwell Publishing Ltd. First edition first published 1994 © Blackwell Publishing Ltd. Registered Office John Wiley Sons Ltd The Atrium Southern Gate Chichester West Sussex PO19 8SQ UK Editorial Offices 9600 Garsington Road Oxford OX4 2DQ UK The Atrium Southern Gate Chichester West Sussex PO19 8SQ UK 111 River Street Hoboken NJ 07030–5774 USA For details of our global editorial offices for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced stored in a retrieval system or transmitted in any form or by any means electronic mechanical photocopying recording or otherwise except as permitted by the UK Copyright Designs and Patents Act 1988 without the prior permission of the publisher. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names service marks trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required the services of a competent professional should be sought. The contents of this work are intended to further general scientific research understanding and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method diagnosis or treatment by health science practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research equipment modifications changes in governmental regulations and the constant flow of information relating to the use of medicines equipment and devices the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine equipment or device for among other things any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom. Library of Congress Cataloging-in-Publication Data Dunning Trisha. Care of people with diabetes : a manual of nursing practice / Trisha Dunning. – 4th ed. p. cm. Includes bibliographical references and index. ISBN 978-0-470-65919-9 pbk. I. Title. DNLM: 1. Diabetes Mellitus–nursing–Handbooks. WY 49 RC660 616.4 ′620231 –dc 23 2013014725 A catalogue record for this book is available from the British Library. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Cover image: iStock © Chris Fertnig Cover design by Grounded Design Set in 9.5/11.5pt Sabon by SPi Publisher Services Pondicherry India 1 2014

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Contents Cure Diabetes in 21 Days Foreword xv Preface xvi Acknowledgements xviii List of Abbreviations and Symbols xix 1 Diagnosing and Classifying Diabetes 1 Key points 1 What is diabetes mellitus 2 Prevalence of diabetes 2 Classification of diabetes 3 Overview of normal glucose homeostasis 4 The metabolic syndrome in children and adolescents 7 Type 1 and Type 2 diabetes 8 Type 2 diabetes in Indigenous children and adolescents 15 Gestational diabetes 15 Example Information Sheet: Preparation for an oral glucose tolerance test 20 Screening for diabetes 21 Preventing Type 2 diabetes 22 Preventing Type 1 diabetes 25 Managing diabetes mellitus 25 Key points 25 Aims of management 27 Exercise/activity 29 Diabetes education 32 Complications of diabetes 33 Aim and objectives of nursing care of people with diabetes 34 Technology and diabetes management 36 A sobering final comment 38 References 38 2 Holistic Assessment Nursing Diagnosis and Documentation 44 Key points 44 Rationale 44 Holistic nursing 45 Care models 45 Characteristics of an holistic nursing history 47 Nursing history 49 Example Health Assessment Chart 50 Instruments to measure health status 54 Documenting and charting patient care 54 Care plans 55

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vi Contents Nursing responsibilities 56 Documentation by people with diabetes 57 References 58 3 Monitoring Diabetes Mellitus 60 Key points 60 Rationale 60 Introduction 61 Monitoring 1: Blood glucose 61 Key points 61 Blood glucose testing checklist 71 Monitoring 2: Urine glucose 73 Key points 73 Monitoring 3: Additional assessment 76 Self-care 80 The annual review 81 References 81 4 Nutrition Obesity and Exercise 84 Key points 84 Rationale 84 The importance of good nutrition 85 Obesity 85 Overview of the pathogenesis of obesity 86 The significance of abdominal obesity 87 Nutrition obesity and stress 88 Methods of measuring weight 88 Managing obesity and diabetes 90 Malnutrition and under-nutrition 90 Method of screening for dietary characteristics and problems 93 Principles of dietary management for people with diabetes 94 Goals of Dietary Management 97 Dietary management: obesity 98 Bariatric surgery 99 Complementary weight loss programmes 101 Factors associated with making dietary changes 101 Nursing responsibilities 102 References 107 5 Medicines Management 111 Key points 111 Introduction 112 Quality Use of Medicines QUM 112 Quality Use of Medicines and Diabetes 113 Oral Glucose-Lowering Medicines GLM 114 The incretin hormones 124 New medicines for type 2 diabetes 125

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Contents vii Medicine interactions 126 When should insulin be initiated in Type 2 diabetes 128 Barriers to insulin therapy 132 Some strategies to overcome the barriers 132 Insulin therapy 133 Types of insulin available 134 Injection sites and administration 137 Mixing short- and intermediate-acting insulins 138 Commonly used insulin regimens 139 Interpreting morning hyperglycaemia 140 Continuous subcutaneous insulin infusion CSII 141 Continuous blood glucose sensors 142 Subcutaneous insulin sliding scales and top-up regimes 143 Uses of insulin infusions 145 Insulin allergy 147 Transplants 148 Stabilising diabetes 148 Stabilising diabetes in hospital 149 Community and outpatient stabilisation 150 Lipid-lowering agents 152 Monitoring lipid medicines 157 Antihypertensive agents 157 Antiplatelet agents 160 Medication safety adherence and medication self-management 161 Enhancing medication self-care 163 Example protocol for outpatient stabilisation onto insulin 166 References 167 6 Hypoglycaemia 174 Key points 174 Rationale 174 Introduction 175 The counter-regulatory response 176 Definition of hypoglycaemia 178 Recognising hypoglycaemia 180 Counter-regulatory hormonal response to hypoglycaemia 181 Causes of hypoglycaemia 181 Preventing and managing hypoglycaemia 182 Hypoglycaemic unawareness 183 Prevalence of hypoglycaemic unawareness 183 Nocturnal hypoglycaemia 184 Relative hypoglycaemia 187 Medicine interactions 187 Objectives of care 188 Treatment 188 Prolonged hypoglycaemia 189 Patients most at risk of hypoglycaemia 190 Psychological effects of hypoglycaemia 191

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viii Consequences of hypoglycaemia 192 Guidelines for administering glucagon 193 Adverse reactions 194 References 194 7 Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA Hyperosmolar Hyperglycaemic States HHS and Lactic Acidosis 198 Key points 198 Rationale 199 Contents Prevention: proactively managing intercurrent illness 199 Self-care during illness 201 Hyperglycaemia 201 Diabetic ketoacidosis DKA 203 Brittle diabetes and hyperglycaemia 210 Euglycaemic DKA 210 Hyperosmolar Hyperglycaemic States 211 Presenting signs and symptoms 212 Lactic acidosis 213 Lactic acidosis associated with Metformin 215 References 216 8 Long-Term Complications of Diabetes 218 Key points 218 Introduction 219 Pathophysiology of diabetes complications 219 Cardiovascular disease and diabetes 221 Key points 221 Rationale 222 Medicines and cardiovascular disease 223 Complementary medicines CAM 226 Other management considerations 227 Mental health and cardiovascular disease 228 Nursing responsibilities 229 Telephone coaching 233 Cerebrovascular disease 233 Signs and symptoms 234 Diabetes and eye disease 235 Key points 235 Rationale 235 Introduction 235 Risk factors for retinopathy 236 Diabetes and renal disease 241 Key points 241 Introduction 241 Stages of chronic kidney disease 241 Risk factors for renal disease 242 Renal failure 243

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Contents ix Renal disease and anaemia 245 Diet and renal disease 245 Renal disease and older people 247 Kidney biopsy 247 Renal dialysis 247 Objectives of care 249 Nursing responsibilities 250 Commencing CAPD in patients on insulin 250 Educating the patient about CAPD 251 Supportive care 252 Renal disease and herbal medicine see also Chapter 19 252 Peripheral and autonomic neuropathy 253 Key points 253 Introduction 253 Vascular changes 254 Infection 255 Diabetes-related peripheral neuropathy 257 Other pain management strategies 258 Stages of peripheral neuropathy 259 Risk factors for developing foot problems 259 Objectives of care 260 Nursing responsibilities 260 Classification of foot ulcers 262 Wound management 262 Wound management techniques under study 264 Rehabilitation 264 Autonomic neuropathy 265 Key points 265 Introduction 265 Diagnosis and management 267 Nursing care 268 References 269 9 Management During Surgical and Investigative Procedures 277 Surgical procedures 277 Key points 277 Rationale 277 Introduction 278 Children with diabetes undergoing surgical procedures 279 Older people with diabetes and surgical procedures 280 Aims of management 280 Preoperative nursing care 281 Major procedures 284 Postoperative nursing responsibilities 286 Minor procedures 287 Insulin pump therapy in patients undergoing surgery 288 Emergency procedures 289 Bariatric surgery 290

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x Investigative procedures 290 Key points 290 Rationale 290 The objectives of care 291 General nursing management 291 Eye procedures Complementary therapies and surgery and investigative 292 procedures 295 Preoperative phase 295 Postoperative phase 296 Implications for nursing care 297 References Example Instruction Sheet 2a: Instructions for people with diabetes on oral glucose-lowering medicines having procedures 297 as outpatients under sedation of general anaesthesia Example Instruction Sheet 2b: Instructions for people with diabetes on insulin having procedures as outpatients under sedation 298 or general anaesthesia 299 Contents 10 Conditions Associated with Diabetes 300 Key points 300 Introduction 300 Enteral and parenteral nutrition 301 Aims of therapy 301 Routes of administration 302 Choice of formula 304 Nursing responsibilities 304 Diabetes and cancer 306 Management 307 Objectives of care 308 Nursing responsibilities 309 Managing corticosteroids in people with cancer 310 Complementary therapies and cancer 311 Smoking alcohol and illegal drug use 312 Smoking 312 Nicotine addiction 314 Assisting the person to stop smoking 315 Medicines to support smoking cessation 317 Alcohol addiction 317 Illegal drug use 319 Effects on diabetes 321 Interactions with medicines 322 Management issues 322 Brittle diabetes 323 Introduction 323 Causes of brittle diabetes 324 Management 324 Oral health and diabetes 325 Introduction 325 Causal mechanisms 326 Management 326 Diabetes and liver disease 327 Introduction 327 Managing people with diabetes and liver disease 328

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Contents xi CAM medicines 329 Haemochromatosis 329 Iron overload 330 Management 330 Diabetic mastopathy 330 Diagnosis 330 Management 331 Diabetes and coeliac disease 331 Signs and symptoms 332 Diagnosis 332 Management 333 Cystic fibrosis-related diabetes 333 Diagnosis 334 Signs and symptoms 335 Management 335 Sleep disturbance and diabetes 335 Diagnosis 336 Management 337 Diabetes and tuberculosis 337 Management 337 Diabetes and HIV/AIDS 338 Management 338 Diabetes and hearing loss 339 Causes of hearing loss 339 Management 340 Diabetes and musculoskeletal diseases 341 Management 342 Corticosteroid and antipsychotic medications and diabetes 342 Key points 342 Introduction 342 Management 344 Antipsychotic medicines 345 Diabetes and driving 346 Prevalence of and risk factors for driving crashes 346 Diabetes-related effects on driving 349 Hypoglycaemia effects on driving 352 Strategies to enhance driving safety 353 Information for people with diabetes to help them drive safely 354 Diabetes and fasting for religious observances 355 Education and counselling 356 References 356 11 Diabetes and Sexual and Reproductive Health 365 Key points 365 Rationale 365 Sexual health 366 Sexual development 367 Sexual problems 367 Possible causes of sexual difficulties and dysfunction 368 Sexuality and older people 369 Women 369 Men 370 Investigation and management 371 Medication management for ED 372 Non-pharmacological therapy 372 Complementary medicines for sexual problems CAM 373 Involving partners in ED management 374 Sexual counselling 374 The PLISSIT model 376 Role of the nurse 377 References 377 12 Diabetes in Older People 379 Key points 379 Rationale 380 Introduction 380

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xii Determining functional status 386 Geriatric syndromes 388 Cognitive functioning 388 Contents Depression and older people with diabetes 394 Dementia 394 Managing diabetes in older people 395 Management aims 395 Factors that affect management decisions 396 Guidelines for administering diabetes medicines with enteral feeds 401 Education approaches 402 Self-care 403 Factors that can affect metabolic control 404 References 414 13 Diabetes in Children and Adolescents 422 Key points 422 Rationale 422 Introduction 423 Managing children and adolescents with diabetes 425 Aspects of care that apply to both Type 1 and Type 2 diabetes in children and adolescents 425 Managing Type 1 diabetes 427 Managing childhood Type 2 diabetes 430 Medication self-management 431 Other conditions associated with diabetes 431 Complementary therapy use in children 432 Strategies for enhancing adherence during adolescence 433 Ketoacidosis in children 434 References 434 14 Women Pregnancy and Gestational Diabetes 438 Key points 438 Rationale 438 Polycystic ovarian syndrome 439 Pregnancy 442 Complications of pregnancy 446 Effects of diabetes on the baby 447 Longer term effects of maternal hyperglycaemia on the child 448 Gestational diabetes 448 Risk factors for gestational diabetes 449 Managing gestational diabetes 450 Type 1 diabetes 451 Type 2 diabetes 452 Menopause and diabetes 452 Signs and symptoms of menopause 453 Managing the menopause 453 Contraception options for women with diabetes 454 Complementary approaches to managing the menopause 456 References 458 15 Psychological and Quality of Life Issues Related to Having Diabetes 463 Key points 463 Rationale 464 Introduction 464 Depression 469 Symptoms of depression 470 Maintaining mental health and managing depression 470 Screening for psychological distress and depression 472 Antipsychotic medicines and diabetes 473 Type 1 diabetes 473 Type 2 diabetes 474

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Contents xiii Compliance/adherence/concordance 475 Psychological distress and cardiovascular disease 476 Quality of life 478 References 479 16 Diabetes Education 483 Key points 483 Rationale 484 Introduction 484 Learning styles 486 Education and other theories/models 489 Communication – the central element of effective teaching and learning 492 Teaching: an art and a process 494 Health literacy 495 Survival skills 498 Sample diabetes education record chart 499 Empowerment 501 Special issues 502 The nurses’ role in diabetes education 502 Insulin administration 504 Guidelines for teaching people about insulin delivery systems 504 Documenting diabetes education 505 Examples instruction sheets 505 Example Instruction Sheet 3: How to draw up insulin from one bottle 505 Example Instruction Sheet 4: How to draw up insulin from two bottles usually a short/rapid acting and an intermediate acting insulin 506 Example Instruction Sheet 5: How to give an insulin injection using syringes or insulin pens 506 Example Instruction Sheet 6a: Managing your diabetes when you are ill: patients with Type 1 diabetes 506 Example Instruction Sheet 6b: Managing your diabetes when you are ill: patients with Type 2 diabetes 508 Evaluating diabetes education 509 References 511 17 Nursing Care in the Emergency Intensive Care Outpatient Departments Community and Home-Based Care and Discharge Planning 516 Key points 516 Community practice and home care nurses are in an ideal position to deliver preventative health care education 516 Rationale 516 The emergency department 517 Intensive Care ICU 519 The outpatient department 519 Community Practice Nursing and Home-Based Care 520 Contents Introduction 520 How to obtain advice 521 General points 521 Disposing of sharps in the home situation 527 Storing insulin 528 Practice nurses 528 Discharge Planning 529 Key points 529 References 530 18 Managing Diabetes at the End of Life 532 Key points 532 Introduction 533

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xiv Palliative care and diabetes 534 Key issues in palliative and end of life care 534 The end of life process 538 Key management considerations for managing diabetes at the end of life 540 Glycaemic targets 541 Blood glucose monitoring 541 Hyperglycaemia 542 Hypoglycaemia 542 Medicine management 543 Type 1 diabetes 543 Type 2 diabetes 544 Nutrition and hydration 545 Diabetogenetic medicines 546 Managing corticosteroid-induced diabetes in palliative care patients 547 Antipsychotic medicines 547 Supporting family/carers 548 Withdrawing treatment 548 Diabetes education 549 References 549 19 Complementary and Alternative Therapies 552 Key points 552 Rationale 552 Introduction 553 CAM philosophy 555 Integrating complementary and conventional care 556 Can complementary therapies benefit people with diabetes 558 Spirituality 561 CAM and surgery 561 Herb/medicine interactions 567 How can complementary therapies be used safely 568 Nursing responsibilities 569 Identifying quality health information on the Internet 570 References 572 Index 575

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Foreword It is with pleasure that I write the Foreword to this publication of Prof. Trisha Dunning. This comprehensive work represents a kaleidoscope of excellence and all professionals involved in the provision and delivery of diabetes care will find it invaluable in their practice. It is a most useful addition to their knowledge and will positively influence their delivery of care in the context of evidence-based practice and person-centred care. Each chapter pertinently addresses the key points as outlined at the beginning and is comprehensively referenced. Each of the 19 chapters can be read individually or in sequence to get the comprehensive view. The burden of diabetes at both an individual and societal level is well documented and therefore this book should prove to be a most useful guide to policy makers at national and international levels. The author is eminent in the field of diabetes research care and contemporary policy development and implementation. She is also a regular and respected contributor at international conferences and serves as a member of significant national and international boards. We are indebted to her commitment to the field of diabetes clinical practice and research. She is richly deserving of our congratulations for this work which I recommend without hesitation. Anne-Marie Felton President and co-founder of Foundation of European Nurses in Diabetes FEND Vice President Diabetes UK Co-Chair European Coalition on Diabetes ECD Preface Science and technology has increased our understanding about the pathophysiology of diabetes its management and the key role of education and self-care in achieving optimal outcomes since it was first described as diabetes maigre bad prognosis and diabetes gros big diabetes. Qualitative research highlights the importance of considering the individual’s beliefs and attitudes their explanatory models for diabetes and life in general their social situations and the key central role they play in their care. Translational research is becoming

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important. Person-centred care is now central to service delivery care standards and best practice. Equally importantly nurses and other health professionals are accountable for the care they provide and must reflect on their own beliefs attitudes and explanatory models because they affect the care and advice health professionals provide and their ability to establish therapeutic relationships with people with diabetes. The strength of the therapeutic relationship is a significant factor in diabetes outcomes. However evidence is not always easy to interpret and may not be readily accessible despite the advances in education and technology and the increasing number of databases of systematic reviews such as the Cochrane Collaboration the Joanna Briggs Institute and the bewildering number of management guidelines many of which make slightly different recommendations that are regularly published. In other ways we have made very little progress. The prevalence of obesity the metabolic syndrome and diabetes are all increasing globally. People are living longer and there is an increasing prevalence of Type 2 diabetes in developing countries and worryingly in children. People with diabetes are still developing devastating complications and premature death. Care of People with Diabetes was revised to reflect the changes in our understanding of the pathophysiology of diabetes and its complications and diabetes care and education since 2009. It is not possible to include every new piece of information and I had to leave a great deal of information out I stress not including work does not mean it is not interesting relevant or worthwhile. A new chapter about diabetes and palliative care has been included. Some information has been removed and some chapters amalgamated. I use the term ‘people/person with diabetes’ in most places in the text to be consistent with the Position Statement A New Language for Diabetes Diabetes Australia. 2011 however the term ‘patient’ still occurs in many places where it seems appropriate such as referring to people in hospital. I am indebted to people with diabetes for teaching me so much about the practicalities of life diabetes and how they live with it. I invite readers to reflect on the following words of a young woman with Type 1 diabetes: Diabetes is a designer disease. It was designed for people with routine lives – and that’s NOT me Preface xvii Her words eloquently illustrate the enduring importance of Hippocrates’ words which reflects the essence of person- centred care: It is more important to know what sort of person has a disease than to know what sort of disease the person has. Hippocrates circa 460–370 bc Both statements highlight the imperative to consider the individual in their life context and involve them in setting relevant goals and planning their care. I sincerely hope the revised edition of the book will continue to contribute to the vast body of information about diabetes. The book was not intended to take the place of the procedures and policies of health professionals’ employing institutions: it will complement them. The book also complements two of my other books: Managing Clinical Problems in Diabetes 2009 and Diabetes Education: Art Science and Evidence 2012 both also published by Wiley-Blackwell. I hope my books will help nurses and other health professionals care for people with diabetes in a holistic caring and sensitive way and that each person who reads the books will find something of value. Finally People get off track. Just have the patience to help them get back on track. That’s what’s important. Rural health TV programme about type 2 diabetes and Aboriginal and Torres Strait Islander People.

slide 19: Acknowledgements To Cure Diabetes Permanently Click Here I sincerely thank Wiley Blackwell for promoting the book and for supporting it since the first edition was published in 1994. I work in a supportive team of doctors and nurses and with wonderful academic colleagues. My special thanks go to them for their friendship and critical comment on various sections of the book. In particular Dr Bodil Rasmussen Dr Sally Savage Susan Streat Nicole Duggan Michelle Robins Heather Hart Patricia Streitberger and Pamela Jones. I am also grateful to Professor Alan Sinclair for his friendship and advice about managing diabetes in older people Professor Peter Martin for his advice about palliative care Lisa-Jane Moody for her comments about hearing impairment and Jessie Joose for her suggestions about nutrition. I acknowledge the generosity of the Australian Commonwealth Department of Health and Aging for permission to reproduce the figure depicting how the Quality Use of Medicines framework can be applied to diabetes management that appears in Chapter 5. My thanks also to Dr Sally Savage Nicole Duggan and Professor Peter Martin for agreeing it would be appropriate to include Table 18.2 and Figure 18.1. The table and figure were first published in Guidelines for Managing Diabetes at the End of Life Dunning Savage Duggan Martin 2010. I am in awe of the people who undertook the work described in this book and other researchers and clinicians who contribute so much information about diabetes that continues to challenge inform and inspire me. I continue to learn a great deal about diabetes from the people who live with diabetes whom I teach and care for and who participate in my research and their families. I thank these people for the privilege of working with them and for the information and stories they share. I appreciate ‘drop in’ visits from Leigh Olsen a man with diabetes who scours bookshops and other places for old medical and nursing texts he thinks I will enjoy. My especial thanks go to Anne-Marie Felton trailblazer dear friend and esteemed colleague for ‘everything’ especially for agreeing to write the foreword for this edition. I am grateful to James Rainbird for his careful editing and attention to detail. Finally I treasure the support and understanding of my family: the furry four-legged ones and feathered two-legged ones. My special thanks and love go to my husband John.

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List of Abbreviations and Symbols ↑ Increased ↓ Decreased ≤ Equal to or less than Less than ≥ Equal to or greater than Greater than ADA American Diabetes Association ADS Australian Diabetes Society BG Blood glucose BMI Body mass index BP Blood pressure BUN Blood urea nitrogen CAM Complementary and alternative medicine CAPD Continuous ambulatory peritoneal dialysis CCF Congestive cardiac failure CCU Coronary care unit CSII Continuous subcutaneous insulin infusion DA Diabetes Australia DKA Diabetic ketoacidosis DUK Diabetes UK ECG Electrocardiogram EN Enteral nutrition FFA Free fatty acids GLM Glucose lowering medicines HbA1c Glycosylated haemoglobin HHS Hyperosmolar Hyperglycaemic States HM Human insulin IAPO International Alliance of Patient Organisations ICU Intensive care unit IDF International Diabetes Federation IV Intravenous therapy

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LFT Liver function test MI Myocardial infarction MODY Maturity onset diabetes of the young xx List of Abbreviations and Symbols NDSS National Diabetes Supply Scheme OGTT Oral glucose tolerance test PCOS Polycystic Ovarian Syndrome SIGN Scottish Intercollegiate Guidelines Network TPN Total parenteral nutrition TPR Temperature pulse and respiration TZD Thiazolidinediones WHO World Health Organization The words are used in full the first time they appear in the text. All abbreviations are widely accepted and recognised.

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Chapter 1 Diagnosing and Classifying Diabetes To Cure Diabetes Click Here Cancer diabetes and heart disease are no longer diseases of the wealthy. Today they hamper the people and economies of the poorest populations…this represents a health emergency in slow motion. Ban Ki Moon Secretary General of the United Nations Key points • Diabetes is the modern pandemic. It represents a considerable global economic and social burden for the person with diabetes and for health services. • The prevalence of the metabolic syndrome Type 1 Type 2 and gestational diabetes is increasing. • The greatest increase in diabetes prevalence is occurring in Africa the Middle East and South East Asia. • The overlapping mechanisms by which obesity leads to the metabolic syndrome and Type 2 diabetes are complex and not yet fully understood. • Not everybody who is obese has insulin resistance or diabetes • Central obesity plays a key role in the progression to insulin resistance and Type 2 diabetes. • Lean people may be at higher risk of morbidity and mortality than obese people. • Primary prevention and early detection are essential to reduce the personal and community burden associated with the metabolic syndrome and diabetes and their complications. • Type 2 diabetes is a progressive disease and complications are often present at diagnosis. Thus insulin will eventually be necessary in most people with Type 2 diabetes. • The prevalence of obesity the metabolic syndrome and Type 2 diabetes is increasing in children. Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning.

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© 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd.

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2 Care of People with Diabetes What is diabetes mellitus Diabetes mellitus is a metabolic disorder in which the body’s capacity to utilise glucose fat and protein is disturbed due to insulin deficiency or insulin resistance. Both states lead to hyperglycaemia and glycosuria. The body is unable to utilise glucose in the absence of insulin and draws on fats and proteins in an effort to supply fuel for energy. Insulin is necessary for the complete metabolism of fats however and when carbohydrate metabolism is disordered fat metabolism is incomplete and intermediate products ketone bodies can accumulate in the blood leading to ketosis especially in Type 1 diabetes. Protein breakdown also occurs and leads to weight loss and weakness and contributes to the development of hyperglycaemia and lethargy. The different types of diabetes have different underlying causal mechanisms and clinical presentation: in general young people are insulin-deficient Type 1 diabetes while older people usually secrete sufficient insulin in the early stages but demonstrate resistance to insulin action Type 2 diabetes. In the early stages of Type 2 hyperinsulinaemia might be present. Type 2 is a progressive disease with slow destruction of the insulinproducing beta cells and consequently insulin deficiency. However 10 of older people with presumed Type 2 diabetes have markers of islet autoimmunity and become insulin dependent early in the course of the disease Turner et al. 1997 see latent autoimmune diabetes LADA later in this chapter Type 2 is becoming increasingly prevalent in children and adolescents as a result of the global obesity epidemic Barr et al. 2005 Zimmet et al. 2007. Type 2 diabetes is the most common accounting for 85 of diagnosed cases Type 1 accounts for 15 of diagnosed cases. Prevalence of diabetes Diabetes is a global health problem affecting 371 million people worldwide International Diabetes Federation IDF 2012 and more than 187 million are unaware they have diabetes. The prevalence is expected to increase to 552 million by 2030 unless the epidemic can be halted. In lower income families 3 out of 4 people have diabetes. The number of deaths attributed to diabetes in 2012 was 4.8 million and global diabetesrelated spending was estimated to be 471 billion US dollars IDF 2012. The three countries with the highest diabetes prevalence are China 92.3 million India 63 million and USA 24.1 million. In Australia AusDiab data show 100 000 people develop diabetes annually Cameron et al. 2003 and the prevalence continues to increase: 7.5 of people over 25 years and 16.8 of people over 65 have diabetes and a further 16.1 65 have impaired glucose tolerance IGT. In addition 200 000 progress from being overweight to obese 3 of adults develop hypertension and 1 develop renal impairment annually and the average waist circumference increases by 2.1 cm particularly in women. The prevalence increases annually by 0.8 Australian Diabetes Society ADS 2012. Thus a significant proportion of the population develops features of the metabolic syndrome with the associated increased risk of Type 2 diabetes and other associated conditions and leads to high health costs Colagiuri et al. 2003 Australian Institute of Health and Welfare AIHW 2005. In the UK an estimated 2.3 million people have diabetes and up to another 750 000 people have undiagnosed diabetes SIGN 2010. In Scotland approximately 228 000 people were registered as having diabetes in 2009 an increase of 3.6 from 2008 SIGN 2010. The reason for the increased prevalence of Type 2 diabetes is due to many inter-related factors including genetic predisposition environmental factors and the ageing population. Type 2 is the most common type accounting for 80–90 of cases. There is wide variation in the incidence rates of newly diagnosed Type 1 diabetes in children in different populations. However Type 1 in children and adolescents is increasing particularly in developed countries EURODIAB 2000 The DIAMOND Project Group 2006

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Diagnosing and Classifying Diabetes 3 Soltesz et al. 2006. The incidence of Type 1 diabetes in children 15 years on the Western Australian Children’s Database has increased gradually over the past 25 years but occurs in peaks and troughs rather than in a linear progression Haynes et al. 2012. For example peak years were 1992 1997 and 2003 in Australia. The incidence of type 1 appears to fluctuate in five-year cycles and might be influenced by circulating viruses especially enterovirus infections or other environmental factors Haynes et al. 2012. The association between ingestion of cow’s milk in infancy and pathogenesis of Type 1 diabetes is discussed in Chapter 13. Recently the role of IRE1∂ in inducing thioredoxin- interacting protein to activate the NLRP3inflammasome and promote programmed pancreatic cell death Lerner et al. 2012. The researchers stated that the findings suggest dietary modification could extend the honeymoon period in Type 1 diabetes or possibly prevent diabetes. Thus the economic burden of diabetes and health care costs are high. Over 9 of people admitted to hospital in Australia have diabetes and rates of 11–25 are reported in other countries. The proportion of people with diabetes admitted to hospital is increasing and they mostly have longer lengths of stay ADS 2012. Some people not known to have diabetes develop hyperglycaemia in hospital. Hyperglycaemia is associated with increased morbidity and mortality independently of diabetes Chapter 7. It is not clear whether hyperglycaemia in people without a diabetes diagnosis is due to undiagnosed diabetes/IGT or whether it is an indicator of underlying critical illness. However because in-hospital hyperglycaemia in non- diabetics may represent undiagnosed diabetes or risk of future diabetes these people should receive education and be followed up. Classification of diabetes Diabetes is broadly classified into Type 1 and Type 2 diabetes and other types. • Type 1 diabetes has two forms:  Immune-mediated diabetes mellitus which results from autoimmune destruction of the pancreatic beta cells leading to absolute insulin deficiency.  Idiopathic diabetes mellitus refers to diabetes forms that have no known aetiologies. Type 2 diabetes mellitus refers to diseases associated with relative insulin deficiency as a result of progressive beta cell failure and insulin resistance. • Impaired glucose homeostasis is an intermediate metabolic stage between normal glucose homeostasis and diabetes. It is a significant risk factor for cardiovascular disease and Type 2 diabetes. Thus early detection and management are important. There are two forms: 1 Impaired fasting glucose IFG where the fasting plasma glucose is higher than normal but lower than the diagnostic criteria. 2 Impaired glucose tolerance IGT where the plasma glucose is higher than normal and lower than the diagnostic criteria after a 75 g glucose tolerance test. IFG and FPG often occur together and are associated with the metabolic syndrome. • Gestational diabetes mellitus which occurs during pregnancy. • Other specific types which include diabetes caused by other identifiable disease processes and other factors:  Genetic defects of beta cell function such as Maturity Onset Diabetes of the Young MODY .  Genetic defects of insulin action.  Diseases of the exocrine pancreas such as cancer and pancreatitis.  Endocrine disorders such as Cushing’s disease and acromegaly.

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4 Care of People with Diabetes  Medicines such as glucocorticoids and atypical antipsychotics have been associated with weight gain but the newest second-generation antipsychotic medications such as aripiprazole are weight neutral Citrome et al. 2005. Possible causes of weight gain associated with medicines include food cravings and eating more changed resting metabolic rate changes in neurotransmitters and neuropeptides such as leptin which regulate appetite and weight loss before medicines are commenced Zimmermann Himmerich 2003. Individuals with schizophrenia are generally more overweight than those without. • Chemical-induced diabetes. Overview of normal glucose homeostasis Blood glucose regulation glucose homeostasis relies on a delicate balance between the fed and fasting states and is dependent on several simultaneously operating variables including hormones nutritional status especially liver and muscle glucose stores exercise tissue sensitivity to insulin and the type of food consumed. Figure 1.1 shows the key features of the fed and fasting states. Insulin release occurs in two phases. The first phase is important to controlling the postprandial blood glucose rise and is lost early in the progression to Type 2 diabetes. Postprandial glucose 7.8 mmol/L is associated with cardiovascular events and plays a role in the development of other co-morbidities IDF 2011. Insulin action is mediated via two protein pathways: Protein 13-kinase through insulin receptors and influences glucose uptake into the cells and MAP-kinase which stimulates growth and mitogenesis. Anabolism fed state Catabolism fasting state • Driven by Insulin and the incretin hormones • Driven by a variety of hormones e.g. catecholamines • Insulin release stimulated by the rise cortisol growth hormone glucagon in blood glucose • Increases endogenous glucose output: 80 liver • Two phase response 20 kidney • Facilitates glucose uptake • Induces insulin resistance • Reduces hepatic glucose output • Reduces glucose utilisation • Insulin output reduced • Protective during hypoglycaemia – Fasting state 12–16 hours after an overnight fast and is an important determinant of day long glycaemia – Postprandial fed state–dynamic regulated by insulin and glucagon especially in the first 30–60 minutes – insulin is secreted in two phases and regulates the rate of glucose entry into cells and removal from the circulation: • Post prandial blood glucose rise is usually transient • Peaks 60–90 minutes • Usually returns to normal within 3 hours • Usually there is very little diurnal variation in the blood glucose level • Isolated post prandial hyperglycaemia occurs in IGT Figure 1.1 Overview of glucose homeostasis showing the key factors operating during the fed and fasting states. Usually the blood glucose is maintained within the normal range by the interplay of the anabolic and catabolic hormones which are in turn influenced by other hormones and a number of factors such as nutritional status and intake. Recently researchers identified the interaction of insulin with its primary binding site on the insulin receptor revealing a conformational switch in insulin once it engages with the receptor Menting et al. 2012. Conformational switching is unusual in the tyrosine receptor kinases. The clinical significance of the finding is not yet clear but it could influence the development of future insulin analogues. The metabolic syndrome The metabolic syndrome consists of a cluster of risk factors for cardiovascular disease and Type 2 diabetes. Several researchers have explored the factors that predict diabetes risk including the World Health Organization WHO IDF Diabetes Epidemiology Collaborative

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Diagnosing and Classifying Diabetes 5 Analysis of Diagnostic Criteria in Europe DECODE 2008 Epidemiology Study on the Insulin Resistance Syndrome DESIR US National Cholesterol Education Programme Adult Treatment Panel NCEP ATP 111 and the European Group for the Study of Insulin Resistance: Relationship Between Insulin Sensitivity and Cardiovascular Disease Risk EGIR-RISC. Key features of the metabolic syndrome • The metabolic syndrome appears to be a result of genetic predisposition and environmental factors which include high saturated fat diets inactivity smoking hormone imbalances contributing to metabolic stress maternal obesity age and some medicines Bruce Byrne 2009. These factors represent a cumulative risk and are largely modifiable. • Central obesity waist circumference: Europoids 94 cm in men and 80 cm in women South Asian and Southeast Asian men 90 cm women 80 cm: Zimmet et al. 2005 childhood/adolescent Body Mass Index BMI 25–29 overweight 30 obese. Interestingly Carnethon et al. 2012 reported overweight people diagnosed with diabetes live longer than leaner people with diabetes in a prospective study to identify cardiovascular risk factors n 2600. The death rate was 1.5 in overweight people compared to 2.8 in lean people after accounting for cardiovascular risk factors such as age hypertension hypercholesterolaemia and smoking. The authors acknowledged the limitations of the study. They also noted Asian people are more likely to be normal weight at diagnosis and stressed the need for extra vigilance in leaner people. Significantly not all obese people develop the metabolic syndrome. See also Chapter 4. • Raised serum triglycerides 1.7 mmol/L. • Low serum HDL-c: 1.03 mmol/L males 1.29 mmol/L women. • Hypertension: systolic 130 mmHg or diastolic 85 mmHg in women. • IFG: 5.6 mmol/L or previously diagnosed diabetes e.g. gestational diabetes GDM. IFG is associated with a 20–30 chance of developing Type 2 diabetes within 5–10 years. The chance increases if FPG is also present. Other key features include: • Increasing age. • Insulin resistance. High serum levels of sugar metabolites amino acids and chlorinecontaining phospholipids are associated with reduced insulin sensitivity and insulin secretion and higher risk of Type 2 diabetes Floegel et al. 2012. A small study suggests people who sleep for 4 hours are 30 more insulin resistant than those who sleep longer Cappuccio Miller 2012. However the sample size was a small one and only one participant was female which could be important because men and women respond to sleep deprivation differently. Thus further research is needed. • Genetic predisposition and the Developmental Origins of Adult Health and Disease DOHaD hypothesis Barker et al. 1990. Maternal obesity at conception alters gestational metabolism and affects placental embryonic and foetal growth and development King 2006 and increases the susceptibility of the child to components of the metabolic syndrome Taylor Poston 2007 Bruce Byrne 2009 Armitage et al. 2008 Nakamura Omaya 2012. Epigenetic changes occur during early foetal development when mothers suffer malnutrition during pregnancy. Their children are more likely to develop metabolic syndrome diabetes obesity and cardiovascular disease. In addition the grandchildren of malnourished mothers are more likely to be low weight at birth regardless of the nutritional status of their mothers see 1996–2012. In addition under-nutrition increases susceptibility to infection and obesity or overnutrition leads to immunoactivation and susceptibility to inflammatory diseases such as diabetes Dandona et al. 2010. Likewise Helicobacter pylori may predispose individuals to

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6 Care of People with Diabetes diabetes Haan et al. 2012. Haan et al. followed 800 Latino non-diabetic adults over age 60 for 10 years 144 developed diabetes. People who tested positive for Helicobacter pylori were 2.7 more likely to develop diabetes compared to other infections. • Hyperinsulinaemia which occurs in the presence of insulin resistance and exaggerates the proliferative effects of the MAP-kinase pathway. • Procoagulent state: elevated plasma fibrinogen and plasminogen activator inhibitor-1 PAI -1. • Vascular abnormalities: increased urinary albumin excretion and endothelial dysfunction which affect vascular permeability and tone. • Inflammation: both over nutrition and infection induce inflammation. Dietary fats and sugars can induce inflammation by activating an innate immune receptor Tolllike receptor 4 TLR4 Omaye 2012. Recent research suggests ‘good’ intestinal bacteria have a preventative role and pre- and probiotics help maintain healthy gut and immune systems 1996–2012 Nakamura Omaya 2012. Inflammatory markers such as cytokines Interleukin adhesion molecules and TNF-alpha alter endothelial function. C-reactive protein is a significant predictor of cardiovascular disease and possibly depression and there is an association among diabetes cardiovascular diseases and depression. In fact some experts suggest depression could be an independent risk factor for Type 2 diabetes Loyd et al. 1997 and accelerates the progression of coronary artery disease Rubin 2002. Depression is associated with behaviours such as smoking unhealthy eating lack of exercise and high alcohol intake which predisposes the individual to obesity and Type 2 diabetes. Peripheral cytokines induce cytokine production in the brain which activates the hypothalamic-pituitary-adrenal axis and the stress response which inhibits serotonin and leads to depression. Inflammation appears to be the common mediator among diabetes cardiovascular disease and depression Lesperance Frasure- Smith 2007 Bruce Byrne 2009. • Hyperuricaemia: More recently liver enzymes such as sustained elevations of alanine aminotransferase ALT and gamma-glutamyl transferase GGT which are associated with non-alcoholc fatty liver disease and low adiponectin have been associated with diabetes and cardiovascular disease. Therefore the relationship is complex. Conversely normal testosterone levels appear to be protective against diabetes in men and low testosterone levels in men with diabetes are associated with a significantly increased risk of death Jones et al. 2011. In women high testosterone indicates greater risk of developing diabetes: high oestradiol levels confer increased diabetes risk in both men and women American Diabetes Association 2007. Consequences of the metabolic syndrome include: • A five-fold increased risk of Type 2 diabetes. • A two- to three-fold increased risk of cardiovascular disease myocardial events stroke and peripheral vascular disease. • Increased mortality which is greater in men but women with Type 2 diabetes have a greater risk than non-diabetic women. • Increased susceptibility to conditions such as:  Gestational diabetes GDM  Foetal malnutrition  Polycystic ovarian syndrome  Fatty liver  Gallstones  Asthma  Sleep problems  Some forms of cancer.

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Diagnosing and Classifying Diabetes 7 The risk of developing cardiovascular disease and Type 2 diabetes increases significantly if three or more risk factors are present Eckel et al. 2005. The metabolic syndrome in children and adolescents The prevalence of metabolic syndrome in children and adolescents is usually extrapolated from adult definitions and may not be accurate. However it is vital that children and adolescents at risk of developing the metabolic syndrome be identified early. Future risk appears to be influenced in utero and early childhood by factors such as GDM low birth weight feeding habits in childhood genetic predisposition and socio-economic factors Burke et al. 2005 Nakamura Omaya 2012. The IDF proposed that the metabolic syndrome should not be diagnosed before age 10 but children at risk should be closely monitored especially if there is a family history of metabolic syndrome diabetes dyslipidaemia cardiovascular disease hypertension and obesity and preventative strategies should be implemented Weiss Caprio. 2005 Zimmet et al. 2007. In the 10–16-year-old age range diagnostic features are waist circumference 90th percentile triglycerides 1.7 mmol/L HDL-c 1.03 mmol/L glucose 5.6 mmol/L OGGT recommended systolic blood pressure 130 mm Hg and diastolic 85 mm Hg. Adult criteria are recommended for adolescents over 16 years. The long-term impact on morbidity and mortality will emerge as young people with the metabolic syndrome become adults. However heart disease may be apparent in children as young as 10 Sinaiko 2006 and early onset of Type 2 diabetes in adolescents is associated with more rapid progression of complications than occurs in Type 1. Management of the metabolic syndrome in children and adults consists of primary prevention through population-based strategies aimed at early detection regular follow-up of at-risk individuals and personalised education. Secondary prevention concentrates on preventing the progression to diabetes and cardiovascular disease. Lasting effects demonstrating reduced cardiovascular and Type 2 diabetes risk has been demonstrated in studies such as the Diabetes Prevention Program DPP the Finnish Diabetes Prevention Study and the Da Quing IGT and Diabetes Study. These studies showed the importance of multidisciplinary team care modifying lifestyle factors that contribute to obesity by improving diet and activity levels to reduce weight 10 body weight in the long term and stopping smoking. Some programmes include health coaching but the cost–benefit has not been demonstrated Twigg et al. 2007. The Transformational Model of Change is frequently used to implement preventative strategies. Medicines might be required for secondary prevention for example to control blood glucose and lower lipids antihypertensives such as statins and weight management medicines in addition to lifestyle modification. Several medicines have been shown to reduce the incidence of diabetes in people with the metabolic syndrome. These include Metformin 850 mg BD which showed a 31 risk reduction in the DPP 100 mg of Acarbose TDS by 25 after three years STOP-NIDDM and women with a history of GDM in the TRIPOD trial were less likely to develop diabetes when they were treated with Troglitazone. Troglitazone was withdrawn from the market because of the tendency to cause liver disease. Other thiazolidinediones such as pioglitazone and rosiglitazone do not have the same adverse effects on the liver. Rosiglitazone reduced the risk of prediabetes progressing to diabetes by 60 over three years in the DREAM study but has since been associated with increased risk of MI and Poiglitizone might increase the risk of bladder cancer the risk appears to be higher with long duration of use NPS 2012 see Chapter 5. Orlistat an intestinal lipase inhibitor taken TDS reduced the risk of progression to diabetes in obese adults with metabolic syndrome by 37 over four years XENDOS study. However compliance with Orlistat is low due to the side effects see Chapter 5.

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8 Care of People with Diabetes The macrovascular risk factors need to be managed proactively and screening programmes are imperative so abnormalities are treated early see Chapter 8. A 75 g OGGT may be performed initially to diagnose the metabolic syndrome and repeated after 12 months to determine whether glucose tolerance changed then the test interval can be increased to every two to three years WHO 1999. However if an individual demonstrates significant changes in weight gain OGGT may be performed earlier. The Consensus Development Conference on Antipsychotic Drugs and Obesity and Diabetes American Diabetes Association et al. 2004 recommended monitoring people on antipsychotic medicines including: • BMI at baseline and every visit for 6 months then quarterly and treat if weight increases by one BMI unit • Blood glucose and lipids at baseline and if weight increases by 7 and then annually • HbA1c 4 months after starting antipsychotic medicines and then annually in people with metabolic syndrome or diabetes risk factors. Type 1 and Type 2 diabetes Type 1 diabetes Type 1 diabetes is a disease of absolute insulin deficiency that usually affects children and young adults but can occur in older people where it usually manifests as latent autoimmune diabetes LADA see the following section. Recent research has indicated that insulin resistance is also a feature in lean people with uncomplicated Type 1 diabetes Donga et al. 2012. However Donga et al.’s sample was small eight people using insulin pumps and eight healthy controls matched for age gender and BMI thus the clinical relevance of the finding is not clear. The symptoms usually occur over a short space of time two to three weeks following a subclinical prodromal period of varying duration where the beta cells are destroyed. The precipitating event may have occurred many years prior to the development of the symptoms. Type 1 diabetes can be due to an autoimmune or idiopathic process. Various researchers have demonstrated that exogenous factors play a role in the development of Type 1 diabetes on the basis that 10 of susceptible people develop diabetes and 40 of monozygotic twins both develop diabetes the 10-fold increase in the incidence of Type 1 diabetes in European Caucasians in the last 50 years and migration studies that show the incidence of Type 1 has risen in people who migrated from low to high incidence regions Knip et al. 2005. This is known as the trigger-bolster hypothesis. Seasonal variations in incidence of new diagnosis occur. The EURODIAB sub-study 2 study group researchers EUROBIAB 1999 suggested low plasma 25-hydroxyvitamin D may be implicated in the development of Type 1 diabetes 1999. Later Stene Jones 2003 suggested there was no link between vitamin D supplementation and lower rates of Type 1 diabetes. A systematic review and meta-analysis of observational studies and a meta-analysis of cohort studies undertaken in 2008 suggest vitamin D supplementation in early childhood might reduce the risk of Type 1 diabetes by 30 Zipitis Akoberng 2008. A recent prospective study in Spain identified a significant inverse association between vitamin D and risk of Type 2 diabetes Gonzalez-Molero et al. 2012. However randomised controlled trials are required to clarify whether there is a causal link and the optimal vitamin D dose duration of treatment and the best time to begin using vitamin D supplements. As indicated earlier in this chapter and in Chapter 13 a range of other environmental triggers has been implicated in the development of Type 1 such as potatoes cow’s milk and

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Diagnosing and Classifying Diabetes 9 various viruses. Thus the cause of Type 1 diabetes appears to be multifactorial due to a combination of genetic predisposition and a diabetogenic trigger that induces an immune response which selectively destroys pancreatic beta cells. Islet cell antibodies ICA glutamic acid carboxylase GAD or tyrosine phosphatase IA-2A antibodies are present in 85 of cases. Type 1 diabetes in children usually presents with the so-called classic symptoms of diabetes mellitus: • Polyuria • Polydipsia • Lethargy • Weight loss • Hyperglycaemia • Glycosuria • Blood and urinary ketones. In severe cases the person presents with diabetic ketoacidosis DKA see Chapter 7. Bed- wetting may be a consequence of hyperglycaemia in children and older people. Classically insulin secretion does not improve after treatment but tissue sensitivity to insulin usually does. Figure 1.2 is a schematic representation of the progression of Type 1 diabetes. It shows the progressive relentless destruction of the beta cells from the time of the initial triggering event. Five to ten per cent of first-degree relatives of people with Type 1 diabetes have beta cell antibodies usually with normal glucose tolerance and some progress to diabetes. Recent studies suggest early infant feeding is associated with the development of Type 1 diabetes-related autoantibodies such as GAD 1A-2A with a male preponderance and is more common in children of mothers with Type 2 diabetes or coeliac disease and with short term breast feeding Zeigler et al. 2003 Wahlberg et al. 2006 Chapter 13.

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10 Care of People with Diabetes Beta cell decline over months to years Figure 1.2 Schematic representation of the slow progressive loss of beta cell mass following the initial trigger event in Type 1 diabetes. Latent autoimmune diabetes LADA LADA is a genetically linked autoimmune disorder that occurs in 10 of people who are often initially diagnosed with Type 2 diabetes. LADA prevalence varies among ethnic groups LADA has some features of both Types 1 and 2 diabetes. The UKPDS 1998 identified that one in 10 adults aged between 25 and 65 presumed to have Type 2 diabetes were GADAb positive and these findings have been evident in other studies Zinman et al. 2004. LADA often presents as Type 2 but has many of the genetic and immune features of Type 1 see the previous section and Table 1.2. People with LADA had a different clinical course from Type 2 diabetes: in a 6-year follow up in the UKPDS 84 of people with GADA required insulin compared to 14 of antibody negative people. LADA is primarily an insulin deficiency state where Type 2 has a long progression to insulin and is characterized by insulin resistance. The clinical features also resemble Type 1 in that people with LADA are not usually obese are often symptomatic and do not have a family history of Type 2 diabetes. However GADA appears to have a bimodal distribution in LADA identifying two LADA subgroups with different distinct clinical autoimmune and genetic features. People with high GADA titers are younger leaner insulin deficient have lower C-peptide and high HbA1c higher prevalence of other diabetes-specific autoantibodies or other autoimmune diseases such as thyroid disease and lower prevalence of metabolic syndrome than people with LADA and low GADA titers Buzzetti et al. 2007. There are no current guidelines for managing LADA Cermea et al. 2009 although an expert panel convened by the ADA suggested C-peptide response is an appropriate measure of beta cell function and response to treatment. Management depends on the GADA titers and clinical presentation and should be individualised. Management considerations include: • Testing lean people presenting with Type 2 diabetes for autoantibodies especially GADA and C-peptide to correctly diagnose LADA treat it appropriately with insulin and prevent episodes of ketoacidosis Niskanen et al. 1995 Cermea et al. 2009. • Introducing insulin early to support insulin secretion and protect the remaining beta cells Cernea et al. 2009. Sulphonylureas appear to achieve similar or worse glycaemic control than insulin alone and lead to the early need for insulin thus Sulphonylureas are not recommended as first line treatment Cremea et al. 2009. • Thiazolidediones may have a beta cell protective/augmentative effect but their benefit in LADA has not been demonstrated and the contraindications need to be considered. • Metformin may be contraindicated because insulin resistance is not always a feature of LADA and because of the potential risk of lactic acidosis in susceptible people Chapter 5. • Diet and exercise relevant to the individual and the treatment mode. • Stress management and regular complication screening and mental health assessment as per Types 1 and 2 diabetes . • Appropriate education and support. Triggering event Loss of first phase insulin response Development of islet-specific T cells and autoantibodies Loss of glucose tolerance Overt presentation of Diabetes –C - peptide detectabl e Honeymoon phase Overt presentation of Diabetes –C - peptide not detectable 0 100

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Diagnosing and Classifying Diabetes 11 Type 2 diabetes Type 2 diabetes is not ‘just a touch of sugar’ or ‘mild diabetes’. It is a serious insidious progressive disease that is often diagnosed late when complications are present. Therefore population screening and preventative education programs are essential. Type 2 diabetes often presents with an established long-term complication of diabetes such as neuropathy cardiovascular disease or retinopathy. Alternatively diabetes may be diagnosed during another illness or on routine screening. The classic symptoms associated with Type 1 diabetes are often less obvious in Type 2 diabetes however once diabetes is diagnosed and treatment instituted people often state they have more energy and are less thirsty. Other subtle signs of Type 2 diabetes especially in older people include recurrent candida and urinary tract infections incontinence constipation symptoms of dehydration and cognitive changes particularly in information processing speed and executive function Spauwen et al. 2012. As indicated insulin resistance often precedes Type 2 diabetes. Insulin resistance is the term given to an impaired biological response to both endogenous and exogenous insulin that can be improved with weight loss and exercise. Insulin resistance is a stage in the development of impaired glucose tolerance. When insulin resistance is present insulin production is increased hyperinsulinaemia to sustain normal glucose tolerance however the hepatic glucose output is not suppressed and fasting hyperglycaemia and decreased postprandial glucose utilisation results in postprandial hyperglycaemia. Insulin resistance is a result of a primary genetic defect and secondary environmental factors Turner Clapham 1998. When intracellular glucose is high free fatty acids FFAs are stored. When it is low FFAs enter the circulation as substrates for glucose production. Insulin normally promotes tryglyceride synthesis and inhibits postprandial lipolysis. Glucose uptake into adipocytes is impaired in the metabolic syndrome and Type 2 diabetes and circulating FFAs as well as hyperglycaemia have a harmful effect on hepatic glucose production and insulin sensitivity. Eventually the beta cells do not respond to glucose glucose toxicity. Loss of beta cell function is present in over 50 of people with Type 2 diabetes at diagnosis United Kingdom Prospective Study UKPDS 1998 Figure 1.2. Figure 1.3 depicts the consequences of insulin resistance. Insulin is secreted in two phases: an effective first phase is essential to limit the postprandial rise in blood glucose. The first phase is diminished or lost in Type 2 diabetes leading to elevated postprandial blood glucose levels Dornhorst 2001 IDF 2011. Postprandial hyperglycaemia 7.8 mmol/L two hours after a meal contributes to the development of atherosclerosis hypertriglyceridaemia and coagulant activity endothelial dysfunction and hypertension and is a strong predictor of cardiovascular disease and contributes to the development of other diabetes complications Ceriello 2003 IDF 2011. Interestingly the beta cells do respond to other secretagogues in particular sulphonylurea medicines. Figure 1.3 Some consequences of the insulin resistance syndrome. These factors lead to increased morbility and mortality unless diabetes is diagnosed early treatment commenced. The net effect of these abnormalities is sustained hyperglycaemia as a result of: • impaired glucose utilisation IGT • reduced glucose storage as glycogen • impaired suppression of glucose-mediated hepatic glucose production • high fasting glucose FPG Insulin resistance syndrome Hyperinsulinaemia Hypertension Hyperglycaemia and Type 2 diabetes Abdominal obesity Atherosclerosi s Systemic low-grade chronic infection Decreased fibrinolysis Endothelial dysfunction

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12 Care of People with Diabetes • reduced postprandial glucose utilisation leading to postprandial hyperglycemia. Various tools and risk calculators are used to detect Type 2 diabetes. They encompass some or all of the following risk factors AUSDRISK Tool Abassi et al. 2012: • have the metabolic syndrome • are overweight: abdominal obesity increased body mass index BMI and high waisthip ratio 1.0 in men and 0.7 in women. The limitations of the waist circumference in some ethnic groups are outlined later in the chapter. Elevated FFAs inhibit insulin signalling and glucose transport see Figure 1.4 and are a source of metabolic fuel for the heart and liver. Binge eating precedes Type 2 diabetes in many people and could be one of the causes of obesity however the prevalence of eating disorders is similar in Type 1 and Type 2 diabetes Herpertz et al. 1998 • are over 40 years of age but note the increasing prevalence in younger people see also Chapter 13 • are closely related to people with diabetes • are women who had gestational diabetes or who had large babies in previous pregnancies • the children of a woman who had gestational diabetes maternal obesity or maternal malnutrition • are inactive high levels of sedentary time is associated with 117 increase in the relative risk of Type 2 diabetes and 147 increase in the risk of cardiovascular disease and 49 increased risk of all-cause mortality Wilmot et al. 2012. Occupational sitting time also represents increased risk of Type 2 diabetes van Ufelen et al. 2010. Other metabolic syndrome-associated risk factors for Type 2 diabetes have already been described. In addition active and former smoking and acanthosis nigricans are associated with hyperinsulinaemia Kong et al. 2007. Baseline and hypertension progression are independent predictors of Type 2 diabetes Conen et al. 2007. Recent research suggests insulin lack might be partly due to the enzyme PK Cepsilon PKCe Rise in blood glucose from • Diet • Body stores Stimulates Glucagon Cortisol Adrenalin

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Diagnosing and Classifying Diabetes 13 Figure 1.4 Diagrammatic representation of insulin binding insulin signalling translocation of GLUT-4 and glucose entry into the cell. GLUT- 4 is a glucose transporter contained in vesicles in the cell cytoplasm. Once insulin binds to an insulin receptor GLUT-4 moves to the cell membrane and transports glucose into the cell. During fasting GLUT-4 is low and increases in response to the increase in insulin. Failure of GLUT-4 translocation could explain some of the insulin resistance associated with Type 2 diabetes. The effects of insulin are mediated by two protein pathways: P13-kinase through the insulin receptors glucose uptake and MAP-kinase which stimulates growth and mitogenesis. which is activated by fat and reduces insulin production. Future medicines may target this deficiency and restore normal insulin function Biden 2007. In addition Swedish researchers Mahdi et al. 2012 demonstrated that people with high serum Secreted Frizzled- Related protein 4 SFRP4 have a 5-fold increased risk of developing diabetes in the following five years. SFR4 plays a role in the inflammatory process and its release from islet cells is stimulated by interleukin-1 β. High serum SFRP4 reduces glucose tolerance. SFRP4 is elevated several years before Type 2 diabetes is diagnosed indicating it could be a useful risk marker for Type 2 diabetes independently of other risk factors Table 1.1 Generally agreed characteristics of Type 1 and Type 2 diabetes mellitus. Type 1 Type 2 Age at onset Usually 30 years a Usually 40 years. But increasing prevalence in children and adolescents Speed of onset Usually rapid Usually gradual and insidious Body weight Normal or underweight often recent weight loss 80 are overweight pancreas to release insulin Insulin attaches to receptors on cell membranes Glucose Receptors facilitate glucose entry by translocation of GLUT-4 to cell wall Glucose used to produce heat and energy or stored as fat GLUT-4 transports glucose into the cell

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14 Care of People with Diabetes Heredity Associated with specific human leukocyte antigen HLA- DR3 or 4 b No HLA association Genetic predisposition which is complex and only beginning to be understood Autoimmune disease and environmental triggers Environmental and lifestyle factors contribute Insulin Early insulin secretion Impaired later may be totally absent Often preceded by the metabolic syndrome see section on ‘The metabolic syndrome’ . Insulin resistance is reversible if appropriate diet and exercise regimens are instituted. Type 2 is associated with slow progressive loss of beta cell function Ketosis Common Rare Symptoms Usually present Often absent especially in the early stages. Acanthosis nigricans is common in some ethnic peoples Frequency 15 of diagnosed cases 85 of diagnosed cases Complications Common but not usually present at diagnosis Common often present at diagnosis Treatment Insulin diet exercise stress management regular health and complication assessment Diet GLM exercise insulin stress management regular health and complication assessment a Increasing incidence of the metabolic syndrome and Type 2 diabetes in children and adolescents. b Occurs in older people see LADA. Vitamin D deficiency may also be a risk factor for diabetes independently of other risk factors in longititudinal studies such as the Australian Obesity and Lifestyle AusDiab study Gagnon et al. 2011. Given the increasing information about the complexity of Type 2 diabetes pathophysiology it is unlikely any single intervention will prevent or treat the disease effectively thus it is not clear whether vitamin D supplementation is likely to modify diabetes risk. Vitamin D deficiency is very common and is also a marker of general health status and may be indicated to manage other concomitant conditions such as osteoporosis. The characteristics of Type 1 and Type 2 diabetes are shown in Table 1.1. Management is discussed in Chapter 2. The majority of people with Type 2 diabetes require multiple therapies to target the multiple underlying metabolic abnormalities and achieve and maintain acceptable blood glucose and lipid targets over the first nine years after diagnosis UKPDS 1998. Between 50 and 70 eventually require insulin which is often used in combination with other glucose lowering medicines GLM which means diabetes management becomes progressively more complicated for people with Type 2 diabetes often coinciding with increasing age when their ability to manage may be compromised which increases the likelihood of non- adherence and the costs of managing the disease for the patient and the health system. Type 2 diabetes in Indigenous children and adolescents Type 2 diabetes in children and adolescents is discussed in Chapter 13 but it is a significant problem in Indigenous children and adolescents. Indigenous Australians like other Indigenous peoples are at high risk of Type 2 diabetes especially when they live in remote communities and it develops at a younger age Minges et al. 2011. Onset is often in early adolescence and frequently asymptomatic. Indigenous children and adolescents with diabetes usually have a family history of Type 2 diabetes are overweight and have signs of hyperinsulinaemia and acanthosis nigricans. There is a high prevalence of misrovascular and macrovascular complications and the associated morbidity and mortality Azzopardi et al. 2012. A number of causative factors are implicated including intrauterine exposure to risk during maternal pregnancy obesity physical inactivity genetic predisposition and socioeconomic and environmental factors. Consequently experts recommend screening Aboriginal and Torres Strait Islander children over age 10 for metabolic syndrome and diabetes. The IDF 2011 criteria for diagnosing Type 2 diabetes in Indigenous children and adolescents are:

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Diagnosing and Classifying Diabetes 15 • Random laboratory venous blood glucose BG 100 mmol/L and polyuria and polydipsia especially when the symptoms occur at night. OR • Fasting laboratory venous BG 7 mmol/L performed after fasting for at least 8 hours. OR • Random laboratory plasma BG .11.1 mmol/L on at least two separate occasions. Oral glucose tolerance tests OGTT are not practical in many remote Indigenous communities. Point-of-care HbA1c might be an alternative but no clear diagnostic recommendations are available for children. Ketones should be checked in newly diagnosed Indigenous children to ensure treatment is appropriate. Management should be individualised taking into account the psychosocial factors that influence adherence. Gestational diabetes Diabetes occurring during pregnancy is referred to as gestational diabetes GDM. GDM occurs in 5 of all pregnancies Rice et al. 2012. The incidence of GDM is increasing with the global obesity epidemic. GDM refers to carbohydrate intolerance of varying degrees that first occurs or is first recognised during pregnancy. Several factors have been implicated in the development of GDM including diet and lifestyle smoking some medicines older age genetic background ethnicity number of previous pregnancies and recently short stature Langer 2006. People at risk of GDM should be screened for diabetes using standard diagnostic criteria at the first prenatal visit. High risk women have impaired fasting glucose 5.6– 6.9 mmol/L and/or impaired glucose tolerance 2-hour OGTT 7.8–11.0 mmol/L. Women with HbA1c 5.7–6.4 are also at increased risk Rice et al. 2102. For more information about GDM refer to Chapter 14. Maturity onset diabetes of the young MODY Maturity onset diabetes of the young MODY is a rare heterogeneous group of disorders that result in beta cell dysfunction. MODY can develop at any age up to 55. It has a genetic basis and at least nine different genes that result in the MODY phenotype which Table 1.2 Classification of single gene mutations resulting in MODY Data from Rice et al. 2012. Genetic variety Prevalence: of overall MODY gene mutations depending on the populations studied Features HNFIA 30–50 Common mutation Progressive beta cell failure 5 mmol/L BG rise at 2 hours on OGTT 75 gram Sensitive to sulphonylureas GCK 30–50 Common mutation Elevated fasting BG with small 3 mmol/L rise at 2 hours on OGTT 75 gram Mild hyperglycaemia and may not require treatment HNF-4A 5 Similar presentation to HNF1A Associated with higher birth weight Transient neonatal hyperglycaemia Progressive beta cell failure Sensitive to sulphonylureas HNF1B 5 Associated with renal disease Urogenital tract abnormalities in girls INS 1 Varied clinical presentation Usually present with neonatal diabetes but can present in childhood and early adulthood IPF1 1 Average age at diagnosis 35 years

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16 Care of People with Diabetes NUEROD1 1 Vary rare Similar to type 2 diabetes Onset mid 20s Development of beta cell failure and reduced insulin production May be overweight CEL 1 Very rare Due to exocrine pancreatic dysfunction but pathophysiology is unknown Adult onset age 36 PAX4 1 Vary rare fewer than five families reported with the genes. suggests MODY is a single entity. MODY accounts for 1–2 of people diagnosed with diabetes but the prevalence could be underestimated because population-based screening programmes have not been performed Gardner Tai 2012. The different genetic aetiologies vary in age at onset hyperglycaemia pattern response to treatment and extrapancreatic manifestations. The varieties of MODY are shown in Table 1.2. People with MODY often have a strong family history of diabetes insulin independence no insulin autoantibodies and evidence of endogenous insulin production low insulin requirement and generally do not become ketotic McDonald et al. 2011. However there are distinct phenotypes which might present differently. Treatment depends on the MODY type but generally includes GLMs diet and exercise although insulin may eventually be required. HNFIA individuals are very sensitive to sulphonylureas. MODY can be difficult to recognise and the diagnosis missed or delayed Appleton Hattersley 1996. This can have implications for the individual and their family in commencing appropriate treatment for the specific type of MODY. Genetic counselling is also advisable. Practice points 1 MODY is a different disease process from Type 2 diabetes that occurs in young people and has a different genetic and inheritance pattern from Type 2. 2 The prevalence of Type 2 diabetes in children is increasing and is associated with obesity and insulin resistance Sinha et al. 2002. 3 MODY has been misdiagnosed as Type 1 diabetes and insulin commenced unnecessarily. 4 MODY has also been diagnosed instead of Type 1 diabetes in the UK Health Service Ombudsman 2000. 5 Type 2 diabetes is a serious insidious life-threatening disease. These points demonstrate the importance of taking a careful clinical history and undertaking appropriate diagnostic investigations. Diagnosing diabetes Urine glucose tests should not be used to diagnose diabetes if glycosuria is detected the blood glucose should be tested. When symptoms of diabetes are present an elevated blood glucose alone is often sufficient to confirm the diagnosis. See Table 1.3 for diagnostic criteria. If the person is asymptomatic abnormal fasting blood glucose values of 7 mmol/L should be demonstrated on at least two occasions before the diagnosis is made note that some guidelines suggest 6.5 mmol/L. Random plasma glucose 11.1 mmol/L and symptoms are diagnostic of Type 2 diabetes. An oral glucose tolerance test OGTT using a 75 g glucose load may be indicated

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Diagnosing and Classifying Diabetes 17 to determine the presence of glucose intolerance if results are borderline. The criteria for diagnosing diabetes according to the World Health Organization are shown in Table 1.3. A protocol for preparing the patient and performing an OGTT are outlined later in the chapter. However some experts suggest 75 g may be too high a load for some ethnic groups such as Vietnamese. Abnormal plasma glucose identifies a subgroup of people at risk of diabetes-related complications. The risk data for these complications is based on the 2-hour OGTT Table 1.3 Diagnostic criteria for non-pregnant adults with diabetes based on the World Health Organization and the American Diabetes Association Guidelines. Stage Fasting plasma glucose Random plasma glucose Oral glucose tolerance test OGTT Normal 6.1 mmol/L 2 hour plasma glucose 7.8 mmol/L Impaired glucose tolerance Impaired fasting glucose – fasting glucose ≥ 6.1 and 7.0 mmol/L Impaired glucose tolerance – 2 hours plasma glucose ≥ 7.8 and 11.1 mmol/L Diabetes ≥ 7.0 mmol/L ≥ 11.1 mmol/L and symptoms 2 hour plasma glucose 11.1 mmol/L Note: In this table venous plasma glucose values are shown. Glucose in capillary blood is about 10–15 higher than venous blood. HbA1c can be used to make the diagnosis instead of or as well as venous blood glucose 6.5 in a laboratory using certified assay method standardised to DCCT criteria. Practice point Hyperglycaemia often occurs as a stress response to serious intercurrent illness such as cardiovascular disease and it may be difficult to diagnose diabetes in such circumstances. However controlling the blood glucose during the illness is important and leads to better outcomes including in non-diabetics Chapters 7 and 9. plasma glucose level. However the fasting glucose of 7.8 mmol/L does not equate with the 2-hour level used to diagnose diabetes. Recently the ADA and the WHO lowered the fasting level to 7.0 mmol/L to more closely align it to the 2-hour level. The WHO continues to advocate routine OGTT screening in at-risk individuals to identify people at risk of complications early in order for early treatment to be instituted. The ADA does not advocate routine OGTT use because it believes that the revised fasting level is sensitive enough to detect most people at risk. Therefore there could be differences internationally about the routine use of the OGTT. The ADA and the WHO do agree on how the test should be performed. Australia supports the continued use of the OGTT when the diagnosis is equivocal and to detect GDM Hilton et al. 2002 Twigg et al. 2007. However OGTT may not always be practical in remote communities Azzopardi et al. 2012. A recent study suggested untrained people could perform self-administered OGTT in the community setting using a specific device n 18 people without diabetes and 12 with Type 2 OGTT were performed unaided in the home twice unaided but observed in the clinic and one OGGT/participant was perfumed by a nurse. The results were verified with simultaneous laboratory values of the 0 and 120-minute samples Bethel et al. 2013. A data recorder attached to the test device recorded information about the test. Device failures meant 0 and 120 minutes BG was only available for 141/180 OGTTs independent of the test setting. Self-performed and laboratory values were similar and reproducible. The clinical implications are unclear at this time. Other prevention measures include providing the public with information about screening and health maintenance programmes and self-risk assessment lists for example checklists from the Agency for Healthcare Research and Quality AHRQ. Checklists can be downloaded from the Internet or The information is based on the US Preventative Services Task Force recommendations.

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18 Care of People with Diabetes HbA1c has an accepted place in monitoring metabolic control in people with diabetes. In addition the WHO IDF and the American Diabetes Association ADA recommend using HbA1c as screening test for Type 2 diabetes. The Australian Diabetes Society ADS Royal College of Pathologists of Australasia and the Australasian Association of Clinical Biochemists released a position statement in 2102 that recommended HbA1c be used to diagnose diabetes if the analysis is performed in a laboratory that meets external quality assurance standards and recommended HbA1c 6.5 48 mmol/mol as the diagnostic cut point. Point-of-care HbA1c tests are useful clinical decision-making tools but they are not recommended for diagnosing diabetes. The ADS noted HbA1c 6.5 48 mmol/mol does not exclude a diagnosis of diabetes based on existing fasting BG or OGTT criteria. The latter remain the diagnostic tests of choice for GDM Type 1 diabetes and when people have conditions that affect the HbA1c result d’smden et al. 2012. In November 2012 a Medicare Consultation paper was released in Australia proposing a rebate of 16.90 when HbA1c was performed as a diagnostic test but the rebate would be limited to one test per year per person an additional confirmatory test would be covered if the result was ≥6.5 48 mmol/mol. The rate of screening in primary care might increase if the rebate is introduced. Advantages of HbA1c as a diagnostic test are people do not need to fast before blood is collected and the test can be performed at any time of the day. HbA1c measures chronic glycaemia and HbA1c levels are strongly associated with retinopathy macrovascular outcomes and mortality d’Emden et al. 2012. HbA1c assays are standardised and generally reliable in most countries. However errors associated with non-glycaemic factors such as haemoglobinopathies and anaemia that affect HbA1c need to be considered when interpreting the findings Saudek et al. 2008. Other markers of hyperglycaemia and diabetes risk include Fructosamine glycated albumin and 15 anhydroglucitol 15-AG which are associated with the development of diabetes independently of baseline HbA1c and fasting glucose Juraschek et al. 2012. It is not clear what place these markers have in diagnosing or monitoring diabetes as yet but they could be useful when HbA1c is not reliable such as haemoglobinopathies. In fact fructosamine is recommended in the latter situation. Other experts suggests the combination of HbA1c 5.7–6.4 39–46 mmol/mol and fasting plasma glucose 5.6–6.9 mmol/L are likely to reduce the likelihood of missing a diagnosis of diabetes and be more likely to identify people with prediabetes fasting plasma glucose 6.1–6.9 and HbA1c 6.0–6.4 42–46 mmol/mol who are likely to progress to diabetes Heianza et al. 2012. Abikshyeet et al. 2012 suggested salivary glucose could be a useful non-invasive diagnostic and monitoring test for diabetes but acknowledged more research is needed before salivary glucose testing is adopted. Most prediction models for the risk of developing Type 2 diabetes appear to identify individuals at high and low risk of developing diabetes but extended models that include conventional biomarkers perform better. Some models overestimate risk Abbassi et al. 2012. Thus it could be important to ensure the screening parameters such as BMI and glycaemic targets are relevant to the target population. Oral glucose tolerance test OGTT An OGTT is used to diagnose diabetes: • When fasting and random blood glucose results are equivocal. • When there is a strong family history of diabetes especially during pregnancy. • If the suspicion of diabetes is high but blood glucose tests are normal/equivocal. An OGTT should not be performed when the person: • Is febrile • Is acutely ill for example postoperatively or uraemic • Has been immobilised for more than 48 hours • Has symptoms of diabetes or an elevated blood glucose before commencing the test. Rationale for OGTT

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Diagnosing and Classifying Diabetes 19 Early diagnosis and treatment of diabetes reduces the morbidity and mortality associated with the hyperglycaemia. Preparing the patient for an OGTT 1 Give specific oral and written instructions to the patient. A sample is given in Example Instruction Sheet 1 below. 2 Ensure the diet contains at least 200 g/day carbohydrate for at least 3–5 days before the test. 3 If possible stop medicines that can influence the blood glucose levels 3 days before the test: some of these will need to be reduced gradually for example corticosteroids Chapter 10. People should be informed about the consequences of stopping their medicines and when to resume taking them after the test: • thiazide diuretics • antihypertensive medicines • analgesic and anti-inflammatory medicines • antineoplastic medicines • steroids. 4 Fast from 12 midnight the night before the test. 5 Avoid physical/psychological stress for 1 hour prior to and during the test. 6 Avoid smoking for at least 1 hour prior to the test. 7 Allow the patient to relax for 30 minutes before beginning the test. Example Information Sheet: Preparation for an oral glucose tolerance test PATIENT INSTRUCTIONS FOR ORAL GLUCOSE TOLERANCE TEST Date of test: Name: Time: I.D. label Location where test will take place: 1 Please ensure that you eat high carbohydrate meals each day for 3 days before the test. Carbohydrate foods are: breads cereals spaghetti noodles rice dried beans and pulses vegetables fruit. These foods should constitute the major part of your diet for the 3 days. 2 Have nothing to eat or drink after 12 midnight on the night prior to the test day except water. 3 Specific information about managing medicines: ……………………………… 4 Bring a list of all the tablets you are taking with you when you come for the test. 5 Do not smoke for at least one hour before the test. The test The test is performed in the morning. You are required to rest during the test which will take approximately 3 hours to complete. A small needle will be inserted into an arm vein for blood sampling. The needle will stay in place until the test is completed. You will be given 300 mL of glucose to drink. This is very sweet but it is important to drink it all over the 5 minutes so that the results of the test can be interpreted correctly. Water is permitted. You will be given a drink and something to eat when the test is finished. The doctor will discuss the results with you. Test protocol 1 The person should rest during the test to avoid dislodging the cannula. 2 Insert a cannula into a suitable vein for blood sampling e.g. the cubical fossa. 3 The blood glucose should be tested before commencing the test. If elevated clarify with the doctor ordering the test before proceeding. Collect two milliliters of blood in fluoride oxalate tubes for laboratory analysis at each test time point. 4 Flush the cannula with normal saline between samples to prevent clots forming in the cannula. One to two milliliters of blood should be withdrawn and discarded before collecting each sample to avoid contaminating the sample with saline left in the tubing. 5 Collect blood samples at the following times. However sometimes only a baseline 0 and a two-hour sample are collected : minutes: -10

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20 Care of People with Diabetes 0 ⇒ 75 g glucose consumed over 5 minutes. Water can be given after the glucose is all consumed. It is very sweet and some people find it difficult to drink. +30 +60 +120 The glucose used for an OGTT is prepacked in 300 mL bottles containing exactly 75 g of glucose. 6 Ensure the person has a follow-up appointment with the referring doctor whose responsibility it is to explain the test results and commence or arrange for appropriate management and education. Screening for diabetes Because of the insidious nature and increasing incidence and prevalence of Type 2 diabetes many countries have instituted population-based education and screening and/or case detection programmes in at-risk populations. Fingerprick blood glucose tests are not generally used to diagnose diabetes: see Table 1.3 for the diagnostic criteria. Many programmes also involve checking for obesity and cardiovascular risk factors. At-risk groups include: • age 55 years • high-risk ethnic groups such as indigenous people Southeast Asians Indians from the subcontinent • women with Polycystic Ovarian Syndrome PCOS • previous GDM • family history of diabetes • people with symptoms but symptoms are often absent in Type 2 diabetes • older people 65 years • People with known diabetes complications such as cardiovascular erectile dysfunction and renal disease • active smokers Willi et al. 2007. Screening for Type 1 diabetes is not usually necessary because it presents differently and has a more rapid onset and symptoms are usually present. First-degree relatives of people with Type 1 diabetes can be tested for risk markers autoantibodies for diabetes but the preventative strategies applicable to Type 2 diabetes do not apply. An example of one screening and preventative model of care is shown in Figure 1.5.

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Diagnosing and Classifying Diabetes 21 Preventing Type 2 diabetes To Cure Diabetes Click Here A number of clinical trials have demonstrated that it is possible to prevent Type 2 diabetes and may in turn prevent the associated morbidity from long-term complications. Most prevention trials were conducted among people with IGT because it is a strong predictor of Type 2 diabetes. These programmes include the Da Qing Study Pan 1997 the Oslo Diet and Exercise Program the Diabetes Prevention Program DPP 2002 and the Finnish Diabetes Prevention Study DPS 2003 which showed a 58 reduction in the progression to diabetes in people who followed a healthy lifestyle and the effects were still present at the four-year follow up. Tuomilehto et al. 2001. The DPS was stopped early because the intervention was so successful but the researchers continued to follow people who did not develop diabetes for up to 10 years. The intervention group achieved a reduction of 40 compared to controls. Elements of these programmes have been adapted and implemented in many countries since the findings were first published especially the DPP for example Go For Your Life and the Life Programme in Australia. However a Cochrane review Nield et al. 2008 stated ‘There is no high quality data on the efficacy of dietary intervention for the prevention of Type 2 diabetes.’ Since causes of the metabolic syndrome and Type 2 diabetes are complex and multifactorial it is not surprising that dietary interventions in isolation are ineffective. Key features of the DPS are weight reduction 5 reducing fat intake to 30 with 10 coming from saturated fats fibre intake of 15 g per 1000 calories and 30 minutes of moderate exercise per day. In the DPS weight loss and exercise appeared to be more important than dietary goals in preventing diabetes. Achieving weight loss and making dietary changes is difficult and only 2 of participants in the DPS achieved four or five targets but no participant who did so developed diabetes compared to 50 of the control group. Weight management strategies are discussed in Chapter 4. Studies concentrating on increasing fibre and magnesium to prevent Type 2 diabetes show inconsistent results despite current guidelines to increase the total fibre intake. The type of fibre consumed may be important in that soluble fibre may enhance gastric emptying and reduce the postprandial glucose rise. A meta-analysis revealed lower diabetes risk with increased intake of cereal fibre but no significant association with fruit and vegetable fibre. Thus including whole grain foods is important in diabetes prevention diets Krishnan et al. 2007 and as indicated pre- and probiotics are emerging Outpatient management preferre d–p rimary care. Treatment according to agreed protocols and guidelines. Regular review. Specific diabetes education to support the individual to comply with treatment and seek advice early. Dietary advice complication screening. Early identification and treatment of long-term complications. Counselling. Hospital care when needed. Rehabilitation when necessary. Counselling. Diabetes education. Continuing management complication screening and education. Behaviour modification using individualised strategies. Regular monitoring. General diabetes education. Targeted screening according to risk factors for Type 2 MODY GDM. Universal screening not usually recommended. Preventative health population-based messages. a Figure 1.5 Example of a screening and preventative model of health care.

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22 Care of People with Diabetes as important considerations for gut health and preventing immune- and inflammatoryrelated diseases such as diabetes. An example of a screening and prevention model is shown in Figure 1.5. Vegetarians appear to have reduced risk of metabolic syndrome and reduced risk of Type 2 diabetes. Nash 2012. Likewise Mediterranean diets while not strictly vegetarian are generally high in fibre prebiotics and whole grains and are associated with reduced risk of Type 2 diabetes. Avoiding liquid calories such as those in sugar sweetened beverages fruit juice and alcohol appears to be important. These liquids also lead to dental caries. Rice is the staple food in many countries such as China where white rice is consumed at 3–4 times per day. The Glycaemic Index of white rice is higher than other whole grains and Basmati type rice. Studies suggest the relative risk of developing diabetes is 1.11 for every serving of white rice consumed per day Hu et al. 2012. Many existing public health screening and prevention models fall into four main categories Lang Rayner 2012: • Sanitary-environmental model. • Biomedical model that can be individual or population focused. • Social behavioural model which rivals the biomedical model. It might not take account of who has the strongest influence on behavior which may be companies like Coca Cola. • Techno-economic model which views health as depending on economic growth and knowledge development. • Ecological model which focuses on interactions among factors that impact on health including climate change and integrates elements of the other four models. Climate change impacts on factors such as food security/availability extreme weather events which displace people and affect their lifestyle and social circumstances IDF 2012. The relative merits of these models have not been tested but current policies do not appear to be halting the exponential rise in the prevalence of the metabolic syndrome and diabetes. In fact Simmons et al. 2012 suggested screening for diabetes does not reduce deaths. The researchers followed a cohort of nearly 12 000 people at high risk of diabetes for 10 years and found they were no more likely to have died than 4000 people who were not screened and there were no significant differences between the two groups for deaths specifically attributable to diabetes. Interestingly benefits for microvascular disease were not analysed. It is unlikely that screening alone would reduce risk unless relevant prevention strategies were used and early diagnosis and management incorporated into the model. Likewise population-wide prevention may not reduce healthcare spending because it does not reduce the risk of serious illness or premature death because of the number of people who need to receive a particular preventive treatment to prevent a single illness Reuters Health Information 2013. Targeted prevention programmes that incorporate environmental and social factors and collaborating with local government and religious institutions and other key stakeholders need to be part of prevention programmes. Two European projects DE-PLAN and IMAGE are addressing implementation processes for diabetes prevention programs and developing a toolkit to help people develop and implement programmes for preventing Type 2 diabetes. The kit includes a practical guideline that targets everybody who could have a role in prevention such as health professionals teachers traditional healers and politicians it explains key aspects of financial management how to identify people at risk as well as educating and training key personnel and monitoring and quality assurance processes that need to be addressed. It will be interesting to determine whether the toolkit makes a difference in actual practice since many prevention programmes already encompass all the elements in the tool kit including education. One important factor that might lead to changes is the Global Monitoring Framework GMF for non-communicable disease which was agreed in November 2012 between the WHO and national governments. The GMF is ambitious and has been dubbed ‘25 by 25’ in recognition of the first target which is to reduce NCD-related deaths by 25 by 2025. Other targets include reducing the: • increase in diabetes and obesity • prevalence of inactivity by 10 • harmful use of alcohol by 10 • consumption of salt by 30 • prevalence of tobacco use by 30 • prevalence of hypertension by 25. Signatory countries to the agreement will be required to report their performance against the agreed targets in 2013. The targets reflect metabolic syndrome risk factors such as hypertension inactivity and smoking. Importantly one target

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Diagnosing and Classifying Diabetes 23 is to halt the increasing prevalence of diabetes and premature mortality from non-communicable diabetes. Important proposed strategies to help meet the Global Framework is to ensure essential medicines and self-management preventative education are available IDF 2012. Meanwhile research is underway to understand the genetics that predispose people to insulin resistance and Type 2 diabetes and help predict the risk for diabetes to better target prevention and management strategies. Significant progress has been made in identifying the variations in DNA sequence involved in the development of diabetes as part of the Genome-wide study GWAS. Sixty-five regions of the human genome associated with diabetes have been identified Morris 2012 however the effects of the variants are too subtle to be used as risk predictors at present. Research to determine how beta cells and insulin-responsive tissues normally develop and function are also progressing for example discovering the relationship between the FTP gene and obesity. Animal studies are underway to determine the mechanisms that affect appetite and metabolism and predispose to obesity. Genetic studies are increasing our understanding of the relationship between SHBG levels and diabetes risk. SHBG is a binding protein produced in the liver that transports testosterone and to oestrogen to some extent to target tissues. SHBG levels are often low in people with Type 2 diabetes. Previously researchers assumed that insulin resistance lowered SHBG however genetic studies suggest low SHBG may have a causal role in Type 2 diabetes Ding et al. 2009. Preventing Type 1 diabetes Research for the elusive cure for Type 1 diabetes continues. Approaches include: • Immune intervention using monoclonal antibodies to prevent the immune system destroying beta cells. People diagnosed early enough to still have some functioning beta cells receive a combination of medicine such as Teplizumab and Otelixizumab. The medicines protect the remaining beta cells and people may need less insulin. The results of clinical trials vary among countries. For example in Europe and America young slim people appear to benefit from the medicines however people from Asia derive less benefit. Genetic differences age and BMI might account for the different responses. • Stem cells: blood stem cells have been used in a similar way to treatment for leukemia in Brazil. Radiation is used to destroy the immune system and fresh blood stem cells are infused to calm the immune system so it no longer destroys beta cells. Early clinical studies show ‘promise.’ The following is more specifically treatment but it is relevant to stem cell research. In Australia researchers have isolated stem cells in the adult pancreas and developed a technique to transform the stem cells into insulinproducing beta cells that release insulin in response to glucose. The hope is people with Type 1 diabetes may be able to regenerate their own beta cells if the immune attack that initially caused diabetes can be prevented. • Reprogrammed liver cells are being researched in animal studies in Israel Jaekel 2012. Managing diabetes mellitus Key points • The person with diabetes undertakes 90 of their diabetes management thus they are experts in their diabetes and their lives. • Visits to health professionals occur at regular intervals and mostly concern assessing physical psychological and metabolic status and making treatment recommendations. • Diabetes education is the cornerstone of management. The phrase generally refers to people with diabetes BUT it applies equally if not more so to the health professionals who provide education and care for people with diabetes. • It is essential to individualise care plans and develop them with the individual concerned. Management strategies for specific aspects of care are discussed in almost every chapter of the book. This section deals with general management information.

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24 Care of People with Diabetes Many ‘diabetes care models’ have been developed as the framework within which to provide diabetes care. These include the Chronic Disease Model and its derivations such as the Flinders Model used in some Australian states. Research suggests effective diabetes care models need to enable early diagnosis and coordinate diagnosis treatment and ongoing management and educate people with diabetes and their health professionals Renders et al. 2012. Effective components of management programs appear to be high frequency of contact with people with diabetes and ability for the people managing the disease primarily the person with diabetes to adjust their medicines and are more effective for people with inadequate glycaemic control HbA1c 8 at baseline Pimouguet et al. 2010. Diabetes education is an essential component of diabetes management and the benefit seems to apply equally to groups and individual education and combinations of both Pimouguet et al. 2010 Chapter 16. Currently the Australian Government is evaluating a new care model: the Diabetes Care Project DCP in a large randomised control trial involving general practices nurses and allied health professionals in Queensland Victoria and South Australia. The DCP consists of two models of coordinated care. General practices that enroll will be randomised to either usual care control or intervention 1 or 2. Intervention 1 will test an electronic tool that creates individualised care plans and enables health professionals and the individual to access the care plan and health record and update information and automated follow-up and review processes. Patient progress will be monitored against their care plan. Health professional compliance with Medicare will also be monitored. Intervention 2 uses the same electronic tool and a new funding model and encompasses a new team member the care facilitator. The new funding model is risk adjusted and enables patients to access diabetes educators and allied health professionals. It will be interesting to track progress of this innovative model. The model appears to comply with Pimouguet et al. 2010 and Renders et al. 2012 criteria for effective models. The diabetes team Effective diabetes management depends on having a collaborative multidisciplinary health care team. The person with diabetes is the central player in the team. Good communication among team members is vital and information the patient receives must be consistent between and within hospital departments health services and health professionals to ensure smooth transition among services and avoid confusing the patient with inconsistent information. The team usually consists of some or all of the following: • Diabetologist • Diabetes nurse specialist/diabetes educator and/or diabetes nurse practitioner • Dietitian • Podiatrist • Social worker • Psychologist • General practitioner. Other professionals who contribute regularly to the diabetes management: • Opthalmologist • Optometrist • Pharmacist • Specialists such as vascular and orthopaedic surgeons neurologists and urologists audiologists • Cultural/traditional health workers for example Aboriginal health workers in Australia and traditional healers in Africa • Exercise physiologists • Hospital physiotherapists. The ward staff who care for the patient in hospital and the community also become team members during presentations to hospital and emergency departments and care in home settings including: • Doctors • Nurses • Dietitians

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Diagnosing and Classifying Diabetes 25 • Community physiotherapists • Occupational therapists. It is easy to understand why people with diabetes can be confused about health professional roles and responsibilities and about their own role and responsibilities in diabetes care if they receive conflicting information from health professionals. Managing diabetes consists of dietary modification regular exercise/activity and in some cases insulin or GLMs. Diabetes education and regularly assessing metabolic control and complication status is essential. In addition general health care is very important and includes dental checks mammograms prostate checks and preventative vaccinations for example fluvax and pneumovax. As indicated many times in this book it is essential to personalize the care plan and individualise management targets to suit the person’s risk status social situation and capabilities. Repetition is one important education strategy. Politicians and marketers also use it Helping people manage their diabetes requires health professionals to be effective marketers politicians and communicators. Aims of management Diabetes management should be determined within the Quality Use of Medicine framework see Chapter 4. Management aims for Australia are defined in the National Diabetes Strategy and a number of other specific guidelines such as those described in the Australian Diabetes Society Position Statements and Clinical Management Guidelines for Diabetes in General Practice. A range of other guidelines produced by various countries and diabetes associations such as the UK Scotland the USA and the IDF some of which are listed in this and other chapters in the book. The aim of diabetes management is to maintain quality of life and keep the person free from the symptoms of diabetes and the blood glucose and blood lipids within in an acceptable range. The blood glucose range needs to be determined on an individual basis usually between 4.0 and 6.0 mmol/L for 90 of tests especially during acute illness and surgery young people and during pregnancy and HbA1c 7 Diabetes Australia DA 2011/12 and Royal Australian College of General Practitioners RACGP 2011/12 Table 1.4. However higher targets might be more appropriate for people at risk of hypoglycaemia Chapter 6 older people Chapter 12 and children Chapter 13. The aim is to obtain results as near as possible to the target blood glucose range but there must be a balance between the food plan medication insulin/GLMs and exercise/activity. Maintaining emotional well-being is essential Chapter 1. General management goals targets are shown in Table 1.4. The regimen should affect the person’s lifestyle as little as possible although some modification is usually necessary. People with Type 1 require insulin in order to survive. Obese people with Type 2 can sometimes be treated effectively with a combination of diet and exercise but research suggests that people managed with diet are not as rigorously monitored and have more hyperglycaemia and hypertension than those on medicines Hippisley-Cox Pringle 2004. Many people with Type 2 diabetes require GLMs and usually eventually insulin due to the progressive loss of beta cell function In the current person-centred empowerment model of diabetes care the person with diabetes is the pivotal person in the management team. Forming a therapeutic Table 1.4 Diabetes management targets but note most current guidelines recommend targets be individualised according to specific microvascular macrovascular and hypoglycaemia risk ADS 2012 ADA 2013 DA/RACPG 2011/12 SIGN 2010 NICE 2008. Glucose: Fasting blood glucose 4–6 mmol/L HbA 1c 7 53 mmol/mol Lipids: LDL-c 2.5 mmol/L triglycerides 1.5 mmol/L HDL-c 1.0 mmol/L total cholesterol 4.0 mmol/L Blood pressure: 130/80 mmHg 125/75 mmHg if proteinuiria exceeds 1 g/day: 140/90 if over 65 years. BMI 25 kg/m 2 ideal waist circumference women 80 cm men 94 cm. Renal function: Urine albumin excretion 20 mm/min in timed overnight collection 20 mm/min spot collection albumin–creatinine ratio 3.5 mg/mmol in women 2.5 mg/mmol men eGFR. Alcohol intake: Women 1 standard drink/day men 2 standard drinks/day. No smoking Exercise/activity: 150 minutes/week at least 30 minutes brisk walking or equivalent/day or on at least five days/week partnership with the individual and accepting their choices is essential to achieving optimal outcomes. Putting the person at the centre of care means respecting their choices even when the

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26 Care of People with Diabetes individual elects not to follow advice after receiving adequate information informed decision- making. Not following advice should not be labeled ‘non-compliant or non-adherent.’ Accepting the person’s decision does not mean the health professional does not continue to provide information and advice. It does mean they might need to change the way they do things and try new strategies. Clinical observation Diabetes is a balancing act. The individual’s physical psychological spiritual and social and relationship needs must be balanced to enable people to undertake the necessary self- management to achieve management targets optimal physical health. In fact the emphasis should be on balance rather than control. Spirituality resilience and positive thinking in particular are important but neglected aspects of current diabetes management strategies and are key to being able to manage life changes turning/tipping points self-empowerment and self-determination Parsian Dunning 2008. Management involves educating the person with diabetes and other family members and carers in order to help them: • Understand diabetes be involved in deciding their care plan and adopt relevant selfcare strategies necessary to maintain optimal health and meet glycaemic targets. • Manage the impact of diabetes on their physical psychological and spiritual functioning to maintain an acceptable quality of life. • Achieve and maintain an acceptable weight. • Achieve acceptable blood glucose levels and HbA1c. • Achieve a normal blood lipid profile. • Relieve symptoms of diabetes polyuria polydipsia and lethargy. This involves helping the person recognise and manage relevant signs and symptoms associated with diabetes and any concomitant condition/s. • Prevent and/or manage hypolycaemia. • Manage intercurrent illnesses sick days. • Prevent complications of diabetes and of treatment. Table 1.5 Guidelines for assessing the patient’s blood glucose testing pattern. The results should be considered as part of the overall situation not as isolated pieces of data. The target HbA 1c is 7 6.5 in some countries. Haemoglobin A1c Glucose mmol/L Control Fasting Two hours after food 4.0–6.0 31–48 mmol/mol 4 7 Excellent or ‘too good’ high risk of hypoglycaemia a 6.0–7.4 48–58 mmol/mol 7 9 Upper limit of target range 7.5–9.4 58–75 mmol/mol 10 14.5 Increased short- and long-term complication risk. 9.5 75 mmol/mol 14 20 Increased short- and long-term complication risk a If fasting glucose is high postprandial glucose is often also high. Postprandial glucose is affected by first phase insulin response glucagons secretion muscle and live glucose stores fat tissue sensitivity to insulin food intake and digestion and absorption of food from the gut.Both affect the HbA1c level. Fasting and postprandial have the same effect on HbA1c when the HbA1c is 7.3–8.4. Fasting glucose has a greater effect when the HbA1c is 8.5. The higher the HbA1c the greater the effect fasting glucose has on HbA1c. Note the HbA1c mmol/mol values are the closest approximations to the HbA1c percentage values. The general target is 53 mmol/mol. • Maintain a healthy independent lifestyle where the person is able to manage the necessary self- care tasks to achieve acceptable glycaemic control and have a good quality of life.

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Diagnosing and Classifying Diabetes 27 • Understand social and legal responsibilities and entitlements such as driving insurance National Diabetes Supply Scheme in Australia. • Plan for life transitions including stopping driving moving to supported or aged care facilities and end of life care. Table 1.4 described the management targets. Table 1.5 provides some glycaemic information to consider when assessing metabolic control. HbA1c is only part of the overall picture and should NOT be considered in isolation. A suggested model for managing diabetes is shown in Figure 1.6. The model is divided into phases and indicates that management education and counselling are required for life. Exercise/activity Exercise plays a key role in the management of Type 1 Type 2 diabetes and GDM as well as people without diabetes including health professionals. It increases tissue sensitivity to insulin aiding in the uptake and utilisation of glucose during exercise and for several hours afterwards. The energy sources during exercise are depicted in Figure 1.7. In addition regular exercise may have beneficial effects on the risk factors that contribute to the development of diabetes complications especially cardiovascular disease Boule et al. 2001. Exercise: • Increases cardiovascular efficiency • Reduces blood pressure • Reduces stress • Aids in weight reduction and appetite control • Promotes a sense of wellbeing • Aids in blood glucose control • Improves strength and reduces the risk of falls in older people which helps them remain independent anaerobic exercise. All of these factors also reduce the risk of developing the long-term complications of diabetes. People are advised to have a thorough physical check-up before commencing

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28 Care of People with Diabetes Figure 1.6 Suggested diabetes management model. Most diabetes management occurs in primary care settings in collaboration with secondary and tertiary care services. Phase 2: After diagnosis Phase 1: Prediagnosis stage Phase 3: If complications occur Secondary or tertiary inpatien t/ outpatient services Person with diabetes Community / primary care services Level of suspicion Diagnos e Assess Advis e Educate Initiate treatment Communicate Collaborate Follow-u p– recall system Symptoms HbA c 1 Blood pressure Lipids Weight Complication status Mood Quality of life Diet Blood glucos e monitoring Exercis e Smoking Insulin management OHA management Identify early Institute treatment Podiatris t Orthotis t Surgeon Wound management Physiotherapis t Psychologis t Diabetes educator Diabetologis t Aims : • Early diagnosis • Collaborative care • Management targets determined Aims : • Achiev e/ maintain management targets • Prevent complication s–s hort and long term • Prevent need for hospital admission • Monitor response to treatment • Monitor specific clinical end points Monitor self-care practices Aims : • Manage complications • Prevent deterioration of complications • Provide rehabilitatio n and counselling • Early referra l

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Diagnosing and Classifying Diabetes 29 Figure 1.7 Normal energy sources during exercise. Note: At rest free fatty acids are the major energy source. As exercise begins muscle glycogen is utilised as the predominant energy source. As exercise continues the blood glucose is utilised reverting to free fatty acids as the major energy source if exercise is prolonged. Blood glucose is maintained by hormonal regulation of hepatic glucose output and lipolysis. an exercise programme in particular the cardiovascular system eyes nerves and feet should be examined. Food fluid and clothing should be suitable for the type of exercise and the weather. Insulin/GLM doses might need to be adjusted. Where the duration of the exercise is 30 minutes adjustments are generally not required. Adjustments are often necessary where the duration of the exercise exceeds 30 minutes Perlstein et al. 1997. Exercise should be decided in consultation with the individual and suited to their preferences and physical capabilities. It is advisable that the person tests their blood glucose before and after exercising and to have some carbohydrate available during exercise in case of hypoglycaemia. Infrequent exercise is not advisable the aim should be to begin with 10–15 minutes exercise and progress to 30–60 minutes of moderate intensity three to five times per week daily if possible. Footwear and clothing should be appropriate to the type of exercise and the feet inspected after exercising. Exercise is not recommended in extremes of temperatures or at periods of hyperglycaemia especially if ketones are present in the urine or blood. People should discuss their exercise plans with the diabetes team and/or exercise physiologist in order to plan an appropriate routine adequate carbohydrate intake and appropriate medication doses. Ensure adequate fluid intake to replace water loss especially in hot weather. In general anaerobic exercise e.g. weight lifting does not significantly enhance glucose utilisation. It does build muscle mass and improve strength but does not improve Practice point Hypoglycaemia can occur several hours after vigorous or prolonged aerobic exercise due to continuing glucose uptake by muscles. People need to be informed about adequate carbohydrate intake and medication dose adjustment as well as recognising and treating hypoglycaemia before and after exercise see Chapter 5. cardiovascular fitness and may reduce falls risk in older people. Anaerobic exercise is unlikely to cause an increase in blood glucose. Aerobic exercise e.g. running cycling swimming uses glucose as the major fuel source and hypoglycaemia can occur. It also confers cardiovascular benefits. Chapter 12 discusses exercise in older people. Falls risks need to be considered in older people. Specific advice about medications and food intake needs to be tailored to the individual. The relationship between hypoglycaemia and exercise is generally well recognised. Hyperglycaemia can also occur if insulin levels are low when exercising. In this situation the counter-regulatory hormones predominate and increase the blood glucose and extra medicine doses might be needed. Insulin is easier to titrate in such circumstances. 100 80 60 40 20 1 0 hours hours 2 3 hours F ree f atty acids Ser um glucose Intramuscular glycogen 4 hours

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30 Care of People with Diabetes Exercise for the person in hospital 1 Encourage as much mobility/activity as the person’s condition allows. 2 Increase movement and activity gradually after a period of being confined to bed. 3 Consider postural hypotension and differentiate it from hypoglycaemia to ensure correct management is instituted. 4 Consult the physiotherapy department for assistance with mobility chair or hydrotherapy exercises. 5 Consider having the occupational therapist undertake a home assessment to ensure safety at home for example following a stroke. Practice point Be aware that resuming normal activity after a period of prolonged inactivity for example in rehabilitation settings constitutes unaccustomed exercise and can result in hypoglycaemia especially if the person is on insulin/GLM and is not eating well or is malnourished. Exercise/activity increases the basal energy requirement by 20. Diabetes education Diabetes education is an integral part of diabetes management. Regular support and contact with the diabetes care team assists people to self-manage their diabetes by providing advice and support when necessary. For more details see Chapter 16. Practice points 1 People with Type 2 diabetes do not become Type 1 when insulin is needed to control blood glucose. The current accepted term is insulin-treated or insulinrequiring diabetes. The basic underlying pathophysiology does not change and usually enough endogenous insulin is produced to prevent ketosis occurring except during severe intercurrent illness. 2 Type 2 diabetes is characterised by progressive beta cell destruction and insulin is eventually required by 50 of people UKPDS 1998. 3 People with LADA often require insulin soon after diagnosis because they are insulin deficient not insulin resistant. Complications of diabetes Many people with diabetes are admitted to hospital because they have an active diabetes complication. The presence of a diabetic complication can affect the duration of the admission and the patient’s ability to care for him or herself. Hence diabetic complications contribute to the overall cost of health care for these patients. In addition they represent significant physical and mental lifestyle costs to the person with diabetes and their family. Complications can be classified as acute or long term. Acute complications can occur during temporary excursions in blood glucose levels. Long-term complications occur with long duration of diabetes and persistent hyperglycaemia especially in the presence of other risk factors. In Type 2 diabetes long-term complications are frequently present at diagnosis. Often there are few symptoms and both the diagnosis of diabetes and the coexisting complication/s can be overlooked Chapter 8. Acute complications 1 Hypoglycaemia refer to Chapter 6. 2 Hyperglycaemia: • diabetic ketoacidosis refer to Chapter 7 • hyperosmolar states refer to Chapter 7.

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Diagnosing and Classifying Diabetes 31 3 Infections can occur if blood glucose control is not optimal. Common infections include dental disease candidiasis and urinary tract infections. 4 Fat atrophy/hypertrophy and insulin allergy occur very rarely with modern highly purified insulins and correct injection site rotation. Long-term complications Two important studies the DCCT in 1993 and the UKPDS in 1998 DCCT 1993 UKPDS 1998 demonstrated the relationship between the development and progression of the long-term complications of Type 1 and Type 2 diabetes respectively. In addition the UKPDS demonstrated the importance of controlling blood pressure to reduce the risk of cardiovascular disease. Diabetes management guidelines and metabolic targets are regularly revised as new evidence emerges. Current management targets are shown in Table 1.4. 1 Macrovascular disease or disease of the major blood vessels for example: • myocardial infarction • cerebrovascular accident • intermittent claudication. 2 Microvascular disease or disease of the small blood vessels associated with thickening of the basement membranes of the small blood vessels for example: • retinopathy • nephropathy. 3 Neuropathy: diabetes can also cause damage to the central and peripheral nerves: • peripheral: decreased sensation in hands and particularly the feet which can lead to ulcers Charcot’s arthropathy and amputation. • autonomic: erectile dysfunction atonic bladder gastroparesis mononeuropathies. 4 Complications of pregnancy: diabetes during pregnancy carries risks for both mother and baby: • mother: toxaemia polyhydramnous intrauterine death and Caesarian section • baby: congenital malformations prematurity respiratory distress hypoglycaemia at birth. A number of other factors might play a role in the development of diabetic complications. For example studies are under way to determine the role of free radicals or reactive oxygen species ROS advanced glycated end products AGE changes in cellular signalling and endothelial humoral components that determine coagulation status and the tendency to form microthrombi. Long term complications are discussed in Chapter 8. It is the responsibility of all health professionals involved in providing care to comprehensively assess the patient including the presence of complications to determine their self-care potential and devise an appropriate achievable management plan in consultation with the individual and to be involved in preventative teaching about reducing risk factors for the development of diabetic complications. Health professionals need to be proactive about identifying opportunities for health screening and education. Practice points 1 Hyperglycaemia and insulin resistance commonly occur in critically ill patients even those who do not have diabetes van den Berghe et al. 2001 ADS 2012. 2 It is important to control these states in people with diabetes during illness because of the extra stress of the illness and/or surgery and their compromised insulin response. Elevated blood glucose in these situations in people without diabetes will require decisions to be made about the diagnosis of diabetes after the acute episode resolves. Aim and objectives of nursing care of people with diabetes In hospital

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32 Care of People with Diabetes Being hospitalised is more common for people with diabetes than those without and they are more likely to stay longer ADS 2012. Current diabetes management guidelines are heavily weighted towards screening and primary care management but recently the ADS 2012 and other diabetes professional associations released guidelines for managing people with diabetes in hospital and these guidelines should be used to guide care. Specific nursing care is described in most other chapters of the book. Factors that complicate diabetes management during illness • Age. • Gender. • Type and duration of diabetes. • Presence of diabetes complications. • Nutritional status. • Potentially erratic insulin absorption especially in Type 1. • Haemodynamic changes in blood flow. • Counter-regulatory stress response to illness hospitalisation treatment pain psychological stress and fear. • Timing of meals and snacks as well as during TPN fasting and renal dialysis and especially in relation to medicine administration. • Duration of time between insulin administration and meals. • Effect of medications on the gut especially narcotics for pain relief. Glucose requirements may need to be increased to compensate for slow transit times to supply sufficient energy and prevent hypoglycaemia. • Increased white cell count and impaired leukocyte function as a result of hyperglycaemia might not indicate the presence of infection. • Presence of ‘silent’ disease such as MI UTI and few classic symptoms of Type 2 diabetes hypoglycaemia or hyperglycaemia. • Delayed wound healing and strength of healing tissue. • Increased risk of thrombosis. • Development of ketoacidosis and/or hyperosmolar states if hyperglycaemia is not reversed. • Impaired cognitive function and lowered mood can make problem-solving self-care and learning difficult. • Depression. People’s stories 1 People with diabetes worry that hospital staff will make mistakes especially with their medication doses and administration times and managing hypoglycaemia. 2 They dislike being made to feel incompetent and not trusted by staff who ‘take over’ the self-care tasks they usually perform for themselves and who do not believe what they say. 3 Conversely some people prefer the nurses to take on diabetes slef-care tasks because it is an opportunity to ‘let go of’ the responsibility for a short time. 4 They find judgmental attitudes about eating sweet things demeaning especially when they are accused of dietary indiscretions when their blood glucose is high. 5 They dislike being labelled non-compliant or uncooperative if they have difficulty learning and remembering information. Aims and objectives of nursing care Aims

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Diagnosing and Classifying Diabetes 33 To formulate an individual nursing management plan so that the person recovers by primary intention maintains their independence and quality of life as far as possible and does not develop any complications of treatment and in some cases helping them prepare for a peaceful death. Recognise the importance of support from the family and other key individuals to the individual’s well-being self-care capacity and ability to take responsibility for their disease. Rationale Early diagnosis of diabetes and monitoring for short- and long-term complications enables early treatment and improved outcomes. The nurse’s understanding of the pathophysiology and classification of diabetes and its complications will improve the care they provide. Objectives 1 Establish a therapeutic relationship based on respect equality and trust. The therapeutic relationship is essential to healing. 2 To assess the person’s: • usual care plan • physical mental and social status • usual glycaemic control • ability to care for themselves • knowledge about diabetes and its management • the presence of any diabetes-related complications including lowered mood and depression • acceptance of the diagnosis of diabetes • presence of concomitant disease processes • medicine regimen including complementary medicines. 3 To encourage independence as far as the physical condition allows in hospital test own blood glucose administer own insulin select own meals. 4 To obtain and maintain an acceptable blood glucose range that minimises hypoglycaemia or hyperglycaemia and keeps the person free from distressing symptoms and fluctuating blood glucose levels. 5 To prevent complications occurring as a result of hospitalisation e.g. falls associated with hypo- and hyperglycaemia and a range of other factors. 6 To observe an appropriate management plan in order to achieve these objectives. 7 To inform appropriate health professionals promptly of the patient’s admission for example diabetes nurse specialist/diabetes educator dietitian or podiatrist. 8 To ensure the patient has the opportunity to learn about diabetes and its management particularly self-management and particularly when their usual care changes and new medicines are commenced. 9 To plan appropriately for discharge including managing medicines and undertaking or referring the person for a home medicine review if they meet the criteria and ensuring they have the equipment necessary to manage their diabetes medicines blood glucose meter insulin devices. 10 To prevent further hospitalisations as a result of diabetes. Technology and diabetes management Technology increasingly supports diabetes management and self-care and health professional learning. Electronic media such as the Internet enables users to retrieve and store information exchange information by participating in virtual communities and networks of practice and communicate with the people they care for Harno 2013. For example health information services peer communities practice guidelines risk assessment tools self-management tools research publications and counselling are available online. Telephone general health care advice services often manned by specially trained nurses and diabetes-specific call centres. In addition electronic media enable people with diabetes to be monitored remotely via teleconferences/telemedicine and by exchanging information such as blood glucose data between the individual and the health professional via email or mobile phone. Electronic patient registers and medical records are a reality in some countries. Research suggests a nurse- led multidisciplinary team can manage a group of people with diabetes in online disease management programmes Tang

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34 Care of People with Diabetes et al. 2012 and patients are generally satisfied with electronic monitoring Mehrotra et al. 2013 but it is possible to misdiagnose the condition and some doctors are not prepared to make a diagnosis without examining the patient. Some doctors use smart phones to photograph health issues such as wounds to track wound healing and eye health and for teaching purposes. Some specific diabetes management technology includes: • A range of increasingly sophisticated blood glucose meters some with connectivity to other electronic systems such as mobile phones and insulin pumps and some with inbuilt management algorithms. • Insulin delivery systems such as pumps. • Automated support algorithms for adjusting medicine doses and carbohydrate intake. • Non-invasive devices to detect nocturnal hypoglycaemia. • Automated portable system to control blood glucose overnight in people with Type 1 diabetes. • Online HbA1c converter tool that converts HbA1c percentages to mmol/mol/. • Health behaviour tracking systems such as stairs climbed kilojules burned some of which link to smart phones which become like a personal trainer. • Many mobile phone apps such as symptom checkers and risk calculators that help people in a range of ways. • Electronic decision-support tools for people with diabetes and health professionals including computer-generated reminders. Interestingly the latter appear to be more effective if they are delivered on paper and if there is space on the reminder for the clinician to document the reminder content or advice Ariditi Rege-Walther et al. 2012. There is no doubt there will be more the exciting technological advances that will enhance the care of for and by people with diabetes. However like most health care options there are risks and benefits that need to be considered. Some risks to consider include: • Not all information on the Internet is accurate or appropriate. People with diabetes need help to identify reliable sites such as the websites of diabetes organisations like Diabetes UK Diabetes Australia the American Diabetes Association and service providers such as Government websites Mayo Clinic and sites that display the Hon Code symbol. • Internet information may improve knowledge but it may not change behaviours Chapter 16 or health professional practice because social cultural and behavioural context are not part of the learning process Kinson 2012 although socialisation might be a feature of online group activities and support groups. • A combination of education about how to use management guidelines decision support tools and patient registers can lead to improved outcomes for people with Type 2 diabetes in general practice settings Barlow 2013. • Adequate back up and data management systems need to be in place so important data are not lost or accessible to people not involved in the individual’s care. That is stringent monitored security systems must be in place wherever confidential information is stored including on mobile phones. • Medicolegal issues such as breeches of privacy and confidentiality for example storing personal patient information including research data on smart phones. There are very significant implications for individuals whose data are not protected and the health professional concerned if the smart phone is lost or stolen. • Using/communicating patient information without consent including in tele/video health professional management conferences case discussions publications and presentations. A sobering final comment OPTIMISE the Optimal Type 2 Diabetes Management Including Benchmarking and Standard Treatment Trial Hermann et al. 2012 compared physician’s individual performance with a peer group to determine whether benchmarking and assessing change in three quality indicators of vascular risk: HbA1c LDL-C and systolic blood pressure improved the quality of Type 2 diabetes care in primary care settings n 3980. The findings show HbA1c targets were only met in 52.2 34.9 for LDL-C and 27.3 for systolic blood pressure. Other studies show older physicians are less likely to follow guidelines or use new medicines Tung 2011 and nurses have inadequate diabetes knowledge Livingstone Dunning 2010 including about medicines and in aged care settings Dunning et al. 2012. These findings are very concerning even allowing for the many confounding variables that affect the ability of people with diabetes to meet targets. As suggested in Chapter 16 patient-related targets may not be the best measure of health professional performance and more appropriate measures should be considered. If they are the best measure of health

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Diagnosing and Classifying Diabetes 35 professional performance health professionals must examine their care practices behaviours and attitudes and the care systems in which they operate to determine whether/how these factors affect their performance. For example general practitioners identified treatment costs to the patient and reluctance to commence insulin as barriers to their ability to achieve optimal management targets in a cluster randomised trial in Asia-Pacific that involved educating doctors about how to use diabetes guidelines Reutens et al. 2011. A great deal of time and money is spent on health professional education if health professionals are ineffective more than 50 of the time we need to determine whether education programmes adequately train health professionals to deliver diabetes education and care and/or are delivered in a manner suitable to health professionals’ learning needs. 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36 Care of People with Diabetes Carnethon M. De Chavez P. Biggs M. et al. 2012 Association of weight status with mortality in adults with incident diabetes. Journal American Medical Association 308 6 581. Chiasson J. Josse R. Gomis R. et al. 2002 Acarbose for prevention of type 2 diabetes mellitus: The STOP-NIDDM randomized trial. Lancet 359 2072–2077. Citrome L. Blonde L. Damatarca C. 2005 Metabolic issues in patients with severe mental illness. South Medical Journal 98 7 714–720. Conen D. Ridker P. Mora S. Buring J. Glynn R. 2007 Blood pressure and risk of developing type 2 diabetes mellitus: The Women’s Health Study. European Heart Journal 28 23 2937–2943. Dandona P. Ghanim A. Chaudhuri A. Dhindsa S. Kim S. 2010 Macronutrient intake induces oxidative and inflammatory stress: Potential relevance to atherosclerosis and insulin resistance. Experiential Molecular Medicine 42 245–253. 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Clapham C. 1998 Insulin resistance impaired glucose tolerance and non- insulin-dependent diabetes pathologic mechanisms and treatment: Current status and therapeutic possibilities. Progress in Drug Research 51 33–94.

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38 Care of People with Diabetes Turner R. Stratton I Horton V. et al. 1997 UKPDS 25 autoantibodies to islet cell cytoplasm and glutamic acid carboxylase for prediction of insulin requirement in type 2 diabetes. UKPDS Study group. Lancet 350 1288–1293. Twigg S. Kamp M. Davis T. Neylon E. Flack J. 2007 Prediabetes: A position statement from the Australian Diabetes Society and Australian Diabetes Educators Association. Medical Journal of Australia 186 9 461–465. UKPDS United Kingdom Prospective Diabetes Study 1998 Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with Type 2 diabetes UKPDS 33. Lancet 352 837–853. van Ufelen J. Wong J. Chau J. 2010 Occupational sitting and health risks: a systematic review. American Journal of Preventative Medicine 39 379–388. 1996–2012 Obesity: Metabolic and Clinical Consequences accessed October 2012. Wahlberg J. Vaarala O. Ludvigsson J. ABIS-study group 2006 Dietary risk factors for the emergence of type 1 diabetes-related autoantibodies in 2 1/2 year-old Swedish children British Journal of Nutrition 95 3 603–608. Weiss R. Caprio S. 2005 The metabolic consequences of childhood obesity. Best Practice Research Clinical Endocrinology Metabolism 19 3 405–419. Willi C. Bodenmann P. Ghali W. Faris P. Cornuz J. 2007 Active smoking and the risk of Type 2 diabetes: A systematic review and meta-analysis. Journal of the American Medical Association 298 2654–2664. Wilmot E. Edwardson C. Achana A. et al. 2012 Sedentary time in adults and the association with diabetes cardiovascular disease and death: Systematic review and meta-analysis. Diabetologia DOI: 10.1007/00125-012-2677- z. World Health Organization WHO 1999 Definition Diagnosis and Classification of Diabetes Mellitus and its Complications: Report of a WHO Consultation. Part 1: Diagnosis and Classification of Diabetes Mellitus. WHO Geneva. Zimmermann U. Himmerich H. 2003 Epidemiology implications and mechanisms underlying drug-induced weight gain in psychiatric patients. Journal of Psychiatric Research 37 193–220. Zinman B. Kahn S. Haffner S. et al. 2004 Phenotypic characteristics of GAD antibody-positive recently diagnosed patients with type 2 diabetes in North America and Europe. Diabetes 53 12 3193–3200. Zimmet P. Alberti G. Shaw J. 2005 Mainstreaming the metabolic syndrome: a definitive definition. Medical Journal of Australia 183 4 175–176. Zimmet P. Alberti G. Kaufman F. et al. IDF Consensus Group 2007 The metabolic syndrome in children and adolescents – An IDF consensus report. Paediatric Diabetes 8 299–306. Further reading Conen D. 2007 Blood pressure may predict incident type 2 diabetes in healthy women. European Heart Journal published online 9–10-2007. Dean L. McEntyre J. 2004a The genetic landscape of diabetes. http// books/bv.fegicallbv.View.ShowTOCriddiabetes. TOC accessed January 2008. Dean L McEntyre J. 2004b The genetic landscape of diabetes http// bv.fegicallbv.View.ShowTOCriddiabetes. TOC accessed January 2008. Donga E. van Dijk M. Hoogma R. Corssmit E. Romijin J. 2012 Insulin resistance in multiple tissues in patients with type 1 diabetes mellitus on long term continuous subcutaneous insulin infusion. Diabetes Metabolism Research Reviews. DOI: 10.1002/dmrr.2343. Dunstan D. Zimmet P. Welborn T. et al. 2002 The rising prevalence of diabetes and impaired glucose tolerance: The Australian obesity and lifestyle study. Diabetes Care 25 829–834. Engelau M Gregg E.2012 Diabetes screening does not reduce deaths. The Lancet 380 9855 www.…/PIIS0140-673612X6048-3 accessed December 2012. Eltisham S. Hattersley A. Dunger A. Barrett T. 2004 First UK survey of paediatric type 2 diabetes and MODY. Archives of Diseases in Childhood 89 526–529. Floegal A. Stefan N. Yu Z. et al. 2012 Identification of serum metabolites associated with risk of type 2 diabetes using a targeted metabolomic approach Diabetes DOI 10.2337/db12-0495. Hermans M. Brotons C. Elisaf M. et al. 2012 Optimal type 2 diabetes mellitus management: The randomized controlled OPTIMISE benchmarking study: Baseline results from six European countries. European Journal of Preventative Cardiology DOI: 10.1177/2047487312449414. Lindstrom J. Ilanne-Parikka P. Peltonen M. 2006 Sustained reduction in incidence of type 2 diabetes by lifestyle intervention: Follow-up of the Finnish Diabetes Prevention Study. Lancet 368 1673. Maynard J. Rohrscheib M. Way J. Nguyen C. Ediger M. 2007 Non-invasive Type 2 diabetes screening: Supervision substudy to fasting plasma glucose and A1c. Diabetes Care 30 5 1120–1126. Nichols G. 2007 Preventing and predicting diabetes. Medscape Diabetes and Endocrinology posted 8.10.2000. Nilsson C. Ursing D. Torn C. Aberg A. Landin-Olsson M. 2007 Presence of GAD-antibodies during gestational diabetes predicts type 1 diabetes. Diabetes Care DOI: 10. 2337/dc07–0157. Oomichi T. Emoto M. Tabata E. et al. 2007 Impact of glycemic control on survival of diabetic patients on chronic regular hemodialysis: A 7-year observational study. Diabetes Care 29 1496–1500. Pradhan A. Rifai N. Buring J. Ridker P. 2007 Hemoglobin A1c predicts diabetes but not cardiovascular disease in nondiabetic women. The American Journal of Medicine 120 8 720–727. Schultz M. 2007 Fiber and magnesium intake protects against developing type 2 diabetes. Archives of Internal Medicine 167 956–965. Snitker S. Watanabe R. Avi L. et al. 2004 Changes in insulin sensitivity in response to troglitazone do not differ between subjects with and without the common functional pro12Ala perixisome proliferator-activated receptor gamma2 gene variant: results from the Troglitazone in Prevention of Diabetes TRIPOD study. Diabetes Care 27 1365–1368.

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Diagnosing and Classifying Diabetes 39 Spanwen P. Kohler S. Verhey F. Stenhonwer C. van Boxtel M. 2012 Effects of type 2 diabetes on 12-year cognitive change. Results from the Maastricht Aging study. Diabetes Care DOI 10.2337/ dc12-0746.

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Chapter 2 Holistic Assessment Nursing Diagnosis and Documentation To Cure Diabetes Click Here Every person who requires health care has a unique set of needs. Key points • An holistic diabetes assessment education and management plan must:  Encompass the physical emotional spiritual family social and environmental factors relevant to the individual and be developed in collaboration with them and significant family members and carers.  Include general nursing and health care needs as well as diabetes management. • Incorporate diabetes-specific factors likely to affect self-care health professional care and outcomes. • Develop and document individual care plans based on the best available evidence and communicate them to other relevant health professionals family and carers keeping in mind the individual’s right to privacy. • Evaluate outcomes relevant to the overall management goals agreed metabolic targets as well as short-term goals formulated within the overall plan for a specific episode of care such as an admission to hospital. • Discharge planning and transitional care among health services should be part of the care plan. Rationale Best practice diabetes education and care relies on a combination of the best available evidence intuition and clinical judgement effective communication skills and the informed participation of the person with diabetes. Careful assessment enables physical psychological spiritual and social issues that impact on care to be identified and Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd.

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Holistic Assessment Nursing Diagnosis and Documentation 41 incorporated into nursing management and discharge/transition plans. Life balance and emotional well-being are essential to achieving metabolic targets. Significantly many care standards now include person-centred and family-centred care. However fee-for-service payment models do not encourage health professionals especially doctors to spend time with patients yet person-centred care depends on health professionals having sufficient time to address the whole patient and his or her concerns. At present most systems expect the individual to engage with the healthcare system but often systems and processes are not integrated or accessible. Holistic nursing Holistic care aims to heal the whole person using art and science to support the individual to mobilise their innate healing potential: that is to become empowered. Healing occurs when the individual embraces and transforms traumatic life events and is open to and/or recognises his or her potential Dossey et al. 1995 p. 40. Transcending traumatic life events such as the diagnosis of diabetes or a diabetes complication is part of the spiritual journey to self-awareness self-empowerment and wholeness. Significantly spirituality is not the same as religion although it may encompass religion Dossey et al. 1995 p. 6 Parsian Dunning 2008 Dunning 2013. Thus in order to achieve holistic care nurses must consider the individual’s beliefs and attitudes because the meaning people attach to their health diabetes and treatment including medicines affects their self-care behaviour and health outcomes. At least eight broad interpretations of illness have been identified: challenge enemy punishment weakness relief irreparable loss/damage value adding and denial Lipowski 1970 Dunning 1994 Dunning Martin 1998. In addition the author has identified other explanatory models during routine clinical care: diabetes is an opportunity for positive change and diabetes is a visitation from God. Care models Wagner et al. 1996a suggested that many care models have limited effectiveness and reach because they rely on traditional education methods and do not support selfmanagement and transition among services. The essential elements needed to improve outcomes encompass: • Evidence-based planned care including management guidelines and policies. • Appropriate service and practice design that encompasses prevention and expedites referral and communication among services. • Systems to support self-management. • Process to ensure practitioners are knowledgeable and competent collaborate and communicate effectively have sufficient time to provide individual care and are supported to do so and where health professional roles are clearly defined and complementary. • Clinical information systems that enable disease registries to be maintained outcomes to be monitored relevant reminders to be sent to patients and performance to be evaluated Wagner et al. 1996a. Many current diabetes management models such as the Lorig and Flinders models the Group Health Cooperative Diabetes Roadmap Kaiser-Permanente in Colorado nurseled case management and various shared care models including computer programs 46 Care of People with Diabetes Interactive Health Communication Applications IHCA encompass these elements and improve patient adherence to management strategies and satisfaction. However their application is still limited by time and resource constraints including timely patient access to health professionals. Research suggests Internet-based support can improve patient-practitioner communication and collaboration and enhance a patient’s sense of being valued and secure Ralston et al. 2004. However more research is needed to determine the best way to use these programmes and their effects in specific patient groups Murray et al. 2005. Generally patients have a better understanding of what is expected of them if they receive both written and verbal information Johnson et al. 2003. The font size colour and language level of any written material provided

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including instructions for procedures and appointments and health professional contact details needs to be appropriate to the age education level and culture of the individual concerned see Chapter 16. In addition health professionals must clearly promote a patient-centred approach to care National Managed Care Congress 1996 that is evident within the service. For example patients are involved in decisions about their care and see the same doctor each time they attend an appointment. They should also be involved in service planning and deciding what constitutes quality care and what metrics to use to measure quality Jones 2013. Most patients want to be cared for by knowledgeable competent and caring health professionals who are approachable and expert communicators yet these issues that are so important to patients are not included in quality metrics. Patient satisfaction surveys fall short of demonstrating person-centred care although such surveys often seek information to help them make services more ‘patient friendly’ they often reflect selection bias and contain multiple confounders and many are not validated in any appropriate way. In addition patient satisfaction does not reflect person-centred care or quality care. Although patient-centred care is difficult to define and achieve often because it is a subjective concept and as indicated because of time constraints it generally refers to: • personalised care rather than ‘one target fits all:’ diabetes management guidelines are beginning to encompass individualised management targets • ensuring care considers the individual’s social mental physical social situation as well as their goals explanatory models capability physical mental spiritual and linguistic and health and general beliefs experiences religion and culture • delivering care that is culturally sensitive and relevant to the individual but which is also family- centred Joint Commission 2010 • using effective communication strategies that account for any disabilities the individual might have and using translators sensitively. Effective communication is a two way process in which messages are negotiated until the information is correctly understood by everybody involved in the communication • developing strategies to help the patient trust their health professionals Wagner et al. 1996a and vice versa • helping patients acquire the information they need to make informed decisions McCulloch et al. 1998 • improving patient adherence to management recommendations Wagner et al. 1996b: also see Chapters 15 and 16 • making collaborative decisions with the patient and communicating them to relevant people. Kleinman et al. 1978 suggested some simple questions that can help create shared understanding between people with diabetes and health professionals. The questions are still relevant today and are in fact recommended by the Joint Commission roadmap for hospitals concerning advocacy and person- and family-centred care 2010 . Such questions encompass : • What do you think caused your illness/problem/s • Why do your think the problem started when it did • How is the problem affecting you • How serious do you think the problem is • What sort of treatment do you think will help • What do you want the treatment to do outcomes • What are your main concerns about the problem • How can I/we help These questions can be supplemented with clarifying questions and by checking assumptions. Specific programs that train health professionals how to deliver patient-centred care improve patient trust in doctors Lewin et al. 2001 McKinstry et al. 2006 and the delivery of patient information Kinnersley et al. 2007. In addition patients may need specific education about how to ask relevant questions during consultations and how to participate in

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Holistic Assessment Nursing Diagnosis and Documentation 43 making management decisions. Both parties may need education about how to negotiate the complex nature of shared decision- making to balance the imperative for evidence-based care with the need to incorporate the individual’s values and preferences Kilmartin 1997. In order to assist the process the Foundation for Informed Decision-Making in the USA 2007 developed a series of interactive videos and written materials for patients about a range of common medical conditions. In order to deliver person-centred care it is necessary to undertake a thorough assessment use appropriate questions and clinical reasoning to identify the patient’s needs and management guidelines to determine whether the recommended treatment is likely to benefit the individual whether the benefits outweigh the risks and whether the individual can/will adhere to the recommendations including their self-care capacity and then recommend appropriate treatment options to the individual. Characteristics of an holistic nursing history The nursing history is actually the individual’s story and health professionals are privileged to learn part of that story. The art of ‘story listening’ is essential to compiling a useful patient history. The history/story: • includes demographic data age gender social situation • collects units of information about past and current individual and family health and family and social relationships see Figure 2.1 to enable individual care plans to be formulated considering the person’s goals and expectations:  obtains baseline information about the person’s physical and mental status before and after and the presenting complaint  collects information about the person’s general health and diabetes-related beliefs and attitudes and the meaning they attach to and the importance they place on symptoms • Should be concise to enable information to be collected in a short time • Should focus on maintaining the person’s independence while they are in hospital e.g. allowing them to perform their own blood glucose tests .

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Figure 2.1 Example of a combination of a genomap information inside the circle and an ecomap information outside the circle of a 50- year-old woman with Type 2 diabetes and a history of childhood molestation and sexual abuse. It shows a great deal of conflict within and outside the family and identifies where her support base is. The findings should be documented in the medical record one should think about that term – does it reflect person-centred care and communicated to the appropriate caregivers. There is an increasing trend towards electronic data collection and management process that enable information to be easily and rapidly transferred among health professionals. Some systems enable patients to access their health information. Most modern electronic blood glucose meters have a facility for marinating a record of blood glucose test results that can be downloaded into computer programs. These systems have the capacity to significantly improve health care however consideration must be given to the privacy and confidentiality of all personal information and appropriate access and storage security mechanisms should be maintained according to the laws of the relevant country. Note: A guideline for obtaining a comprehensive nursing history follows. However it is important to listen to the patient and not be locked into ‘ticking boxes’ so that assumptions can be checked and non-verbal messages and body language noted and clarified and vital and valuable information is not overlooked. Most of the information is general in nature but some is specifically relevant to diabetes e.g. blood glucose testing and eating patterns. The clinical assessment in the example guideline is particularly aimed at obtaining information about metabolic status. Assessing the person with diabetes does not differ from assessing people with any other disease process. Assessment should take into account social physical and psychological factors in order to prepare an appropriate nursing care plan including a plan for diabetes education and discharge/transition. Any physical disability the patient has could affect their ability to self-manage their diabetes inject insulin inspect feet test blood glucose. Impaired hearing and psychological distress and mental illness may preclude people attending group education programmes. Management and educational expectations may need to be modified to accommodate disabilities. If the person has diabetes however metabolic derangements may be present on admission or could develop as a consequence of hospitalisation. Therefore careful assessment enables potential problems to be proactively identified alerts to be flagged if necessary a coordinated collaborative care plan to be developed and appropriate referral to other health professionals medical specialist podiatrist diabetes nurse specialist/diabetes educator dietitian and psychologist to take place. A health ‘problem list’ that ranks problems in order of priority can also assist health professionals to plan individualised care that addresses immediate and future management goals. The first step in patient assessment is to document a comprehensive health history. Nursing history A nursing history is a written record of specific information about a patient. The data collected enable the nurse to plan appropriate nursing actions considering the individual patient’s worldviews and needs. A good patient care plan will enable consistent care to be delivered within and among nurses and service departments. An example patient assessment chart follows. It was formulated to collect relevant diabetes-specific data which could be used in conjunction with other relevant tools such as those shown in Table 2.1. Some electronic data management systems enable some information to be collected electronically from existing records when the patient has attended the service before.

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Holistic Assessment Nursing Diagnosis and Documentation 45 Example Health Assessment Chart Formulated for people with diabetes in hospital but most issues are relevant in any health care setting. Other systems-based assessment may also be necessary for example respiratory renal nervous and gastrointestinal systems. A. Demographic data Name ………………………………………………………………………………......................…... Age ……………… Gender  Male  Female Type of diabetes  Type 1  Type 2  Other …………………..........................… Duration of diabetes ………………………… years Known allergies ……………………………………………………………......................………..… Social Language spoken: …………………………….……………………………......................…………. Command of English/language of relevant country:  Written  Spoken Important cultural practices e.g. fasting dietary requirements practices related to dying and death Marital status …………………………………….………….…………........................…..………… Living arrangements  With partner  Alone  Other Support systems …………………………………………………………….......................………… Age and health status of significant other/carer …………………................……………………. Work type …………………………………………………………………......................…………… Responsibility in the home ……………………………………….……...................…….…….…… Hobbies …………………………………….………….….......................……….…………...……… Education level ……………………………………………......................…………………………… Religion and religious practices e.g. prayer …….....................……….…………………………… Spiritual practices e.g. meditation Meals Regular meals  Yes  No Food allergies ..………………………………………………….………..……......................…….... Usual diet ………………………………………...………………………..….......................……..… Appetite generally ………….....……………......…. currently ……..........………………………… Who does the cooking ………….………….………….………….….......................…....………… Who does the shopping ……………………………………..................………………....………… Eating out ………….………….………….………….…….…......................…….……....………… Current nasogastric tube …………………....… TPN ……..…………. IV …………....………...… Alcohol consumption  Yes  No How much ……….……..……….............… How often ……….….................……………… Smoking  Yes  No Cigarettes/pipe ……….……................................................……………… How many per day ………..........…………….…… Marijuana: ……….…….............……....…… Current medications Record dose and dose frequency for each medicine when they administer it in relation to food and exercise whether they miss doses if so how often and why whether they alter doses if so how often and why. Check insulin injection sites Insulin delivery system used …….………….……………….……...........................……………… Insulin administration technique/accuracy ……….………...................……….…….....………… Preparing injection using usual system …………...................…………………………………….. Patient can name type/s of insulin  Yes  No. Do they adjust their insulin dose Why ..………………......……. What criteria do they use to adjust doses ....…….............……. Complementary therapies: name of the product/therapy why they are using it and what they are using it for. If on insulin or oral hypoglycaemic agents: ask whether they have hypoglycaemia. How often Do they ever lose consciousness during a hypoglycaemic episode

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46 Care of People with Diabetes Do they recognise the signs and symptoms of hypoglycaemia What signs/symptoms do they experience When does it usually occur What is the blood glucose level before they treat the hypo How do they treat the hypo Do they always have some form of glucose with them …………..…………..………............…. Usual activity level Sports ……….…….……………….……………….........................…….....……………………….. Gardening ……………….……………….…………......................…….…….....………………….. Walking …………….……………….………………..........................…….....…….……………….. Other ……………….……………….……......................………….…….....……....……………….. Sleep pattern Approximately how long do they sleep for Do they have trouble getting to sleep Do they have trouble staying asleep Do they need to get up at night to go to the toilet ……...................…………………… How often Can they go back to sleep after going to the toilet What prevents them from sleeping Do they use anything to help them sleep …………....…………… What …….............……… Disabilities What activities are limited .…….….……………….……………….……...........................…….... To what degree .…….….……………….……………….…….....……........…......................…..... 1 General .…….….…….……….……………….…….............................……………………… 2 Hearing .…….….…….……….……………….…….....…………………........................…… 3 Related to diabetic complications …………………….…..................……….…….....…….. Reduced vision  glasses  contact lenses  registered blind Neuropathy a Peripheral …......................…………………………………………………….... b Autonomic ……………………………………….....................................….... Vascular a Cardiac ………………………………………………….................................... b Legs and feet …………………………….............................……………...….. Kidney function …………………………………………….....................……………….…...…...... Sexuality a Erectile dysfunction ………………………………………….................………. b Sexual difficulties .....………………………………….................….….………. 4 Mobility and flexibility 5 Dexterity fine motor skills Self-monitoring of diabetes status testing methods ............................................................................................................................................... Tests own blood glucose  Yes  No Tests blood ketones during illness Yes  No  Testing frequency ……………………………………………....................………………………… System used Blood glucose meter type …………………………………………………….................…….…… Testing accuracy …………………………………………....................…………………….....…… Psychological status Anxiety Depression Adjustment to diabetes  Anxious  Denial  Depression  Well adjusted Usual mental state …………………….......… Current mental state ………………….…..........… Current stressors ………………………………………………………………….......................…… Coping mechanisms …………………………………………………......................…………..…… Diabetes knowledge

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Holistic Assessment Nursing Diagnosis and Documentation 47 Previous diabetes education  Yes  No How long ago …….................…………..… Attendance at education support groups  Yes  No Name of group ……………………………………………………………...................……….….… Patient’s stated reason for being in hospital ............................................................................................................................ ............................................................................................................................ B. Clinical and laboratory examination A detailed physical examination is essential. Particular attention should be paid to the following areas. 1 General inspection • Conscious state • Temperature pulse and respiration • Blood pressure lying and standing note any postural drop • Height • Weight and history of weight gain/loss BMI ….…………Waist circumference • Hydration status skin turgor • Presence of diabetic symptoms thirst polyuria polydipsia lethargy • Full urinalysis • Blood glucose • Presence of ketones in blood  urine  2 Skin • Pigmentation Acanthosis nigricans • Skin tone/turgor colour • Presence of lesions rashes wounds ulcers • Inspect injection sites including abdomen note any thickening lumps bruises 3 Mouth • Mucous membranes dry/moist • Lips • Infection halitosis • Teeth: evidence of dental caries loose teeth red gums incorrectly fitting dentures 4 Feet and legs • Temperature of feet and legs noting any differences between two legs and parts of the feet and legs • The skin of the feet and legs may be hairless and shiny due to poor circulation • Muscle wasting • Ulcers or pressure areas on soles of feet and toes including old scars • Loss of pain sensation that may be due to nerve damage estimate the size and depth of any ulcers using a template filed in the medical record note their location and how long they have been present • Presence of oedema • Infection including fungal infection inspect between the toes • Condition of nails and general cleanliness of feet • Type of footwear • Record podiatry contact or referral if any Laboratory tests Full blood count Glucose

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48 Care of People with Diabetes HbA ic Lipid profile Kidney function Liver function Urea and electrolyte Other relevant tests Table 2.1 Some commonly used assessment instruments. The content of the instruments the purpose of the assessment and the particular patient population should be considered when selecting instruments even when they are valid and reliable. Some are available in languages other than English. Details of most of the diabetes-specific instruments can be found on Tool.html 2006 and Garrett et al. 2001. Generic instruments Diabetes-specific instruments Sickness Impact Profile Bergner et al. 1976 Audit of Diabetes-dependent Quality of Life ADDQoL Bradley et al. 1999 Nottingham Health Profile Hunt McKenna 1985 Appraisal of Diabetes Scale ADS Carey et al. 1991 Short Form Health Survey SF-36 Ware et al. 1992 Diabetes Health Profile DHP-1 DHP-18 Meadows et al. 1996 Quality of Life After Acute Myocardial Infarction Oldridge et al. 1991 The Diabetes Impact Measurement Scale DIMS Hammond Aoki 1992 K10+ depression scale which is sometimes used as part of the psychosocial profile developed by the Department of Human Services Victoria Australia Diabetes Quality of Life DQOL Jacobson et al. 1988 Diabetes Specific Quality of Life Scale DSQOLS for Type 1 diabetes Mulhauser et al. 1998 Perceived Therapeutic Efficacy Scale PTES Spiritual Assessment Tool Dossey et al. 1995 Hospital Anxiety and Depression Scale HADS Self Assessment Health Status EQ-5D Center for Epidemiological Studies Depression Scale CESD Radloff 1997 Patient Health Questionnaire PHQ-9 Pfizer Inc 2003 Questionnaire on Stress in Diabetic Patients QSD-R Duran et al. 1995 Well-being Enquiry for Diabetics WED Mannucci et al. 1996 Problem Areas in Diabetes PAID Polonsky et al. 1995 Diabetes Treatment Satisfaction Questionnaire DTSQ Bradley 1994 Diabetes Care Profile DCP Fitzgerald et al. 1996 Diabetes-39 Questionnaire D-39 Boyer Earp 1997 Spirituality Questionnaire for young adults with diabetes SQ Parsian Dunning 1997 which is not listed on the RCMAR website Note: permission to use some of these tools may be needed before the tools can be used and specific training in analysing and interpreting the data is needed with some instruments. Other useful instruments include pain scales falls risk tools activities of daily living and mental assessment such as Folstein’s Minni Mental. The Victorian Department of Human Services now Department of Health and Aging DOHA 2006 produced a range of profiles such as the Psychosocial Profile which encompasses mental health and well-being and the Health Behaviours Profile that are used in many Australian DOHA funded projects. Other important information to obtain might include functional status whether the person has an advanced care plan and other proxy decision-making tools and what special provision might be required to fulfill religious observances e.g. fasting for Ramadan or Buddhist lent and how to care for the body after death. These issues are often difficult to discuss but they are an essential part of person-centred care. Instruments to measure health status Some specific instruments can be very helpful to determine health status quality of life QOL beliefs and attitudes and satisfaction. QOL is a complex multifactorial and individual construct encompassing the individual’s physical

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Holistic Assessment Nursing Diagnosis and Documentation 49 social and mental functioning satisfaction with life and whether/how these factors are affected by illness and its management Salek 1998. Significantly social well being is strongly correlated with emotional well being. A range of instruments generally designated as generic and disease-specific is available. Generic instruments were designed for use in a wide range of patients and populations. Disease-specific instruments have a narrower focus on particular illnesses in this case diabetes see Chapters 4 12 and 15. Table 2.1 presents an overview of generic and diabetes specific instruments commonly used to collect important subjective information from individuals about their health status and beliefs. The instruments have all been extensively validated. Documenting and charting patient care Documenting in the health record Documentation is an essential part of health management. Alternative methods of documenting care are emerging for example charting by exception where only events outside the normal expected progress are recorded. This form of charting requires supportive documentation in the form of guidelines flow charts care plans and care maps. They can avoid duplication and streamline documentation. The use of care pathways is becoming increasingly common in Australia and in the UK O’Brien Hardy 2000. Other ways of documenting holistic care incorporate genomaps and ecomaps see Figure 2.1 which can effectively convey a great deal of information about the social relationship and support base aspects of an individual’s life Cluning 1997. They are particularly useful for long-term chronic diseases such as diabetes where these factors affect management outcomes see Chapters 15 and 16. They also record information that is often passed on anecdotally during handover or in the ‘corridor’ which means vital information that could assist in planning care is not available or is misinterpreted. Genograms illustrate how an individual relates to other people in the family and ecomaps place the family in the context of the wider social situation in which they live. Ecograms and ecomaps can be simple or convey complex and detailed information. Together they give a great deal of information about: • the individual’s environment • their relationships with people in their environment • family structure • family and extended support • family health history • family functioning • health service utilisation • social orientation. This information helps determine how social support and other networks influence the person’s self-management and the assistance they can rely on for example to manage serious hypoglycaemia and intercurrent illness. Care plans The employing institution’s policy regarding the method of documentation should be followed. Good documentation enables the required care to be communicated to all staff. In the future changes will occur to the methods of documenting care for example focus charting and flow charts may replace narrative notes. Flow charts are designed to enable all healthcare providers to document care on a single care plan which reduces duplication and may enhance communication. Many health services now use electronic documentation and communication processes. Standardised care plans of common medical and nursing diagnosis are being developed to serve as blueprints and may reduce the time spent on documentation. Despite the fact such care plans encompass ‘charting by exception’ they are not consistent with personalised care. For example a patient consulted the author about her electronic ‘personalised’ care plan that was generated in primary care by her general practitioner who printed a copy of the care plan for her to keep. She did not understand what the information meant. The care plan contained the standard

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50 Care of People with Diabetes blood glucose lipid blood pressure and weight targets and indicated she should have no more than one glass of alcohol per day. When the information was explained to her she became very upset and agitated crumpled the care plan into a ball and threw it in the bin. She said: ‘well it is not personalised for me. I am a former alcoholic. I have not had any alcohol for 5 years now my target is one glass a day. If I had one glass I could not stop.’ The move towards computerised or ‘paperless’ documentation is daunting and exciting but due consideration must be given to data security. Confidential information should be labelled as such in the medical record. Extra care is required with mobile technology such as smart phones laptops and palm pilots to ensure patient confidentiality is protected if any patient data are stored and/or communicated via these media. Nursing notes Due consideration needs to be given to standard policies for good documentation and the laws governing privacy and confidentiality and people’s right to access their medical records. Medical notes are a record of the patient’s encounter with a service provider in any setting and hospital admission the care they received and the outcomes of the care provided and acts as a guide for discharge planning. Handwritten documentation should be written legibly and objectively. Medical records are not legal documents but can subpoenaed for a court hearing. In such cases good documentation can help the health professional recall the situation. Documentation should contain the following: • The condition of the patient recorded objectively for example describe wounds in terms of size and depth. • Quantification of the patient’s condition recording swelling oedema temperature pulse and respiration TPR and blood pressure BP using objective measures. • All teaching the patient receives and that still required. • The patient’s response to treatment. • All medications received and any associated adverse events. • Removal of all invasive medical devices e.g. packs drains IV lines. • Psychological spiritual and social factors. Clinical observation In some cases it is possible to refer to standard protocols in medical records if there is a set procedure documented and regularly revised for example there is a standard procedure for performing an oral glucose tolerance test. The documentation could note relevant details such as the time date and person’s name and then state ‘OGGT performed according to the standard protocol’. Where any deviation from the protocol occurred it should be recorded. If required the standard protocol could be produced. Documenting metabolic status ‘diabetic charts’ The purposes of ‘diabetic charts’ are: • To provide a record of blood glucose measurements so the blood glucose pattern can be identified and used to adjust insulin/glucose lowering medicine GLM doses dose forms and the dose regimen. • To record blood ketone measurements to detect risk of ketoacidosis especially in Type 1 diabetes. • To provide a record of the dose and time insulin and other GLMs were administered. • To record episodes of hyper or hypoglycaemia and how they were managed. Frequency of blood testing depends on the patient’s status and the management plan see Chapter 3. Practice point

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Holistic Assessment Nursing Diagnosis and Documentation 51 A common error is that medication doses are not recorded on the ‘diabetic chart’ which makes it difficult to interpret the blood glucose pattern without the medication information. Nursing responsibilities 1 Write legibly. Avoid using unauthorised abbreviations. Insulin doses should be documented as ‘units’ not u/s. 2 Accurately record all medication doses and dose intervals. 3 Record hypoglycaemic episodes symptoms treatment time activity and food omission in the appropriate column. Hypoglycaemia should also be documented in the patient’s unit record. 4 Do not add unnecessary details. 5 Sign and include the date and time of all entries. Figure 2.2 depicts example charts for a frequent testing and b testing 4-hourly or less often.

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52 Care of People with Diabetes infusion b 4-hourly or less frequent testing. Documentation by people with diabetes People with diabetes also document a great deal of information about their disease. They use a variety of written and electronic record-keeping methods including blood glucose monitoring diaries complication screening records and other management information such as medication lists and the results of investigative procedures. These records are a vital part of the documentation process. They not only supply written information they also contain a great deal of information about an individual’s self-care ability for example a blood glucose diary covered with blood smears could mean the person is having difficulty placing the blood on the strip. Discussing the issue with the patient Figure 2.2 Sample diabetes record charts for a 2-hourly testing e.g. when using an insulin DIABETIC FREQUENT MONITORING IDENTIFICATION TIME INSULIN BLOOD SUGAR URINE NURSING COMMENT S E.g. Adverse reactions or food omission DOSE a DATE TYPE GLUCOSE 0 10 / 1 / 1 4 / 1 2 1 2 IDENTIFICATION INSTRUCTIONS TYPE OF INSULIN BLOOD GLUCOSE AND URINE TESTS MUST BE RECORDED IN FULL. COMMENTS 1100 1600 2100 0700 Date Insulin type Dose Blood glucose mmol/L Urine glucose Ketones Insulin type Dose Blood glucose mmol/L Urine glucose Ketones b

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Holistic Assessment Nursing Diagnosis and Documentation 53 might reveal that they often get the shakes and their vision is blurred due to hypoglycaemia. It is important however that all such assumptions are checked. Importantly the information in the individual documents must be valued and used in the clinical encounter. It is a tangible record of the hard work of self-care. References Cluning T. 1997 Social assessment documentation: genomaps and ecomaps. In Nursing Documentation: Writing What We Do ed. J. Richmond Chapter 7. Ausmed Publications Melbourne. Dossey B. Keegen L. Guzzetta C. Kolkmeier L. 1995 Holistic Nursing: A Handbook for Practice. Aspen Publishers Maryland pp. 20–21. Dunning P. 1994 Having diabetes: young adult perspectives. The Diabetes Educator 21 1 58–65. Dunning P. Martin M. 1998 Beliefs about diabetes and diabetes complications. Professional Nurse 13 7 429–434. Dunning T. 2013 Turning points and transitions: Crises and opportunities. Chapter 8 in Diabetes Education: Art Science and Evidence ed. T. Dunning Wiley Blackwell Chichester pp 117–131. Foundation for Informed Medical Decision Making 2007 http:// accessed December 2007. Hunt S. McKenna J. 1985 Nottingham Health Profile. html accessed January 2008. Johnson A. Sandford J. Tyndall J. 2003 Written and verbal information versus verbal information only for patients being discharged from acute hospital settings to home. Cochrane Database of Scientific Reviews. Issue 4 Art No Cd003716. DOI 10. 1002/14651858. CD 003716. Kilmartin M. 1997 Evidence is lacking on shared decisions. Journal of Health Services Research and Policy 2 2 112–121. Kinnersley P. Edwards A. Hood K. et al. 2007 Interventions before consultations for helping patients address their information needs. Cochrane Database of Scientific Reviews Issue 3 Art. No. CD 004565 . DOI 10. 1002/14651858. 2. Kleinman A. Eisenberg L. Goode B. 1978 Culture illness and care: Clinical lessons from anthropological and cross cultural research. Annals of Internal Medicine 88 2 251–258. Lewin S. Skea Z. Entwistle V. Zwarenstein M. Dick J. 2001 Interventions for providers to promote a patient-centred approach in clinical consultations. Cochrane Database of Systematic Reviews Issue 4 Art. No. CDOO 3267. DOI 10. 1002/14651858.CDOO3267. McCulloch D. Price M. Hindmarsh M. et al. 1998 A population based approach to diabetes management in a primary care setting: Early results and lessons learned. Effective Clinical Practice 1 1222. McKinstry B. Ashcroft R. Car J. Freeman G. Sheik A. 2006 Interventions for improving patients’ trust in doctors and groups of doctors. Cochrane Database for Systematic Reviews Issue 3 Art. No. CDOO4134. DOI: 10. 1002/14651858.CDOO4134.pub2. Murray E. Burns J. See Tai S. Lai R. Nazareth I. 2005 Interactive health communication applications for people with chronic illness. Cochrane Database of Systematic Reviews Issue 4 Art. No. CDOO4274. DOI: 10. 1002/4651858.CDOO4274.pub4. National Managed Health Care Congress NHCG 1996 The Disease Management Strategic Research Study and Resource Guide. NHCG Washington. O’Brien S. Hardy K. 2000 Impact of a care pathway driven diabetes education programme. Journal of Diabetes Nursing 4 5 147– 150. Parsian N. Dunning T. 2008 Spirituality and coping in young adults with diabetes. Diabetes Research and Clinical Practice 79 182 S82–S121. Ralston J. Revere D. Robins L. 2004 Patients’ experience with a diabetes support program based on an interactive electronic medical record: Qualitative survey. British Medical Journal 328 115–162. Salek S. 1998 Compendium of Quality of Life Instruments. John Wiley Sons Chichester UK. The Joint Commission 2010 Advancing Effective Communication Cultural Competence and Patient- and Family-Centered Care: A Roadmap for Hospitals. Oakbrook Terrace IL USA: The Joint Commission. Wagner E. Austin T. Davis C. et al. 1996a Improving outcomes in chronic illness. Managed Care Quarterly 4 2 1225. Wagner E. Austin T. et al. 1996b Organising care for patients with chronic illness. The Milbank Quarterly 74 4 51–54. Further reading Bradford K. 2013 Patients need to be involved in quality metrics. Primary Care Progress blog accessed February 2013. Garratt A. Schmidt L. Fitzpatrick R. 2002 Patient-assessed health outcome measures for diabetes: A structured review. Diabetic Medicine 19 111.

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Chapter 3 Monitoring Diabetes Mellitus To Cure Diabetes Naturally Click Here Key points • Regular assessment of the individual’s physical emotional social spiritual relationship status and their capability to perform their usual activities of daily living and self-care is essential to enable proactive management strategies to be implemented. • Structured regular complication screening programmes that encompass mental health self- care driving safety and a structured medication review should be undertaken at least annually. In some cases the health and well-being of spouses need to be considered especially older spouses who provide care and support. • Diabetes education and management programmes should be evaluated and revised regularly to ensure they remain current. People with diabetes should be involved in the evaluation processes. • The people with diabetes has a responsibility to undertake appropriate selfcare to manage their disease. Rationale Proactive monitoring programmes enable blood glucose and lipid patterns complication status and self-care capability to be identified and the management regimen appropriately tailored to the individual. The accuracy of blood glucose self-monitoring technique and appropriate maintenance of equipment is an important aspect of the individual’s ability to manage their diabetes and helps ensure management decisions are based on the best available data when used in conjunction with laboratory investigations and physical and mental assessment. Self-monitoring enables people with diabetes to identify the effects of diet exercise and other factors on their blood glucose levels and gives them greater insight into and control over their disease.

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Monitoring Diabetes Mellitus 55 Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. Monitoring and meeting management targets is also a key quality management activity and funding and the service accreditation processes are often based on health professionals and governments meeting targets and complying with guidelines and care standards. The new Non-Communicable Disease Global Monitoring Framework IDF 2012 was discussed in Chapter 1. In addition health services in Australia will have to demonstrate person-centred care in all of the 12 new accreditation standards. These regulatory expectations put pressure on service managers clinicians clerical staff and ultimately people with diabetes. Introduction Monitoring blood glucose is an important part of diabetes management. The results obtained form the basis for adjusting medication food intake and activity levels. Urine glucose is not a reliable method of assessing metabolic control but might still be useful for some people and in some countries where no other method is available provided the renal threshold for glucose has been established. Most glucose circulating in the blood is reabsorbed in the renal tubules however the capacity to reabsorb glucose is exceeded during hyperglycaemia and glucose appears in the urine. The renal threshold for glucose is fairly constant about10 mmol/L but may be higher in older people and during pregnancy Sonksen et al. 1998. Glucose in the urine represents the amount of glucose that collects in the urine since the bladder was last emptied and is therefore a retrospective value. Practice point Urine glucose testing cannot detect hypoglycaemia. People with diabetes are expected to and do manage their diabetes at home that is they are responsible for over 90 of diabetes management decisions. Thus each individual is an expert in his/her diabetes. People should be encouraged to continue to self-monitor blood glucose in hospital if they are well enough to do so. If health professionals perform the test they should always inform the patient about the result unless they are too ill to understand the information. In addition blood glucose testing time can be used as a teaching opportunity and an opportunity to assess the individual’s testing technique. The results of blood and urine tests are only useful if the tests are accurately performed. Monitoring 1: Blood glucose Key points • Follow correct procedure when performing tests. • Perform meter control and calibration tests regularly. • Clean and maintain equipment regularly. • Record and interpret results according to the clinical situation. The role of blood glucose monitoring in the care of diabetes Blood glucose monitoring provides insight into the effectiveness of the diabetes management plan. It enables direct feedback to the patient about their blood glucose. Some experts suggest the cost and time associated with blood glucose self-monitoring is not cost effective even when patients are taught to adjust their management regimen. For example the DiGEM investigators undertook a randomised control trial involving people with treated Type 2 diabetes over age 25 treated with diet or GLMs which showed no statistically significant difference in HbA1c at 12 months but there was a significant change in total cholesterol Farmer 2007. Subjective parameters such as quality of life and sense of control

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56 Care of People with Diabetes were not measured. Other researchers also show that people who monitor their blood glucose are younger at diagnosis and present with a higher HbA1c than people who do not test Franciosi et al. 2005 Davis et al. 2006. In contrast the ROSSO study Schneider et al. 2006 showed metabolic control improved in people with Type 2 diabetes who performed frequent blood glucose tests and demonstrated a 51 lower risk of death and a 32 lower risk of microvascular and macrovascular complications. In addition people who monitored were more aware of their blood glucose levels and sought advice from health professionals sooner. Likewise Karter et al. 2006 demonstrated improved HbA1c after home blood glucose testing was instituted in the Kaiser Permanente study. Other researchers show lower rates of self-blood glucose monitoring in men and people with low education level those who do not have health insurance in countries where equipment is not subsidised as well as those not on insulin those taking GLMs having less than two consultations with the doctor annually and not attending diabetes education programmes Centers for Disease Control and Prevention CDC 2007. These studies suggest there may be gender and age differences in the rates of blood glucose self-monitoring but the rates are similar in different countries. Nevertheless most management guidelines continue to recommend blood glucose self-monitoring as an integral part of the management plan. Testing frequency should be individualised depending on glycaemic control and health status in Type 2 diabetes but at least daily when insulin and/or GLMs are used. People with Type 1 should monitor at least TDS Canadian Diabetes Association 2008. Blood glucose testing is performed to: • Monitor the effectiveness of diabetes therapy and guide adjustments to the food plan OHAs/insulin dose exercise/activity mental well being and quality of life see Chapter 2. • Detect hyperglycaemia which can be confirmed by laboratory blood glucose tests and elevated HbA 1c levels a marker of the average blood glucose over the preceding three months and more recently A1c- derived average glucose. • Achieve blood glucose targets which has a role in preventing or delaying the onset of diabetes-related complications and maintaining independence and quality of life. • Diagnose hypoglycaemia including nocturnal hypoglycaemia which can present as sleep disturbances snoring restlessness or bad dreams. • Establish the renal threshold for glucose to determine the reliability of urine testing in those rare cases where people still test their urine glucose. • Achieve ‘tight’ control in pregnancy and thereby reduce the risks to both mother and baby. • Provide continuity of care following hospitalisation. Blood glucose monitoring is of particular use in: • Frequent hypoglycaemic episodes and hypoglycaemic unawareness. • Unstable or ‘brittle’ diabetes. • Managing illnesses at home and when recovering from an illness. • GDM pregnancy and in neonates born to women with GDM and diabetes. • Establishing a new treatment regimen. • Stabilising OHA and/or insulin doses:  patients with renal failure autonomic neuropathy cardiovascular or cerebrovascular insufficiency where hypoglycaemia signs can be masked or not recognized  during investigations such as angiograms and surgical procedures  detecting actual or potential medicine/medicine or medicine/herb interactions  during travel. Clinical observation In the home situation blood glucose testing enables the person with diabetes to take more responsibility for and control over their disease and is a tool they can use to maintain their quality of life. It is not a means by which health professionals control people with diabetes. It is only one aspect of an holistic individualised assessment see Chapter 2.

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Monitoring Diabetes Mellitus 57 The target blood glucose range and frequency of testing should be assessed individually when people with diabetes are in hospital. The aim is to achieve a blood glucose pattern as close to normal as possible. Generally accepted blood glucose targets are: pre-meal 5 mmol/L and two-hour post prandial 7.8 mmol/L IDF 2007. However the management regimen must target both fasting and post prandial blood glucose to achieve optimal control and reduce the risks associated with hyperglycaemia see Chapters 1 7 and 8. Hyperglycaemia in hospitalised people with and without diabetes is associated with more morbidity and mortality in general surgical IVU and cardiology settings Australian Diabetes Society ADS 2012. ADS guidelines generally recommend blood glucose range between 5 and 10 mmol/L in most situations but the individual’s needs must be considered. Increasing emphasis is being placed on reducing post prandial hyperglycaemia because it is associated with increased risk of retinopathy cardiovascular disease increased risk of cancer and impaired cognitive function in older people IDF 2007. Significantly elevated postprandial hyperglycaemia is present before Type 2 diabetes is diagnosed and partly accounts for why cardiovascular complications are frequently present at diagnosis. Management of postprandial hyperglycaemia is discussed in Chapters 5 and 8. Likewise glucose variability is also associated with diabetes complications and mortality therefore the aim is to try to reduce swings in blood glucose between hyperglycaemia and hypoglycaemia Chapter 7. The medicine regimen is often intensified when the individual is in hospital to reduce optimise metabolic control. Such intensification is associated with lower 30-day readmission/emergency presentation risk and lower HbA1c on outpatient follow-up Wei et al. 2013. Although the focus is on achieving optimal blood glucose control to prevent or delay the onset of diabetes complications optimal control is often not achieved. The person is usually blamed for not ‘complying’ with recommendations. However the progressive nature of Type 2 diabetes and clinical inertia also play a part Grant et al. 2004. Clinical inertia refers to health professionals recognising a problem but failing to act. Like ‘noncompliance’ clinical inertia is a derogatory term for a complex phenomenon where behaviours are influenced by factors such as competing demands in the clinical setting including time constraints and patients presenting with multiple problems that cannot all be addressed at the same time Parchman et al. 2007. However clinician inertia combined with patient non-adherence might increase the risk of poor control and may be mutually causative. Factors that influence blood glucose levels 1 Food: times of last food intake quantity and type of carbohydrate/fibre consumed in relation to meals and activity. 2 Exercise: timing with respect to food medication and insulin doses injection site type of exercise and blood glucose level when commencing exercise. 3 Intercurrent illness for example influenza urinary tract infection. 4 Medications used for diabetes control blood glucose: oral agents insulin. 5 Other medicines for example corticosteroids oral contraceptives beta blockers and non-prescription medications that contain glucose ephedrine pseudoephedrine or alcohol for example cold remedies and glucose lowering complementary medicines see Chapters 5 and 19. 6 Alcohol: type relationship to food intake amount consumed. 7 Insulin type injection site injection technique. 8 Complementary medicines/therapies for example glucose lowering herbs stress management techniques see Chapter 19. 9 Emotional emotional dwelling and physical stress – not only stress itself but medications used to treat stress. 10 Accuracy of monitoring technique. 11 Pregnancy in people with diabetes and gestational diabetes. 12 Childhood: erratic swings in blood glucose levels are common. 13 Adolescence: hormonal factors during adolescence can make control difficult. 14 Renal liver and pancreatic disease. 15 Other endocrine disorders for example thyroid disease Cushing’s disease and acromegaly. 16 Parenteral nutrition. 17 Obtaining the blood sample from unwashed fingers for example after the patient or health professional treated a hypoglycaemic event with oral glucose.

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58 Care of People with Diabetes Clinical observation Insulin absorption can be delayed if insulin is injected into an oedemateous or ascitic abdomen. The delayed absorption can affect the blood glucose level. The thigh or upper arm may be preferable sites in this instance. Guidelines for the frequency of blood glucose monitoring 1 In care settings capillary blood glucose tests should be performed only by adequately qualified health professionals or the person with diabetes. 2 Medical staff and sometimes diabetes educators are usually responsible for interpreting the results and adjusting the diabetes management plan. Over time many people with diabetes become expert at adjusting their insulin doses to account for carbohydrate intake Dose Adjustment for Normal Eating DAFNE and during illness and exercise. The following recommendations are guidelines only the policies and procedures of the employing institution should be followed and the regimen should be tailored to the individual’s needs and hospital setting for example frequent monitoring is required when IV insulin infusions are used and in surgical and ICU settings. Suggested protocol in hospital settings. Blood glucose tests performed before meals and before bed e.g. 7 a.m. 11 a.m. 4 p.m. and 9 p.m. in order to obtain a profile of the effectiveness of diabetes therapy. Occasionally urine glucose will be measured at these times for 24 hours to establish the renal threshold. As indicated testing two hours after food especially in Type 2 diabetes may be preferable in order to provide information about glucose clearance from the blood stream after a meal as an indicator of cardiovascular risk. Blood glucose tests may be performed at 2 a.m. or 3 a.m. for two to three days if the blood glucose is high before breakfast and there is a possibility of nocturnal hypoglycaemia see Chapter 6. Blood ketones should be monitored in all patients with Type 1 diabetes and in Type 2 people during severe stress for example surgery infection and myocardial infarction if blood glucose tests are elevated. Urine ketone tests might still be used in some places but are a less reliable indicator of ketosis than blood ketones. Each person’s needs should be assessed individually and the testing schedule tailored to individual requirements where work routines and staffing levels allow. One way to achieve an individualised monitoring regimen is to allow the patient to perform their own blood glucose tests where their condition permits them to do so. Regimen for patients on insulin. Initially for 48 hours monitor at 7 a.m. 11 a.m. 4 p.m. and 9 p.m. to assess the effectiveness of the prescribed insulin therapy. Review after 48 hours and alter the testing frequency if indicated. If the insulin regimen is altered review again after 48 hours. Note: The timing of blood glucose monitoring depends on the insulin regimen and the action profile of the prescribed insulin see Chapter 5. Patients using insulin pumps and those on IV insulin infusions require more frequent monitoring. Patients on oral GLM. Initial monitoring as for insulin-treated patients. Review after 48 hours and reduce monitoring frequency to twice daily daily or once every second or third day alternating the times of testing as indicated by the level of control and the general medical condition of the patient. Patients managed on diet and exercise. Initially twice daily monitoring decreasing to daily or once every second or third day unless the patient is having total parenteral nutrition TPN diagnostic procedures is undergoing surgery or is actually ill. In the acute care setting patients are usually ill and require at least 4-hourly monitoring. The frequency can often be reduced in rehabilitation mental health and care facilities for older people and in the end stages of life. Special circumstances. These might require a prescription from the medical staff. They include: 1 Insulin infusion: tests are usually performed every 1–2 hours during the infusion and reviewed every 2 hours. Reduce to 3–4 hourly when blood glucose levels are stable see Chapter 5.

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Monitoring Diabetes Mellitus 59 2 People on corticosteroid therapy because these medicines induce insulin resistance and increase hepatic glucose output which might be greater in people who already have insulin resistance and hyperglycaemia and may be a risk factor for hyperosmolar states see Chapters 7 10 and 18. Ketones should also be monitored in Type 1 diabetes because some corticosteroids also induce lipolysis and increase the risk of ketoacidosis. a Non-diabetic patients: regularly screen for hyperglycaemia. The effects on blood glucose depend on the formulation dose dose frequency and duration of action and the response of the individual to the particular preparation used. Often the blood glucose increases during the day and is higher in the afternoon Dunning 1996 Diabetes UK 2012. Oral preparations have a greater impact on blood glucose than IV preparations which usually do not cause a great rise in the blood glucose. b People with diabetes: see protocols in the preceding sections ‘Regimen for patients on insulin’ ‘Patients on GLMs’ or ‘Patients managed on diet and exercise’. 3 TPN guidelines suggest: a Routine blood glucose testing for the first 48 hours: 7 a.m. 11 a.m. 4 p.m. and 9 p.m. until the patient is stable on TPN then revert to protocol in section Regime for patients on insulin or Patients on oral hypoglycaemic agents. b Monitor blood for ketones: 7 a.m. 11 a.m. 4 p.m. and 9 p.m. Practice point Never prick the feet of an adult because it causes trauma and increases the risk of infection. Heel pricks can be performed on babies. Blood glucose meters Blood glucose meters are devices used to monitor blood glucose in the home or at the bedside in hospital. The first capillary blood glucose meter was introduced in 1974. Over the following decades the technology of both meters and test strips has changed rapidly. Staff should become familiar with the system used in their place of employment. Consult the diabetes educator/specialist team or manufacturer for specific advice. Where meters are used a blood glucose meter quality management programme with a centralised coordinator is desirable Figure 3.1. As part of such a programme it is recommended that: • Individual nurses and other users demonstrate competence to use the system in operation. • Meters are subject to regular control testing and calibration according to the manufacturer’s recommendations and are calibrated as required usually when a new pack of strips is opened and are appropriately cleaned and maintained and that these processes are documented. • A procedure for dealing with inaccurate results and meter malfunction is in place. Most meters can be programmed to read in mmol/L or mg/dL which is used in the United States. Most meters also store a record of blood glucose tests and other information that can be downloaded into computer software programs that enable the data to be displayed in a range of ways. Increasingly they include other functions that enable personalised information to be entered and decision aids to help people with diabetes manage their diabetes. Sequential tests with control high and low solutions Both tests within limits Proceed with patient testing Both tests exceed limits • Check expiry dates of strips and control solutions • Check calibration if appropriate • Review operator technique

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60 Care of People with Diabetes Incorrect technique Repeat tests in duplicate Supervisor should with new vials of control evaluate and explain 3. Proceed with patient testing for reporting faults Figure 3.1 An example of a quality control flow chart for checking blood glucose meters. Modern meters are small and light easy to operate and only require a very small amount of blood. Particular meters are designed specifically for particular target audiences such as children and older people who have different requirements. For example large result display screens and ‘talking’ meters for vision- impaired people. Test strips require a minimal amount of blood. Therefore many of the systems errors associated with early meters have been eliminated. However inaccuracies still occur and are mostly due to technique errors. Meter technology changes rapidly and health professionals need to be aware that the system in use in the hospital may be different from the system the person uses at home and should be aware that: • Although blood glucose readings obtained from the fingertip most closely correlate with arterial glucose there are usually small differences in test results between capillary and venous blood. • There are often small differences between blood glucose tests performed on different meters at the same time. Several factors account for the difference such as squeezing the finger to obtain a second drop of blood. Usually a difference of 3 is acceptable. People may need to be reassured that their meter is not at fault. The individual’s needs and understanding and likely reaction need to be considered before comparing results on different meters in the presence of the person with diabetes. • Alternative site testing from sites other than the fingertip such as the forearm abdomen and thigh are available and cause less discomfort but only yield a small quantity of blood 3 mL. However blood glucose levels vary among different sites. For example there is a lag in increases and reductions in blood glucose by up to 30 minutes at the forearm compared with the fingertip which can lead to delay in detecting and treating hypoglycaemia Jungheim Koschinsky 2002. Less variation occurs between the palm and ball of the thumb. • Heat and light affect strip accuracy. Correct technique solution correct technique Repeat tests T ests exceed limits Repeat tests with a new batch of strips Check calibration code if appropriate T ests within limits T ests exceed limits Discontinue use of the instrument Follow procedure Within limits Discard problem solution Proceed with patient testing 1 . Examine storage procedure with strips and solutions 2 . Discard the faulty batch of strip s

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Monitoring Diabetes Mellitus 61 Practice point ‘Glucometer’ is not a generic term for blood glucose meters. It was the name of a specific meter that has not been available on the market for at least 10 years. A more appropriate term is ‘blood glucose meter’ or use the name of the particular meter. Continuous glucose monitoring systems The technology to enable continuous glucose monitoring is developing rapidly towards the ultimate ‘closed loop system’. Fingerprick blood glucose tests may miss many hypoglycaemic and hyperglycaemic levels: continuous blood glucose monitoring systems enable ‘real-time’ continuous blood glucose levels to be identified. Sampling generally occurs from interstitial and tissue sites. Interstitial glucose concentrations are often lower than capillary concentrations during the night compared with capillary glucose Monsod et al. 2002. However continuous monitoring enables the trend toward hyperglycaemia or hypoglycaemia trend analysis to be monitored and preventative action to be taken. Continuous glucose monitoring system CGMS The original CGMS system consists of a pager-sized glucose monitor disposable subcutaneous glucose sensor and a cable connecting these two components to a com munication system that stores data which is downloaded into a computer software program that enables the results to be displayed in graph form. Glucose concentrations are measured every 10 seconds: an average of those values is saved in the meter every five minutes for 72 hours. CGMs is usually performed over three days. Glucose targets can be assigned the duration and frequency of hypo- and hyperglycaemic episodes and modal time determined using modern software. This provides important information that can help health professionals and patients understand the differences between their home blood glucose testing results and HbA1c and detect unrecognised hypoglycaemia. Previously CGMS was primarily used to determine blood glucose profiles before using insulin pumps during GDM in paediatrics and to detect unrecognised hypoglycaemia rather than for routine home monitoring because of the cost. CGM meters are still more expensive than other blood glucose meters but the technology has advanced significantly. Four CGM systems were recently introduced and show real time glucose levels on the monitor every five minutes and have hypo- and hyperglycaemia alarms. A significant advantage of CGM is the ability to monitor glucose variability and adjust diabetes management regimen to reduce it because glucose variability is associated with increased risk of complications and mortality Chapter 8. HbA1c does not measure glucose variability. The four CGMS meters are not all available in every country at the time of writing. The four CGMs meters are: • Freestyle Navigator Abbott Diabetes Care. • Gardian Real-Time Medtronic MiniMed. • Dexcom SEVEN Dexcom. • GlucoDay Menarini. A competent trained team is essential to correctly attaching CGMS explaining the system to the individual and ensuring they are competent to operate it. Currently CGM is not recommended for routine use in people with diabetes SIGN 2010. A system that links CGMS and an insulin pump has been developed which makes personalised intensive management possible for those who can afford it. The CGMS system is attached to the body or inserted into the body. Blood glucose information is transferred to the insulin pump which controls the insulin dose Kim et al. 2012. Interpreting different results Patients often comment that their blood glucose results are different from the results obtained using the meter in the outpatient clinic and doctor’s rooms or at when they retest their blood glucose after a few minutes. Blood glucose meter tests only reflect individual points in time and may not detect fluctuations in blood glucose especially post prandially and overnight. CGMS is useful to detect such fluctuations.

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62 Care of People with Diabetes Different meters give different results even when the tests are performed correctly and close together in time but generally should not differ by more than 5. Squeezing the finger to obtain a drop of blood can dilute the sample with tissue fluids and affect the accuracy of the test result. Likewise capillary glucose values are likely to differ from laboratory values reported on venous blood. Capillary glucose is 5 higher than venous glucose. Laboratory values can be affected by glycolysis. Glucose in whole blood decreases by 5–7 per hour because of the glycolytic enzyme activity in red blood cells. Thus venous samples should be sent to the laboratory promptly or kept at 4 °C for short periods if it is not possible to transport the sample immediately. Preservatives such as fluoride in blood tubes slow but do not stop glycolysis in blood samples. People are often confused by the different ways of reporting blood glucose mmol/L or mg/dL and HbA1c and mmol/mol. Meter blood glucose results may not give an accurate indication of the average blood glucose level or of the minute fluctuations that occur minute-by-minute. Discrepancies between blood glucose meter readings and HbA1c could be used as an opportunity to explore testing technique other factors that affect the results of both testing methods and the individual’s feelings about diabetes and its management. The differences may be a sign of underlying stress especially in adolescents Rose et al. 2002 see Chapter 13. Practice point Incorrect operator technique inadequate quality control testing incorrect meter calibration and using out-of-date test strips are the major causes of inaccurate results using blood glucose meters. Reasons for inaccurate blood glucose results Inaccurate blood glucose readings can occur for the following reasons: 1 Meters and test strips • using the incorrect strip for the meter • using the incorrect calibration or code although several meters no longer need to be coded • using an unclean meter • low or flat battery • inserting the strip incorrectly or facing the wrong way • insufficient blood on the strip will give a false low reading with some older meters • quality control tests/calibration are not performed • strips used after the expiry date • failure to wash hands before testing especially if sweet substances have been handled • humidity and high temperatures affect some meters and/or strips. If in doubt repeat the test or confirm biochemically. Practice points • It is not necessary to swab the finger with alcohol prior to testing because it can dry the skin. Alcohol swabbing does not alter the blood glucose results Dunning et al. 1994. • The hands should be washed in soap and water and dried carefully before testing especially if the person has been handling glucose for example in an accident and emergency department/casualty when the person presents with hypoglycaemia. Monitoring blood ketones A 10-second capillary blood ketone testing meter is a useful adjunct to blood glucose testing for people with Type 1 diabetes during illness and enables them to detect ketosis and institute treatment or seek a health professional early to

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Monitoring Diabetes Mellitus 63 prevent ketoacidosis see Chapter 7. Blood ketone testing is increasingly being used in the clinical setting for the same reasons as well as giving an indication of the adequacy of the treatment during illness Wallace et al. 2001 ADS 2012. Blood ketone monitoring is required during sustained hyperglycaemia and can reduce attendances at emergency departments for example SIGN 2010 quoted a 50 reduction in the need for a hospital admission for DKA in people testing blood ketones compared with people using urine ketone testing but the event rates in most trials are small SIGN 2010. Thus many guidelines still indicate there is not enough evidence to recommend routine ketone testing in Type 1 Type 1 or Type 2 diabetes. However there is enough clinical experience to suggest it is warranted in acute illness including in hospital. Blood ketones are raised after fasting in the morning during starvation may indicate a UTI in non-diabetic patients after hypoglycaemia not due to excess insulin some inborn errors of metabolism and ketoacidosis which is most commonly due to diabetes. Ketosis characteristic of untreated Type 1 diabetes and can occur in LADA and Type 2 diabetes. The main ketone bodies are : • Acetoacetate which is an end product of fatty acid metabolism. • Acetone which is formed from spontaneous decarboxylation of acetoacetate. Acetone is volatile and is expelled in expired air. It is the ketone responsible for the acetone smell of ketoacidosis. • Beta-hydroxybutyrate B-OHB which is a reduced form of acetoacetate and the major ketone formed in acidosis. Acetoacetate and beta-hydroxybutyrate are important energy substrates for many tissues especially the brain particularly during fasting and inadequate food intake. Blood ketone testing for B-OHB is more reliable than urine ketone testing Fineberg et al. 2000. Currently available urine ketone test strips do not measure B-OHB and laboratory ketone testing often does not do so either unless it is specifically requested. The ketone meter measures capillary B-OHB which is the most abundant ketone body and the best guide to the patient’s metabolic status: Levels 1 mmol/L require further action for example extra insulin levels 3 mmol/L require medical assessment. Blood glucose testing checklist Nursing actions 1 Assemble materials and prepare environment according to hospital policy and testing system used: • test strip removed from vial and cap replaced immediately or open foil package • dry cotton or rayon ball or tissue to blot the test site if required • disposable fingerpricking device or a device with disposable end cap to avoid the possibility of cross-infection from blood left on the device. 2 Explain procedure to patient. Obtaining a drop of blood 3 Wash patient’s hands with soap and warm water dry carefully. 4 Choose a site on any finger near the side or tip. Avoid using the pad of the finger where nerves and arteries are concentrated: it is more painful. 5 Prick finger firmly using a fingerprick device. 6 ‘Milk’ along the length of the finger to well up blood at the puncture site. Avoid squeezing too hard. 7 Allow the drop of blood to fall onto the strip or be drawn up by capillary action depending on the type of meter and strips in use. 8 Dispose of sharps into an appropriate sharps container. Documenting the results 1 Record test results on diabetes chart and in any other pertinent record. 2 Communicate results to appropriate person for example the doctor and the patient. Tips

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64 Care of People with Diabetes a Warm hands bleed more readily. b If peripheral circulation is deficient obtaining blood can be difficult. Trap blood in fin gertip with one hand by milking the length of the finger and applying pressure with finger before pricking. c Excess squeezing can dilute the red cells with plasma and lead to inaccurate results. d Check with biochemistry result if the result does not match the clinical picture. Table 3.1 Blood ketone levels and potential management. It should be noted that these levels are an indication and are not evidence-based Data from Laffel L. Kettyle W. 2000. Blood ketone level B-OHB Potential management Normal 0.5 mmol/L Elevated 0.5–1.5 mmol/L and blood glucose ≥16 mmol/L Ketosis risk/impending ketosis insulin dose may need to be increased Food intake might be low due to fasting poor intake or anorexia Acidosis 1.5 mmol/L and blood glucose 16 mmol Ketones established and ketoacidosis risk medical review required Insulin required possibly as an IV infusion Infection could be present People with Type 1 diabetes are advised to test for ketones during illness hyperglycaemia pregnancy if polyuria polydipsia and lethargy are present and if they have abdominal pain. Abdominal pain is common in ketoacidosis and usually resolves as the ketosis clears. If it persists it could indicate an abdominal emergency see Chapter 7. Type 1 patients with hyperglycaemia and HbA1c 8.5 in association with B-OHB are insulin deficient and at risk of ketosis. Normal blood B-OHB is 0–0.5 mmol/L. Table 3.1 depicts normal and abnormal ketone levels and suggests the management required. Testing for ketones is important during illness in: • all people with Type 1 diabetes • people with Type 2 who are severely ill • during fasting • after severe hypoglycaemia:  severe stress  TPN feeds high in glucose or lipids  in the operative period. The rate of fall of B-OHB using blood ketone strips can potentially avoid these situations and improve self-care and enable preventative action to be taken early to avoid ketoacidosis. Blood ketone strips can be used as an indicator of the adequacy of the treatment in acute care settings. Clinical observation Lower than actual capillary blood glucose levels can be recorded using some blood glucose meters in the presence of moderate-to-heavy ketosis. The reason for this finding is not clear. As a consequence health professionals and patients can underestimate the severity of the hyperglycaemia miss developing ketoacidosis and delay appropriate treatment. Practice points

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Monitoring Diabetes Mellitus 65 1 Ketones are present in non-diabetic individuals during fasting and can be detected in 30 of first voided morning urine specimens of pregnant women. 2 Ketone test strips using nitroprusside reagents used on urine test strips give false- positive ketone results in the presence of sulphydryl drugs such as captopril. 3 Insulin replacement corrects the acidosis by facilitating the conversion of B-OHB into acetoacetate and indicates the ketosis is resolving. However urine ketone tests can indicate the ketones are still high. That is urine ketone clearance lags behind actual blood ketone levels. 4 Urine ketone test strips give false-negative results when they have been exposed to the air for some time have passed their expiry date and if the urine is highly acidic such as in a person taking large doses of vitamin C. Monitoring 2: Urine glucose Key points Urine glucose testing is not recommended except in countries that do not have ready access to blood glucose meters or for people who cannot afford to buy a blood glucose meter. Meters are sometimes supplied without charge in some countries but strips have to be purchased. If it is used: • Establish renal threshold to determine the reliability of urine tests. • Fluid intake hydration status urine concentration and time since last voiding affect results. • Double voiding is unnecessary. • However a full urinalysis can provide important clinical information such as the presence of infection which is often silent in people with diabetes haematuria and indicates jaundice. In the presence of normal kidney function glycosuria is correlated to the blood glucose concentration. Glycosuria occurs when the tubular maximum reabsorption is exceeded usually around 8–10 mmol/L blood glucose. The test reflects the average glucose during the interval since the person last voided rather than the level at the time the test is performed. This is called the renal threshold for glucose and varies within and between individuals. The renal threshold may be changed by: • increasing age • renal disease • long-standing diabetes. Therefore: • The blood glucose can be elevated without glycosuria being present. • Traces of glucose in the urine can indicate loss of control. • The renal threshold can be low in children and glycosuria present when blood glucose is normal. It is important to establish the renal threshold during a period of good control normoglycaemia by simultaneously testing blood and urine glucose. Practice points

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66 Care of People with Diabetes • Urine glucose monitoring is not an accurate reflection of the blood glucose level. In addition it does not give warning of impending hypoglycaemia. • A negative urine glucose finding does not indicate hypoglycaemia. • Double voiding prior to testing is not necessary. Indications for urine glucose tests 1 If a person refuses to monitor their blood glucose or cannot afford the equipment. 2 When the aim is to avoid glycosuria. Monitoring kidney function Diabetic nephropathy is the leading cause of end-stage renal disease thus early identi fication of declining renal function is imperative see Chapter 8. Twelve- and 24-hour urine collections are used to monitor kidney function and detect early kidney damage by monitoring creatinine clearance rates and microalbumin excretion rates. Microalbuminuria reflects abnormally elevated albumin level not detectable on urine dipsticks. It is the earliest marker of the onset of kidney and cardiovascular damage and predicts deteriorating renal function Krolewski et al. 1995. Up to 30 of newly diagnosed people with Type 1 diabetes already have high urine albumin levels of these 75 have microalbuminuria and 25 have overt nephropathy. People with Type 2 in the MICRO-Hope study HOPE 2000 had a 20 risk of progression from normal to microalbuminuria to nephropathy over 5 years which is similar to Type 1. Early diagnosis and treatment can delay the onset by 24 years and decrease the need for dialysis and increase life expectancy Borch-Johnsen et al. 1993. Seventeen per cent of people with essential hypertension develop proteinuria despite satisfactory treatment Ruilope et al. 1990. Methods of screening for microalbuminuria Several methods are available and include: • Timed 12- or 24-hour urine collections. • Spot urine tests. The first voided morning specimen is often used for initial screening Jerums et al. 1994. • Random urine tests using dipsticks or automated urine analysers to measure microalbumin and calculate the microalbumin–creatinine ratio normal level in males is 2 mg/mmol and 2.8 mg/mmol in women. These tests should be negative for protein Sheldon et al. 2002. • Micral-Test dipstick tests Boehringer Mannheim GmbH Mannheim Germany is an immunochemical- based urinary dipstick used to test for microalbuminuria and can be used in the ward situation. Compared to radioimmunoassays Micral-Test has a sensitivity of 92.2 specificity of 92.3 and a positive predictive value of 37.8 in predicting an albumin excretion rate 20 m/minute Jerums et al. 1994. However it is not often used clinically in Australia. • Glomerular filtration rate GFR. The degree of reduction in the GFR is linked to the development of renal disease. GFR is used as the index to classify the severity of renal disease see Chapter 8. • Serum creatinine which is used as a surrogate marker of GFR is relatively inaccurate Chadban et al. 2003. Significantly serum creatinine is not reliable in older people especially those with lean muscle mass who can have creatinine in the normal range despite severely compromised renal disease Mathew 2003. • Estimated GFR e-GFR is calculated using a predictive equation that uses serum creatinine age and gender. It is less accurate in Chinese people and possibly other Asian peoples and Indigenous Australians Zuo et al. 2005. In the US the Modification of Diet in Renal Disease MDRD is a valid method of determining e-GFR and classifying renal disease National Kidney Foundation 2002. e-GFR may be unreliable in the following situations:  acute changes in kidney function  people on dialysis  high protein and high vegetable diets and those who take creatinine supplements  skeletal muscle diseases such as paraplegia and amputees.  those with high muscle mass  in the presence of severe liver disease  when the e-GFR is 60 mL/min/1.73 m 2

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Monitoring Diabetes Mellitus 67  children 18 years  Asian peoples  Maori and Pacific Islander peoples  Aboriginal and Torres Strait Islander peoples. Microalbuminuria is diagnosed when the urine albumin level is 30 mg/dL and is expressed as the quantity of albumin excreted in a given time 20 m/minute or as a concentration 20 m/L urine. Most experts prefer the albumin–creatinine ratio because the other tests can be affected by the concentration of the urine. Nurses have a role in screening and detecting declining renal function and educating the person about appropriate preventative measures. If timed urine collections are needed the procedure for collecting the urine should be explained to the patient carefully. Written instructions should be supplied if the collection is to be performed at home. Collections are best obtained at a period of good control and normal activity not during illness or menstruation therefore the urine is often collected on an outpatient basis. The opportunity can be taken during a hospital admission to collect 12- or 24-hour timed urine collections when people repeatedly fail to collect them as outpatients. In some cases the first early morning voided specimen will be collected 50 mL. Ensure the correct containers are used for the collection and the specimen is correctly labelled. Monitoring 3: Additional assessment In addition to blood and urine testing diabetic status is assessed by: 1 Psychological and emotional health and wellbeing Chapter 15. 2 Self-care capacity. 3 Regular weight checks. Height is also required to calculate BMI. Waist circumference is preferred and sometimes arm circumference in older people. 4 Regular physical examination especially: • blood pressure lying and standing to detect any postural drop that could indicate the presence of autonomic neuropathy • eyes retina and visual acuity • cardiac status • feet • kidney function • driving safety especially in older people. 5 Regular education about: • diet • self-monitoring techniques • injection sites • general diabetes information especially new technology and research findings that need to be discussed in the context of the individual see Chapter 16 • changes to diabetes care as a result of research. Specific age groups such as children Chapter 13 and older people Chapter 12 require additional assessment such as physical and mental functioning and psychological status Chapter 15. Practice point Normal ranges for the tests described differ among laboratories depending on the assay methods used. It is helpful if people attend the same pathology service to have blood and urine tests performed.

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68 Care of People with Diabetes Nursing responsibilities 1 To have a basic knowledge of the tests in order to be able to explain them to the patient. 2 Ensure patients who are required to fast are given appropriate written instructions before the test about their medications and any other preparation required. 3 To ensure the correct collection technique appropriate amount of blood and correct tubes are used. 4 Mix the sample by inverting the tube two or three times if an anticoagulant tube is required. Vigorous shaking causes haemolysis of red blood cells which affects the results. 5 To ensure the specimen reaches the laboratory within 30 minutes of collection or be refrigerated to prevent glycolysis occurring and consequent inaccurate results. 6 To ensure results are available for medical evaluation. 7 To know the effects of illness and stress on the results of the test. 8 To ensure the appropriate sterile blood collection technique is used. 9 To ensure appropriate disposal of used equipment and to protect themselves from needlestick injury. 10 To ensure patients are given their medication and something to eat after completing tests when fasting is required and that they are informed about when to recommence any medications that were temporarily stopped and the doses to take. Blood glucose Venous glucose is measured to: • Screen for and diagnose diabetes. • Monitor effectiveness of and determine the need for glucose lowering medicines and the dose and dose frequency. • Evaluate glycaemic control. • Confirm high/low capillary glucose result. Glycosylated or glycated haemoglobin HbA 1c It is most useful to have the HbA1c result at the time the person is assessed by the doctor/ diabetes educator. Blood can be drawn from a vein and measured in the laboratory before the clinic/doctor visit so the result is available at the time of the consultation. Alternatively blood can be drawn from a fingerprick sample at the time of the visit using devices such as the DCA 2000 Bayer analyser. Circulating blood glucose attaches to the haemoglobin in the red blood cells and undergoes an irreversible non- enzymatic interaction with amino groups of lysine and valine residues in haemoglobin Amadori reaction whereby the glucose becomes permanently fixed to the haemoglobin glycosylation. The glycosylated haemoglobin HbA 1c A1c in the US can be measured and quantified to give an indication of the average blood glucose concentration over the preceding 3 months normal 4–5.9 and to predict risk of long-term diabetes complications Bloomgarden 2007 Kilpatrick et al. 2007. Currently four main assays and 20 different measurement methods are used that measure different glycated products and report different units HbA1c HbA1 and total GHb Colman et al. 2008. The four assay methods are: ion-exchange chromatography electrophoresis affinity chromatography and immunoassay. Fasting prior to obtaining the blood sample for HbA1c is not necessary. Tests are usually performed at least three months apart but can be done sooner to gauge the effect of a treatment modification and in research. Kirkpatrick et al. 2007 pointed out that HbA1c is a proxy measure of average blood glucose and can be misleading because individuals are higher or lower glycosylators at specific mean blood glucose levels which emphasises the importance of considering the individual and the overall clinical picture. Current assay methods use a mixture of glycated haemoglobins to determine the HbA 1c. Representatives from the American Diabetes Association The European Association for the Study of Diabetes the International Diabetes Federation and the International Federation of Clinical Chemistry and Laboratory Medicine IFCC have been discussing methods of standardising HbA1c measurement for a number of years and released a consensus statement in Milan in 2007 Consensus Committee 2007. Key recommendations were: • Standardising the method of measuring HbA1c and the reference system used to report results.

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Monitoring Diabetes Mellitus 69 • The IFCC reference system is the only currently valid method of measuring HbA1c and should be used as the basis to standardise HbA1c measurements. • The results should be reported in IFCC units mmol/mol and derived national Glycohaemoglobin. Standardisation Program Units NGSP should be calculated using the IFCC-NGSP master equation. • Laboratories should be able to maintain a CV 3 at HbA1c between 6 and 9 and manufacturer’s assays should have a CV 5 Colman et al. 2008. • If the ongoing ‘average plasma glucose study’ using frequent capillary glucose measurements and continuous glucose monitoring due to be published in early 2008 fulfills its priori-specified criteria an A1c-derived average glucose value ADAG should also be reported Nathan 2007. The ADAG value is calculated from the individual’s A1c result to deduce an estimate of their average blood glucose O’siordan 2007. • That clinical guidelines be revised and glycaemic targets be expressed as IFCC units derived NGSP units and ADAG. Consequently education programmes for health professionals and people with diabetes are being developed and a smart phone app is available to convert HbA1c to mmol/ mol the new measurement units. Glycaemic targets should not be considered independently of other risk factors for complications such as hyperlipidaemia hypertension and smoking age and comorbidities. HbA1c targets differ slightly among various guidelines. It is generally accepted that targets should be: • As low as possible to reduce the likelihood of microvascular complications. Most recommend 6.5 or 7 for most people with Type 2 diabetes. • Individualised for specific patients after discussing the risks and benefits with them. For example children older and frail people and those with limited life expectancy might require higher targets 8 and those at very high risk of microvascular complications may need lower targets range 7–7.5. • Avoid adverse events such as frequent hypoglycaemia. Practice points • People who experience frequent hypoglycaemic episodes may have a low HbA1c that might not reflect their complication risk. • HbA1c results should be evaluated as part of the total clinical picture and not viewed in isolation. • HbA1c does not represent the blood glucose profile but gives an average level. It is considered to be the ‘gold standard’ for monitoring metabolic control. Table 3.2 lists some factors that might affect HbA1c results. Fructosamines The fructosamines are a group of glycosylated blood and tissue proteins that reflect the average blood glucose levels within the preceding three weeks. Fructosamine results can be lower in patients with low serum albumin cirrhosis of the liver or haemoglobinopathies. Table 3.2 Non-glycaemic factors that can affect results of glycosylated haemoglobin assays. False high False low

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70 Care of People with Diabetes Chronic alcohol abuse Foetal haemoglobin Hyperlipidaemia Hyperbilirubinaemia Renal failure Splenectomy Anaemia Abnormal haemoglobins such as HbS HbC HbD found in some ethnic groups Chronic blood loss Haemolysis Haemorrhage Recent blood transfusion Fructosamine estimations are not performed very often but they are useful for monitoring: • diabetes during pregnancy • initial response to diabetes medication • patients with chronic anaemia • patients with haemoglobinopathies. Serum lipids Serum lipids are usually elevated if the blood glucose is elevated. Three classes of lipids are measured as shown with the target range in brackets: 1 Cholesterol 4.0 2 Triglycerides 1.5 3 Lipoproteins: • very low-density lipoprotein VLDL • low-density lipoprotein LDL 2.5 • high-density lipoprotein HDL 1.0. Although it is generally accepted that fasting blood lipid levels are most useful recent research suggests non-fasting levels correlate more closely with cardiovascular risk Bansal et al. 2007 Vardo et al. 2007. However there are many forms of hypertriglyceridaemia and more research is needed to determine the exact relationship with atherosclerosis. High lipids especially elevated triglycerides and LDL and low HDL is a common lipid profile in people with poorly controlled Type 2 diabetes which may be secondary to hyperglycaemia and is a clinical useful measure of the need for lipid-lowering medications such as fibrates fish oil concentrates or nicotinic acid depending on the type of lipid abnormality present see Chapter 5. Alcohol should not be consumed for 24 hours before the blood sample for serum lipid measurements is taken. C-peptide C-peptide is the connecting peptide which determines the folding of the two insulin chains during insulin production and storage in the pancreas. It splits off in the final stages and can be measured in the blood. It is used to measure endogenous insulin production to determine the type of diabetes along with various antibodies see Chapter 1 if it is not clear in the clinical presentation. C-peptide is present in normal or elevated amounts in Type 2 diabetes indicating that insulin is being produced and that diet and/ or OHAs with exercise could achieve acceptable control. However progressive beta cell loss occurs in Type 2 diabetes and C-peptide levels fall proportionally. C-peptide is absent or low in people with Type 1 diabetes and can be a useful indicator in slow onset Type 1 diabetes LADA occurring in adults Cohen 1996 see Chapter 1. C-peptide is not changed by injecting exogenous insulin. Fasting results are most useful. Islet cell antibodies Islet cell antibodies ICA are found in most newly diagnosed people with Type 1 diabetes indicating that diabetes is an autoimmune disease. The beta cells of the pancreas are the specific target in diabetes and other pancreatic functions are not affected. In the laboratory impaired insulin release can be demonstrated when ICA are present but the clinical implication is still unclear.

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Monitoring Diabetes Mellitus 71 ICA are present in the prediabetic state before the disease is clinically obvious. They can also be present in close relatives who are at high risk of developing diabetes if they have ICA. GAD antibodies are also present in 80 of people with Type 1 diabetes and enable it to be distinguished from Type 2 diabetes Cohen 1996 see Chapter 1. Creatinine clearance and urea As indicated creatinine clearance is used to estimate renal function. It is also used to determine nutritional status in relation to protein especially during TPN and continuous ambulatory peritoneal dialysis CAPD. An increase in the blood urea nitrogen BUN may indicate impaired renal function however the BUN can also be increased if the patient is dehydrated has internal bleeding or is on steroids. Anorexia a low protein diet and fasting can lead to a decrease in urea. Self-care The key aspects of self-care are discussed in Chapter 16. Generally assuming responsibility for self-care is an iterative process that falls into three main categories: 1 Focusing on diabetes after diagnosis to acquire the knowledge and skills master the self-management tasks and make life adjustments needed to perform diabetes self-care which involves individuals and their family/carers. It takes time to accept diabetes and master these significant life changes. Some people take a long time others adapt quickly depending on social environmental and a range of other factors. 2 Activating resources which encompasses being able to identify relevant resources and using them effectively to support their self-care activities. Resources might be family friends health professionals Internet and other media as well as local resources such as libraries churches meals on wheels and transport. 3 Living with diabetes: people cope with diabetes and successfully integrate it into their lifestyle and grow as individuals Schulman-Green et al. 2012. This essential stable phase can easily be disrupted by life events and when a complication develops and the person needs to readapt. Nurses can ask four simple questions to help make a decision about an individual’s diabetes self-care capacity: 1 Does the individual have the knowledge and skills to manage their diabetes to the best of their ability 2 Has the individual access to appropriate resources equipment support and health professional advice 3 Is the individual satisfied with their life at present 4 Are their cultural issues that need to be considered Nurses are in an ideal situation to help determine the barriers to optimal self-care and potential medicine non-adherence Chapter 5. Barriers might be physical financial/ economic psychological cognitive health literacy/numeracy social and environmental Baumann Dang 2012. Motivational interviewing active listening reflecting clarifying being present in the moment fully focused on the individual and their story and involving the individual in making management decisions and setting goals and targets is essential. The annual review The annual review is a structured nursing and medical review undertaken in general practice to: • review management goals • assess diabetes complication status • determine whether referral to one of more specialists is warranted. • revise the immunisation schedule • undertake other important monitoring process as indicated Diabetes Australia/ Royal Australian college of General Practitioners 2011/12.

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72 Care of People with Diabetes Many of the assessments discussed in this chapter are encompassed in the annual review. References Australian Diabetes Society ADS 2012 Position statement individualization of HbA1c targets for adults with diabetes mellitus. ADS Canberra. Bansal S Buning S Rifai N. et al 2007 Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. Journal of the American Medical Association 18 298 309–316. Baumann L. Dang T. 2012 Helping patients with chronic conditions overcome barriers to care. Nurse Practitioner 37 3 32–38. Bloomgarden Z. 2007 Glucose variability. Comment on sessions presented during the 67th American Diabetes Association Scientific Sessions June 22–26 Chicago Illinois. viewarticle/560754 accessed January 2008. Borch-Johnsen K. Wenzel H. Vibert G. Mogensen C. 1993 Is screening and intervention for microalbuminuria worthwhile in patients with IDDM British Medical Journal 306 1722–1725. Canadian Diabetes Association 2008 Reduce your risk of serious complications associated with diabetes. www.canadiandiabetes accessed on 9 January 2008. Chadban S. Briganti E. Kerr P. 2003 Prevalence of kidney disease in Australian adults: the AusDiabe kidney study. Journal of the American Society of Nephrologists 14 7 Suppl. 2 S121–S138. Cohen M. 1996 Diabetes: A Handbook of Management. International Diabetes Institute Melbourne. Colman P. Goodall I. Garcia-Webb P. Williams P. Dunlop M. 2008 Glycohaemoglobin: a crucial measurement in modern diabetes management. Progress towards standardization and improved precision of measurement. EMJA colman. html acessed February 2008. Consensus Committee 2007 Consensus Statement on the Worldwide Standardisation of the Haemoglobin A1c Measurement. The American Diabetes Association European Association for the Study of Diabetes International Federation of Clinical Chemistry and Laboratory Medicine International Diabetes Federation. Diabetes Care 30 2399–2400. Davis T. Bruce D. 2006 Is self-monitoring of blood glucose appropriate for all Type 2 diabetic patients The Freemantle Diabetes Study. Diabetes Care 29 1764–1770. RACGP/DA Royal Australian College of General Practitioners Diabetes Australia 2011/12 Diabetes Management in General Practice: Guidelines for Type 2 Diabetes DA RACGP Canberra. Diabetes UK 2012 End of life diabetes care. Diabetes UK London. Dunning T. Rantzau C. Ward G. 1994 Effect of alcohol swabbing on capillary blood glucose. Practical Diabetes 11 4 251–254. Dunning T. 1996 Corticosteroid medications and diabetes mellitus. Practical Diabetes International 13 6 186–188. Farmer A. 2007 Self-monitoring of blood glucose does not improve HbA1c levels in patients with noninsulin treated diabetes: The DIGEM study. Presented during the 67th American Diabetes Association Scientific Sessions June 22–26 Chicago Illinois. Also published in the British Medical Journal Online June 6 2007. Fineberg S. 2000 Comparison of blood beta-hydroxybutyrate and urine ketones in 4 weeks of home monitoring by insulin-requiring children and adults. American Diabetes Association Scientific Meeting USA June. HOPE Outcomes Prevention Evaluation Study Investigators 2000 Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes. Results of HOPE and MICRO-HOPE substudy. Lancet 355 253–259. International Diabetes Federation IDF 2007 Guideline for Management of Postmeal Glucose. IDF Brussels. International Diabetes Federation IDF 2012 The Global NCD Framework. IDF Brussels. Jerums G. Cooper M. O’srien R. Taft J. 1994 ADS Position Statement 1993: Microalbuminuria and diabetes. Medical Journal of Australia 161 265–268. Jungheim K. Koschinsky T. 2002 Glucose monitoring at the arm: Evaluation of upper dermal blood glucose kinetics during rapid systemic blood glucose changes. Hormone Metabolism Research 34 325–329. Kilpatrick E. Rigby A. Atkin S. 2007 Variability in the relationship between mean plasma glucose and HbA 1c: Implications for the assessment of glycaemic control. Clinical Chemistry 53 897–901. Kim H.S. Shin J.A. Chang J.S. et al. 2012 Continuous glucose monitoring: current clinical use. Diabetes Metabolism Research Reviews 28 Suppl 2 73–78. Laffel L. Kettyle W. 2000 Frequency of elevations in blood b-hydroxybutyrate B-OHB during home monitoring and association with glycaemia in insulin-treated children and adults. Proceedings ADA Scientific Meeting USA. Monsod T. Flanagan D. Rife F. 2002 Do sensor glucose levels accurately predict plasma glucose concentrations during hypoglycaemia and hyperinsulinaemia Diabetes Care 15 899–893. Nathan D. 2007 The problem with ADAGE A1c-derived average glucose equivalent. 67th American Diabetes Association Scientific Sessions June 22–26 Chicago Illinois. O’siordan M. 2007 Average blood glucose instead of HbA1c Change appears to be coming for diabetes care. Heartwire July 3. accessed December 2007. Parchman M. Pugh J. Romero R. Bowers K. 2007 Competing demands or clinical inertia: The case of elevated glycosylated hemoglobin. Annals of Family Medicine 5 3 196–201. Rose M. Fliege H. Hildebrandt M. Schirop T. Klapp B. 2002 The network of psychological variables in patients with diabetes and their importance for quality of life and metabolic control. Diabetes Care 25 35–42. Ruilope L. Alcazar J. Hernandez E. Rodico J. 1990 Does an adequate control of blood pressure protect the kidney in essential hypertension Journal of Hypertension 8 525–531. Schneider M. Heinemann B. Lodwig L. et al. 2006 The ROSSO Study group: self-monitoring of blood glucose in Type 2 diabetes and long term outcome: An epidemiological study. Diabetologia 49 271–278.

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Monitoring Diabetes Mellitus 73 Schulman-Green D. Jases S. Martin F. 2012 Self-management in chronic illness. Journal of Nursing Scholarship 44 136–144. SIGN Scottish Intercollegiate Guidelines Network 2010 SIGN Management of Diabetes: a national Guideline Edinburgh. Sonksen P. Fox C. Judd C. 1998 Diabetes at Your Fingertips. Class Publishing London p. 105. Varbo A Benn M Tybjaerg-Hansen A. et al. 2007 Nonfasting triglycerides and risk of myocardial infarction ischemic heart disease and death in men and women. Journal of the American Medical Association 18 298 299–308. Wallace T. Meston N. Gardnert S. Matthews D. 2001 The hospital and home use of a 30-second hand-held blood ketone meter: Guidelines for clinical practice. Diabetes Medicine 18 8 640–645. Wei N. Wexler D. Nathan D. Grant R. 2013 Intensification of diabetes medication and risk for 30-day readmission. Diabetes Medicine 30 2 e56–62. Zuo L. Ma Y. Zhou Y. 2005 Application of GFR – estimating equations in Chinese patients with chronic kidney disease. American Journal of Kidney Diseases 45 463–472. Further reading Garg S. Potts R. Ackerman et al. 1999 Correlation of fingerstick blood glucose measurements with Glucowatch biographer glucose results in young subjects with Type 1 diabetes. Diabetes Care 22 1708–1714. Kolb H. Schneider B. Heinemann L. Lodwig V. Martin S. 2007 Is self-monitoring of blood glucose appropriate for all Type 2 diabetic patients Comment on the the Freemantle Diabetes Study. Diabetes Care 30 183–184. McGowan K. Thomas W. Moran A. 2002 Spurious reporting of nocturnal hypoglycaemia by CGMS in patients with tightly controlled Type 1 diabetes. Diabetes Care 25 1499–1503. Weinstein R. Schwartz S. Brazg R. et al. 2007 Accuracy of the 5-day Freestyle navigator Continuous Glucose Monitoring system: Comparison with frequent laboratory reference measurements. Diabetes Care 30 1125–1130.

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Chapter 4 Nutrition Obesity and Exercise To Cure Diabetes Naturally Click Here Key points • Obesity is an increasing global health issue. • Obesity is associated with more than 30 medical conditions and affects many other conditions. Weight loss can improve some obesity-related conditions including the metabolic syndrome Type 2 diabetes hypertension and reduce cardiovascular risk. • The relationship between weight health outcomes and life expectancy is complex and is affected by genetic make-up and significantly environmental factors which may play a more dominant role. • Population-based and targeted screening and prevention programmes are required to address the problem. • Dietary advice for people with diabetes is applicable to the whole population. However specific dietary advice should be individualised • Diet and exercise continue to be the cornerstone of diabetes management even when medicines are required. • Regular dietary assessment is advisable. Rationale Good nutrition is vital to health and well being and is an essential basis of diabetes management. Obesity is a significant health problem and a major risk factor for serious disease including Type 2 diabetes. Managing obesity is difficult. Regular nutritional assessment is important to maintain the optimal health of people with diabetes as their general health age and diabetes-related circumstances change.

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Nutrition Obesity and Exercise 75 Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. The importance of good nutrition Good nutrition is essential to health. Inadequate nutrition leads to many diseases and affects the primary condition and response to treatment Sydney-Smith 2000. Sixty per cent of deaths are related to nutritional factors for example diabetes-associated cardiovascular disease Middleton et al. 2001. In particular micronutrients and protein intake are often inadequate and mineral deficiencies are common in Australia especially in people living in poverty. Diets low in vitamins and minerals are also deficient in antioxidants that modulate oxidative tissue damage. Oxidative tissue damage is implicated in the development of long-term diabetes-related complications and is compounded by smoking excess alcohol intake and chronic inflammatory diseases see Chapter 8. Vitamins C E and A and some plant chemicals phytochemicals are naturally occurring antioxidants derived from a well-balanced diet. Obesity Obesity is defined as excess body fat and is now recognised as a disease in its own right Marks 2000 James Coster 2011. Obesity is emerging as a complex phenomena caused by a number of inter-related factors including high fat energy-dense diets inadequate amounts of exercise and genetic hormonal and environmental factors Brunner McCarthy 2001 Bouchard et al. 2004 Freyling 2007 Unger Scherer 2010. The estimated risk of becoming obese using data from the Framlingham Study suggests a normal weight person has a 50 long-term risk of becoming overweight and 25 risk of becoming obese Reynolds et al. 2005. However a number of studies suggest underweight might confer greater health risks especially in older people Diehr et al. 1998 2008. A recent study suggests normal weight people with Type 2 diabetes are more likely to die from any cause than heavier people with Type 2 diabetes over 10–30 years after adjusting for demographic factors smoking and cardiovascular risk Carnethon et al.2012. Cardiovascular mortality risk in normal weight individuals was higher by 50 and non-cardiovascular risk more than double of than those in overweight individuals which is consistent with the so called ‘obesity paradox.’ Unlike most researchers Carnethon 2012 measured BMI when diabetes was diagnosed which helped control for the effect of diabetes duration on complication status. However lower body weight might be associated with underlying illness or nutritional deficiencies that predisposes individuals to morbidity and mortality risk. Some medicines such as corticosteroids antipsychotics birth control medicines insulin sulphonylureas and thiazolidinediones TZDs contribute to weight gain see Chapter 5. There is increasing evidence that ethnicity environmental factors social isolation being teased about weight low self-esteem and low global self-worth contribute to obesity in children Goodman Whitaker 2002 Eisenberg et al. 2003. Contributing environmental factors include sedentary behaviour including excess television viewing Wilmot et al. 2012 insufficient physical activity which might be influenced by living in unsafe areas and high consumption of fast foods Burdett Whitaker 2005. The prevalence of overweight and obesity are increasing globally but there are differences among populations and among ethnic groups within populations. Rates of overweight and obesity are also increasing in children and adolescents. A child with one overweight parent has a 40 chance of becoming overweight and the risk increases to 80 when both parents are overweight. A recent Dutch study showed that more than 75 of severely obese children younger than 18 already has one or more cardiovascular risk factors. Significantly 62 of severely obese children younger than 12 years have one or more cardiovascular risk factors. Many also have hypertension low HDL cholesterol and impaired fasting glucose Chapter 13. Obesity prevents people from undertaking many self-care tasks and activities of daily living and increases the burden on joints leading to pain and discomfort that limits exercise capability. In addition obesity makes it difficult for health professionals to perform some preventative health care interventions such as cervical smears and mammograms and overweight women are more likely to have false-positive results in these tests than non-obese women Elmore et al. 2004.

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76 Care of People with Diabetes Overview of the pathogenesis of obesity As indicated environmental factors play an important role in the development of obesity and its related diseases. A simplistic explanation is: increased food intake leads to weight gain and obesity which lead to insulin resistance and impaired insulin action in muscle liver and fat tissue. The pancreas compensates by secreting extra insulin hyperinsulinaemia. In the long term the beta cells become exhausted and hyperglycaemia and hypertriglyceridaemia develop James Coster 2011. In addition a novel hypothesis suggests diet-induced obese people homeostatically guard their weight Spreadbury 2012. Abdominal fat is not inert. It produces signalling molecules adipokines which exacerbate endothelial dysfunction. A number of adipokines are produced see Table 4.1. In addition the endocannabinoid CRB neuroregulatory system influences the activity of other neurotransmitter systems including hormone secretion and modulates immune and inflammatory responses. Likewise understanding of the role of Table 4.1 Effects of adipokines and changes that occur in the presence of abdominal obesity which demonstrates their role in the development of insulin resistance Type 2 diabetes and cardiovascular disease. Name of adipokine Effects in the body Effect of increasing abdominal obesity on adipokine levels Tumour necrosis factor- alpha Disrupts insulin signalling processes in the cell membranes Reduces endothelial vasodilatation by reducing nitric oxide Higher Interleukin-6 Stimulates rate of C-reactive protein release from the liver Induces insulin resistance Damages endothelial function Higher Plasminogen Activator Inhibitor-1 Enhances prothrombotic state Higher Leptin Regulates: • appetite • energy expenditure • insulin sensitivity Stimulates the sympathetic nervous system Acts as a signalling factor in hypertension Higher Adiponectin Improves tissue sensitivity Anti-inflammatory Reduces atherogenesis Lower Angiotensinogen Contributes to hypertension Higher leptin-resistance on satiety mediators and white adipose tissue in regulating body metabolism insulin sensitivity and food intake has increased rapidly over the past few years Spreadbury 2012. The CRB system consists of many endocannabinoids including CB1 and CB2. CBI occurs through the body including in the brain adipose tissue vascular endothelium and sympathetic nerve terminals. CB2 mostly occurs in lymph tissue and macrophages. In addition a number of endocannabinoid subtypes exist whose function is yet to be determined. Endocannabinoids regulate metabolism in a number of ways. Blocking CB1 reduces food intake abdominal fat triglycerides LDL C-reactive protein CRP and insulin resistance and it increases HDL. Activating CB1 has the opposite effect. Data from the RIO-Europe Trial showed significant weight reductions and reduction in cardiometabolic risk factors such as waist circumference triglyceride levels and elevated HDL using the CB1 blocker Rimonabant compared to controls van Gaal 2005. The latter effects occurred independently of weight loss. People taking Rimonabant averaged 4.7 kg weight loss after a year and were more likely to achieve a 10 weight loss than controls. White adipose tissue has many functions including acting as a storage depot for triglycerides. It is regarded as an endocrine organ that secretes a range of adipokines which influence weight inflammation coagulation fibrinolysis

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Nutrition Obesity and Exercise 77 tissue response to insulin and contributes to the development of metabolic syndrome and Type 2 diabetes. Energy balance is impaired and obesity results if white adipose tissue function is disrupted Iqbal 2007 see Table 4.1. Ghrelin is produced in the stomach and mediates hunger. Restricting calories and exercising increases Ghrelin levels Leidy et al. 2007. Adipose tissue has a major role in hormone metabolism such as synthesising oestrogen in postmenopausal women which is protective against osteoporosis Moyad 2004. Likewise replacing testosterone preserves skeletal muscle and reduces abdominal obesity in non-obese men over 50 years whose testosterone level is 15 nM Allan 2009 . Thus it contributes to overall well-being. The significance of abdominal obesity People with central or abdominal obesity are at increased risk of obesity-related diseases such as metabolic syndrome Type 2 diabetes dyslipidaemia fatty liver and therefore are at significant risk of cardiovascular disease. Obesity is a risk factor for shortened life expectancy in younger but not older people Heiat et al. 2001 and the importance of overweight and obesity as predictors of health status decline in people 65 years. In fact some research indicates being overweight is associated with better quality of life and health status in older people Stevens 2000. Waist circumference is significantly correlated with triglyceride levels CRP cholesterol and glucose but not HbA1c in healthy women Behan Mbizo 2007. Likewise the INTERHEART Study Group 2005 demonstrated that waist circumference is strongly related to myocardial infarction but the level of risk is unclear. Physical fitness may reduce the inflammation associated with abdominal obesity and reduce cardiovascular risk Zoeller 2007. Various cardiovascular risk scores have been developed based on parameters such as age gender total cholesterol LDL systolic blood pressure being treated for hypertension and smoking for example The Framlingham Risk Score Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults 2002 and the Systemic Coronary Risk Evaluation SCORE Third Joint Taskforce of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice 2003. However a 12-year US study of people in their sixties suggests obese people live as long as people of normal weight and are less likely to develop diabetes or lipid abnormalities if they are fit. However at BMI 30 people experience difficulty performing usual activities of daily living and develop other obesity-related disorders such as musculoskeletal disease that cause pain lower muscle strength and reduce cardiovascular fitness ABC Health and Well Being 2007. Thus the focus on weight management must also include reducing/managing obesity-related disability. Other obesity-related diseases include osteoarthritis rheumatoid arthritis and other musculoskeletal diseases some forms of cancer for example breast oesophagus colorectal endometrial and renal cell cancers sleep apnoea and daytime sleepiness Chapter 10 gout urinary stress incontinence and surgical complications. Significantly maternal obesity is associated with a higher incidence of birth defects Chapters 1 and 14. Nutrition obesity and stress There is a complex association among nutrition stress and overweight/obesity. Stress affects eating behaviour: most people eat more and gain weight 30 reduce weight Stone Brownell 1994 but the reasons for the increased intake are unclear. Likewise Fiegal et al. 2002 found people are concerned about life stress and 50 eat more calorie dense food when they are stressed and undertake less activity. A suggested mechanism for the effect of stress on weight is that cortisol levels increase during stress which stimulates appetite: managing stress reduces stress-related intake. In addition chronic low level stress reduces insulin sensitivity and contributes to abdominal obesity and the metabolic syndrome. Significantly 45 of women and 23 of men think they are overweight and 20 of underweight women think they are overweight and are dieting to lose weight Better Health Channel January 2008. People use a range of self-initiated strategies to lose weight which are often successful initially but regain half to two thirds of the weight lost in the first 12 months and nearly all within 5 years. In contrast the NHANES 1999–2002 showed 58 of people who lost 5 of their bodyweight maintained the weight loss for up to 5 years. Factors associated with weight gain in NAHANES included:

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78 Care of People with Diabetes • Mexican-American peoples • significant weight loss • fewer years since reaching their maximum weight • long time spent watching TV: children and adults • attempting to control weight • sedentary lifestyle • frequent attempts to diet were associated with increased risk of developing an eating disorder. Ethnic differences could partly explain the different findings. In addition people who are supported to lose weight are more likely to stay motivated than those who ‘go it alone.’ Selfperception and body image influence quality of life and mood and there is a pervasive association among perception of being overweight depression and disordered body image. Methods of measuring weight Measuring obesity is difficult. A number of methods are used. Each has advantages and disadvantages. Crude weight Weighing people is the simplest way to estimate obesity using height/weight standards. It does not take into account muscular builds at different heights or that lean body mass weighs more than fat tissue. Mild obesity 20–40 overweight moderate obesity 41–100 and severe obesity twice the actual weight for height. Crude weight and BMI are useful to track weight changes over time but weighing is best undertaken using the same scales at the same rime of day wearing the same clothing. Body mass index The Body Mass Index BMI sometimes referred to as Quetelet’s Index is a simple method of assessing obesity but like crude weight it does not take into account muscular builds at different heights. However despite the limitations BMI 30 generally indicates excess adipose tissue. BMI should be interpreted according to growth charts in children. BMI is calculated using the following formula: weight in kilograms divided by height in metres squared. Waist-hip ratio The waist-hip ratio WHR is measured with the person standing and specifically measures abdominal obesity. The waist is defined as the largest abdominal circumference midway between the costal margin and the iliac crest. A WHR 90 in men and 80 in women is generally regarded as an accurate predictor of obesity-related disorders independently of the BMI. WHR can be affected by postprandial status time of day and depth of inspiration to an unknown degree. It includes both intra-abdominal fat the area of interest and subcutaneous fat but it is not clear how to adjust the WHR for subcutaneous fat. There are also differences among ethnic groups that need to be considered. It is useful to record the WHR on a regular basis. Other ways of measuring body fat include: • Dual energy X-ray absorptiometry DEXA which is often used in research and to determine risk of osteoporosis. Lean body mass skin fold thickness densitometry hydrostatic weighing and bioelectrical impedance analysis are other ways to measure obesity. Strategies used to measure food consumption: A number of tools are used to estimate food intake over various time periods. These include: • Food records: the individual keeps a detailed record of their intake for varying periods from three to seven days. Maintaining a food record can be burdensome and requires the person to be literate. In addition actually recording intake often influences the person to consider what they eat and change their usual eating pattern. • Food frequency questionnaires FFQ to retrospectively estimate usual dietary intake over time usually 6–12 months. Information is collected about specific types of food and the quantities and frequency with which they

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Nutrition Obesity and Exercise 79 are consumed. Short 60 foods and long 100 foods FFQs are used. FFQs must be culturally relevant and a number of culturally relevant forms exist. Modified FFQs identify dietary fat fibre fruit and vegetable intake. • Dietary recall often over 24-hours to estimate current intake. Accuracy is influenced by the individual’s ability to recall the type and quantity of food consumed. Most people underestimate their intake. • Visual estimation where trained observers monitor an individual’s food choices classifies foods using a rating scale and estimates serving sizes. This is intimidating and may influence the individual’s food selection. Nurses can undertake this type of monitoring process. • Plate waste methodology which has been used extensively in studies of food intake in school children but is not practical in clinical practice. Managing obesity and diabetes Obesity and Type 2 diabetes are chronic conditions and long-term management strategies are needed. Usually a combination of strategies is most effective especially when they are developed in consultation with the individual. In the first instance energy-dense food intake such as simple carbohydrates and saturated and trans fats should be reduced exercise increased and possibly more sleep Lamberg 2006. Exercise needs to be enough to increase total energy expenditure to 160–180 of the resting metabolic rate Erlichman et al. 2002. Increasing exercise with or without a weight loss diet induces a modest weight loss. People with diabetes should have a thorough physical assessment before undertaking exercise and weight loss programmes that need to be individualised for best effect. Along with diet exercise prescriptions Elfhag et al. 2005 and wearing a pedometer Richardson et al. 2008 can help the individual achieve weight loss. Counselling and behavioural strategies that encompass support exercise and dietary counselling are effective and in Australia are supported through some health benefit funds. For example commercial diet-oriented weight loss programmes such as Step into Life Lifestyle Integrated Functional Exercise LIFE Mass Attack Weight Loss Program Lite n’ Easy ClubOptiSlim. Some of these programmes deliver nutritionally balanced portion controlled low fat meals to the individual’s home. Prepared low-energy meals or meal replacements that replace some or all of the individual’s diet can be useful as an initial weight loss strategy or to avoid refeeding syndrome after severe calorie restriction or bariatric surgery. However they can be expensive in the long term. Avoiding fructose and corn syrup which are common forms of sugar added to foods and non-alcoholic beverages in the USA. Self-help programmes often combine lifestyle change computer-assisted interventions packaged programmes such as Internet correspondence courses and take-home weight loss kits. Self-help programmes are difficult to measure but Latner 2001 claimed 45 of people using such programmes lose weight and keep it off. Knowledgeable clinicians can support individuals likely to benefit from a self-help approach Tan et al. 2006. Significantly public health programmes that involve health providers legislators the food industry and health insurers are needed and must include children and adolescents. Weigh loss strategies may need to include strategies to keep people physically active in the longer term and recent research suggests it could be important to minimise exercise variation because maintaining exercise at a consistent level moderates age-related weight gain in proportion to the amount of exercise performed Williams 2008. Even fit people tend to gain weight with increasing age thus the amount of exercise may need to be increased to reduce age-related weight gain Williams 2008. Significantly stopping exercise leads to weight gain. Malnutrition and under-nutrition The focus in diabetes prevention and management is usually on obesity overnutrition but malnutrition is a significant problem especially in older people. Malnutrition prevalence ranges from 10–30 in the community 20– 50 in acute care settings 30–50 in rehabilitation settings and 40–70 in aged care facilities in Australia Dietitians Association of Australia 2009. Malnutrition is associated with increased costs and adverse outcomes and is often under-recognised. Importantly overweight people can be malnourished. Dietary management: diabetes Diet and exercise is the mainstay and first line of treatment of Type 2 diabetes to control blood glucose and manage cardiovascular and other health risks. The aim is to achieve a healthy weight range for the individual. The aim is to

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80 Care of People with Diabetes achieve an appropriate weight within the healthy weight range for the individual but focusing on weight might mean that under-nutrition is not considered which as indicated might confer more health risks than overweight especially in older people. Expert dietary advice is essential but the changing role of the nurse and the focus on the preventative aspects of healthcare mean that nurses have a responsibility to develop knowledge about nutrition and its role in preventing disability and disease. A number of basic screening tools can be used to identify dietary intake and nutritional characteristics and can be incorporated into usual nursing assessment and patient care plans and enables useful information to be communicated to the dietitian. The general dietary principles apply to the whole population as well as all people with diabetes. Precise advice depends on the individual’s age gender lifestyle eating habits cultural preferences and nutritional requirements. It is important that realistic targets are negotiated with the patient particularly if weight control is necessary. The goal is to achieve gradual progressive weight loss to reduce weight by 5–10 which is usually achievable and improves the health profile Pi-Sunyer 2006. The effect of medications fasting for procedures and gastrointestinal disturbances such as diarrhoea and vomiting on food absorption and consequently blood glucose levels is an important consideration especially during illness. Optimal nutritional care is best achieved by collaboration among the individual and their family nurses other health professionals and the dietitian to decide the most appropriate management regimen. Nurses have the greatest continuous contact with the patient in hospital consequently they have an invaluable role in nutritional management by: 1 Identifying patients at high risk of nutritional deficiencies for example poor nutritional intake and/or unintentional weight loss. Approximately 30 of all patients in hospital are undernourished Kondrup et al. 2003a. People with Type 1 diabetes who have repeated admissions to hospital for ketoacidosis Chapter 7 might have an eating disorder that could be triggered by underlying psychological stress or unrealistic perceptions of obesity. Sensitive discussion with the individual and his or her family and relevant investigations are needed. 2 Screening patients’ nutritional characteristics to identify actual and/or potential problems for example: • Inappropriate erratic and over-eating and those with eating disorders. Screening processes should be connected to relevant actions. For example if the person is eating appropriately arrange for regular screening at specified intervals. If the person is at risk of an eating disorder an appropriate nutrition plan needs to be determined. If functional metabolic or diabetes-related complications are present standard nutrition plans may not be appropriate and dietitian advice will be needed Kondrup et al. 2003b. The following factors need to be considered when deciding the level of risk: the current condition whether the condition is stable weight loss/gain can be assessed from the health history the significance of the condition and whether it is likely to deteriorate or improve and any disease processes that affect nutritional status such as appetite diabetes complications and hyperglycaemia. Managing eating disorders is challenging because people often do not consider their eating behaviour as a problem or deny they have an eating problem. Repeated episodes of ketoacidosis DKA could indicate an eating disorder and needs to be investigated. Young people with diabetes often run their blood glucose levels high to lose weight which puts them at risk of DKA see Chapters 7 and 13. Cognitive behaviour therapy may be a useful strategy when the eating disorder is mild to moderate. The complex underlying issues need to be ascertained and managed. • Those with domestic financial and/or employment problems. 3 Providing ongoing patient monitoring on a meal-to-meal basis. Example questions to ask when taking a diet history are shown below. The questions should be asked sensitively as part of a nutritional assessment. Do you have regular meals • It is important to clarify what the individual means by ‘regular’ and whether they skip meals and if they do when and why. For example a nurse with diabetes working in the operating theatre might find it difficult to always predict when the operation will finish. Do you have a good breakfast • Poor morning appetite can indicate nocturnal hypoglycaemia and catecholamine production to maintain the falling blood glucose.

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Nutrition Obesity and Exercise 81 • People who do not eat breakfast often snack later in the day on energy-dense foods and can be protein- deficient. • Missing breakfast interferes with work performance. How often do you eat takeaway foods • Takeaway foods tend to be high in fat salt and sugar and low in fibre protein and essential vitamins and minerals. Do you eat cream biscuits chocolates or lollies • This question is a way of checking the individual’s intake of sugar and fat. Can you tell me some of the foods you eat that contain carbohydrate • Regular carbohydrate intake is important when the individual is using insulin or insulin oral glucose lowering medicines. A minimum of 130 g carbohydrate per day is required to meet the brain demand for glucose ADA Guidelines. The information collected from screening investigations and questions provides the basis from which nursing staff can quickly and effectively refer patients to the dietitian who can support nursing staff by: • Setting dietary management goals for the individual consistent with their health status lifestyle and healthcare goals. • Identifying possible nutritional problems. Estimating caloric intake is difficult because people generally underestimate their caloric intake by as much as 50 despite trying to keep accurate food records Fabricatore 2004 but three-day food records can be helpful to health professionals and the person with diabetes. • Identifying causes of possible nutritional problems and suggesting strategies to overcome them. • Counselling and educating the patient about how to reduce the risks associated with these problems. • Supporting nursing and medical staff on an ongoing basis to ensure most effective nutritional management is achieved and maintained Dunning Hoy 1994. The person with diabetes is in control of what they eat and their activity level and must be actively engaged in planning meals and exercise regimens. Dietary requirements change with increasing age activity level health status pregnancy and lactation and during specific disease processes for example renal and cardiac disease. Method of screening for dietary characteristics and problems Nutritional status 1 Identify whether the person is overweight or underweight and whether the person’s health is affected by their weight status. For example calculate BMI and/or waist-hip ratio. 2 Review any current haematological and biochemical measurements which reflect the person’s nutritional status such as haemoglobin and serum albumin levels creatinine folate and cholesterol. Clinical signs such as tiredness fatigue and obesity can indicate inadequate protein intake and can be confirmed by blood urea nitrogen BUN and serum creatinine levels. Low creatinine suggests protein intake is low. Low BUN and creatinine suggests a catabolic state such as hyperglycaemia. Consider coeliac disease in people with Type 1 diabetes see Chapter 10. Recent research indicates malnourished patients have a longer length-of-stay are older and have increased mortality rates compared with well-nourished patients. Most malnourished patients are not identified as being at risk Middleton et al. 2001. Clues to nutritional deficiency are: • Weight loss. • Low lymphocyte count. • An illness lasting longer than three weeks. • Serum albumin 3.5 g/dL. Note serum albumin usually falls during acute illness and is not a stand-alone measure of nutritional deficiency.

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82 Care of People with Diabetes • A comprehensive nutrition history and assessment including medicines and possible food-medicine interactions malabsorption oral health anorexia dysphagia mental health and functional ability to identify factors that could contribute to under- nutrition which are likely to be multifactorial. If a patient is identified as being malnourished their nutritional status should be monitored by weighing them regularly using the same scales and with the person wearing similar clothing by monitoring nitrogen balance and using appropriate screening tools such as those listed below. Nutritional supplements may be needed. Dietary characteristics The tools and questions described earlier in this chapter can be used to determine: • the regularity/irregularity of meals and/or snacks • whether the person consumes foods and fluids containing refined sugar • whether the person omits any of the major food groups. If one or more problems are identified the person should be referred to the dietitian for further dietary analysis and advice. Screening tools Screening tools are used to measure overall risk of malnutrition rather than food consumption and include: • Malnutrition Screening Tool MST which is widely used in Australia. • Malnutrition Universal Screening Tool MUST for adults Malnutrition Advisory Group MAG 2000. • Simplified Nutritional Assessment Questionnaire SNAQ. • Nutritional Risk Screening NRS-2002 for hospital settings. • Mini Nutritional Assessment MNA © for the elderly Vellas et al. 1999. • The Healthy Eating Index HEI and Modified HEI for children and adolescents Feskanich et al. 2004. • Biomarkers to identify specific food components in body fluids or tissue which independently reflect intake of the particular food. Principles of dietary management for people with diabetes A number of dietary guidelines have been developed such as the American Diabetes Association the Diabetes and Nutrition Group of the European Association for the Study of Diabetes The Canadian Diabetes Association Diabetes UK the Indian Council of Medical Research National Heath and Medical Research Council NHMRC and Diabetes Australia. The macronutrient content of these guidelines varies despite the fact they are all evidencebased and largely draw on the same evidence. Not surprisingly socio-economic factors and food availability appear to influence the dietary advice health professionals provide and what people consume perhaps more than nutrition guidelines Kapur Dunning 2007. Diets such as the traditional Mediterranean Okinawan Dietary Approaches to Stop Hypertension DASH antihypertensive anti-inflammatory diet South Beach diet Atkins type diet Omniheart Onish and Onish Zone A to Z diets all appear to improve metabolic risk factors by reducing lipids and weight to various degrees Carey et al. 2005 Gardner et al. 2007 Fung 2007 Tay et al. 2008 although they include different combinations of macronutrients. Interestingly ancestral diets high in acellular carbohydrates could promote an inflammatory microbiota and could be the primary cause of leptin resistance and obesity Spreadbury 2012. Likewise consuming high fat dairy products may reduce obesity risk in Europeans compared to Americans. The difference could partly be attributed to the different feeding practices adopted in the two countries. Dairy farms are more likely to be highly industrialised in the US where the cows are kept indoors and fed on high protein energy-dense fodder and have little or no exercise. Thus the milk from US cows has a higher fat content that cows raised on traditional European dairy farms. Ruminant fat consists of more than 400 different fatty acids and is the most complex form of fat in the human diet. These findings are interesting considering NHMRC and other guideline recommendations to consume low fat dairy products where possible. Likewise vegetarian and vegan diets which are high in fibre low in saturated fat and have a low glycaemic index and lower haem iron are associated with reduced risk of Type 2 diabetes less weight gain and better cardiovascular

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Nutrition Obesity and Exercise 83 outcomes. However vegetarian diets may lack essential B group vitamins and iron thus supplements might be required. Vegetarian people treated with Metformin are at increased risk of vitamin B12 deficiencies because Metformin affects absorption of vitamin B 12 see Chapter 5. Although iron is found in vegetables such as spinach and pumpkin from eggs it is not absorbed as well as haem iron from red meat. Thus iron supplements might be required Marsh 2008. There are various methods of counting carbohydrate for example exchanges portions and carbohydrate counting that help ensure an even distribution of carbohydrate and appropriate ratio of carbohydrate to exercise and glucose lowering medicines doses and administration times when planning meals for individuals. An exchange is equal to 15 g and a portion 10 g of carbohydrate. Exchanges are sometimes used in the UK while Australia often uses glycaemic index GI and glycaemic load. More recently portions are making a comeback in programmes such as The German Diabetes Training and Treatment Program DTTP and its counterpart the Dose Adjustment for Normal Eating Program DAFNE. These programmes are being widely adopted and adapted for example OzDAFNE in Australia and in group education programmes such as the Royal Derby Hospital in the UK Shorrock Hannah 2011. Using the information they learn in such programmes people with diabetes estimate their carbohydrate intake based on 10 g portions and calculate their short-acting insulin doses as a ratio to carbohydrate consumption. Basal insulin doses are adjusted to address preprandial and bedtime blood glucose targets see Chapter 1. HBA1c reductions of 1 and improved quality of life have been demonstrated without increasing hypoglycaemia or weight Muhlhauser et al. 2002 DAFNE Study Group 2002. In general people with diabetes should: • Eat foods high in complex carbohydrate with low GI 50–60 of total intake high fibre unprocessed foods. Rapidly digested carbohydrates cause a rapid rise in blood glucose and a greater demand on the pancreas to release insulin to maintain the normal blood glucose range. Low GI foods are associated with a lower risk of diabetes and the related complications Brand-Miller et al. 2003. GI is a method of ranking foods based on their immediate effect on the blood glucose level. Foods that enter the blood stream quickly have a high GI for example sugars. Foods that enter more slowly are known as low GI for example cereals. The GI is the area under the glucose response curve measured after ingestion of a test food and multiplied by 100. Foods with a GI 55 are classified as low GI 56–69 as moderate GI and 70 are high GI foods. In general the lower the GI the smaller the impact on the blood glucose level. However many factors affect the rate at which carbohydrate is absorbed including the types of sugar and starch in food the degree of processing cooking methods and the presence of other nutrients such as fat and fibre and the particular combination of foods. Foods high in fat have a low GI because the fat delays their digestion and they are absorbed slowly but high fat foods are not recommended. Low GI foods are the preferred basis of a well-balanced diet. They slow food absorption from the gut so the postprandial glucose load is reduced cause satiety and help control weight reduce HBA1c improve insulin sensitivity and help control lipids BrandMiller et al 2003. People with diabetes are advised to include low GI foods in at least one meal each day. Simple sugars do not have to be excluded using the GI food plan. The move to GI-based diets is not universal and GI can be difficult for some people to understand. Generally if people are accustomed to working in portions or exchanges and have reasonable metabolic control they should not be expected to change particularly if they are elderly. Scientists are currently undertaking research to reduce the GI of some foods such as rice by altering their amylopectin structure to improve consumer acceptability Rahman et al. 2007. GI is not related to the quantity portion size of carbohydrate which is measured by glycaemic load GL. GI is taken into account when determining GL. That is GI indicates how rapidly the food enters the blood as glucose and the GL indicates how much carbohydrate is in a portion/serving both are important to understanding the effect of a particular carbohydrate on blood glucose. The type of dietary fibre influences GI water-soluble fibres such as hemicellulose mucilages gums and pectins have low GI because they slow digestion and absorption of carbohydrate. Recent advances in blood glucose meter and insulin pump technology and other technological advances include algorithms that calculate insulin doses based on the insulin to carbohydrate ratio correction factors and illness and activity levels. Carbohydrate counting is very important when people use insulin pumps. • Be low in fat 10 of total energy value especially saturated fat and trans fatty acids see Tables 4.2 and 4.3 which depict the main types of dietary fats and their effects on blood lipids respectively. Some fat is necessary

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84 Care of People with Diabetes to supply essential fatty acids and fatsoluble vitamins A D E and K. Despite an overall reduction in dietary fat the mean Australian serum cholesterol has not fallen since 1980 National Heart Foundation 2008. Omega 3 and 6 fatty acids are crucial to healthy brain function normal growth and development and skin and hair growth bone health regulating metabolism and

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86 Table 4.3 Effect of high carbohydrate alcohol and fibre on blood fats. Carbohydrate Fibre a Alcohol Non-nutrient components b Increases VLDL and triglycerides Reduces cholesterol Increases triglycerides and VLDL and possibly cholesterol HMG-CoA-like activity Lowers HDL Small increase in HDL Reduces cholesterol and LDL a Effects depend on the type of fibre. Insoluble fibres only have a small effect on lipoproteins soluble fibre has a favourable effect. b For example allicin saponins isoflavonoids phyto-oestrogens and anthocyanins. Individually they only have a small LDL lowering effect but combining several components may produce a cumulative effect. maintaining reproductive function. Omega 6 fatty acids have an important role in modulating the inflammatory response by generating eicosanoids prostaglandins and leukotrienes and cytokines interleukins. For example gamma-linolenic acid omega 6 synthesised from linolenic acid reduces inflammation. There is strong evidence that replacing saturated fatty acids with omega 3 and 6 reduces cardiovascular disease in people with diabetes and non-diabetics Eddy 2008. Dietary sources are not high in gamma-linolenic acid. Some are found in green leafy vegetables and nuts. The richest sources are borage oil blackcurrant and evening primrose oil and breast milk. The conversion of linolenic acid into gamma-linolenic acid is inefficient in older age diabetes high alcohol consumption eczema viral infections excess fat intake hypercholestrolaemia and deficiency of vitamin B6 zinc magnesium calcium and biotin. Deutsch 2007 suggested Euphasia superba krill is a better source of omega-3 than plant sources and rapidly reduces C-reactive protein a marker of inflammatory disease. However compared to fish oils krill oil has less omega 3 so larger doses are needed and krill is more expensive. Sources of omega 3 6 and 9 are shown in Table 4.4. • Contain adequate protein 15 of total intake. • Be low in simple sugar less than 25 g/day. • Ensure a variety of food is eaten daily from each of the five food groups. • Ensure that complex carbohydrate is consumed at each meal to reduce the postprandial blood glucose rise and the likelihood of hypoglycaemia in patients on insulin or diabetes medication. • Limit salt. A typical western diet contains about 10 g of salt per day and 75 of salt consumed is added salt. The National Health and Medical Research Council NHMRC 2003 and The Heart Foundation recommend an upper level of 6 g of salt per day. The 2003 NHMRC Guidelines have been reviewed and should be available in 2013 but the content is expected to be similar. High salt diets are leading causes of cardiovascular disease and hypertension WHO 2002 and reducing salt intake reduces blood pressure. • Reduce alcohol. Small amounts of alcohol 0.5–1 drink/day can reduce cardiovascular risk and post prandial blood glucose levels if consumed with the evening meal containing carbohydrate. Greater quantities impairs glucose metabolism and contributes to hyperlipidaemia In Australia the current recommendation is two standard drinks per day for men and one standard drink per day for women. Goals of Dietary Management The goals of dietary management are to: • improve the person’s overall health • attain optimal body weight Care of People with Diabetes Table 4.4 Sources of omega-3 -6 and -9 essential fatty acids. And daily intake recommended RDI by the National Health and Medical Research Council 2006. A variety of foods high in essential fatty acids should be consumed each day. Omega-3 EPA RDI 50–200 mg/day Omega-6 RDI 150–1500 mg/day Omega-9 RDI 50 g/day Fresh tuna Safflower Olive oil

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Nutrition Obesity and Exercise 87 Halibut Evening primrose Avocado Sardines Sunflower Almond Mackerel Corn and maize Apricot Herring Hempseed Canola Trout Walnut Peanut Krill Pumpkin seed Butter Cod liver oil a Borage Lard Blackcurrant Eggs Soya bean Milk Flax and linseed Coconut RDI recommended daily intake. The RDI varies among publications. Consider the quantity of EPA and DHA in omega-3 supplements rather than the total quantity of fish oil in the product. Different types of fish contain different quantities of omega- 3. Consider the risk of bleeding before recommending supplements if the person is on anticoagulant medicines or has bleeding conditions. a Cod liver oil may be contraindicated in pregnancy without medical advice. • attain lipid and blood glucose levels as close to normal as practical considering hypoglycaemia risk and its consequences: see Chapter 6 • ensure normal growth and development in children • decrease the risk of diabetes- and obesity-related complications and comorbidities • identify nutrition-related disorders that can affect diabetes management and interpreting investigative procedures for example anaemia. Dietary management: obesity Public health strategies are required to have a significant impact on the health wellbeing and obesity levels of the population see Chapter 1. Individual dietary advice should be age- gender- and culture- specific and achievable which means addressing environmental issues such as access to healthy food safe accessible areas to exercise and accurate understandable food labels. As well as diet and exercise a combination of behaviour change strategies tailored to the individual and support are required. Diets high in fruit vegetables whole grains legumes and low in fat are generally safe and effective and promote fullness and satiety National Institute of Health 2000. However 20 of people trying to lose weight consume these foods. As indicated commercial weight loss programmes such as Weight Watchers The slim-fast plan Dr Atkin’s New Diet and the Rosemary Conley Program result in significant weight loss and lower WHR after six months compared to controls who gained an average of 0.6 kg. However the improvements were not sustained after the trial was completed. More sustained benefit was noted in programmes that included a support group Truby Baic 2006. Other popular diets include the following which all have advantages and disadvantages. People with diabetes should be advised to discuss these diets with a dietitian and/ or their doctor before they try them: • High protein-low carbohydrate ketogenic diets. • Meal replacement plans where 1–2 meals per day are replaced with meal supplements. • Dairy diet. Preliminary data suggest 3 servings/day of calcium-rich food enhances weight loss through a variety of mechanisms but more research is needed to confirm these preliminary results Zemel 2003. Fish oil supplements 3 g fish oil containing 1.8 g polyunsaturated fatty acids have been shown to reduce adiposity and atherogenic risk factors in a randomised controlled trial of women with Type 2 diabetes Rizkalla 2007. However fish oil may affect the INR in patients taking anticoagulants.

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88 If the BMI is 30 or BMI 27 and diabetes or cardiovascular risk factors are present and diet and exercise is ineffective medicines such as lipase inhibitors Xenical or serotonin reuptake inhibitors such as Sibutramine can be used but they only reduce weight by 10. Sibutramine can increase blood pressure Donohoe 2008. Research into future weight loss medicines is likely to focus on the hormones involved in regulating satiety leptin ghrelin and CRBs. Fucoxanthin an antioxidant obtained from brown seaweed which is commonly used in Asian cuisine has been shown to induce weight loss and increase omega-3 fatty acid levels in rats Miyashita 2006 but its application in humans is unknown. Bariatric surgery Gastric bypass surgery bariatric surgery is increasingly being recommended for people with Type 2 diabetes who have a body mass index 35 where lifestyle and medical treatments for obesity and uncontrolled diabetes have not been effective provided they are fit and over 18 years Proietto et al. 2012. Bariatric surgery refers to a variety of surgical procedures that induce weight loss by: • reducing the size of the stomach to restrict the amount of food that can be consumed • delaying digestion and absorption of food in the intestines • causing a feeling of fullness and satiety due to stimulation of nerves in the stomach or through the hormones that control hunger or both. Types of procedures include: • adjustable gastric banding the most commonly used procedure • partial or sleeve gastrectomy • gastric bypass Roux-en-Y and bilopancreatic diversion see Table 4.5. Who is suitable for bariatric surgery People most suited to bariatric surgery: • have Type 2 diabetes • are obese with a BMI .35 • have tried lifestyle and medical treatments with no success significant weight loss • are over 18 years

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Nutrition Obesity and Exercise 89 Table 4.5 Bariatric surgical procedures and the postulated weight loss mechanisms. Complication rates are reported to be low: 1 for gastric banding to between 2 – 10 for the other more complex procedures. Risks increase with increasing age degree of obesity and concomitant medical conditions. Bariatric procedure Outline of the procedure Postulated weight loss mechanism Adjustable gastric band An adjustable gastric band is paced around the upper section of the stomach that creates a small pouch that can only hold a small amount of food. Restricts the quantity of food consumed Sleeve gastrectomy Removal of two thirds of the stomach Restricts the quantity of food consumed. Affects hunger by stimulating nerves or altering hormones that induce satiety. Gastric bypass: Roux-en-Y procedure Restricts the quantity of food consumed Affects hunger by stimulating nerves or altering hormones that induce satiety. Delays digestion and reduces absorption of nutrients. • are fit enough to undergo surgery • understand the procedure and the commitment needed for ongoing care and followup and to maintain lifestyle changes after surgery • obese adults with a high risk of Type 2 diabetes and BMI 35 and another obesityrelated- condition or BMI 40 who meet the other preceding criteria. The benefits and risks associated with bariatric surgery for people with diabetes has not been established and should be considered on an individual basis. Bariatric surgery appears to improve blood glucose control through weight loss reduced insulin resistance and improved insulin sensitivity Proietto et al. 2012. Blood glucose normalises in up to 75 of people especially if they had Type 2 diabetes for a short period before undergoing surgery. Procedures such as gastric bypass that involve the small intestine appear to induce hormonal effects apart from weight loss that improves blood glucose control within a few days. Bariatric surgery effectively reduces weight and improves quality of life and lowers the risk of comorbidities after two years compared to controls Adams 2006 and with 12 months of medical therapy prior to bariatric surgery achieved glycaemic control in obese people with uncontrolled Type 2 diabetes n 150 Schauer et al. 2012. Schauer et al. did not find significant differences in total and LDL cholesterol levels 12 months post-bariatric surgery or a significant reduction in the number of medicines needed to manage hyperlipidaemia. Adverse events included blood clots requiring surgery nausea and vomiting and gastric leak after sleeve gastrectomy. However they did not report any deaths serious hypoglycaemia malnutrition or excessive weight loss. However some serious adverse events can occur over time and include: • The gastric band slipping or less commonly the band eroding into the stomach wall. • Vitamin and mineral deficiencies due to inadequate nutrition or reduced absorption Encinosa et al 2006. Improved mood has been demonstrated using the Beck Depression Inventory Mitka 2003. Several procedures are used such as Roux-en-Y gastric bypass stapled gastroplasty and

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90 Care of People with Diabetes adjustable gastric banding all of which reduce the stomach size and control caloric intake. Although the risks are high people lose weight and blood glucose levels normalise Encinose et al. 2006. Despite these promising findings long-term outcomes are not yet available and it is not clear whether glucose control will be maintained in the long term. Significantly access to an experienced interdisciplinary team is essential for ongoing follow up and to minimise complications. Complementary weight loss programmes Many complementary weight CAM loss strategies are similar to conventional programmes and these are beneficial and effective. However many CAM medicines have limited evidence of any benefits Egger 2005 and some are dangerous for example weight loss products that contain ephedra should be avoided and have been banned in some countries. Likewise creams soaps and body wraps are unlikely to lead to weight loss. They may improve body image and self-concept and help the individual mentally. Hypnosis and acupuncture may be useful adjuncts to some other strategies. People also use topical creams and ‘anticellulite’ fat preparations to improve their body image and research is continuing into the effectiveness such medicines. Caruso et al. 2007 reported 11 reduction in waist circumference compared to 5 after 12 weeks in controls with equal reductions in women and men using a 1200-calorie balanced diet a walking programme and 0.5 topical aminophylline cream applied to the waist BD. The diet and exercise could confound the results. Likewise the study was not blinded. Thus there is no compelling evidence to recommend using currently available anticellulite preparations and some that con tain aminophylline could affect heart rate and rhythm which might be undesirable in people with diabetes. In Australia weight control products complementary and conventional must conform to the Weight Management Industry Code of Practice http://www.weightcontrol. org/browse.asppage349. People should be advised to check whether products conform to this Code before they purchase the product. In addition websites the show the HonCode logo are likely to contain accurate unbiased information. Factors associated with making dietary changes Kapur et al. 2008 described a number of factors associated with positive dietary changes in India. These included: • being older • a shorter time since being fit and of acceptable weight • having strong family support • having a less busy work life • being conscious of their health • having received dietitian advice and frequent visits to a dietitian • being interested in overall health not just diabetes. Motivational interviewing in addition to diet and exercise leads to weight loss in African- American in a randomised prospective trial in women. HbA1c was correlated Table 4.6 Medicines whose absorption can be modified by food. Reduced absorption Delayed absorption Increased absorption Aspirin Aspirin Diazepam

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Nutrition Obesity and Exercise 91 Cephalexin Cefaclor Dicoumarol Erythromycin Cephalexin Hydrochlorothiazide Penicillin V and G Cimetidine Hydrochlorothiazide Phenacetin Digoxin Metoprolol Tetracycline Indoprofen Nitrofurantoin Theophylline Metronidazole Propranolol with weight loss at six months but was not sustained at 18 months Smith-West 2007. Galuska et al. 1999 demonstrated cost savings in people being counselled and suggested frequent reminders and support were essential. These findings suggest important issues for health professionals to consider when developing weight management strategies and delivering dietary advice. They might also indicate that health professionals also need to make some behaviour changes and become better educated about nutrition and how to deliver dietary and weight loss advice. Nursing responsibilities 1 To assess dietary and nutritional characteristics and problems such as poor intake under- or overweight and unexplained weight loss/gain and refer to a dietitian as required for example at a change from tablets to insulin if there are frequent high or low blood glucose levels the diagnosis of a complication such as renal disease if the patient displays inadequate knowledge or when the person requests a referral. 2 To observe and if necessary record food intake with particular reference to carbohydrate intake of patients on glucose lowering medication. 3 To promote general dietary principles to patients in accordance with accepted policies and procedures. 4 To ensure the meals and carbohydrate content are evenly spaced throughout the day. 5 To ensure adequate carbohydrate intake for fasting patients and those with diminished intake to avoid hypoglycaemia. 6 Administer medicines at an appropriate time in relation to food. 7 To know that the absorption of some medicines can be modified by food especially antibiotics and their effectiveness may be diminished or increased see Table 4.6. The pharmacological response to medicines is influenced by the individual’s nutritional status. In turn medicines can affect the nutritional status. The sense of smell and taste play a significant role in adequate dietary intake. Both these senses diminish with age and can be changed by disease processes and some medicines. Gastrointestinal GIT disorders can lead to malabsorption pH changes alter the bioavailability of nutrients and medicines inhibit medicine binding and chelation and impair the metabolism and excretion of medicines NHMRC 1999. Interactions can also occur with commonly used dietary supplements see Chapter 19 and the International Bibliographic Information on Dietary Supplements National Institute of Health. 8 To observe for signs and symptoms of hyper- and hypoglycaemia and correct the blood glucose level by appropriate nutritional management as part of the management plan. Table 4.7 Some food-medicine interactions 11 Food Medicine Possible effects Black liquorice in large doses Digoxin Diuretics Calcium channel blockers Irregular heart rhythm Hypertension High serum sodium Muscle pain Weakness

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92 Care of People with Diabetes Aged cheese such as brie parmesan Roquefort Sauerkraut Over ripe avocadoes Pepperoni MAO antidepressants Hypertension Grapefruit juice Calcium channel blockers Lipid-lowering medicines Some oral contraceptives Some psychiatric medicines Modifies medicine metabolism Orange juice Aluminium-containing antacids Antibiotics Increases aluminium Milk and other dairy products Tetracycline Digitalis Laxatives containing bisacodyl Enhanced effects Oatmeal and high fibre cereals Many oral medicines including antihypertensive agents Can affect absorption Leafy and green vegetables high in vitamin K Warfarin and other anticlotting medicines Interferes with blood clotting Caffeinated foods such as tea coffee chocolate Asthma medications Quinolone antibiotics Some oral contraceptives Excessive excitability Alcohol Medicines containing pseudoephedrine Antidepressant medicines Antipsychotics Muscle relaxants Sedatives Glucose-lowering medicines Excitability Sedation Hypoglycaemia High salt foods Steroids Fluid retention Iodine-rich food Thyroid medicines Reduced efficacy Might affect blood glucose through its effect on the thyroid see also Chapter 5. Note: Alcohol interacts with almost all medicines. Some medicines increase the risk of nutritional deficiencies. For example metformin leads to vitamin B-12 deficiency cholestyramine increases excretion of folate and vitamins A D E and K and antacids interfere with the absorption of many essential minerals. Thus the person being prescribed medicines should be advised about when to take them in relation to food. People at high risk of a food– medicine interaction are older taking medicines for chronic diseases such as diabetes have hypertension depression hypercholesterolaemia renal disease or congestive heart failure. Inadequate nutrition and low protein stores can delay the healing process. Some food- medicine interactions are shown in Table 4.7. ‘Sugar-free’ foods ‘Sugar-free’ usually refers to the sucrose content of foods. Other sugars are often used to sweeten foods labelled sugar-free e.g. dextrose fructose maltose lactose galactose. Recent evidence suggests fructose which is used to sweeten most soft drinks causes a greater increase in triglycerides and LDL than glucose American Dietetic Association 2004 Havel 2007. The study was undertaken in overweight and obese individuals but the findings are likely to apply to non-obese people because fructose is more likely to pass into the

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Nutrition Obesity and Exercise 93 lipogenic pathway than glucose after being metabolised in the liver. More research is needed to confirm these findings to determine the percentage of total energy consumption at which fructose has an atherogenic effect. These foods may not be appropriate for people with diabetes. Low calorie and artificially sweetened foods are generally recommended. Alternative sweeteners Alternative sweeteners elicit a pleasurable sensation without affecting the blood glucose and are generally safe if used at the recommended doses. They may also play a role in reducing dental caries American Dietetic Association 2004. They are an acceptable alternative to sugar for people with diabetes. However a small amount of sugar included in a balanced diet does not adversely affect the blood glucose. There are two types of alternative sweeteners: non-nutritive or artificial and nutritive. Non-nutritive sweeteners are kilojoule free for example: • Saccharin • Acesulphame-K • Aspartame Equal • Cyclamate • Isomalt • Neotame • Sucralose Splenda • Alitame • Neotame These products are safe to use. If used in cooking they are best added after cooking because heat can change the taste. The best choices for pregnant women are Acesulphame-K Alitame Aspartame and Sucralose. Nutritive sweeteners are usually derived from different types of carbohydrate and products containing these sweeteners are often labelled ‘carbohydrate modified’. Nutritive sweeteners include: • Sorbitol • Fructose Sweetaddin • Mannitol • Xylitol • Maltilol • Isomalt • Polydextrose Litesse • Maltodextrin hydrolysed corn syrup • Thaumatin Many nutritive sweeteners are sugar alcohols for example sorbitol. These sweeteners can cause diarrhoea in high doses. Likewise ‘diet’ products containing alternative sweeteners can be high in fat. Stevia Stevia rebaudiana a herb much sweeter than sugar is being promoted as a suitable sugar alternative for people with diabetes and may have glucose lowering effects but it has not been extensively evaluated in clinical practice. Only very small quantities are required. Larger doses may cause diarrhoea. Food additives

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94 Care of People with Diabetes Many people are allergic to food additives which can result in sensitivities or in severe cases analphylaxis. Different additives are used for different classes of foods. A list of food additives and their code numbers can be obtained from www.foodstandards. gov. au. Types of additives include acidity regulators antioxidants bulking agents colourings flavourings emulsifiers gelling agents humectants preservatives and thickeners. Some of these additives are also used in some medicines. It is important to learn to read labels and to get to know the alternative names for foods and additives that commonly cause allergies such as cow’s milk soy nuts and gluten as well as alternative names for fat and sugar. Key information on a food label people need to look for includes: • The nutrition claims for example fat free high fibre low fat reduced fat cholesterol free low in salt low in sugar and sugar free. • How to interpret the list of ingredients. • How to interpret the allergy information. • The country of origin. • Use by dates and storage recommendations. • Understand the nutrition information. • How to interpret information about recommended daily intake. • Understanding the figures and symbols such as the GI symbol genetically modified foods and the Heart Foundation tick. These key aspects should be part of routine dietary advice or the person can be referred to Reid 2007 for further information. Alcohol Alcohol reduces hepatic glucose output but does not have a direct affect on insulin secretion or glucose disposal Shai 2007. It is recommended that alcohol consumption be limited because of its potential to affect blood glucose and contribute to or mask hypoglycaemia see Chapter 6. Sweet alcoholic drinks can lead to hyperglycaemia while the alcohol itself leads to hypoglycaemia. The hypoglycaemic effect may depend on the nutritional state and glucose stores. Alcohol should never be consumed on an empty stomach. Alcohol supplies considerable calories and provides little or no nutritional value. In addition alcohol clouds judgment and can lead to inappropriate decision-making. Drunkenness can resemble hypoglycaemia and treatment of hypoglycaemia may be delayed. Appropriate education about hypoglycaemia risk with alcohol consumption is essential. Alcohol has a range of other physical effects including liver cirrhosis malnutrition and peripheral neuropathy. Although moderate amounts of alcohol may reduce cardiovascular risk the current recommended intake still applies: in Australia two standard drinks per day for men and one standard drink per day for women. See also Chapter 10. Exercise/activity Exercise has an important role in controlling the blood glucose and increasing overall fitness. It should be combined with a suitable diet. Higher levels of sedentary behaviour are associated with 112 increased risk of developing diabetes 147 increased risk of developing cardiovascular disease and 49 risk of all cause mortality Wilmot et al. 2012. There is an association between occupational sitting and health outcomes including diabetes cardiovascular disease and mortality van Uffelen et al. 2010. However although TV viewing is often cited as a risk factor for diabetes and other diseases it is a poor measure of overall sedentary behaviour and may underestimate the true effect of over all sitting-related sedentary behaviour Wilmot et al. 2012. However people who watch a lot of TV often eat large

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Nutrition Obesity and Exercise 95 quantities of energy-dense snacks that increase their risk of obesity and consequently obesity- related diseases. Thus exercise programmes should include information about how to reduce occupational and TV-related sitting. People commencing an exercise programme should first have a medical assessment. Structured aerobic and resistance training programmes improve blood glucose levels and lower HbA1c by 0.6 and reduce cardiovascular risk in Type 2 diabetes Krause Levine 2007. A 1 reduction was associated with 15–20 reduction in major macrovascular events and 37 reduction in microvascular events. In addition exercise has mental health benefits such as improved body image and feelings of self-worth Goldfield et al. 2007. Exercise capacity is an independent predictor of non-fatal cardiac events and mortality of patients referred for treadmill testing ETT Peterson et al. 2008. For example low exercise capacity is associated with increased risk of MI on ETT but it is not clear whether limited exercise capacity indicates underlying cardiovascular disease or whether it is a marker of cardiovascular events. Exercise can result in hypo- or hyperglycaemia. Under normal circumstances exercise stimulates hepatic glucose output and glucose utilisation to maintain glucose in the normal range. However if exercise occurs in times of metabolic stress the sympathetic drive can be stimulated which leads to reduced glucose utilisation van de Veire et al. 2006. Before exercising people should check their blood glucose levels. It is important to make a gradual start to the exercise. Strenuous activity can cause hypoglycaemia extra carbohydrate may be needed. Various strategies are suggested to help people begin and maintain an exercise/ activity regimen. The beneficial effects of exercise are less evident if exercise is the sole focus of the intervention Conn et al. 2007. Effective strategies include: • Providing exercise education. • Setting achievable goals and focusing on achieving one goal at a time. • Providing individual supervision is as effective as group programmes and is more acceptable to some people. • Suggesting written ‘exercise prescriptions’ that take account of the individual’s interests gender age and capabilities. • Wearing a pedometer especially when combined with a step goal diary. Reduction in BMI of 0.38 kg/m 2 and reductions in blood pressure by 3.8 mm Hg have been described Bravata et al. 2007. A recent meta-analysis suggests people lose an average of 0.05 kg representing 2–3 of body weight over 12 months and continues if the individual continues to wear the pedometer Richardson et al. 2008. People often hope to lose much more weight than this so it is important that they realise even small weight loss is beneficial and to set reasonable goals. Steps walked increased from 2000 to 4000 per day on average in Richardson et al.’s meta-analysis. Pedometers provide feedback on the number of steps a person takes per day but exercise duration intensity and frequency and the long-term benefits are unknown. • Combining exercise with rehabilitation programmes. • Tai Chi particularly in older people and those in wheelchairs has a range of benefits such as: improved muscle strength flexibility balance and range of movement lower risk of falls improved cardiovascular fitness and reduced cholesterol and abdominal fat. In addition people have a younger vital age ICCMR 2008 see Chapter 19. More recently combination programmes such as Lifestyle Integrated Functional Exercise LIFE that teach the principles of balance and lower limb strength training have been shown to be beneficial especially for older people Clemson et al. 2012. Such programmes help reduce falls and improved functional capacity.

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96 Care of People with Diabetes References Adams T. Walker J. Litwin S. Pendelton R. 2006 Two-year improvement in morbidity following gastric bypass surgery. NAASO: The Obesity Society Annual Scientific Meeting Dallas Texas. Abstract 16-0R October. Allan C. 2009 Testosterone reduces visceral fat gain in non-obese older men. Journal of Clinical Endocrinology and Metabolism. 30: 139–146. American Dietetic Association ADA 2004 Guidelines for the use of nutritive and non-nutritive sweeteners. ADA 104 2 255–275. Behan K. Mbizo J. 2007 The relationship between waist circumference and biomarkers for disease in healthy non-obese women. American Society for Clinical Pathology 38 7 422–427. Better Health Channel 2008 Better Health Channel Fact Sheet: Weight Loss – Common Myths. Available at: htpp:// accessed January 2008. Brand-Miller J Hayne S petocz P Coalgiuri S. 2003 Low glycaemic index diet in the management of diabetes: a meta-analysis of randomized controlled trial. Diabetes Care 26 8 2261–2267. Bravata D. Smith-Sprangler C. Sundaram V. 2007 Using pedometers to increase physical activity and health. A systematic review. Journal of the American Medical Association 298 2296–2304. Bouchard L. Drapeau V. Provencher V. Lemieux S. 2004 Neuromedin beta: A strong candidate gene linking eating behaviours and susceptibility to obesity. American Journal of Clinical Nutrition 80 6 1478– 1486. Burdette H. Whitaker R. 2005 A national study of neighbourhood safety outdoor play television viewing and obesity in preschool children. Pediatrics 116 3 657–662. Dietitians Association of Australia 2009 Evidence based practice guidelines for the nutritional management of malnutrition in adult patients across the care continuum. Nutrition and Dietetics 66 Supp S4–S10. Donohoe M. 2008 Weighty matters: Public health aspects of the obesity epidemic. Medscape Obstetrics and Gynaecology and Women’s Health. Available at acccessed January 2008. Carnethon M. de Chaves P. Biggs M. et al. 2012 Association of weight status with mortality in adults with incident diabetesJournal of the American Medical Association 3086 581–590 Carey V. Bishop L. Charleston J. 2005 Rationale and design of the optimal macronutrient intake heart Omni-Heart trial. Clinical Trials 2 6 529–537. Caruso M. Pekarovic S. Raum W. Greenway F. 2007 Topical treatments for fat reduction do they work A best evidence review. Diabetes Obesity and Metabolism 9 300–303. Clemson L. Fiatarone Singh M. et al. 2012 Integration of balance and strength training into daily life activity to reduce falls in older people the LIFE study: Randomized parallel trial. British Medical Journal 345e4547 DOI:10.1136bmj.e4547. Deutsch L. 2007 Evaluation of the effect of Neptune krill oil on chronic inflammation and arthritis symptoms. Journal of American College of Nutrition 26 1 39–48. Conn V. Hafdahl A. 2007 Metabolic effects of interventions to increase exercise in adults with Type 2 diabetes. Diabetologia 50 913–921. DAFNE Study Group 2002 Training in flexible intensive insulin management to enable dietary freedom in people with Type 1 diabetes: Dose adjustment for normal eating DAFNE randomized controlled trial. British Medical Journal 325 746. Diehr P. Bild D. Harris T. 1998 Body mass index and mortality in non-smoking older adults. The cardiovascular effects. Journal of Public Health 88 623–629. Diehr P. O’seara E. Fitzpatrick A. Newman A. 2008 Weight mortality years of healthy life and active life expectancy. Journal American Geriatric Society 56 1 76–83. Dunning T. Hoy S. 1994 What To Do Till the Dietitian Gets There. Servier Australia Melbourne. Eddy S. 2008 Omega-6 and 9 fatty acids. Journal of Complementary Medicine 7 2 34–39. Egger G. Thorburn A. 2005 Environmental policy approaches: Methods of dealing with obesity in Clinical Obesity in Adults and Children 2nd edn eds Kopleson P. Caterson I. Deitz W. Blackwell Publishing Oxford. Erlichman J. Kerbey A. James W. 2002 Physical activity and its impact on health outcomes. Paper 2: prevention of unhealthy weight gain and obesity by physical activity: An analysis of the evidence. Obesity Review 3 273–287. Elmore J. Carney P. Abraham L. 2004 The association between obesity and screening mammography accuracy. Archives of Internal Medicine 164 1140–1147. Feskanich D. Rockett H. Colditz G. 2004 Modifying the healthy eating index to assess diet quality in children and adolescents. Journal of the American Dietetic Association 104 9 1375–1383. Fung T. 2007 DASH-style diet may reduce risk of CHD and stroke. American Heart Association Scientific Sessions Abstract 2369. November 5th. van Gaal L. Rissanen A. Scheen A. 2005 RIO-Europe Study

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Nutrition Obesity and Exercise 97 group. Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: 1-year experience from the RIO-Europe Study. Lancet 365 1389–1397. Galuska D. Will J. Serdula M. Ford E. 1999 Are health care professionals advising obese patients to lose weight Journal of the American Medical Association 282 1576–1578. Gardner C. Kiazand A. Alhassan S. 2007 Comparison of the Atkins Zone Ornish and LEARN diets for change in weight and related risk factors among overweight premenopausal women: The A to Z Weight Loss Study: A randomized trial. Journal of the American Medical Association 297 969–977. Goldfield G. Mallory R. Parker T. Cunningham T. Legg C. 2007 Effects of modifying physical activity and sedentary behaviour on psychosocial adjustment in overweight/obese children. Journal of Pediatric Psychology 32 7 783–793. Havel P. 2007 Fructose but not glucose consumption linked to atherogenic lipid profile. American Diabetes Association 67th Scientific Sessions Abstract 0062-0R June. ICCMR 2008 International Council Complementary Medicine Research march. 29–31 Sydney. Iqbal O. 2007 Endocannabinoid system and pathophysiology of adipogenesis: Current management of obesity. Personalised Medicine 4 3 307–319. James D. Coster A. 2011 Identifying the enemy in the battle against diabetes and obesity. Diabetes Management Journal 37 68. Kapur K. Kupur A. Ramachandran S. et al. 2008 Barriers to changing dietary behaviour. Journal of the Association of Physicians in India 56 27–32. Kapur K. Dunning T. 2007 Global nutritional recommendations: A combination of evidence and food availability. Practical Diabetes International 24 9 1–8. Kraus E. Levine B. 2007 Aerobic and resistance training improves glycaemic control in Type 2 diabetes. Annals of Internal Medicine 147 357–369 423–425. Kondrup S. Allison S. Elia M. Vallas B. Plauth M. 2003a EPSEN guidelines for nutrition screening 2002. Clinical Nutrition 22 4 415–421. Kondrup J. Rasmussen H. Hamberg O. 2003b Nutritional risk screening NRS 2002: A new method based on an analysis of controlled clinical trials. Clinical Nutrition 22 321–336. Lamberg L. 2006 Rx for obesity: eat less exercise more and – maybe get more sleep. Journal of the American Medical Association accessed February 2008. Latner J. 2001 Staff help in the treatment of obesity. Obesity Review 2 87–97. Malnutrition Advisory Group MAG 2000 MAG – Guidelines for Detection and Management of Malnutrition. British Association for Parenteral and Enteral Nutrition Redditch UK. Marks S. 2000 Obesity management. Current Therapeutics 41 6. Marsh K. 2008 Vegetarian diets and diabetes. Diabetes Management Journal 26 14–15. Middleton M. Nazarenko G. Nivison-Smith I. Smerdely P. 2001 Prevalence of malnutrition and 12- month incidence of mortality in two Sydney teaching hospitals. Medical Journal of Australia 31 455–461. Mitka M. 2003 Surgery for obesity: Demand soars amid scientific ethical questions. Journal of the American Medical Association 289 1761–1762. Miyashita K. 2006 Brown seaweed may burn away brown fat. American Chemical Society 232nd National Meeting and Exposition San Francisco 10–14th Sept. Moyad M. 2004 Fad diets and obesity-Part 1: Measuring weight in a clinical setting. Urology Nurse 24 2 114–119. Muhlhauser I. Berger M. 2002 Patient education –evaluation of a complex intervention. Diabetologia 45 1723–1733. National Health and Medical Research Council NHMRC 1999 Diet for Older Australians. Commonwealth of Australia Canberra. National Health and Medical Research Council NHMRC 2003 Dietary Guidelines for Australian Adults. NHMRC Ref. No. N29-N34. National Health and Medical Research Council NHMRC 2006 Healthy eating Club Fact Sheets: fat cholesterol. accessed January 2008. Peterson P.N. Magid D.J. Ross C. 2008 Association of exercise capacity on treadmill with future cardiac events in patients referred for exercise testing. Archives of Internal Medicine 168 174–179. Pi-Sunyer F. 2006 Use of lifestyle changes treatment plans and drug therapy in controlling cardiovascular disease and obesity. Obesity 14 Suppl 3 135S–142S. Proietto J. Aly A. Barton M. Spalding A. Hagger V. 2012 Diabetes Australia position statement on bariatric surgery. Diabetes Management Journal 39 26–30. Rahman S. Morell M. Topping D. et al. 2007 Low glycaemic response cereals for enhanced human health. International Diabetes Monitor 19 3 21–25. Reynolds S. Yasuhukio S. Crimmins E. 2005 The impact of obesity on active life expectancy in older Americans. Gerontologist 45 438–444. Richardson C. Newton T. Abraham J. Sen A. Swartz M. 2008 A meta-analysis of pedometerbased walking interventions and weight. Annals of Family Medicine 6 1 69–77. Reid C. 2007

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98 Care of People with Diabetes Rizkalla S. 2007 Fish oil supplements cut adiposity in Type 2 diabetes. American Journal of Clinical Nutrition 86 1670–1679. Schauer P. Kashyap S. Wolski K. et al. 2012 Bariatric surgery versus intensive medical treatment in obese patients with Type 2 diabetes. New England Journal of Medicine DOI 10.1056/NEJM oa1200225. Shorrock I. Hannah J. 2011 Carbohydrate counting and insulin dose adjustment –group education for people with Type 2 diabetes. Journal of Diabetes Nursing 15 6 239. Stevens J. 2000 Impact of age on associations between weight and mortality. Nutrition Review 58 129–137. Smith-West D. 2007 Motivational interviewing improves weight loss in women with Type 1 diabetes. Diabetes Care 30 1018–1087. Spreadbury I. 2002 Comparison with ancestral diets suggest dense acellular carbohydrates promote an inflammatory microbiota and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metabolic Syndrome and Obesity 2012 5 175189. Stone A. Brownell K. 1994 The stress eating paradox: Multiple daily measurements in adult males and females. Psychological Health 9 425–436. Sydney-Smith M. 2000 Nutritional assessment in general practice. Current Therapeutics 41 9 13–24. Tay J. Brinkworth G. Noakes M. 2008 Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. American Journal of Cardiology 51 59–67. Truby H. Baic S. 2006 Randomised controlled trial of four weight loss programmes in the UK: Initial findings from the BBC “diet trials”. British Medical Journal 332 1309–1314. Third Joint Taskforce of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice 2003 European guidelines on cardiovascular disease prevention in clinical practice. European Journal of Cardiovascular Prevention Rehabilitation 10 Suppl. 1 S1–S78. van Uffelen J. Wong J. Chau J. 2010 Occupational sitting and health risks: A systematic review. American Journal of Preventative Medicine 39 379 – 388. Unger R. Scherer P. 2010 Gluttony sloth and the metabolic syndrome: A roadmap to lipotoxicity. Trends in Endocrinology and Metabolism 216 345–352. van de Veure N. de Winter O. Gir M. et al. 2006 Fasting blood glucose levels are related to exercise capacity in patients with coronary artery disease. American Heart Journal 152 3 486–492. Vellas B. Guigoz Y. Garry P. 1999 The Mini Nutritional Assessment MNA and its use in grading nutritional state of elderly patients. Nutrition 15 116–122. Williams P. 2008 Asymmetric weight gain and loss from increasing and decreasing exercise. Medicine Society for Sports Exercise 40 2 296–302. Wilmot E. Edwardson C. Achana F. et al. 2012 Sedentary time in adults and the association with diabetes cardiovascular disease and death: A systematic review and meta-analysis. Diabetologia DOI:10.1007/s00125-012-2677-z World Health Organisation WHO 2000 The World Health Report – Reducing Risk Promoting Healthy Life. WHO Geneva Switzerland. Zemel M. 2003 Role of dietary calcium and diary products in modulating adiposity. Lipids 38 139–146. Zhong X.L. Sikaris K. 2011 Vitamin D deficiency and diabetes: A review of recent data from the AusDiab study. Diabetes Management Journal 37 18–19. Further reading Australian Government 1991 Australian Dietary Guidelines Australian Government Publications Canberra. Barclay A. 2012 Fructose. Diabetes Management Journal 39 1213. Block G. 1982 A review of validations of dietary assessment methods. American Journal of Epidemiology 115 492–505. British Diabetic Association 1992 Dietary recommendations for people with diabetes. Diabetic Medicine 9 189–202. Encinosa W. Bernard D. Steiner C. Chen C. 2006 Healthcare utilization and outcomes after bariatric surgery. Medical Care 44 706–712. Grontved A. Hu F.B. 2011 Television viewing and risk of Type 2 diabetes cardiovascular disease and all- cause mortality: A meta-analysis. Journal of the American Medical Association 305 2448 – 2455. Jespersen I. 2001 The effect of dietary oils on blood lipids and the risk of ischemic heart disease with special emphasis on olive oil. A literature review. Ugeskr Laeger 163 35 4736–4740. Katan W. 1990 Biochemical indicators of dietary intake. European Journal of Clinical Nutrition 52 S5. Keleman L. Jacobs D. Cerham J. 2005 Association of dietary protein with disease and mortality in a prospective study of postmenopausal women American Journal of Epidemiology 161 3 239–249.. National Cholesterol Education Program NCEP Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults 2002 Adult Treatment Panel 111 Final Report. Circulation 106 25 3143– 3421.

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Nutrition Obesity and Exercise 99 National Institutes of Health NIH Office of Dietary Supplements IBIDS database. Available at: accessed January 2008. Tsai A. Wadden T. 2005 Sytematic review: An evaluation of major commercial weight loss programmes in the United States. Annals of Internal Medicine 142 56–66. Weiss E. 2007 Certain factors associated with weight regain after weight loss. American Journal of Preventative Medicine Online June 5th 2007. Available at: anneweiss/ accessed December 2012.

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100 Care of People with Diabetes Chapter 5 Medicines Management To Cure Diabetes Naturally Click Here All things are poison and nothing is without poison. Only the dose distinguishes the killer from the cure. Paracelsus circa 1493–1541 Key points • Medicines should be managed within the principles of the Quality Use of Medicines and pharmacovigilance. • Understanding the pharmacology of the different glucose-lowering medicines and other medicines enables meals activity and medicine administration times to be planned appropriately to suit the individual. • Medicines are the cause of many preventable adverse events including death of people in hospital. • Medicine-related outcomes need to be proactively monitored according to management targets the indications for their use and individual benefits and risks. • Type 2 diabetes is a progressive disease of beta cell decline and insulin will eventually be needed by 50 of people with Type 2 diabetes. • Polypharmacy is common in diabetes especially Type 2 and older people and could be considered best practice but it increases the risk of adverse events including medicine interactions. • Medicine-related non-adherence is common complex and multifactorial. It has its basis in patient and health professional-related issues as well as environmental and system-related issues. • People with diabetes frequently use complementary medicines/therapies CAM which needs to be considered when selecting diabetes management options. Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning.

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© 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. Introduction The main ‘diabetes medicines’ listed below are discussed in this chapter. Other medicines are described in the relevant chapters: likewise the management targets for blood glucose HbA1c lipids blood pressure and weight are described in Chapter1. 1 Oral glucose-lowering medicines GLM 2 Insulin 3 Lipid lowering agents 4 Cardiovascular agents 5 Antiplatelet agents. The author prefers to use the term ‘medicines’ rather than ‘drugs’ which is reserved for describing illegal drugs. Medicines should be managed within a quality use of medicine framework QUM which is an holistic risk management approach that encompasses all types of medicines and recommends using non-medicine options first. The other key principle is pharmacovigilance to reduce the risk of adverse events and monitor medicine use appropriately to achieve optimal outcomes. People with diabetes also frequently use complementary medicines CAM and these are discussed throughout the book but principally in Chapter 19. Medicines are also mentioned in other chapters throughout the book where relevant. Quality Use of Medicines QUM The information in this section was adapted from The Quality Use of Medicines in Diabetes QUM 2005 a paper developed by the Pharmaceutical Health and Rational use of Medicines PHARM Committee a Committee of the Australian Commonwealth Department of Health and Ageing DOHA. The figure is reproduced with DOHA’s permission. The Australian medicines system has been reviewed and revised since 2005 and PHARM no longer exists but QUM is still central to medicines use and policies in Australia and has been adopted in many other countries. QUM also encompasses complementary medicines Dunning 2005. QUM aims to help health professionals and consumers make the best possible use of medicines to improve their health outcomes. QUM recognises the central role of the consumer in medicines use and that many people maintain their health without using medicines while for others medicines are important to their health and well-being. It also recognises that medicines may be needed for prevention as well as treatment. QUM means: • ‘Selecting management options wisely • Choosing suitable medicines if a medicine is considered necessary • Using medicines safely and effectively’ which includes monitoring the outcomes dose adjustments undertaking structured medicine reviews and de-prescribing when indicated DOHA 2002. Thus QUM highlights health professional’s responsibility for safe effective medicines use in addition to the need to consider patient adherence which is influenced by health professionals’ knowledge attitudes behaviours and communication and teaching skills. Medicines Management 113 Quality Use of Medicines and Diabetes Medicines are central to effective diabetes management to control metabolic abnormalities and managing the complications of diabetes and other concomitant conditions. However even when medicines are required lifestyle factors diet exercise and smoking cessation are necessary to achieve optimal outcomes. Prevention programmes have a central primary and ongoing role DOHA 2001. Medicines are used in four main areas in diabetes:

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102 Care of People with Diabetes 1 Primary prevention focuses on lifestyle factors to prevent or delay the need for medicines in those at risk of diabetes and its complications. However medicines may be needed for prevention for example lipid-lowering and antihypertensive medicines and flu vaccine to prevent intercurrent illness in at-risk individuals. 2 Secondary prevention where medicines are usually necessary to reduce the risk of diabetes complications such as renal disease atherosclerosis and retinopathy. 3 Clinical care which involves using medicines to achieve optimal metabolic psychological and quality of life targets by appropriately selecting management options including choosing suitable medicines if they are required obtaining informed consent enhancing informed decision-making by ensuring people have the information and skills needed to actively participate in medicine self-management and monitoring the outcomes to ensure medicines are used safely and effectively. Educating the individual with diabetes and their carers and supporting them to manage their diabetes generally and medicines in particular are key aspects of QUM. Medicines prescribed for other conditions self-initiated non-prescription medicines and CAM use need to be considered as part of a holistic assessment and care plan. Significantly polypharmacy is usually necessary to achieve optimal outcomes for/with people with diabetes and may be considered best practice. However polypharmacy increases the complexity risks and costs of the management regimen. Therefore as few medicines as possible should be used. Insulin and sometimes other medicines are needed at diagnosis in Type 1 diabetes and for many people with Type 2 and LADA. Type 2 diabetes is a progressive disease and consequently the medication regimen becomes progressively complex with increasing duration of the diabetes. 4 Clinical trials commonly investigate new medicines and other interventions before they are licensed for use to ensure they are safe and efficacious and to determine cost-benefit. Information from trials is also used to develop clinical practice guidelines and consumer and health professional information. Health professionals are often asked to help recruit participants for clinical trials. The fact that an individual is participating in a clinical trial should be clearly documented in the person’s medical record. QUM is a useful framework for reducing polypharmacy and duplicate prescribing and for de-prescribing because it encompasses prevention using non-medicine options regular medication reviews and effective communication among health professionals and with people with diabetes National Prescribing Service 2000. Medicines are selected taking into account: • The individual’s social physical and mental health status. • Whether there is a suitable non-medicine option. • The risks and benefits of using medicines for the individual including health literacy and functional and cognitive ability. • Dosage dose interval and duration of treatment. • Other medicines CAM and therapies that the individual might be using or considering. • The process required to monitor the outcomes of medicine use including adverse events medication self- management and other relevant self-care such as blood glucose monitoring processes for communicating the medication plan among the relevant health professionals when the individual makes transitions among health providers and services and strategies for regularly reviewing the continued benefits and risks of the medication regimen and the individual’s self-care capacity. • The costs to the individual the community and the health system. A process for integrating QUM into existing care is shown in Figure 5.1. Oral Glucose-Lowering Medicines GLM Different OHAs target the various underlying abnormalities of glucose homeostasis in Type 2 diabetes Chapter 1. They are not appropriate for Type 1 diabetes. Type 2 diabetes is a progressive disease of beta cell decline thus the medication regimen needs to be constantly monitored and adjusted and medicines included and de-prescribed as necessary. The UKPDS study Turner et al.1999 showed monotherapy was ineffective in 75 of people with Type 2 diabetes. Importantly an appropriate diet and exercise regimen are essential regardless of whether medicines are required. Sulphonylureas were the first GLMs to become available in the 1940s. The Biguanides followed in the 1950s. The value of these medicines has been established and they have been consistently improved over time with new

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generations of the original sulphonylureas. In addition new classes of GLMs have been introduced some of which might extend the life of the remaining beta cells and delay the need for insulin Dornhorst 2001. GLMs target the different underlying abnormalities of glucose homeostasis associated with Type 2 diabetes. These GLM are: • Biguanides which reduce hepatic glucose production and might improve peripheral glucose disposal and promote weight loss. It activates the energy regulating enzyme AMP-kinase in liver and muscle. Metformin is the medicine of first choice in overweight people with Type 2 diabetes UKPDS 1998. Biguanides are insulin sensitisers. • Sulphonylureas and Glitinides which are secretagogues that stimulate insulin release from the beta cells. Therefore the beta cells must be capable of responding by producing insulin. First generation sulphonylureas such as Chlorpropraminde and Tolbutamide are now rarely used in many countries and have been removed from the market in others. Secretagogues might be first-line treatment in people who are not overweight or who have contraindications to Metformin. • Alpha-glucosidase inhibitors which slow carbohydrate digestion and glucose absorption from the gut by inhibiting alpha-glucosidases in the brush border of the small intestine. Alpha-glocosidaises are essential to the release of glucose from complex carbohydrates. Alpha-glocosidaises reduce postprandial glucose levels. • Meglitinides which act on the same beta cell receptor as the sulphonylureas but are chemically different. • Thiazolidinediones TZD which increase whole-body sensitivity to insulins by activation of nuclear receptors and prompting esterifiation and storage of free fatty acids in subcutaneous fat tissue. They reduce daytime preprandial hyperglycaemia and have some effect on the fasting blood glucose. The two main TZDs are Rosiglitazone and Pioglitazone. The latter can be added to Metformin and sulphonylureas or substituted for these medicines if the individual is intolerant of them. Consider whether medicines have a role in primary prevention and investigations for diabetes. Primary prevention Lifestyle prescriptions. Regular sereening of people at risk. Identification of early signals and reduce risk factors Diabetes mellitus by education lifestyle modifications and regular diagnosed monitoring and screening. Type 1 Type 2 Gestational Assess risk factors Assess complications Diabetes specialist Disbetes educator Dietician and other specialist review Plan of management as indicated Education Diet Exercise Consider referral Adequate control Yes No Review by GP regularly Acute care Medications Hospitalisation Complication status needed Consider need for medicines in addition to lifestyle prescription. Type 1 insulin ± other medicines Type 2 OHA ± other medicines GDM insulin if lifestyle modification is not effective Initiate and titrate according to agreed guideliness Referral to specialist if necessary. Assess risk factors including body mass index age family history ethnicity symptoms including increased risk of heart attack. stroke erectile dysfunction and foot problems from high BGL. Consider contraindications to medication use if complications develop e.g. renal disease. Selecting medicines wisely when needed for investigative purposes or management. Educating consumer about medication management and sources of medication information and support in a format appropriate to the individual. Provide and discuss CMI with the individual. Develop a medication management plan. Review medication use. Monitor effectiveness – HbA 1c lipids BP weight BG self-monitoring and medicines self-management.

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104 Care of People with Diabetes Revise lifestyle self-care and medicines selfmanagement. Titrate dose and/or dose interval. Add other agents if indicated. Consider insulin in Type 2 if maximum dose of OHA or there are Cls to OHA. Manage intercurrent illness and/or behavioural cause of not meeting management targets. Monitor effectiveness. Consider HMR or RACMR. Document a medication history including current and past medicines self-prescribed and complementary therapies and any adverse drug events or risk factors for adverse events. Medication risk assessment – knowledge and attitudes vision dexterity communication mental functioning complication status – renal liver mental function. Medication action and discharge plan and follow-up procedures. Management of hypoglycaemic episodes. Develop medication template for self-care. Consider referral for HMR. CMIs† for new medicines. Discharge plan. Figure 5.1 The Quality Use of Medicines process applied to diabetes care reproduced from the Quality Use of Medicines in Diabetes Pharmaceutical Health And Rational use of Medicines PHARM Committee Commonwealth Department of Health and Ageing 2005. The medication regimen should be reviewed each time a new medicine is required if an adverse event occurs and at least annually as part of routine diabetes complication procedures included with permission. HMR home medicines reviews † CMI consumer medicines information. • Dipeptidyl peptidase-4 inhibitors DPP-4 which inhibit the activity of DPP-4 an enzyme that prolongs the activity of endogenous glucagon like peptide 1 GLP -1. • GLP-1 agonists GLP-1 is an incretin hormone secreted in the gut in response to food. GLP-1 amplifies insulin secretion from the beta cells and inhibits inappropriate glucagon secretion. GLP-1 also slow gastric emptying which slows post prandial food absorption and helps control postprandial blood glucose and reduces appetite. GLP-1 agonists mimic the activity of endogenous GLP-1 but are more resistant to being broken down by DDP- 4 which prolongs their action. • Sodium-glucose cotransporter-2 SGLT-2 acts independently of insulin secretion or action and target glucose reabsorption and induce glycosuria Whaley et al. 2012. Some SGLT-2 agents have been approved for use in Europe and the US but they are not yet approved in other countries. • Insulin. Various insulin preparations are available. Insulin can be used alone or in combination with metformin. In Type 2 diabetes Metformin and sometimes sulphonylureas are continued when insulin is initiated but the risk of hypoglycaemia must be considered when insulin and suphonylureas are combined NHS 2008 SIGN 2010 ADAESAD 2012 NPS 2012. The commonly available GLM are listed in Table 5.1. Blood glucose and HbA1c monitoring are essential to assess whether when and which GLM should be commenced and when insulin is required. When GLMs are commenced it is necessary to monitor the blood glucose in order to appropriately adjust the dose and dose interval. However the other factors that affect blood glucose and HbA1c must be considered. Normal endogenous insulin secretion consists of two components: 1 Basal secretion a constant low secretion rate to suppress hepatic glucose production between meals and overnight fasting. 2 Bolus secretion which occurs in response to increasing glucose levels after meals postprandial. These insulin boluses also consist of two phases: first phase an initial high spike which is lost early in the development of Type 2 diabetes and a lower more prolonged second phase. Insulin release is influenced by DPP-4 and GLP- 1.

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The different GLMs and insulins target the different components of glucose homeostasis. Testing the blood glucose is a key to determining medicine effectiveness. HbA1c only provides an overall average blood glucose level and does not account for glucose variability which influences complication risk see Chapters 3 and 8. Thus both measures provide important information as part of the total situation. Key blood glucose testing times are: 1 Before breakfast to assess the fasting blood glucose an indicator of overnight hepatic glucose output. 2 Postprandial usually two hours after food to assess glucose disposal. Postprandial hyperglycaemia is common in Type 2 diabetes because of the loss of first phase insulin response early in the course of the disease. Sometimes testing at both of these times will be required and sometimes overnight 2–3 a.m. to detect nocturnal hypoglycaemia see Chapter 6.

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106 Care of People with Diabetes

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108 Care of People with Diabetes

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110 Care of People with Diabetes

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Biguanides Biguanides are the medicine of first choice for overweight people with Type 2 diabetics when the HbA1c is 7. Metformin effectively lowers all-cause mortality and diabetes complications among overweight people with diabetes UKPDS 1998. It is also used to manage insulin resistance associated with PCOS where it may delay the progression to Type 2. Metformin is the most commonly used Biguanide. It acts by: • impairing the absorption of glucose from the gut • inhibiting hepatic glucose output • increasing glucose uptake in peripheral tissues muscle and fat • increasing the effects of insulin at receptor sites • suppressing the appetite mild effect. Practice points 1 Biguanides do not stimulate the production or release of insulin and therefore are unlikely to cause hypoglycaemia. 2 They have favourable effects on the lipid profile and slow glucose absorption from the intestine. 3 They do not stimulate the appetite and are unlikely to cause weight gain. 4 They have similar effects on HbA1c as sulphonylureas Table 5.1. Possible side effects 1 Nausea and/or diarrhoea occur in 10–15 of patients. Most patients tolerate Biguanides if they are started at a low dose the tablets are taken with or immediately after food and the dosage is increased gradually. • Lactic acidosis is the most significant side effect but it is rare and could be prevented by appropriate assessment monitoring and prescribing see Chapter 7. It occurs in at-risk people during acute infections acute kidney injury and decompensated heart failure which are independently associated with lactic acidosis Iedema Russell 2011. Although lactic acidosis is rare 48 cases were reported to the Australian Adverse Drug Reactions Advisory Committee ADRAC between 1985 and 2001. Of these known risk factors were present in 35 of the 48 cases Jerrall 2002. Salpeter et al. 2006 found no cases of lactic acidosis in a systematic review of comparative trials and cohort studies n 59320 patient years of metformin use. Salpeter et al. estimated the upper limit of true incidence of lactic acidosis per 100000 patient years was 5.1 in people using Metformin and there was no difference in lactate levels for Metformin compared with nonMetformin therapies. However the true clinical incidence is unknown and could be higher because not all adverse events are reported. Nisbet et al. 2004 identified 13 cases of lactic acidosis possibly related to Metformin since 2000. Of these two died three required dialysis for renal failure and one had severe neurological deficits and required nursing home care. The average age was 67 and average serum creatinine was 0.31 mmol/L normal 0.05–0.11 women 0.06– 0.12 men mmol/L. Nisbet et al.’s study highlights the importance of appropriate clinical assessment before prescribing or represcribing medicines especially in older people. The risk of lactic acidosis is increased in people with diseases likely to cause hypoxia such as alcohol abuse and liver renal and cardiac disease. However Ekstrom et al. 2012 found a reduced risk of all-cause mortality in an

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112 Care of People with Diabetes observational study of people on Metformin monotherapy with eGFR 45–60 ml/ min/1.73 squared and no increased risk of all-cause mortality acidosis serious infection or cardiovascular disease in people with eGFR 30–45 ml/min/1.73 squared n 51675. The authors concluded the benefits of Metformin outweigh the risks. Early signs of lactic acidosis include: anorexia nausea and vomiting abdominal pain cramps • weight loss • lethargy • respiratory distress. 2 Biguanides should not be prescribed: • during pregnancy • for people with chronic renal failure • Type 1 diabetes • any disease likely to cause hypoxia such as severe respiratory diseases and hepatic or cardiovascular disease. There is some evidence that at higher doses and longer duration of use Metformin inhibits absorption of vitamin B12. The metformin dose is the strongest predictor of vitamin B12 deficiency Ting et al. 2006. However Ting et al. did not assess calcium intake or measure vitamin B12 metabolites homocysteine and methylmalonic acid which could have affected the results. Nevertheless Vitamin B12 deficiency should be considered in people at high risk of malnourishment for example older people and those with eating disorders people who have been on Metformin for long periods of time especially at high doses and those with malabsorption syndromes such as coeliac disease. Biguanides should be ceased for two days before IVP CAT scans and investigations that require IV-iodinated contrast media to be used Calabrese et al. 2002. Sulphonylureas Sulphonylureas can be used alone or combined with Metformin. They can be used as first line therapy in non-obese people who are intolerant of or have contraindications to Metformin SIGN 2010. They are usually well tolerated but there is a tendency for people to gain weight especially with older sulphonylureas although these are rarely used nowadays. Weight gain occurs to a less extent with newer sulphonylureas Inzucchi 2002. They generally have a rapid onset of action except for long-acting formulations. Hypoglycaemia is a risk especially in older people on long-acting agents although these are rarely used and are no longer available in some countries. However Glibenclamide is available in combination with Metformin Glucovance. People with renal impairment and those who are malnourished are also at risk of hypoglycaemia. Sulphonylureas act by: • stimulating insulin secretion from the pancreatic beta cells • increasing the effects of insulin at its receptor sites • sensitising hepatic glucose production to inhibition by insulin. Possible side effects 1 Hypoglycaemia may result due to over-secretion of insulin if the dose of the medicine is increased food is delayed meals are missed or activity is increased see Chapter 6. 2 Liver dysfunction. 3 Nausea vomiting. 4 Various skin rashes.

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Medicines Management 113 5 Increased appetite. 6 Rarely agranulocytosis and red cell aplasia can occur. Note: points 2–6 are very uncommon. Sulphonylureas are contraindicated in pregnancy although they are used during pregnancy in some countries. They are mostly metabolised in the liver and severe liver disease is a contraindication to their use. Caution should be taken in people who are allergic to ‘sulphur medicines’ because the sulphonylureas have a similar chemical makeup. Meglitinides These medicines increase insulin secretion at meal times and they should only be taken with meals usually 2–3 times per day. They have the same effect on the beta cell receptor but a different chemical structure. They are short acting and have a low hypoglycaemic risk but hypoglycaemia is possible. They have not been assessed for beneficial effects on reducing micro-and macrovascular disease and are generally more expensive then other GLMs SIGN 2010. Meglitinides target early phase insulin secretion which is essential for postprandial glucose and control the postprandial glucose load Dornhorst 2001. In this way they initiate an insulin response pattern close to normal. They can be used in combination with Biguanides and possibly Thiazolidinediones TZD. The two main formulations are Repaglinide and Nataglinide. These medicines are rarely used in Australia because they are not listed on the PBS. However because of their short duration of action and the requirement to take them with meals they could be very useful in older people at high risk of hypoglycaemia. Thiazolidinediones The thiazolidinediones TZD are also known as peroxisome-proliferator-activated receptor PPAR- γ. TZDs lower fasting and postprandial blood glucose by increasing insulin sensitivity in muscle fat and liver cells. Some improve lipid profiles enhance insulin sensitivity and may restore the beta cell mass. They are given as a daily dose. It takes several days before they show an effect. There are two forms Pioglitazone and Rosiglitazone. Pioglitazone can be used as dual therapy in combination with Metformin OR a sulphonylurea in Type 2 diabetes when the HbA1c is 7 when combining Metformin and a sulphonylurea is contraindicated. Pioglitazone can be combined with insulin in Type 2 diabetes if the HbA1c is 7 despite treatment with OHAs and insulin OR insulin alone OR if Metformin is contraindicated. Rosiglitazone can be combined with Metformin AND a sulphonylurea in Type 2 diabetes when the HbA1c is 7 despite maximum tolerated doses of these medicines. TZDs reduce HbA1c by 1–2 Ko et al. 2006 with similar improvements to adding insulin. If adding a TZD does not adequately reduce HbA1c to 8 5 in three months insulin should be commenced Nathan Buse 2006. It is usual to start at low dose and monitor the person closely for signs of heart failure especially those with pre-existing cardiovascular disease. Significant cardiovascular disease is a contraindication to TZDs. Rosiglitazone might prevent or delay the transition to Type 2 diabetes in at-risk individuals DREAM 2006. However subsequent modelling of the DREAM data suggests people taking Rosiglitazone to prevent diabetes would end up taking more medicines than those who start medicines after diabetes is diagnosed and are at risk of TZD side effects Montori Isley 2007. SIGN 2010 stated there is no convincing evidence that Rosiglitazone as monotherapy has benefits over Metformin and sulphonylureas. Pioglitazone is associated with the risk of bladder cancer in people who use the medicine for over 12 months Lewis et al. 2011. The risk is greater in people with bladder cancer or a

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114 Care of People with Diabetes history of bladder cancer. People should be advised of the risk when discussing their medicine options. Pharmaceutical companies have revised their product information to reflect the risk. Side effects • Localised oedema which can be significant and may occur to a greater extent in people treated with TZD and insulin SIGN 2010. • Congestive cardiac failure and heart failure. People with diabetes are 2.5 times more likely to develop heart failure than non-diabetics Nichols et al. 2001 and TZDs increase the risk of heart failure. Rosiglitazone doubles the risk among those with pre-existing cardiovascular disease Home et al. 2009. Both TZDs are contraindicated in people with New York Heart Association Class III or IV heart failure. The person should be closely monitored for signs of heart failure such as oedema and rapid weight gain and importantly informed about these risks. • Myocardial infarction and death associated with Rosiglitazone Nissen Wolski 2007. This report caused significant debate among diabetes experts and stress for patients prescribed Rosiglitazone. The risk appears to be small DREAM 2006. The information should be used in the context of individual risk. For example Rosiglitazone might increase the risk of MI in people with ischaemic heart disease those on insulin or nitrates those with an atherogenic lipid profile and those at high risk of MI ADRAC 2007. Pioglitazone does not appear to carry the same risk because it has fewer adverse effects on lipids Dormandy et al. 2005. The RECORD study 2009 suggested there is a possible increase in cardiovascular events with Rosiglitazone in people with existing heart disease but the association was not statistically significant. The European Medicines Agency EMA 2010 reviewed all medicines containing Rosiglitazone that concluded the risks of Rosiglitazone outweigh the benefits and recommended marketing authorisation for all products containing Rosiglitazone be suspended across the European Union Rosi2011. Likewise the US Federal Drug Administration FDA added information about the cardiovascular risks of Rosiglitizone to the physician labelling and medication guide US FDA 2011. • Reduced red and white cell count. • Weight gain especially deposition of subcutaneous fat while visceral obesity is reduced. Weight gain appears to continue as long as TZDs are continued. Gains between 2 and 5 kg are reported Dormandy et al. 2005. However insulin also causes weight gain 3 kg as do sulphonylureas 4 kg. Weight gain is lower when patients are taking Metformin before a TZD is added Strowig et al. 2004. • Hypercholesterolaemia especially LDL-C Rosiglitazone. • Liver damage although it is uncommon. TZDs are contraindicated if liver disease is present or serum transiminase is 2.5 times the upper limit of the normal. Liver function tests should be performed before starting a TZD and then monitored regularly while the patient remains on TZDs. Signs of liver toxicity include nausea vomiting jaundice dark urine and right upper abdominal discomfort. • Macular oedema European Medicine Agency Press 2005. Macular oedema is a known complication of diabetes and there some reports the condition worsens with TZD. • Fractures occurring in the arms and lower leg usually in women Meier et al. 2008 however the risk is small. Fracture risk may be significant in older women at risk of osteoporosis and increase the risk of falls if the fractures occur in the feet or legs. People prescribed TZD especially women should be informed about the risk. • Women with polycystic ovarian disease should be counselled about contraception because TZDs may improve fertility in these women. • They are contraindicated in pregnancy and during breast feeding. • Care should be taken in lactose intolerant people because TZDs contain a small amount of lactose.

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Medicines Management 115 • Hypoglycaemia is possible because TZDs reduce insulin resistance and enhance the effectiveness of endogenous insulin. These data suggest a thorough assessment including a medication review is warranted before commencing TZDs. Health professionals and people with diabetes should be alert to the possibility of silent MI. Alpha-glucosidase inhibitors These medicines are usually taken in a TDS regimen. They act by slowing glucose uptake of many carbohydrates by inhibiting alpha- glucosidase which slows the metabolism of complex and simple carbohydrates in the brush border of the proximal small intestine so glucose absorption is spread over a longer time frame. Alpha-glucosidase inhibitors reduce fasting and postprandial glucose Rosak Mertes 2012. Their major side effects are due to the arrival of undigested carbohydrate in the lower bowel – bloating flatulence and diarrhoea. These symptoms can be distressing and embarrassing and people often stop their medications because of these side effects. Taking the medicines with meals starting with a low dose and increasing slowly to tolerance levels and careful explanation to the patient can reduce these problems. Hypoglycaemia is possible if alpha-glucosidase inhibitors are combined with other GLMs. They may be contraindicated or need to be used with caution in people with gastrointestinal disease such as gastroparesis coeliac disease and irritable bowel syndrome. Practice point Oral glucose may not be an effective treatment for hypoglycaemia occurring in people on alpha-glucosidase inhibitors because absorption from the gut will be delayed. IM Glucagon is an alternative. The incretin hormones The incretins enhance glucose-mediated insulin secretion by the beta cells. Approximately 60 of insulin secreted in response to food is due to the activity of incretins. The incretin effect is due to peptide hormones released by K and L cells in the intestine directly into the blood stream. The incretins include: 1 Glucose-dependent insulinotropic peptide GIP secreted by the K-intestinal cells. Postprandially GIP levels are 10 times higher than GLP-1 and have similar insulinotrophic actions when the glucose level is 6 mmol/L but its effects are limited at blood glucose levels 7.8 mmol/L. GIP does not inhibit glucagon secretion. 2 Glucagon-like peptide GLP-1 is secreted by the L-cells in the intestine. It primarily regulates postprandial glucose by slowing gastric emptying and reducing glucagon. It reduces appetite and may induce weight loss SIGN 2010 and it may stimulate beta cell proliferation Abraham et al. 2002. GLP-1 binds to its specific receptor but has a very short half-life 60–90 seconds because it is rapidly broken down by dipeptidyl peptidase- 4 DPP-4. Exanetide liragulitide and Lixisenatide are GLP-1 receptor agonist analogues and may improve metabolic control in people with BMI 30 kg/m squared with Type 2 diabetes. Lixisenatide is administered daily. GLP-1 agonists may not be beneficial in

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116 Care of People with Diabetes people with inadequate glycaemic control for 10 years: insulin may be the medicine of choice in these people SIGN 2010. 3 DPP-4 inhibitor analogues are oral GLMs such as Sitagliptin Vildagliptin and Saxagliptin that inhibit the action of DDP-4 and consequently increase postprandial GLP concentration which increases insulin secretion reduces glucose-dependent glucagon secretion and reduces HbA1c 0.5–0.8 Nathan Buse 2006: Inzucchi et al. 2012. DPP- 4 are listed in most countries as add-on therapy with Metformin or a sulphonylurea where a combination of the latter two medicines is contraindicated and particular prescribing recommendations may apply in particular countries NICE 2008 SIGN 2019 NPS 2011. Recently The European Commission approved the combination of Metformin and Linagliptin a DPP-4 inhibitor. Side effects • The effects on long term outcomes are not yet known. Side effects include nasopharyngitis and upper respiratory tract infections which are common and hypersensitivity reactions. • Pancreatitis has been reported with Sitagliptin and Vildagliptin although a causal association has not yet been confirmed NPS 2011 and 2012. • Vildagliptin and Saxagliptin should be avoided in people with renal impairment creatinine clearance 50 ml/mim. • Vildagliptin is not recommended in people with liver disease. Sitagliptin should be used cautiously in people with liver disease. • Sitagliptin has been associated with anaphalyxis angioedema rashes urticaria and exfoliative skin conditions but these side effects are rare NPS 2011. • Weight gain can occur when the gliptins are used with a sulphonylurea. • Hypoglycaemia can occur when the gliptins are used with a sulphonylurea. • Gastrointestinal side effects. New medicines for type 2 diabetes Sodium-glucose cotransporter-2 SGLT2 inhibitors SGLT2 inhibitors are a new class of GLM that target renal glucose reabsorption and induce glucose excretion in the urine independently of insulin secretion or action and are used in type 2 diabetes Whaley et al. 2012. Trials show SGLT2 medicines reduce hyperglycaemia fasting and postprandial blood glucose and HbA1c hypertension and weight. They have a low hypoglycaemia risk and may be able to be combined with insulin and other GLMs Whaley et al. 2012. SLGT2 include Dapagliflozin and Canagliflozin and are administered one per day. Side effects Clinical experience with SLGTs is limited at present. Reported side effects include: • Increased incidence of urinary tract infections which could put individuals with automomic neuropathy affecting the bladder at particular risk. • Increased incidence of genital fungal infections. • Polyuria in volume-sensitive people which could predispose them to dehydration e.g. older people. • Canaglifozin may appears to be less effective in people with renal impairment. • Concerns have been raised about the risk of cardio-and cerebrovascular disease because of the effects on cholesterol. • Canaglifozin increases LDL cholesterol but it also increases HDL though it is not clear whether the benefits outweigh the risks at this stage.

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Medicines Management 117 Canaglifozin was approved by the FDA in March 2013. The US FDA did not approve Dapagliflozin in 2012 because of safety concerns such as increased risk of breast and bladder caner but it was approved in Europe in 2012 under the brand name Forxiga. Antibody 2H10 Antibody 2H10 appears to slow or reverse the progression to Type 2 diabetes in mice. 2H10 may block a protein called vascular endothelial growth factor BVEGF-B which influences fat transport and storage in body tissue such as the heart. Thus 2H10 appears to target insulin resistance. However the antibody is in the very early stage of medicine development and has not yet been tested in humans. Medicine interactions Some possible interactions between GLMs and other commonly prescribed medicines are shown in Table 5.2. Some medicines interact with GLM and can cause hypo- or hyperglycaemia. A number of mechanisms for the interactions are known and they include: • displacing the medicine from binding sites • inhibiting or decreasing hepatic metabolism • delaying excretion • reducing insulin release • antagonising insulin action. Potential medicine and herb or herb/herb interactions and food/medicine interactions should also be considered when introducing a new medicine or reviewing the medicine regimen see Chapter 19. For example over 95 medicines administered by mouth can interact with grapefruit including antihypertensive agents some antibiotics cancer and cardiovascular medicines Bailey 2012 and interactions can occur even if grapefruit is taken several hours before taking the medicine. In addition other citrus fruits may also interact but have not been widely studied to date. Interactions can also lead to micronutrient deficiency Braun Rosenfeldt 2012. Potential interactions have not yet fully emerged for TZIs and the incretins gliptins. Medicines that alter hepatic enzymes have the potential to cause interactions with these GLMs because they are metabolised in the liver. Medicines that interfere with access to the gut by alpha-glucosidase inhibitors can inhibit their action for example charcoal digestive enzymes Cholestyramine Neomycin and some CAM medicines such as slippery elm. Table 5.2 Potential medicine interactions between glucose-lowering medicines and other medicines Data from Shenfield 2001. Medicine Possible mechanism Medicines that increase blood glucose Clonidine Adrenergic response Clozapine Impaired insulin secretion Corticosteroids Oppose insulin action Diuretics especially Thiazides Oppose insulin action Nicotinic acid Unknown Nifedipine Delays insulin action Oral contraceptives Unknown Phenytoin Impairs insulin secretion

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118 Care of People with Diabetes Glucocorticoids Antipsychotics especially atypical antipsychotics Cause insulin resistance and weight gain Sugar-containing medicines for example cough syrup Medicines that lower blood glucose Increase blood glucose ACE inhibitors Enhance insulin action Alcohol Reduce hepatic glucose production Fibrates such as gemfibrosil Unknown MOA inhibitors Unknown Salicylates in high doses some herbal medicines contain salicylic compounds Unknown Practice points 1 The clinical relevance of some postulated medicine interactions is uncertain. 2 Other miscellaneous interactions that should also be considered are: • beta blockers can mask tachycardia and other signs of hypoglycaemia resulting in delayed recognition and treatment increasing the risk of hypoglycaemic coma. • chronic alcohol consumption can stimulate the metabolism of sulphonylureas and delay their effectiveness cause hypoglycaemia mask signs of hypoglycaemia and with Metformin predispose the individual to lactic acidosis. It may also increase the bioavailability of ACE-1. Combining GLMs and insulin Any combination of currently available GLM only lowers HbA1c by 3 American Association of Endocrinologists 2011 thus people with HbA1c 10 are unlikely to achieve management targets using GLM alone. Therefore insulin is assuming an increasingly important role in Type 2 diabetes. As indicated most people with Type 2 diabetes have progressive beta cell dysfunction and a decline in beta cell mass. Proposed mechanisms for these defects include the interplay among a range of factors that reduce beta cell mass and secretory function such as hyperglycaemia elevated free fatty acids and inflammatory processes associated with adipocyte-derived cytokines. Apoptosis appears to be a key underlying mechanism Leiter 2006. In addition lifestyle factors concomitant diseases and often medicines compound the metabolic abnormalities. In some cases medication non- adherence may be a factor and should be assessed in a nonjudgmental manner. Goudswaard et al. 2004 showed continuing Metformin when insulin is commenced is associated with lower HbA1c by up to 0.6 and less weight gain without increasing hypoglycaemia risk. Continuing sulphonylurea when initiating a daily insulin dose was associated with a greater HbA1c reduction than monotherapy. Likewise continuing Metformin sulphonylurea or both when insulin is commenced results in lower insulin requirements compared with monotherapy. Various algorithms are available for initiating insulin and continuing one or more GLM NICE 2008 SIGN 2010 DA-RACGP 2011/12 NPS 2012. The medicines selected and the dose and dose regimen must be tailored to the individual’s needs. Generally bedtime NPH or a basal insulin analogue should be used when adding insulin to Metformin and/or a sulphonylurea depending on the hypoglycaemia risk SIGN 2010. Practice points • GLMs including insulin are not substitutes for healthy eating weight management and regular exercise.

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Medicines Management 119 • Medication administration times should be planned so that GLMs are administered with or before meals to reduce the risk of hypoglycaemia. When should insulin be initiated in Type 2 diabetes Commencing insulin should be a planned proactive decision and should not be delayed. Some experts refer to ‘tablet failure’ as a reason for initiating insulin. The choice of words should be considered carefully when conveying the need for insulin to a person with diabetes: they may interpret ‘tablet failure’ to mean they have failed Diabetes Australia 2011/12. Clinical observations • The challenge for health professionals is to balance the optimal time to initiate insulin with the time the individual is ready to accept insulin. • Culture literacy beliefs experience and social situation are some of the factors that affect people’s readiness to accept insulin. • Interestingly doctors and probably other health professionals frequently do not follow recommended guidelines for various reasons such as resource and time constraints because they are ‘slow adopters’ or because they use complex individual decision-making heuristics Choudhry Fletcher 2005 Tung 2011. The time of day to administer insulin in Type 2 diabetes depends on the individual’s blood glucose pattern HbA1c adherence to medicines and complication status especially cardiovascular and renal status and willingness to use insulin. Often a basal insulin is initiated at bedtime and the dose adjusted according to the fasting prebreakfast blood glucose. Prandial insulin before one or more meals is added if HbA1c and blood glucose targets are not achieved. A general guide to deciding insulin requirements when initiating insulin follows but individual needs and blood glucose pattern and frequency of hypo- and hyperglycaemia must be considered. Indications for insulin include: • Women with Type 2 diabetes who become pregnant and sometimes women with gestational diabetes see Chapter 14. • When the person actually has LADA see Chapter 1. • As rescue therapy in DKA HHS during other acute illnesses and surgical procedures see Chapters 7 and 9. • Persisting hyperglycaemia indicated by elevated fasting blood glucose and/or elevated postprandial blood glucose and HbA1c above the individual’s target e.g. HbA1c 7 . • Symptoms especially polyuria polydipsia and weight loss. • GLM intolerance or contraindication for example Metformin if creatinine is high. • People on two GLMs and not achieving targets where insulin may be preferable to adding a third GLM given that most people with Type 2 diabetes eventually need insulin especially if the GLMs are at maximal doses. However there is no consensus about whether the second agent added to Metformin should be another GLM or insulin. Insulin might be preferable if the HbA1c is 8.5 or the person is very symptomatic Nathan Buse 2006 or when there is a high tablet burden polypharmacy. In such presentations LADA should be considered especially if the individual is thin. The National Prescribing Service advised health professionals to be ‘… more aggressive in their management of people with Type 2

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120 Care of People with Diabetes diabetes’ NPS media release 26 March 2008 a sentiment echoed by other experts. However the benefits of ‘insulin aggression’ need to be balanced against the risks such as hypoglycaemia and its consequences falls in older people MI effects on cognition. • Recent research suggests insulin may have anti-inflammatory properties in addition to its other actions Dandona et al. 2008. The goals are to achieve optimal control without causing hypoglycaemia or excessive weight gain and with minimal impact on lifestyle. Thus understanding the individual’s perspective is essential. For some people commencing insulin and ceasing GLMs may represent a simpler more manageable medication regimen for others it represents ‘the end of the line’ or ‘the last resort.’ Insulin is often added to the GLM regimen at bedtime to reduce fasting glucose levels Riddle et al. 2003 Janka et al. 2005. The dose is titrated according to the fasting blood glucose pattern including self-adjustment by the person with diabetes to achieve targets with minimal hypoglycaemia according to a simple algorithm Yki-Jarvinen et al. 2007. Yki- Jarvinen et al. showed insulin could be successfully initiated in groups and achieve glycaemic targets. In addition group insulin initiation was acceptable to patients. The specific initiation process depends on the policies and guidelines of individual health services. Over recent years research has demonstrated the efficacy of several processes for initiating and titrating insulin in Type 2 diabetes using various insulins and usually starting with small doses. They all used a stepwise approach and include: • The Treat-to-Target study used basal Glargine at bedtime and titrated the dose weekly in 10 weeks Riddle et al. 2003. This regimen is suitable for older people because it is associated with fewer hypoglycaemic events and is well tolerated Janka et al. 2005. Isophane insulin can also be used as the basal insulin but has a higher risk of hypoglycaemia. • The 1-2-3 study which used daily bedtime doses of NovoMix 30 initially and subsequently added doses pre-breakfast then pre-lunch if necessary to achieve targets Raskin et al. 2005. • The INITIATE study that used BD doses of NovoMix 30 Jain et al. 2005. The stepwise approach is also used with insulin analogues such as long-acting basal lantus Detemir and Degludec an ultra long acting preparation currently in phase three clinical trials and rapid acting prandial insulins such as Novorapid. The advantage of using basal bolus insulin dose regimens is that they usually achieve better postprandial control but eating after injecting the insulin is important. BD Lispro/ isophane mix and Metformin also improves pre- and postprandial blood glucose with few episodes of nocturnal hypoglycaemia Malone et al. 2005. Many researchers have compared different brands of insulin and dose regimens. Overall the findings suggest the pharmacokinetic differences among insulin brands may not be clinically relevant and there are likely to be variations in individual patient’s response to the different formulations Zeolla 2007. The ultralong acting basal insulin in phase three testing Degludec appears to cause less nocturnal hypoglycaemia in Type 1 and Type 2 diabetes and reduce fasting glucose Wang et al. 2012. In reality the choice of insulin may actually be made according to prescriber preference and local availability. Despite the similarities indiscriminate switching between different insulin brands or using different brands together is not generally recommended. Outpatient or community-based insulin initiation is preferable except in specific circumstances. A proforma initiation process is outlined in this chapter that can be adapted as necessary and a simple algorithm for commencing insulin in Type 2 diabetes is shown in Table 5.3 and Figure 5.2. Often GLMs are continued with basal insulin regimens if there are no

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Medicines Management 121 contraindications to their use. When bolus insulin doses are added insulin secretagogue doses usually need to be reduced or the medicines discontinued. The algorithm is based on the premise that the individual undertakes blood glucose monitoring relevant monitoring and assessments are undertaken relevant education is provided and the response to therapy is monitored at each step. Consider LADA if the person is not overweight loses weight has significant hyperglycaemia and is very symptomatic because insulin should not be delayed in these people see Chapter 1. Management aims: 1 Proactively initiate insulin. Insulin should not be delayed. 2 Control fasting and postprandial hyperglycaemia without causing serious hyperglycaemia. 3 Achieve HbA1c target relevant to the age of the individual generally 7 but maybe higher in older people. 4 Normalise lipids to reduce cardiovascular risk. 5 Control symptoms. GLM glucose lowering medicines TZD Thiazolidinediones.

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Table 5.3 Simple decision-general guide to deciding insulin doses and dose regimen when commencing insulin NICE 2008 DA-RACGP 2011/12 however guidelines and protocols in use should be followed. Insulin doses are adjusted by 2–4 units according to the blood glucose pattern every 3–4 days to reach the target blood glucose range and avoid hypoglycaemia. Issues to consider HbA 1c Insulin doses and administration times Consider current diabetes management and glycaemic status Decide on a safe blood glucose target range for the individual Decide whether to administer insulin as a daily basal dose and/or bolus doses and when the insulin will be administered on the basis of the amount of insulin required per day and whether oral GLMs will be continued 7 7 Insulin in units/kg depending on pre insulin treatment and weight diet alone 0.2 GLMs 0.3 diet alone 0.3 GLMs 0.4 Morning blood glucose high and evening blood glucose acceptable Morning blood glucose acceptable and evening blood glucose high Morning blood glucose high and evening blood glucose high Pre-bed basal insulin Morning basal insulin Basal bolus regimen that could be with a long acting analogue before bed or before breakfast and TDS rapid acting insulin OR BD premixed insulin OR morning Isophane insulin and TDS rapid-acting insulin Diagnosis Add one GLM Diet and exercise +/– GLM Metformin in overweight individuals Trial for 3 months Trial for 3 months Add second medicine usually an GLM e.g. sulphonylurea Trial for 3 months HbA 1C ≥6.5–7 HbA 1C ≥7.3 Add a third GLM e.g. a TZD Add insulin e.g. OR Basal long-acting analogue at bedtime and titrate the Initiate insulin: preferred if HbA 1C8 dose weekly Do not use GLM above maximal OR doses Isophane 6–10 units at bedtime and adjust the dose by Trial for 3 months 2 –4 units every 3–4 days to gradually achieve the targets Aim for fasting blood glucose 4.0–6.0 mmol/L Monitor for 3 months If the target is not achieved with 50 units of basal insulin add a second dose of insulin e.g. premixed insulin 30/70 Give 2/3 of total dose before breakfast and 1/3 before evening meal OR Institute basal bolus regimen depending on the patient: rapid-short-acting before each meal and long-acting analogue of Isophane at night Cease GLM Figure 5.2 Algorithm for achieving blood glucose targets in Type 2 diabetes that encompasses a Quality Use of Medicines approach and adopts a proactive stepwise approach to initiating insulin.

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Medicines Management 123 Barriers to insulin therapy There are many barriers to initiating insulin therapy in Type 2 diabetes: most relate to the individual with diabetes and some to health professional factors. Although patients often view insulin negatively early explanations about the nature of Type 2 diabetes from diagnosis and with support and encouragement most people usually accept they need insulin. However their fears and concerns must be acknowledged respected and explored. People often regard insulin as ‘the last resort’ and fear hypoglycaemia and weight gain Dunning Martin 1999. The DAWN study Rutherford et al. 2004 showed that people on insulin worried about hypoglycaemia more than non-insulin users and insulin was associated with worse quality of life in people with Type 2 diabetes. This finding continues to emerge in other studies for example MILES 2011. Type 2 diabetes is a silent disease with few symptoms thus it is often difficult for people to accept they have a serious progressive disease. Many worry about weight gain associated with insulin use. They are often reluctant to test their blood glucose frequently and feel blood glucose monitoring and insulin interferes with their lifestyle. For some people the stigma associated with needles is an issue. Many doctors are reluctant to use insulin in Type 2 diabetes and often compound the patient’s concerns albeit usually unintentionally by delaying insulin initiation. Such health professional behaviour has been referred to as ‘clinical inertia’ Shah et al. 2005 and like non-adherence is a complex multifactorial issue Tung 2011. Other health professional- related barriers include inadequate knowledge lack of time support and resources worry about causing hypoglycaemia and complicating the management regimen. For example UK practice nurses felt commencing insulin in primary care was beneficial for patients but lack of time support and confidence and concerns about medico-legal implications and personal accountability made it difficult to achieve Greaves et al. 2003. Some strategies to overcome the barriers The therapeutic relationship between the patient and the health professional has a significant effect on health outcomes and patient behaviours including adherence to medicines and improved safety Worthington 2003 Dunning . Thus a first step is to establish a non- judgmental trusting relationship. Specific approaches depend on the individual and the circumstances in which insulin is required. Health professionals need to acknowledge that: • People’s previous experience of insulin and beliefs about insulin. • Managing insulin is a complex process and is only one self-care and life task the person is expected to fulfill. • ‘Things might get worse before they get better’. For example vision often deteriorates temporarily. • The ability to self-care changes over time due to physical and mental functional changes: normal age-related changes and changes associated with diabetes complications. • Insulin side effects especially hypoglycaemia. • There are usually added costs involved. The transformational model of change can be a useful framework for addressing the need to commence insulin especially if it is integrated with aspects of the health belief model QUM and holistic care where insulin is discussed as one aspect to be addressed not an isolated event in a person’s life. Research suggests timing is important when trying to initiate change. That is it needs to be linked to an individual’s stage in the change process Prochaska Velicer 1997 and significant life transitions which are often also accompanied by changes in identity and behaviour George 1993 Dunning .

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124 Care of People with Diabetes Providing personalised and customised advice and written information is most useful when it is delivered in a caring relationship where the individual’s concerns are acknowledged and they are invited to suggest ways they could address the issues they identify. Thus listening clarifying and following up by asking about progress are essential. However despite the focus on patient-centred care the patient’s views are often not sought and they are inadvertently placed in a passive rather than an active role particularly when communication barriers such as language religion culture health literacy and numeracy hearing impairment or other disabilities are present. Identifying and discussing the person’s concerns is essential. For example ‘needle phobia’ weight gain and hypoglycaemia. Demonstrating the various insulin delivery devices often helps reduce some concerns about needles. People on insulin gain more weight than those on diet for over 10 years Mayfield White 2004 partly due to better glycaemic control and losing less glucose in the urine the fact that insulin is an anabolic hormone lower metabolic rate and people may eat more to prevent hypoglycaemia Birkeland et al. 1994. Levemir appears to cause less weight gain in both Type 1 and Type 2 diabetes Dornhorst et al. 2007 whereas Glargine is associated with a modest weight increase and hypoglycaemia ORIGIN 2012. Strategies to avoid weight gain include selecting insulin formulations and other medicines least likely to contribute to weight gain if possible regular exercise perhaps using a pedometer and individualised nutrition advice. Once symptoms are controlled people often feel more active and exercise helps control weight and blood glucose. Understanding and exploring the person’s concerns about hypoglycaemia and helping them identify strategies to reduce hypoglycaemic episodes. Although the UKPD showed the frequency and severity of severe hypoglycaemia was lower in people with Type 2 diabetes than Type 1 diabetes UKPDS 1998 more recent research suggests hypoglycaemia is a significant risk in both types of diabetes Chapter 6. The risk increases when the HbA1c is 7.4 and with insulin and oral insulin secretagogues. Carefully identifying hypoglycaemia risk factors with the individual and helping them develop strategies to minimise their individual risk is important. Vision can deteriorate when insulin is commenced. Sight is not usually threatened but it is very distressing for the person with diabetes and they need a careful explanation and reassurance to help them understand. Activities of daily living such as reading and driving can be affected. Visual changes occur because the lens absorbs excess glucose in much the same way as sponge soaks up water. Changes in the amount of glucose in the lens can lead to blurred vision and can occur with high and low blood glucose levels. This phenomenon is quite different from diabetic retinopathy which can threaten the sight. The starting dose may not be the ‘right’ dose and the ‘right’ dose changes according to specific circumstances and individual need. Insulin therapy Insulin is a high risk medicine Dooley et al. 2011 and is associated with significant adverse events including in hospitals and aged care facilities. For example 30 of unplanned hospital admissions for older people are associated with medicine-related adverse events Australian Commission on Safety and Quality in Health Care 2010. High risk medicines are likely to cause significant harm or death when given incorrectly. Even when used correctly insulin can cause significant harm. Over one third of medical errors that result in death involve insulin use within 48 hours of the death Anon 2005. Thus when considering insulin the individual’s risk of harm must be considered and preventative strategies used when possible. Overview of insulin action

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Medicines Management 125 Insulin is a hormone secreted by the beta cells of the pancreas. Normal requirements are between 0.5 and 1.0 units/kg/day. Insulin synthesis and secretion are stimulated by an increase in the blood glucose level after meals. Insulin attaches to insulin receptors on cell membranes to facilitate the passage of glucose into the cell for utilisation as fuel or storage and reduces hepatic glucose production. Insulin also stimulates the storage of fatty acids and amino acids facilitates glycogen formation and storage in the liver and skeletal muscle and limits lipolysis and proteolysis. Therefore insulin deficiency results in altered protein fat and carbohydrate metabolism also refer to Chapter 1. Insulin is vital to survival for people with Type 1 diabetes and is eventually required by most people with Type 2 diabetes. Objectives of insulin therapy 1 To achieve blood glucose HbA1c and lipid levels within an acceptable individual range by replacing absent insulin secretion in Type 1 and supplementing insulin production in Type 2 diabetes see previous section. 2 To approximate physiological insulin secretion and action. 3 To avoid the consequences of too much insulin hypoglycaemia or too little insulin hyperglycaemia . 4 Improve quality of life and reduce the risk of long-term diabetes complications. Types of insulin available Insulin cannot be given orally at this stage. It is a polypeptide. Polypeptides are digested by gastric enzymes and do not reach the circulation. Research is currently underway to coat insulin in a substance that can withstand gastric juices and enable it to pass unchanged into the intestine before breaking down. Inhaled insulin is also the subject of research but is not generally used in clinical practice and some nasal insulin trials have been abandoned. A number of different brands of insulins are available for example Novo Nordisk Eli Lilly and SanofiAventis. As indicated the insulins are all effective and safe. Animal insulins bovine and porcine are rarely used nowadays but still available in some countries often under special access schemes. ‘Human’ insulin HM is manufactured by recombinant DNA technology. The amino acid sequence of HM insulin is the same as that of insulin secreted by the beta cells of the human pancreas. Rapid acting insulin analogues prandial insulins have been developed that give a more physiologic response after injection and improve the blood glucose profile for example Humalog Aspart and Apidra. The advantages of these insulins are reduced postprandial hyperglycaemia and reduced risk of hypoglycaemia. Long-acting analogues are Glargine and Levemir. Glargine has a slower onset than Isophane insulins and a smooth peakless action profile for up to 24 hours Buse 2001. Levimir may be shorter acting than Glargine and has its maximal effect between 3 and 14 hours. Recently and ultra-long acting insulin Degludec was introduced but clinical experience with this insulin outside research trial is limited. These insulins enable greater management flexibility and lower risk of hypoglycaemia. Rapid-acting insulin Rapid-acting insulin should be clear and colourless. Examples are: • Lispro Humalog • Novorapid Aspart • Glulisine Apidra.

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126 Care of People with Diabetes They have a rapid onset of action within 10–15 minutes peak at 60 minutes and act for 2– 4 hours. They need to be given immediately before meals and are used in basal bolus regimes in combination with intermediate acting insulin and long–acting analogues or used in combination with OHAs or in insulin pumps. Combining rapid-acting insulin with alpha-glucosidase inhibitors which reduce glucose absorption from the gut can increase the risk of hypoglycaemia. The first hour after injection and 2–3 hours after exercise are other peak times for hypoglycaemia. Short-acting insulin This should be clear and colourless. Examples are: • Actrapid • Humulin R • Hypurin neutral beef. They begin to take effect in 20–30 minutes after injection and act between four and eight hours. Rapid- and short-acting insulins can be used: • Alone two to four times per day • In combination with intermediate- or long-acting insulins • For correction doses • As IV insulin infusions • In continuous subcutaneous insulin infusions via insulin pumps. Intermediate-acting insulin Intermediate-acting insulins must be mixed gently before use and should be milky after mixing. Examples are: • Protophane • Humulin NPH • Hypurin isophane They begin to act in 2–3 hours. The duration of action is between 12 and 18 hours. They can be used: • In combination with short-acting insulin – this is the usual method. • Alone for patients who are sensitive to short-acting insulin or in combination with oral hypoglycaemic agents. Long-acting insulin • Glargine Lantus • Detemir Levemir as described in the preceding section. Ultra-long acting insulin • Insulin Degludec currently in phase 3 trials. Biphasic insulins Biphasic insulins are often prescribed for people with Type 2 diabetes.

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Medicines Management 127 These contain both short- or rapid- and intermediate-acting insulins in various combinations. They must be mixed before using. They do not enable independent adjustment of the short or intermediate components. Examples are: • NovoMix 30 30 Aspart /70 protamine. • Humalog Mix 25 Lispro 25/Lispro protamine 75. • Humalog Mix 50 Lispro 40/ Lispro protamine 50. • Humalin 30/70 Humulin 30/Isopahane 70. • Mixtard 30/70 Actrapid 30/Isopahne 70. Many insulins are available in prefilled disposable insulin devices. Each insulin administration device has advantages and disadvantages and patient preference should be considered. The diabetes educator can help individuals decide which device and therefore to some extent which insulin suits them best. Generally the insulin device should be used with the insulin designed by the same manufacturer. Insulin syringes still have a role and some people with diabetes prefer to use syringes. Storing insulin The temperature at which insulin is stored is important to maintaining its efficacy. Insulin should be stored according to the manufacturer’s directions. Unopened vials should be stored in the refrigerator at 2–8 °C. Insulin vials in use can be stored out of the refrigerator for example in the patient’s medication drawer provided they are not stored near a source of heat or light Campbell et al. 1993 see individual product prescribing information. People with diabetes need to be educated about correct storage and handling of insulin as well as sharps disposal as part of their education about insulin therapy. Exposure to heat and light accelerates the formation of insulin transformation products ITP and denatures insulin. Insulin undergoes a chemical transformation in solution and ITP are formed. The main ITPs are deanimated insulin covalent dimmers and oligomers Pryce 2009. Practice points 1 Long-acting analogues cannot be mixed with other insulins. Nor can they be injected in the same site. 2 They are clear and great care must be taken to ensure they are not mistaken for rapid- or short-acting insulins. Look-alike medicine alert policies should be initiated. For example consider storing them in a different part of the refrigerator and clearly flagging them with a ‘look-alike’ medication alert label. 3 Carefully check the dose to be administered of NovoMix 30 and Humalog Mix 25 or 50 and do not mistake the numbers in the name of the insulin for the insulin dose which has occurred and led to serious adverse medicine events. Clinical observation Hyperglycaemia can occur when using incorrectly stored insulin and insulin that has passed the expiry date.

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128 Care of People with Diabetes Injection sites and administration Administer at the appropriate time before the meal. The abdomen is the preferred site but upper arms thighs and buttocks can also be used. Injection sites must be rotated to avoid lipoatrophy and lipodystrophy and should be checked on a regular basis. Injection sites should also be rotated when people use insulin pumps. How to inject The insulin injection technique can influence insulin absorption and therefore its action. Insulin should be administered subcutaneously. IM injections lead to unstable blood glucose levels Vaag et al. 1990. • Pinch up a fold of skin dermis and subcutaneous tissue between the thumb and index finger. • Inject at a 90-degree angle. If the needle is long pinch up may not be needed and a 45- degree angle can be used to avoid giving an IM injection. • Release the skin remove the needle and apply gentle pressure to the site. • Document dose and time of the injection. • Injection sites should be regularly checked for swelling lumps pain or leakage of insulin. Practice points 1 A range of needle sizes is available. Needle size is important to people with diabetes. They usually prefer small fine gauge needles. 2 Injection with fine gauge needles is relatively painless. 3 Giving the first injection is often very difficult for people with diabetes. Support and encouragement and allowing them to take their time and inject at their own pace is important. 4 If insulin tends to leak after the injection release the skin fold before injecting. Pressure from holding the skin fold sometimes forces the insulin back out of the needle track. Withdraw the syringe quickly to allow the skin to seal. Do not cover so that any insulin leakage can be observed. 5 The loss of even small amounts of insulin can result in unpredictable increases in the blood glucose and inappropriate dose adjustment especially in lean people and children. Careful observation and estimation of the amount of insulin lost is necessary to make appropriate adjustments to the individual’s injection technique – this applies to both patients and nurses. 6 The larger the volume of insulin to be injected the greater the likelihood of some insulin leaking back along the needle track. Likewise leakage can occur if the injection is too shallow or given intradermally. 7 To minimise the risk of insulin loss during injection inject slowly and leave the needle in place for 3–6 seconds after the insulin is delivered. 8 Long-acting and pre-mixed insulins dispensed in insulin pens must be mixed gently before administration. Instructions for teaching people how to draw up and administer insulin using a syringe appear in Chapter 16. Refer also to the manufacturer’s instructions and patient information material. Practice points 1 Insulin syringes and pen needles are approved for single use only.

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Medicines Management 129 2 Pen needles should be removed after administering an insulin dose and a new needle used for the next dose especially with premixed insulins which can block the needle. 3 Most insulin administration devices except syringes were designed to enable patients to administer their own insulin. In hospital patients should remove the needle and place it in the sharps container after injecting to avoid needle stick injury to staff. 4 In hospital aged care and community settings staff should NOT recap needles. 5 If the patient cannot remove the needle from the pen a removal device should be used or the insulin administered using a syringe until the patient is well enough to self-inject again. Mixing short- and intermediate-acting insulins General points There is less need to ‘mix insulins’ now due to the range of modern premixed insulin combinations and insulin analogues. However it is still necessary in some settings and in some countries. Mixing short- and intermediate-acting insulins before injecting may diminish the effect of the short-acting peak which is more marked when there is substantially more long-acting insulin in the mixture as is usually the case especially if the insulin is left to stand for a long time before being injected. The clinical significance of these changes is unknown. It is more likely to apply to in home situations where home-care/domiciliary nurses or relatives draw up doses for several days in advance for people to self-administer see Chapter 18. This practice may not be ideal but it does enable people to retain a measure of independence where syringes are still the device of choice. The long-acting insulin analogues cannot be mixed with other insulin or injected into the same site. Commonly used insulin regimens Daily injection A combination of: • Rapid- or short- and long-acting insulin combinations which are usually given before breakfast. Biphasic premixed insulins such as Mixtard 30/70 are sometimes used. • Long- or intermediate-acting insulin is often given at bedtime when it is combined with GLMs for Type 2 diabetes. Daily regimes are commonly used for:  older people  those not willing to have more than one injection per day  some situations where people require assistance to inject are living in aged care facilities or depending on home nursing care when staff are not available to inject more than once per day. • Daily regimens are not recommended for people with Type 1 diabetes. It can be difficult to attain good control using biphasic insulin because the dose of the individual insulins in the mix cannot be altered which can increase the risk of hypoglycaemia if eating is erratic the carbohydrate intake is low or after vigorous exercise. However premixed insulins can reduce the medicine burden on individuals. BD regimens

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130 Care of People with Diabetes A combination of rapid- or short- and intermediate or long-acting insulin is usually given before breakfast and before the evening meal. Biphasic insulins are commonly used but do not allow a great deal of flexibility in adjusting doses. The evening dose may effectively control overnight hyperglycaemia. There is a risk of nocturnal hypoglycaemia see Chapter 6 . Usually two-thirds of the total dose is given in the morning and one-third in the evening. Figure 5.3 depicts the action profiles of the various insulins. Understanding the action profile enables hypoglycaemia risk times to be identified so that meals activity and medication administration times can be planned accordingly. They also help decide which insulin to adjust when considered in conjunction with the blood glucose profile. Consideration should always be given to other factors that affect blood glucose levels see Chapter 3. Practice point Rapid-acting insulins act very quickly. They should be given immediately before a meal or within 15 minutes after the meal to reduce the risk of hypoglycaemia. Basal bolus regimen Basal bolus regimens simulate the normal pattern of insulin secretion that is a small amount of circulating insulin is present in the blood and restrains gluconeogenesis and glycogenolysis this is the basal insulin. A bolus amount of insulin is stimulated by the blood glucose rise after a meal. Bolus injections of rapid- or short-acting insulin are given before each meal. The longer-acting insulin often an analogue is often given before bed to supply the basal insulin requirement and restrain hepatic glucose output overnight and control the pre-breakfast blood glucose fasting level. Basal bolus regimens offer more flexibility to adjust insulin doses and meal times and therefore lifestyle is not affected as much. The amount of insulin given at each dose is long-acting insulin Intermediate/ long- acting insulin Figure 5.3 Diagrammatic representation of insulin action showing different regimens: a daily b twice a day c basal bolus using short-acting insulins and d basal bolus using rapid-acting insulins. Note: The Breakfast a Lunch Dinner Bed b Breakfast Lunch Dinner Bed c Breakfast Lunch Dinner Bed Intermediate/

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Medicines Management 131 broken line depicts short-acting insulin the unbroken line intermediate/long- acting insulin. The arrows indicate the time of injection. usually small therefore the likelihood of hypoglycaemia is reduced. Basal bolus regimens are commonly used for young people with Type 1 diabetes and increasingly for Type 2. Despite the number of injections per day basal bolus therapy using analogues may be safer for older people with a lower risk of hypoglycaemia and falls. Nocturnal hypoglycaemia is less frequent when long-acting analogues are used. Interpreting morning hyperglycaemia There are three main reasons for fasting hyperglycaemia: 1 Insufficient basal insulin to restrain overnight hepatic glucose output. It is a common finding with daily insulin regimens when the insulin is given in the morning. A larger dose of insulin may be needed or a second dose of insulin introduced at lunch or bedtime or if the person is on GLM and a basal anaglogue insulin the insulin could be given at night. 2 The Somogyi effect which is due to the counter-regulatory response to nocturnal hypoglycaemia. The cause needs to be sought see Chapter 6 but the basal insulin dose may need to be reduced. 3 ‘Dawn phenomenon’ reflects insufficient insulin and insulin resistance. There is a normal physiological increase in many hormones early in the morning. However elevated fasting blood glucose may indicate general hyperglycaemia. A thorough assessment is needed and the medication regimen adjusted. Continuous subcutaneous insulin infusion CSII Insulin pumps continuously deliver subcutaneous insulin usually a rapid-acting analogue at a pre-programmed steady basal rate or rates through a needle inserted subcutaneously which stays in place for about three days. Bolus doses are delivered before meals or as corrective doses for hyperglycaemia. Bolus doses can be preprogrammed or delivered manually when needed. Insulin pumps enable a more physiological insulin profile to be attained and greater flexibility in meeting individual insulin requirements and lifestyle. Insulin pumps use rapid- or short-acting insulin only therefore if they malfunction or are removed for example during surgery the patient must be given insulin via another method to avoid hyperglycaemia. For example subcutaneously or via an IV insulin infusion depending on the circumstances. Modern insulin pumps are generally reliable and have an inbuilt alarm system that identifies a number of faults such as kinks/blockages in the tubing tubing disconnections from the pump and low batteries so that malfunctions can be identified early and appropriate steps taken to avoid hyperglycaemia. Some do not alarm if the tubing disconnects from the insertion site. If this occurs insulin is not delivered and can go unnoticed until the blood glucose is tested. In people with Type 1 diabetes hyperglycaemia can occur quickly and increase the risk of DKA. Reported rates vary between 2.7 and 9 episodes per 100 patient years. d Breakfast Lunch Dinner Bed

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132 Care of People with Diabetes Pumps are expensive and require a great deal of commitment on the part of the person with diabetes to use them safely and effectively. Health professional support and the ready availability of advice are vital. People need time to adjust to the pump regime and become accustomed to not having intermediate-acting insulin. Pumps offer a great deal of flexibility and can have significant psychological benefits. However pumps do not suit everybody and some people dislike the thought of being constantly connected to a device. People need to learn to count carbohydrates when they commence using an insulin pump. Structured education programmes such as Dose Adjustment for Normal Eating DAFNE DAFNE Study Group 2002 are often used to help individuals learn how much insulin is required per meal 0.5 units/10 g of carbohydrate. DAFNE is based on 10 g of carbohydrate. Recently a blood glucose meter and smart phone apps have appeared on the market and can be useful decision-aids for people with diabetes. Combining continuous blood glucose monitoring with an insulin pump is becoming a reality and will be welcomed by people with diabetes. Practice points 1 Insulin pumps are not a cure for inadequate metabolic control but they can help some people achieve better control. 2 They enable the insulin regimen and food intake to be matched to individual requirements and greater flexibility. 3 Hypoglycaemia unawareness may be reversed and hypoglycaemia frequency and severity may be reduced. 4 Insulin injections are not required. 5 Blood glucose monitoring at least 4-hourly is necessary unless the person uses continuous blood glucose monitoring. 6 Training and readily available support and advice from skilled pump experts are essential. 7 People with existing psychological problems do worse on pumps than on other insulin regimes DCCT 1993. 8 Pumps are expensive to purchase and the ongoing cost of consumables is high. In Australia some health insurance funds subsidise the initial outlay for the pump according to specified guidelines. The cost of consumables is subsidised by the Commonwealth government under the National Diabetes Supply Scheme but subsidies for diabetes products is currently under review and could change in the future. Currently there is no national Australian guideline for selecting which patients could benefit from using a pump but most diabetes centres offering pump therapy have guidelines for selecting patients and initiating pump therapy. NICE 2003 recommended that pumps be funded for people with Type 1 diabetes who suffer recurrent severe hypoglycaemia. Continuous blood glucose sensors Continuous glucose monitoring is a step towards a closed-loop system that links continuous blood glucose measurements to a computer-driven insulin infusion system to approximate normal glucose homeostasis. Modern sensors consist of a disposable sensor probe which is inserted into subcutaneous tissue using an insertion device and connected to a battery-powered transmitter. The transmitter sends a signal to a receiver which displays the blood glucose reading. The sensors last for 3–5 days. After the sensor is attached to the transmitter warm-up periods between 2 and 10 hours are required and capillary blood glucose testing is required to calibrate the system. There are at

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Medicines Management 133 least three sensors on the market and each manufacturer recommends ongoing calibration. In addition abnormal sensor readings need to be confirmed with a Table 5.4 Some commonly encountered factors that affect insulin absorption. Accelerated Delayed Type of insulin Type of insulin Exercise Low body temperature High body temperature Condition of injection sites Condition of injection sites Poor circulation Massage round injection site Smoking Depth of injection Long-acting insulins capillary test before corrective action is taken. Thus the current sensors are adjuncts to rather than replacements for capillary blood glucose testing but they enable people to have several days break from finger pricking. The cost is prohibitive for many people. The choice of regimen and insulin delivery system depends on personal preference management targets and the willingness and ability of the patient to monitor their blood glucose. Many factors can influence insulin absorption and consequently blood glucose some of these factors are shown in Table 5.4. Subcutaneous insulin sliding scales and top-up regimes A sliding scale refers to subcutaneous insulin doses administered to reduce hyperglycemia detected on routine blood glucose monitoring. Sliding scales are reactive and retrospective rather than prospective and proactive Hirsch et al. 1995. Sliding scales are not recommended especially for older people American Geriatrics Society Beers Criteria 2012. Sliding scales should not be confused with supplemental insulin administered at meal times based on blood glucose tests according to an algorithm Hirsch et al. 1995. Sliding scales continue to be used especially in hospital despite there being no evidence of any benefit and evidence of harm. In fact diabetes experts have been advocating for a proactive prospective approach to managing hyperglycaemia in hospital rather than using sliding scales since 1981 Queale et al. 1997. Sliding scales treat hyperglycaemia after it occurs. They may predispose the patient to hyperglycaemia-related adverse events particularly given the fact that insulin doses are rarely adjusted and the underlying causes and predisposing factors that lead to hyperglycaemia are not addressed Queale et al. 1997. Using subcutaneous sliding scales in day-to-day management can lead to disassociation between the insulin regimen and the other parameters that affect the blood glucose such as the timing of meals effects of illness and medications for example corticosteroids and the counter-regulatory response to hypoglycaemia. Using sliding scales to stabilise blood glucose for newly diagnosed unstable or brittle diabetes is not generally recommended Katz 1991. It is preferable to monitor the blood glucose over 24–48 hours and adjust the insulin regimen according to the emerging pattern considering the action profile of the various insulins and other factors that affect the blood glucose level. Top-up or stat doses of insulin Top-up or stat doses of insulin refer to temporary supplementary doses of insulin usually rapid- or short-acting given to correct existing hyperglycaemia found on routine blood glucose monitoring. Like traditional sliding scales top-up dosing is reactionary and does not

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134 Care of People with Diabetes address the underlying causes of hyperglycaemia. When necessary extra supplementary insulin correction dose is best added to the next due dose of insulin rather than being given in isolation. Adopting a proactive problem-solving approach considering the management regimen and nursing/medical actions occurring at the time will provide important insight into the cause/s of the hyperglycaemia which can be appropriately treated. For example hyperglycaemia might be a consequence of pain or fear in which case the most effective strategy would be to manage the pain/fear. In addition non-medicine options might be effective. Often top-up doses continue for days before the overall blood glucose profile and medicine requirements or the underlying causes are considered. Practice points 1 There are no documented benefits of insulin sliding scales in people in hospital Gearhart et al. 1994 Queale et al. 1997 or top-up doses. 2 Insulin sliding scales are associated with a 3-fold higher risk of hyperglycaemia especially when basal insulin is not used Queale et al. 1997. 3 Sliding scales are not recommended for older people American Geriatrics Society Beers Criteria 2012. 4 Sliding scales could help maintain acceptable blood glucose levels in hospital if they are used proactively according to a logical algorithm based on the action profiles of the relevant insulin regimen and delivered in relation to meals. 5 IV insulin infusions require a sliding insulin scale and are an example of proactive hyperglycaemia management. Intravenous insulin infusions The IV route is preferred for very ill patients because the absorption of insulin is rapid and more reliable than from poorly perfused muscle and fat tissue. Absorption may be erratic in these patients especially if they are hypotensive. The aims of the insulin infusion are to: • Prevent the liver converting glycogen and fatty acids into glucose and therefore avoid hyperglycaemia that is restrain hepatic glucose output. • Prevent utilisation of fatty acids and therefore limit ketone formation. • Reduce protein catabolism and therefore limit production of glucose substrates. • Enhance wound healing by limiting protein catabolism and normalising neutrophil function. • Reduce peripheral resistance to insulin. • If hyperglycaemia is present gradually lower the blood glucose concentration to 10 mmol/L without subjecting the patient to hypoglycaemia. Intravenous insulin infusions are associated with lower morbidity and mortality in surgical settings see Chapter 9 during acute illness such as MI see Chapter 8 in patients requiring parenteral nutrition Cheung et al. 2005 and in intensive care settings Quinn et al. 2006. In fact van den Berghe et al. 2001 demonstrated improved outcomes using insulin infusions in acutely ill non-diabetics as well as people with diabetes. Two main insulin delivery methods are used: 1 Insulin given via an infusion pump and fluid administered separately. 2 Insulin glucose potassium and fluids are combined GIK which is efficient and safe. The glucose component is usually 5 or 10 dextrose depending on the calories required Dagogo-Jack Alberti 2002. The medication order for the infusion must be clearly and legibly written on the treatment sheet. Insulin doses for IV insulin infusions are usually 0.1 unit/kg/hour. Sometimes an initial bolus of 5–10 units is given. In general a low-dose infusion such as this has been shown to

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Medicines Management 135 reduce the blood glucose and prevent ketosis and acidosis as effectively as high-dose regimens without the added risk of hypoglycaemia. The rate at which the insulin is to be administered should be written in mL/hour and units to be delivered. Several protocols exist the following is one example only. People with insulin-treated Type 2 diabetes may require 1–2 units/hour if they are overweight and insulin resistant. The infusion rate is adjusted according to the patient’s blood glucose results tested 1 –2- hourly. For example : Blood glucose mmol/L Insulin units/hour 0–5.9 0 6–11.1 1 12–15.1 2 16–19 3 19.1 4 24 Notify doctor The insulin order and blood glucose results should be reviewed regularly. The duration of the infusion depends on the clinical status of the patient. Preparing the insulin solution to be infused Two people should check and make up the solution according to the medication order and hospital protocols. In many cases it is prepared and labelled in the pharmacy. Practice points 1 Only clear rapid- or short-acting insulin is used for insulin infusions. Great care should be taken not to use clear long-acting insulin analogues in insulin infusions. 2 Insulin is known to bind to plastic. Flushing the first 50 mL through the giving set tubing prevents this non-specific absorption into the infusion equipment. Uses of insulin infusions General use during surgical procedures Insulin is added to 4 dextrose in 1/5 normal saline or 5 dextrose. The infusion is often given via burette or more commonly an infusion pump at 120 mL/hour i.e. 8-hourly rate see previous example scale. Monitor blood glucose 1–2-hourly and review with medical staff regularly. Special needs • Myocardial infarction. In many areas an IV insulin infusion is commenced when the patient presents to the emergency department and continues for 24 hours after which time subcutaneous insulin is commenced Malmberg 1997 see Chapter 8. • Open heart and other surgery. • Ketoacidosis. • Hyperosmolar states. • Severe septicaemia or other infections • Intensive care unit ICU situations.

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136 Care of People with Diabetes These situations always require the use of a controlled-rate infusion pumps to ensure accurate insulin dosing. It is often necessary to limit the amount of fluid administered to avoid cerebral oedema in these situations especially in young children and the elderly. Standard regimens include: 1 Haemaccel 100 mL + 100 units rapid or fast-acting insulin 1 unit/1 mL used in ICU and administered via an infusion pump. 2 Haemaccel 500 mL + 100 units rapid or short-acting insulin 1 unit/5 mL via an infusion pump. People who are insulin-resistant such as those who: • have liver disease • are on corticosteroid therapy • are obese • have a serious infection • may require more insulin that is a high-dose infusion more units per hour. Practice points • Subcutaneous insulin must be given before removing the infusion and the patient must be eating and drinking normally to avoid hyperglycaemia because of the short half-life of insulin given IV. • Ceasing the infusion before a meal enables a smooth transition to subcutaneous insulin. Risks associated with insulin infusions • hypoglycaemia • cardiac arrhythmias • sepsis at the IV site • fluid overload and cerebral oedema especially in children which is associated with high morbidity and mortality rates. Factors affecting insulin delivery via IV infusions: • accuracy of the system including blood glucose testing • stability of the solution • circulatory insufficiency. Mistakes associated with insulin infusions 1 Where a burette is used and if insulin is added to the burette rather than the bag of IV fluid refilling the burette from the bag results in no insulin being administered and hyperglycaemia results. 2 An incorrect amount of insulin added to the bag/burette can be a result of inadequate checking not using an insulin syringe to draw up the insulin or failing to Insulin infusion

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Medicines Management 137 Figure 5.4 Possible results of a blockage in the IV cannula and three-way adaptor during the concurrent administration of insulin and dextrose/saline. check illegible medical orders especially where insulin doses are written as ‘U/s’ instead of ‘units’ and the dose is misinterpreted. 3 Problems can arise if the insulin infusion is run at the same time through the same site as other intravenous fluids for example 4 dextrose in 1/5 normal saline. The most common method is to infuse the different fluids through the one IV cannula using a three- way adaptor octopus: see Figure 5.4. Usually the dextrose or saline is running at a faster rate than the insulin infusion. Problems can arise if there is a complete or partial blockage of the cannula. The force of gravity pushing the fluid towards the vein can actually cause the dextrose/saline to flow back up the slower- flowing insulin line resulting in high blood glucose levels. Figure 5.6 depicts the result of a blockage in the IV cannula and three-way adaptor during the concurrent administration of insulin and dextrose/saline. If hyperglycaemia occurs during an insulin infusion check: • that the tubing and adaptors are patent • that insulin has been added to the burette/bag • that the amount of insulin added is correct • possible sources of infection for example UTI the feet. Insulin allergy Insulin allergies are rare with modern highly purified insulins but they do occasionally occur. Two types of reaction have been reported: 1 localised weal and flare with itching due to antihistamine reactions 2 generalised anaphylaxis which is rare. Clinical observation Indicating insulin doses by writing ‘U/s’ still occurs despite the known association with adverse events and incorrect in some cases fatal insulin doses being administered. Incorrect usually excess insulin has been administered and can result in serious hypoglycaemia. For example in Australia in an aged care facility a patient died and a court case ensued. Both the nurse who administered the insulin and the doctor who wrote V ein Cannula Flo w of fluid up the insulin line De xtrose/saline line line Clamp Bloc kage par tial completed or kinks in this area h yperglycaemia

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138 Care of People with Diabetes the prescription were found to have contributed to the person’s death. There were other issues involved with the particular patient but the case highlights the importance of accurate documentation and the nurse’s responsibility to check. Insulin doses should always be indicated by writing or typing ‘units’ after the amount to be given. Allergic reactions are most likely to occur where people have been on insulin previously for example during GDM surgery or acute illness in people with Type 2 diabetes where insulin is used intermittently for example during surgery and with corticosteroid medications and when injection sites are not rotated. The reaction may be due to the preservatives and other incipients in insulin rather than insulin itself. To diagnose insulin allergy a careful case history is required. The person should be given insulin and observed where resuscitation equipment is available. Any reaction should be carefully documented. Blood test for IgG and other immune response factors can be helpful. If insulin allergy is present a desensitisation programme may be required. Local reactions can be managed by using a different insulin and antihistamine creams Williams 1993 Dunning et al. 1998. Transplants Pancreas transplants of either the whole pancreas or islet cells or the pancreas and kidneys is available to some people with diabetes for example those with autonomic neuropathy causing life-threatening hypoglycaemic unawareness and end-stage renal failure. Immunosuppresive therapy is required and if rejection does not occur the response is good. The transplanted pancreas/beta cells secrete insulin and HbA1c normalises in three months. Obtaining pancreases for transplantation or to harvest islet cells is difficult as is actually separating the islet cells from pancreatic tissue and other options are under study for example beta cell engineering and stem cell cloning. Islet cell transplants have been undertaken successfully in Canada Australia USA and in the UK and an international islet cell consortium has been established to try to reproduce positive results. Stabilising diabetes Rationale Optimal blood glucose control can prevent or delay the onset of long-term complications. Insulin is frequently required by people with Type 2 diabetes to achieve optimal control as indicated. Stabilising diabetes refers to the process of achieving an optimal blood glucose range helping the person acquire appropriate diabetes knowledge and managing diabetic complications either acute or chronic but the term usually specifically refers to commencing insulin NHMRC 1991. Stabilisation may occur at initial diagnosis of diabetes when a change of treatment is indicated for example transfer from GLM to combination therapy or insulin and for antenatal care in GDM. In most cases stabilising diabetes can be achieved without admitting the person to hospital. Managing diabetes in primary care settings as far as possible is a core component of both the Australian and UK diabetes management strategies MacKinnon 1998 NDS 1998. This process is known as outpatient stabilisation. Outpatient stabilisation requires staff to have the appropriate knowledge specific protocols and ample time if it is to be successful. It can result in considerable cost benefits and reduces the stress and costs associated with a hospital admission.

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Medicines Management 139 There are considerable psychological and quality of life benefits for the person with diabetes. Home/outpatient stabilisation enables insulin to be adjusted according to the individual’s usual lifestyle and reduces the risk of the person having to assume ‘sick role’ behaviours. However some patients will continue to be admitted to hospital for stabilisation of their diabetes for example complex issues that cannot be identified in outpatient settings where clinical observation is necessary or where the person is admitted with a concurrent illness or is diagnosed during an admission and commences insulin while in hospital. Stabilising diabetes in hospital People admitted to improve their metabolic control stabilisation are not generally ill and should be encouraged to: 1 keep active 2 wear clothes instead of pyjamas 3 perform diabetes self-care tasks such as blood glucose monitoring and insulin administration. They will require support encouragement and consistent advice. The time spent in hospital should be kept to a minimum. Nursing responsibilities 1 Inform the appropriate staff about the person’s admission especially the diabetes nurse specialist/diabetes educator specialist team and dietitian soon after they are admitted. 2 Assess the patient carefully refer to Chapter 2. 3 Monitor blood glucose according to usual protocols for example 7 am 11 am 4 pm and 9 pm. In some cases postprandial levels are also performed see Chapter 3. 4 Supervise and assess the patient’s ability to test their own blood glucose and/or administer insulin or teach these skills if the person is newly diagnosed. 5 Ensure diabetes knowledge is assessed and updated and select an appropriate diet: new learning may include insulin techniques sharps disposal hypoglycaemia and home management during illness. 6 TPR daily or every second day. 7 BP lying and standing daily. 8 Ensure all blood samples urine collections and special tests are performed accurately. The opportunity is often taken to perform a comprehensive complication screen and education assessment while the person is in hospital especially if they often miss appointments with health professionals or it has not been performed for some time. Inspection of injection sites and assessment of the person’s psychological status should be included. These tests include ECG eye referral spot urine collection for creatinine and microalbumin and blood tests such as lipids HbA1c and kidney function. 9 Ensure the patient has supplies for example test strips lancets insulin device before discharge and that the appropriate follow-up appointments are made. 10 Ensure they have a contact telephone number in case they need advice. Community and outpatient stabilisation The types of outpatient service provided for people with diabetes include: • diabetes education

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140 Care of People with Diabetes • commencement on diabetes medication GLM insulin • complication screening and assessment • blood glucose testing • consultations with dietitian diabetes nurse specialist/diabetes educator or diabetes specialist • clinical assessment • education is a key factor in a person’s understanding and acceptance of diabetes. Diabetes educators often know the person well from the outpatient service and can assist ward nurses to plan appropriate nursing care and understand the person’s needs. Practice point The specific protocol and policy of the relevant health care setting should be followed and all contacts including telephone advice documented. An example protocol for insulin stabilisation in the community or on an outpatient basis is shown on pages 166 and 167. Objectives of outpatient stabilisation onto insulin Short-term objectives: 1 To reassure the individual and their family and allay the fear that everything about diabetes must be learned at once. 2 Lifestyle should be modified as little as possible. 3 To establish trust between the patient and the diabetes team. 4 To gradually normalise blood glucose and lipids. 5 To teach the ‘survival skills’ necessary for the person to be safe at home: • how to draw/dial up and administer insulin • blood glucose monitoring • recognising and treating hypoglycaemia • sick day management • how and when to obtain advice e.g. provide contact telephone number. Long-term objectives The aim in the long term is for the patient to: 1 Develop appropriate coping and problem-solving skills and resilience to manage their diabetes and life in general. 2 Accept diabetes as part of their life and recognise their role and responsibility in the successful management of the diabetes. 3 Be able to make appropriate changes in insulin doses carbohydrate intake and activity to maintain acceptable blood glucose levels. 4 Be able to maintain an acceptable range of blood glucose HbA1c and lipids. 5 Be able to maintain a healthy weight range. 6 Modify risk factors to prevent or delay the onset of the long-term complications of diabetes and therefore the need for hospital admissions. 7 Attend regular medical/education appointments. 8 Receive ongoing support and encouragement from the diabetes team. 9 Maintain psychological wellbeing and quality of life.

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Medicines Management 141 Clinical observations • People are often overwhelmed unsure what to do and confused by conflicting or inaccurate advice from health professionals family and friends and the media or obtained on the Internet. • These issues frequently need to be addressed and clarified before commencing the insulin stabilisation process. • The therapeutic relationship and trust between health professional and the person with diabetes is a vital aspect of their adjustment to having diabetes and changes in their diabetic management or status. Therapeutic relationships should be cultivated nurtured and treasured. Rationale for choosing community/outpatient stabilisation Community/outpatient stabilisation onto insulin is preferred for the following reasons: 1 To avoid the ‘sick role’ which is often associated with a hospital admission. 2 It is cost effective that is does not require a hospital bed. 3 It involves less time away from work and usual activity for the patient who can therefore be stabilised according to their usual routine rather than hospital routines and food. 4 To encourage self-reliance and confidence. Patient criteria The patient must be: • Able to attend the service for the required period which depends on the individual service. In some cases twice a day visits may be necessary. Telephone contact should be maintained as long as necessary. • Physically and mentally capable of performing blood glucose monitoring and insulin administration or have assistance to do so. In addition some social/family support is helpful initially for older people and is required for children. The process of stabilisation 1 The process should involve members of the diabetes team and relatives/carers as appropriate. 2 Communication especially between the doctor practice nurses diabetes nurse specialist/diabetes educator dietitian and patient is essential. 3 Patients should be assessed on an individual basis so that appropriate education goals and blood glucose range can be determined. The insulin regime and insulin delivery system will depend on individual requirements follow-up advice and early assessment must be available. 4 Formal teaching times should take account of the individual’s commitments as far as is practicable. 5 Adequate charting and documentation of progress should be recorded after each session: blood glucose results ability to manage insulin technique goals of management. 6 Effective education strategies should be used. Stabilisation might be undertaken in groups see Chapter 16. A sample protocol for outpatient stabilisation is shown at the end of this chapter. It is included here to give nurses an overview of the kind of information required and the complex issues

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142 Care of People with Diabetes people with diabetes have to deal with often when they feel vulnerable. Other protocols also exist. Practice points 1 People of all ages forget how to manage emergencies. 2 Health professionals and well-meaning family and friends often give inaccurate advice that either confuses the person with diabetes or causes them to ignore all advice. 3 People with Type 1 diabetes are at risk of ketoacidosis but often do not have ketone testing equipment at home or if they do it is out of date Sumner et al. 2000 Tay et al. 2001. 4 Constant diplomatic reminders are important. An episode in hospital represents an opportunity to remind people about diabetes self-management. Traditionally initiation of insulin occurred on an individual basis. Recent reports suggest that group education programmes for commencing insulin can be effective and achieve reductions in HbA1c and competent insulin self-care by individuals Almond et al. 2001 Yki- Jarvinen et al. 2007. Such programmes could be a cost effective way to manage the increasing numbers of people being commenced on insulin as a result of the DCCT and UKPDS trials provided competent facilitation is available. Lipid-lowering agents Normalising the lipid profile is an essential component of diabetes management guidelines. People with diabetes especially Type 2 are at significant risk of cardiovascular disease which is often present at diagnosis unless the blood glucose and lipids can be kept within normal limits. Generally the aim is to reduce cholesterol especially LDL-c and triglycerides and increase HDL-c. HDL helps remove LDL cholesterol but it might also have anti-inflammatory and antithrombotic properties. HDL-c is inversely related to triglycerides in that high triglyceride levels are associated with the removal of cholesterol from HDL-c to more atherogenic lipoproteins and lipoprotein precursors. HDL-c is often low in Type 2 diabetes partly because of the increased production of triglyceride-rich lipoproteins. LDL-c may not be elevated because of the increased level of cholesterol LDL which suggests relying on LDL-c levels may underestimate the cardiovascular risk in people with Type 2 diabetes Sullivan 2008. High LDL significantly increases the risk of myocardial infarction but other risk factors such as obesity and inflammatory processes are important and are often exacerbated by low levels of HDL Colquhoun 2002. The cholesterol content of HDL HDL-c could be protective in that it reflects removal of cholesterol from atherosclerotic plaque. Low HDL-c is an independent risk factor for cardiovascular disease Anderson et al. 1991. Weight loss reducing saturated fat in the diet exercise and stopping smoking all effectively raise HDL-c. Alcohol increases HDL-c but excess consumption is associated with significant health risks because it causes weight gain especially around the abdomen liver damage contributes to malnutrition and reduces LDL-c and triglycerides and increases the risk of breast cancer in women. Controlling blood glucose is integral to controlling lipids Lipid Study Group 1998. Current lipid targets aim for total cholesterol 4 and triglyceride and LDL 3 in patients with existing heart disease National Heart Foundation 2001. The American Diabetes Association 2007 recommended using statins to prevent cardiovascular disease in all people with Type 2 diabetes particularly reducing LDL-c 100 mg/dL and initiating statins in people with diabetes over 40 years without cardiovascular disease to reach the LDL-c target. Likewise the CARDS study suggested statins are indicated in most people with Type 2 diabetes whereas The ASPEN study Knopp et al. 2006

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Medicines Management 143 suggested people at low risk of cardiovascular disease might receive less benefit from statin therapy. Not all people with diabetes have the same 10-year risk of cardiovascular disease thus lipid lowering therapy needs to be commenced according to individual level of risk Grundy 2004. However lipid-lowering agents including statins must be used with an appropriate diet and exercise regimen Ridker 2012. Major cardiovascular prevention trials include: • Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial ALLHAT which was one of the first trials to assess the efficacy of statins Pravostatin in people with and without diabetes. It failed to show a significant reduction in mortality but there was a trend towards a higher mortality risk in people with LDL-c 130 mg/dL. The findings were similar for those with and without diabetes. • Heart Protection Study which also included people with and without diabetes. The all-cause mortality and major cardiovascular event rate were significantly lower in the Simvastatin group. The outcomes were similar for those with and without diabetes in the Simvastatin group but people with diabetes in the placebo group had more vascular events than non- diabetics and the risk was additive. The researchers suggested people with diabetes have a risk equivalent to those with pre-existing cardiovascular disease and that statin therapy is beneficial for people with diabetes without cardiovascular disease and LDL-c close to the target. • Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm ASCOT- BPLA compared two antihypertensive regimens in people with at least three cardiovascular risk factors. A substudy LLA-ASCOT compared Atorvastatin to placebo. ASCOT was stopped after an average of 3.3 years because there was no significant difference in the primary endpoints. There was an overall benefit from using Atorvastatin but it was not significant in people with diabetes. However the researchers recommended statin therapy should be considered in people with Type 2 diabetes and hypertension. • CARDS included people with Type 2 diabetes LDL-c no history of cardiovascular disease and one additional cardiovascular risk factor and used 10 mg of Atorvastatin. There was a trend which failed to reach significance towards lower all-cause mortality and LDL-c was lower 100 mg/dL in the Atorvastatin group than in the placebo group. CARDS researchers suggested that there was no specific LDL-c threshold at which statins should be initiated in people with Type 2 diabetes. CARDS was used as the basis of American Diabetes Association 2007 recommendation that people with diabetes age 40 and no cardiovascular diseases should be commenced on a statin regardless of their LDL-c level. The Canadian Diabetes Association CDA 2006 recommended the LDL-c target for people with diabetes be lowered to 2 mmol/L from 2.5 mmol/L and placed less emphasis on the LDL/HDL ratio as a primary endpoint of treatment. The triglyceride level at which treatment should be commenced was also revised to 10 mmol/L from 4.5 mmol/L. The CDA suggested fenofibrate be commenced to reduce the risk of pancreatitis and a second lipid-lowering agent be added if targets were not achieved after 4–6 months. • ASPEN included people with Type 2 diabetes and a history of cardiovascular disease and compared 10 mg Atorvastatin with placebo. The protocol was amended to include people with no history of cardiovascular disease following changes in the cardiovascular management guidelines. The results were not statistically significant but there was a trend towards clinical improvements. The researchers concluded that the level of risk presence of multiple risk factors affects the degree to which statins reduce the cardiovascular risk in Type 2 diabetes without cardiovascular disease. • Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial VA-HIT indicated low HDL-c is a treatable risk factor in people with and without diabetes. VA-HIT results indicate fibrates reduce cardiovascular risk by lowering LDL-c but only had a small effect on increasing HDL-c. • FIELD study which used fenofibrate showed reductions in the rates of macular oedema and proliferative retinopathy but did not show a significant increase in HDL-

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144 Care of People with Diabetes c. It lowered LDL-c and there was a reduction in major cardiovascular events in the intervention group Field study 2005. Statins were added in the placebo group which may have influenced the results. • The Framingham Study indicated that low HDL-c is an independent risk factor for cardiovascular disease in people with diabetes and non-diabetics and developed a cardiovascular disease risk calculator Anderson et al. 1991. • PROSPER which studied the effects of Pravastatin on all-cause mortality in people aged 70–82 years with cardiovascular risk factors or cardiovascular disease but failed to show a reduction in all-cause mortality. However a later meta-analysis that included the 4S CARE LIPID HPS trials and unpublished data from PROSPER showed a reduction in all-cause mortality by 22 as well as cardiovascular mortality by 30 non-fatal MI by 26 and the need for revascularisation by 30 and stroke by 25 Afilalo et al. 2008. Afilalo et al. also suggested that older people do not have higher rates of serious adverse events than younger people but they did experience higher rates of myalgia in the statin and placebo groups. Masoudi 2007 showed Ruvastatin reduced LDL-c and C-reactive protein but did not significantly reduce the combined risk of cardiovascular disease in older people mean age 73 years and there were fewer admissions to hospital than in the placebo group. • Other studies such as the West Scotland Coronary Prevention Study WESTCOPS Air Force/Texas Coronary Athersclerosis Prevention Study AFCAPS/TexCAPS also showed cardiovascular benefits Ridker 2012. Management strategies should be based on the absolute risk rather than the lipid level alone. Individual risk assessment should include cardiovascular status age gender the presence of hypertension smoking and family history of hyperlipidaemia hypertension and cardiac disease Chapter 8. Management strategies consist of: • Dietary modification including reducing salt alcohol and saturated fat in the diet and increasing omega-3 fatty acids see Chapter 4. • Low-dose aspirin to reduce platelet aggregation. • ACE inhibitors to control blood pressure and other antihypertensive agents as indicated. • Stopping smoking see Chapter 10. • Lipid-lowering agents are recommended when the absolute cardiovascular risk is 15 in the next 5 years or when the risk is 10–15 in people with a family history of premature heart disease or who have metabolic syndrome National heart Foundation and Cardiac Society of Australia and New Zealand 2005. Most people will be commenced on a statin unless they are contraindicated. Diet and exercise therapy must continue even when lipid- lowering medicines are indicated. Metformin and TZDs might have some small effect on increasing HDL-c and Rimonabant is associated with significant improvements in HDL-c possibly because of the associated weight loss.  Statins reduce LDL-c and have some effect on HDL. They reduce the risk of future cardiovascular disease by 30. However long-term adherence to statins is poor and many older people are not commenced on these agents despite the improved cardiovascular outcomes Diamond Kaul 2008.  Nicotinic acid very effectively increases HDL-c but is associated with side effects and non-adherence is significant. In addition it increases blood glucose. Although the increase is not significant it contributes to overall increased cardiovascular risk.  Ezetimibe can be administered with a statin but it only has a modest effect on HDL-c.  Fibrates.  A new class of lipid-lowering agents Cholesterol Ester Transfer Protein CEPT which block the transfer of cholesterol from HDL-c to more atherosclerotic lipoproteins is under trial. The first agent Torcetrapib significantly raised HDL-c but did not prevent the progression to atherosclerosis. The trial ILLUMINATE was stopped early due to the rate of cardiovascular events in the treatment group Nissen et al. 2007. The adverse results triggered debate about the advisability of using medicines to treat HDL. Other lipid-lowering agents under trial include Liver-X-receptor agonists which promote cholesterol transport and reduce atherosclerosis in animal models endothelial lipase

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Medicines Management 145 inhibitors which raise HDL-c and apolipoprotein A-1 mimetic peptides that improve HDL function in animal models Zadelaar et al. 2007. • Coaching. Table 5.5 depicts the major classes of lipid-lowering agents Colquhoun 2000 2002. Side effects The side effects of lipid-lowering agents often contribute to non-adherence to these medicines: • Statins: tendonitis and myositis occurs in 2 of people Marie et al. 2008. Regular assessment to detect these side effects should occur especially during the first year. Poor sleep quality has been associated with Simvastatin but not Pravastatin Golomb 2007. Taking Simvastatin earlier in the day may reduce these effects. Simons 2002 Table 5.5 Lipid-lowering agents. Lipid-lowering agent and main action Management considerations HMG-CoA reductase inhibitors statins: reduce LDL-c and have a modest effect on triglycerides and HDL may increase bone mineral density for example: Atorvastatin Simvastatin Fluvastatin Rouvastatin Test liver function on commencing and 6 months after commencing Use caution if liver disease is present Reduce the dose if the patient commences cyclosporine. Monitor creatinine kinase CK and effects on muscles and tendons. Generally not recommended during pregnancy a Ezetimebe reduces LDL-c by 18 and by up to 20 if combined with a statin Ezetimebe combined with simvastatin Prescribing authority is required in Australia and specific criteria need to be met. Fibrates: Reduce cholesterol and triglycerides and increase HDL-c for example: Fenofibrate Gemfibrosil Can be combined with HMG-CoA after a trial on monotherapy but the risk of muscle toxicity is increased if used with statins or other fibrates Monitor CK and liver function 6 weeks after starting and again in 6 months Bile acid sequestrants Resins Enhance LDL-c lowering effects of HMG-CoA agents – reduce triglyceride and HDL-c for example: Cholestyramine Cholestyramine hydrochloride Allows lower doses of the resins to be used Slows absorption of oral hypoglycaemic agents Increases hypoglycaemia risk when used with these agents. Administer 1.5 hours apart They can impair the absorption of other medicines such as statins fat-soluble vitamins and thyroxine Can be used with a statin Low-dose nicotinic acid Can be given with HMG-CoA agents Note: The main classes of lipid-lowering medicines are depicted. Relevant prescribing information should be consulted. Combinations of statins and antihypertensive agents are also available for example amlopipine bensylate with Atorvastatin in eight dose combinations which are indicated for people with hypertension and/or angina who meet the prescribing criteria for lipid-lowering agents. Educating and supporting the person to maintain a healthy lifestyle and enhance their medication self-management and improve medication adherence is essential. a Karamermer Roos-Hesselink 2007. suggested measuring creatine kinase CK before commencing statins and then 6-monthly when lipids are checked could help interpret minor changes in muscle enzymes especially in people at risk of muscle effects such as in women and those with a small body frame multisystem disease polypharmacy perioperative interactions with medicines such as Cyclosporin azole antifungals macrolide antibiotics some antidepressants large amounts of grapefruit juice and alcohol. The American College of Cardiology American Heart Association and National Heart Lung and Blood Institute 2002 recommended:  Advising people with no symptoms and raised CK to immediately report generalised muscle aches and pains.

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146 Care of People with Diabetes  Monitoring the individual if the CK is normal and the muscle effects are mild or change to another statin or another lipid-lowering agent.  Referring people with very high CK to a lipid specialist but continue statin therapy until the individual is assessed.  Carefully monitoring muscle enzymes in people with raised CK and muscle aches. Discontinue statin therapy if clinically indicated for example severe symptoms such as fatigue significant pain or an interaction with statin occurs.  Stop statins if CK is ≥10 upper limit of normal. • GIT disturbances Clofibrate. Many people discontinue taking their lipid-lowering agents because they are unconvinced about the need perceive that they have poor efficacy or dislike the associated side effects. Nurses can play a key role in encouraging people to adhere to their medications by explaining the reason they need them and suggesting ways to limit minor side effects. For example Tai Chi might help reduce the muscle effects of statins. Monitoring lipid medicines Current lipid and other management guidelines recommend that blood lipids should be tested at diagnosis and then at least yearly. People using lipid-lowering agents should have their lipid levels measured more frequently. Lipid targets were discussed in Chapter 3. Not achieving targets is not necessarily failure: any reduction in lipid levels has a beneficial effect. Blood glucose should also be monitored and glucose-lowering medicines adjusted as needed to reach blood glucose targets. Persistent hyperglycaemia can cause hypertriglyceridaemia which usually falls along with cholesterol if blood glucose and weight improve. Mixed hyperlipidaemia is best treated with a statin or a fibrate initially depending on the underlying lipid abnormality. Doses are usually adjusted at four-week intervals. For example more than 80 of the lipid-lowering effect of statins is achieved at 50 of the maximal dose Jackowski 2008. Liver function tests and creatine kinase CK should be tested before commencing lipid- lowering therapy then in 4–8 weeks and subsequently when doses are adjusted or if clinically indicated. For example renal impairment older people severe muscle weakness. Statins may need to be temporarily ceased if the person requires macrolide antibiotics. Stopping statins is associated with an increased risk of a cardiac event especially in the first weeks Rossi 2007. If the triglycerides are 4.0 mmol/L or between 2 and 4 mmol/L and HDL is 1 mmol/L gemfibrozil may be the medicine of choice. Consider whether vitamin A D E and K the fat- soluble vitamins supplements are needed if bile acid resins are used in high doses for long periods of time. Omega-3 fish oils 2–5 mg/day effectively lower triglycerides Rossi 2007 and may be a beneficial addition to other agents for hypertriglyceridaemia or mixed hyperlipidaemia. However several products are available on the market and doses are not the same in all products or brands. It is important that people read labels and seek professional advice when using these medicines. In addition they can interact with other medicines. Antihypertensive agents Hypertension is a significant risk factor for cardiovascular disease. Thus achieving and maintaining normotension is a major therapeutic goal. There are many medicines that reduce blood pressure. Therefore the particular antihypertensive agent used depends on the underlying cardiovascular abnormality/ies and specific benefits and risks to the individual. Diabetes is associated with several cardiovascular abnormalities thus several agents are often required. Generally beta blockers are started at a low dose and the dose gradually increased depending on the agent used to improve left ventricular function and reduce the risk of death in patients with heart failure Jackowski 2008. Side effects of beta blockers include:

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Medicines Management 147 • Fluid retention which might be exacerbated by concomitant use of TZDs NSAIDs and COX –2 selective agents. • Hypotension which might increase the risk of falls and may be the result of an interaction with another antihypertensive agent or tricyclic antidepressants. • Bradycardia. • Severe fatigue other causes should be considered such as depression hypothyroidism and hyperglycaemia. • Bronchospasm can occur with beta blockers in patients with asthma and COPD. • Weight gain with some beta blockers such as atenolol which was still apparent at the 20- year follow up of the UKPDS Standl et al. 2012. Atenolol was also associated with a slight increase in tryglycerides and a mean HbA1c increase of 0.6 that required an increase in GLM doses in the UKPDS. ACE inhibitors ACEI are considered first-line therapy in diabetes because they have renoprotective cardioprotective and probably retinoprotective properties as well as reducing blood pressure. In addition they might improve insulin sensitivity. ACEI and metabolites are predominantly excreted via the kidney and doses may need to be adjusted or another antihypertensive agent used if renal function is impaired. Post hoc data analysis suggests ACEI and angiotensin-11 receptor blockers reduce the risk of progression to Type 2 diabetes however there may be different effects in different racial groups. For example Wright et al. 2006 reported lower risk of progression to diabetes in African-Americans receiving Ramipril compared to Amlodipine and Metoprolol. However in the DREAM trial Ramipril did not reduce the incidence of diabetes in nonAfrican-Americans with impaired fasting glucose or glucose tolerance although it did increase the regression to normoalbuminuira Bosch et al. 2006. The ACCOMPLISH trial 2008 to determine the effects of the ACE inhibitor Benazepril and a calcium channel blocker amlodipine on morbidity and mortality was stopped early because the combination treatment was more effective than an ACE inhibitor and a diuretic Jamerson 2008. Cardiovascular morbidity and mortality was reduced by 20. The main side effects of ACEI are: • The ‘ACEI cough’ is a well-known side effect that is benign but often irritating to the individual and family/friends. It is less common with some of the newer agents. • Diabetes is often associated with hyporeninaemic hypoaldosteronism syndromes particularly if renal impairment is present. The syndrome presents with unexplained hyperkalaemia which can be exacerbated by concomitant ACEI use. • Using an ACEI in the presence of renal artery stenosis RAS may critically reduce glomerular filtration. Prevalence of RAS does not appear to be higher in people with diabetes but it may be associated with though not a cause of hypertension. Risk factors include male gender smoking and peripheral vascular and coronary artery disease. Ensuring absence of RAS is important in such patients before commencing ACEI. Plasma potassium and creatinine should be regularly monitored in all patients on ACEI prior to and within one week commencing therapy Gilbert et al. 1998. Long term use of antihypertensive agents is associated with zinc loss which may be clinically relevant if people are already at risk of low zinc for example people with Type 2 diabetes alcoholism renal insufficiency and malabsorption syndromes Braun Rosenfeldt 2012. Antihypertensive medicines associated with zinc loss are thiasizide diuretics ACE inhibitors angiotension-2 receptor antagonists and is especially noticeable with Captopril. Zinc deficiency is associated with anorexia poor appetite compromised immune function and changes in smell and taste and can complicate neurological diseases and age–related degenerative diseases. Improving the diet to include foods that contain zinc and supplements might be indicated and could be trialled and evaluated and continued if benefits were demonstrated. The main types of antihypertensive medicines are shown in Table 5.6.

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Table 5.6 Antihypertensive medications. Often more than one antihypertensive agent will be required in diabetes to manage the underlying cardiovascular abnormalities. Prescribing information should be followed. Class of medicine Generic name Diuretics used for hypertension Thiazide diuretics Hydrochlorothiazide Sulphonamide diuretics Chlorthalidone Diuretics used for heart failure Indapamide hemihydrate High ceiling diuretics Frusemide Aryloxyacetic acid derivatives Ethacrynic acid usually used if the person is sensitive to other oral diuretics Potassium sparing agents: Aldosterone antagonists Amiloride hydrochloride Eplerernone Amiloride hydrochloride Combination potassium sparing agents and low ceiling diuretics Hydrochlorothiazide with amiloride hydrochloride Hydrochlorothiazide with triamterene Non-selective beta blockers used for hypertension Oxyprenolol Hydrochloride Pindolol Propranolol hydrochloride Selective beta blockers used for hypertension Atenolol Metoprolol tartarate Alpha beta blocking agents Beta blocking agents used in heart failure Labetalol hydrochloride Alpha and beta blocking agents Carvedilol Selective beta blocking agents Bisoprolol fumarate Metropolol succinate Beta blocking agents used as antiarhythmics Calcium channel blockers a Sotalol hydrochloride Selective calcium channel blockers with predominantly vascular effects – Dihydropyridine derivatives Amlodipine bensylate Felodipine Lercanidipine hydrochloride Nifedipine Selective calcium channel blockers with direct cardiac effects – phenylalkylamine derivatives Verapamil hydrochloride Calcium channel blockers with cardiac and vascular effects Agents acting on the Renin–Angiotensin System ACE inhibitors ACEI a Diltiazem hydrochloride Plain ACEI Captopril Enalapril maleate Fosinopril sodium Lisinopril Perindopril Quinapril hydrochloride Ramipril Tandolapril ACEI and diuretic combinations Enalapril maleate with Hydrocholorothiazide Fosinopril sodium with Hydrocholorothiazide Perindopril erbumine with Indapamide hemihydrate Quinapril hydrochloride with Hydrocholorothiazide

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Medicines Management 149 Continued Table 5.6 Continued Class of medicine Generic name Angiotensin-11 antagonists Candesartan cilexetil Eprosartan mersylate Irbesartan Telmisartan Angiotensin-11 antagonist combinations Candesartan cilexetil with Hydrocholorothiazide Eprosartam mesylate with Hydrocholorothiazide Irbesartan with Hydrocholorothiazide Telmisartan with Hydrocholorothiazide Centrally acting antiadrenergic agents Methyldopa Imidazoline receptor antagonists Clonidine Moxonidine Peripherally acting antiadrenergic agents Prazosin hydrochloride Hydrazinophthalazine derivatives Hydralazine hydrochloride Pyramidine derivatives Minoxidil a May be contraindicated in pregnancy. Antiplatelet agents Antiplatelet agents are indicated to reduce cardiovascular risk. Commonly used antiplatelet agents are: • Aspirin Salicylate. Salicylates were traditionally used to reduce inflammation fever and pain. They are also commonly used as antiplatelet agents to reduce the risk of cardiovascular disease particularly in people at high risk such as those who had a MI smoke have hypertension and/or high cholesterol. Aspirin may be contraindicated if the individual has a bleeding disorder and sometimes asthma. Aspirin occasionally causes indigestion and a tendency to bleed freely for example from blood glucose testing nosebleeds and bruises. • Clopidogrel hydrochloride sulphate is used if aspirin poses a significant risk of bleeding and is usually used to prevent recurrent stroke TIA or ischaemic event. • Dipyridamole can be used alone or with low-dose aspirin or where aspirin represents a bleeding risk. A combination formulation is available – Dipyridamole with aspirin. These agents are used to prevent recurrent stroke TIA or ischaemic event. • Warfarin and heparin. These agents are rarely combined with antiplatelet agents except when the individual is at high risk. A recent study suggests aspirin is associated with increased risk of macular degeneration MD in a prospective 15 year study involving 2389 participants Liew et al. 2013. Two hundred and seventy five were on aspirin 63 of whom developed MD. Adjusting for age and other confounders suggest the cumulative risk of MD is 9.3 in aspirin users versus 3.7 risk in non-users and this is a dose– response effect. The risk of stopping aspirin must be weighed against the cardiovascular benefits and should be carefully discussed when aspirin is commenced. Caution may be required in people at risk of MD but no such warnings have been issued at the time of writing. It is important for people to understand how their medicines work and the potential interactions with complementary medicines such St John’s wort and glucosamine which might potentiate the action of warfarin and lead to bleeding. Regular INR monitoring is essential and frequent dose adjustment may be required. Home INR monitoring systems are available but regular medical review is essential.

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150 Care of People with Diabetes Medication safety adherence and medication self-management Factors that affect medication safety and contribute to harm are complex and can be patient-related system/environment- related product-related and health-professional related therefore risks in all these categories must be considered and managed. Strategies for reducing health professional-related medicine-related errors include: • Identifying individuals at risk. • Using QUM as a decision-making framework. • Considering safety standards guidelines and advisories such as NICE US Institute of Safe Medicine Practice prescribing information and the Beers Criteria AGS 2012. • Using computerised prescribing ALERTs and reminders. • Implementing automated ALERT systems e.g. to allergies high risk medicine alerts. • Educating health professionals. Education is more effective if it is interactive and clinically based. • Implementing ward-based pharmacies which enhance interprofessional communication. • Undertaking regular comprehensive medicine reviews including home-based reviews. • Using structured medicine validation processes in hospital. • Ensuring practice environments are supportive. Supportive practice environments enhance nurses’ ability to intercept medicine errors before they occur Flynn et al. 2012. • Improving communication among professionals especially when the individual is discharged and during transitions among care facilities Dooley 2011 Dunning 2013a. • Team briefings e.g. concerning medicine alerts high risk patients and new medicines. Medication self-management is an essential aspect of diabetes self-care. It becomes increasingly complex as more medicines are added to the regimen often as the individual grows older. Medicine non-adherence is widely documented. For example two out of three people with diabetes adhere to 80 of their insulin doses Donnelly et al. 2007. The preceding information indicates that polypharmacy is common and is probably best practice diabetes care. Polypharmacy is variously defined as using 2–10 medicines depending on the source sometimes including prescribed over-the-counter and CAM medicines. Polypharmacy contributes to: • Difficulty remembering the medicine regimen which affects medicine adherence medication reviews and complicates prescribing. • Increased risk of medicine interactions. • Increased risk of non-adherence. Approximately half the medicines prescribed for people with chronic conditions are not taken. Krapek et al. 2004 reported people with high scores on the Moirsky Scale denoting adherence had lower HbA1c levels. Non-adherence results in high HbA1c and related health risks Grant et al. 2007. Non-adherence to cardiovascular medications is high: 10–25 discontinue medicines within six months of starting increasing to 21–47 by 24 months Australian Institute of Health and Welfare AIHW 2007. Significantly people who do not have their prescriptions filled after discharge from hospital post-MI are more likely to die within a year than those who have their prescriptions filled Jackevicius et al. 2008. Non-adherence to lipid-lowering agents is also high often because people are not sure they have any benefits feel health professionals are not interested in the individual’s input into their management plan and the associated side effects McGinnis et al. 2007. These findings suggest actually prescribing and monitoring medicines in the spirit of the newer term ‘concordance’ which denotes shared decision-making and agreement might be more effective than current strategies. • Increased likelihood of presenting to emergency or being admitted to hospital with a medication-related event. Budnitz Knight 2007 reported one third of all presentations to emergency in the US involved older people with adverse medication events. • Increased risk of a medication-related error in hospital. As already stated insulin warfarin and digoxin are the top three high-risk medicines all of which are frequently prescribed in diabetes. Adverse medicine-related events occurred in 28 500 hospital admissions in 2004–2005 predominantly in people 65 years and is probably an under estimation AIHW 2007. • High medicine costs. • Increased risk of falls.

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Medicines Management 151 • Increased risk of driving accidents. • Relying on medicines rather than continuing mandatory healthy lifestyle. • Reduced quality of life and well-being. • Health professionals not prescribing needed medicines on the basis of inadequate patient self-care Grant et al. 2007 or because they do not want to complicate the regimen or for other individual decision heuristics Tung 2011. Other factors that contribute to patient non-adherence include: • Low health literacy and health numeracy Chapter 16. • Sensory deficits such as vision and hearing loss. • Reluctance to take medicines and a desire to minimise medicine intake Pound et al. 2005. • Cultural and other beliefs and attitudes about medicines. • Inadequate or unclear medicines education especially when the education is not personalised for the individual and for each medicine Dunning 2013. • Misinterpreting medicine labels and medicine information which is common even when labelling requires minimal reading skills Davis et al. 2008. For example instructions to take medicine twice daily which is imprecise because ‘daily’ means once per day or every 12 hours means people have to make addition decisions about what the words actually mean. ‘Take medicines as directed’ is even more difficult to interpret Dunning 2013. People are more likely to understand specified medicine administration times such as 8 a.m. 6 p.m. but using time periods might suit some people better Davis et al. 2008. Complex medicine regimens independently predict the likelihood people will misinterpret medicine instructions advice or education. • Variations in medicine colour and appearance e.g. when generic medicines are substituted for the individual’s usual medicine Kesslheim et al. 2012. Kesslheim et al.’s study concerned antiepileptic medicines but the concept is likely to apply to all medicines. Earlier studies show many people identify their medicines by the colour size and shape. • Medicine costs. Medicine non-adherence is higher among people who do not attend appointments and is associated with increased rates of all-cause mortality Currie 2012. Currie’s study concerned insulin adherence but most of the findings are likely to apply to other medicines. In addition medicine non-adherence was common in a web-based survey of community pharmacy patients in the US n 2000 Shrank et al. 2011. Caregivers were more likely to report they did not adhere to their medicine regimens than noncaregivers 38 of Shrank’s et al.’s sample described themselves as caregivers and most were women. The finding suggest health professionals may need to consider caregiver behaviours and the potential effect on their medicine adherence and possible the adherence of the person they care for. Enhancing medication self-care Adherence is a complex mixture of acceptance adherence and persistence – not merely taking a medicine. In addition each component is itself complex. For example acceptance involves informed-decision making that can be affected by the health professional’s assessment diagnostic prescribing and communication skills. Significantly agreement of all people involved in medicine adherence is essential to optimal compliance. Barriers to appropriate medication self-care include the complexity of the regimen the number of medicines prescribed the dose frequency not understanding the regimen or when or how to take the medicines poor communication inadequate information or information in a format the individual does not understand beliefs and attitudes to medicines. Adherence to beneficial medicines reduces morbidity and mortality which suggests adherence is a surrogate marker of healthy behaviour Johnson Shalansky 2007. Several meta-analyses have been undertaken but few show a benefit of any one strategy which is not surprising given the complex and changing nature of managing diabetes medicines and more importantly the fact that most strategies focus on changing patient’s behaviour rather than also considering health professional’s contribution to non-adherence. A truly concordant strategy would/should also address health professional- and systems-related factors that affect medicine adherence. Nevertheless a number of strategies for measuring and promoting patient-related medication adherence have been proposed. Some show short-term benefits but longterm benefits are unclear. Strategies include:

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152 Care of People with Diabetes • AIDES method based on a meta-analysis of 53 studies which suggested no single strategy is more effective than any other but strategies that combine cognitive behavioural and affective interventions are more likely to be effective Roter et al. 1998. However the AIDES method appears complicated and there is limited evidence to support its benefit. • Federal Study of Adherence to Medications in the Elderly FAME Lee et al. 2006 which specifically addressed people 65 years and encompasses education regular follow up and customised blister packs. The strategy was based on a review of 12 interventions and was associated with improved adherence over six months from 61 at baseline to 96 and significant reductions in systolic blood pressure and LDL-c. • Education materials such as those developed by the Australian National Prescribing Service Consumer Medicines Information CMI which are available for all PBS listed medicines in Australia Internet sites such as and the International Alliance of Patient Organisations however these are largely passive and their effect on medicines use is unclear. Part of medicines education is helping people understand risks and benefits and putting these into their individual context. Woloshin Schwartz 2007 developed a booklet designed to help people understand risks using colon cancer and medical investigations as examples. It was said to be user-friendly and used 8th grade literacy level. The booklet was tested in a high socioeconomic group and the investigators reported ‘significant improvements in participants’ ability to interpret risk’. It is not clear whether the information would be applicable to lower socioeconomic groups or whether behaviour changed as a consequence of enhanced ability to interpret risk. • Education programmes for health professionals such as improving adherence to cardiovascular medicine National Heart Foundation of Australia 2011. From these strategies relevant meta-analysis and the author’s clinical experience using a QUM approach the following strategies are useful. They can be used alone or in combination depending on the individual’s need and agreement. That is patient-centred medication self-management. • Understand the health professionals’ impact on patient adherence. • Understand the individual’s beliefs and attitudes towards medicines their capabilities and their life goals. • Understand their usual lifestyle and daily activities. • Assess their physical and mental capability to manage medicines whether help is available and whether they will accept it if it is. • Identify triggers to non-adherence for example on more than 5 medicines complex dosing regimen sound-alike medicine names look-alike medicines low literacy cognitive deficits and being a carer. • Develop strategies to address specific issues. These should be developed in consultation with the individual for example ‘How do you think you could remember to take your insulin’ Some useful strategies include personal cues reminders and medicine boxes such as blister packs. • Provide medicine information in a relevant format and language level using appropriate words suitable for the individual. Work through the information with the individual and ask them to repeat back what they learned. Explain the benefits and risks but apply them to the individual’s context that is personalise the information. Information could include:  Why the medicines were prescribed which will include stressing the importance of maintaining a healthy lifestyle.  The name of the medicine the difference between generic and other medicines and what brand names mean.  What the medicine is expected to do outcomes and how the person will know if it is effective.  How soon an effect will show.  The dose and dose frequency.  Special instructions such as when to take the medicine in relation to meals.  What to do if they forget a dose.  When to stop taking the medicine if relevant.  Where and when to seek medicine advice for example fasting for a procedure or investigation.  Common side effects how to recognise them and what to do about minimising or reporting them.  Storing and disposing of unused medicines or medicines that have passed their useby date. • How to use other self-care information to interpret the effects of medicines adherence and non-adherence on relevant outcomes for example their blood glucose pattern. • How to keep their medication list up-to-date and ensure it includes over-the- counter and CAM medicines.

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Medicines Management 153 • Help them formulate questions to ask their doctor at the next appointment if necessary. • Follow-up medicines self-management regularly. Clinical observation From the list of strategies it is clear that person-centred individualised medicine education is complex time consuming and probably not accomplished in the majority of people with diabetes. Reflect on how you and/or your team could improve the way you provide medicine education. Strategies that can be used to monitor medicine adherence In research settings MEMs medicine containers are used. MEMs containers have microprocessors in the lid that record the date and time the container was opened. Opening the container is a proxy measure of medicines’ actual use. MEMs also acts as a behavioural intervention people are more likely to adhere if they think they are being ‘watched’. However MEMs is impractical in clinical settings. Other strategies involve: • Providing appropriate education with behavioural support. • Using case management and effective interprofessional communication. • Systems approaches to reducing the cost of medicines. • Discussing medicine use using open communication blood glucose and other selfmonitoring and laboratory results in a non-judgemental way. • Knowing the ‘right’ questions to ask. • Using open neutral language and choose words and sentences carefully and avoid passive language and ambiguity to enhance memory and understanding. • Using questionnaires such as the:  Brief Medication Questionnaire BMQ that measures current and potential nonadherence and can be self-completed by the individual.  The Morisky Scale which measures attitudinal and behavioural factors that affect adherence. However the language is judgemental e.g. Are you careless at times about taking your medicine It has low internal reliability.  Medication Adherence report MARS whch views medicine use on a continuum.  Beliefs about Medication questionnaire BaMQ.  Revised Illness Perception questionnaire IPQ-R. Reflecting on their own medicine-related behaviours might help them understand people with diabetes medicine-related behaviours. After all health professionals fall into the category of carers: caring is a known risk factor for non-adherence. Based on the preceding information about adherence one could ask: 1 Is adherence a patient problem 2 Is adherence a health professional problem 3 Is adherence an inter-related responsibility of the individual the health professional service providers and funders 4 Should we be promoting rights and responsibilities rather than merely adherence Example protocol for outpatient stabilisation onto insulin SUGGESTED PROTOCOL These are guidelines only and should be modified to suit individual needs. The information can be delivered individually or in groups and over various time frames and include other information relevant to the individual. 1 Introduce the diabetes team and area facilities. 2 Test blood glucose the individual should test their own blood glucose if possible.

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154 Care of People with Diabetes 3 Insulin dose/frequency is determined in consultation with the doctor. 4 The educator demonstrates insulin technique and explains the procedure to the patient and encourages the patient to practice them. 5 It is important to encourage the patient to discuss their feelings about diabetes and to assess current diabetes knowledge learning capacity style psychological status and social situation. Education goals 1 To give a basic explanation of what diabetes is and what an acceptable blood glucose range is. 2 To explain the reason for instituting insulin therapy. 3 To explain the effects of insulin on blood glucose levels that is insulin action and the role of long- and short-acting insulin in control of blood glucose levels. 4 To explain insulin technique: • preparing the dose depending on the insulin delivery system chosen • sites for injection • expiry dates of insulin bottles/cartridges • care and storage • appropriate sharps disposal. 5 To explain why insulin must be given by injection and allow patient to handle insulin device or bottles and practice preparing the insulin dose. 6 To explain hypoglycaemia: • recognising symptoms of low blood glucose levels • causes and prevention • effective management • patient should carry carbohydrate for ‘emergencies’. 7 Blood glucose monitoring should be encouraged to provide feedback to the patient and enable them to telephone in the afternoon with a result if necessary. The role of monitoring should be explained as well as the timing of testing and how to record results. 8 Basic introduction to a food plan: role of carbohydrate in blood glucose control and the need to reduce fat and the need for regular meals. 9 Explain and enrol the patient in the National Diabetes Supply Scheme. 10 Explain responsibilities with respect to self-care medicine management complication screening and driving. a 11 Ensure patient has the equipment to administer insulin and monitor blood glucose and knows how and where to obtain future supplies and knows who to contact for advice. Other important self-care issues 1 Discuss how to manage illness at home in relation to: b. who to contact c. effects of illness on blood glucose d. emergency diet e. monitoring and recording of blood glucose and urine or blood ketones f. adjusting/continuing insulin g. need to rest. 2 Discuss precautions to be taken relating to driving work etc. 3 Discuss the role of exercise/activity in controlling blood glucose levels. 6 Encourage patient to wear some form of identification. 7 Ensure that patient has a contact telephone number and knows who to contact for advice. 8 Provide appropriate follow-up appointments for doctor nurse specialist/educator according to patient needs. 9 Provide ongoing individual teaching as required. 10 Ensure patient knows about other services available for people with diabetes for example diabetes associations and relevant support groups. 11 Arrange for consultation with family if necessary. a Point 10 above: the National Diabetes Supply Scheme only applies in Australia.

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158 Care of People with Diabetes Nicholson G. 2002 Statins decrease fractures and increase bone mineral density. Archives of Internal Medicine 163 537–540. Nisbet J. Sturtevant J. Prons J. 2004 Metformin and serious adverse events. Medical Journal of Australia 180 2 53–54. Nissen S. Wolski K. 2007 Effect of Rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. New England Journal of Medicine 10.1056/NEJMoa072761. Nissen S. Tardif J. Nicholls S. 2007 Effect of Torcetrapib on the progression of coronary atherosclerosis. New England Journal of Medicine 356 1304–1316. ORIGIN 2012 Basal insulin and cardiovascular and other outcomes in dysglycaemia. New England Journal of Medicine 367 319–328. Pound P. Britten N. Morgan M. et al. 2005 Resisting medicines: A syntheses of qualitative studies of medicine taking. Social Science and Medicine 61 133–155. Prochaska J. Velicer W. 1997 The transtheoretical model of health behaviour change. American Journal of Health Promotion 12 38–48. Pryce R. 2009 Diabetic ketoacidosis caused by exposure of insulin pump to heat and sunlight. British Medical Journal 338 1077–1078. Queale W. Seidler A. Brancati F. 1997 Glycaemic control and sliding scale insulin use in medical inpatients with diabetes mellitus. Archives of Internal Medicine 157 545–552. Quinn J. Snyder S. Berghoff J. Colombo C. Jacobi J. 2006 A practical approach to hyperglycaemia management in the intensive care unit: Evaluation of an intensive insulin infusion protocol. Pharmacotherapy 26 10 1410–1420. Raskin P. Rendell M. Riddle M. 2001 A randomised trial of Rosiglitazone therapy in patients with inadequately controlled insulin treated Type 2 diabetes. Diabetes Care 24 7 1226–1232. Raskin P. Allen E. Hollander P. et al. 2005 The INITIATE study group: Initiating insulin therapy in Type 2 diabetes: A comparison of biphasic and basal insulin analogues. Diabetes Care 28 260–265. Richter B. Bandeira-Echtler E. Bergerhoff K. Lerch C 2008 Dipeptidyl peptidase-4 DDP-4 inhibitors for Type 2 diabetes mellitus. Cochrane Database of Systematic Reviews www.ncbi.nlm. Cochrane Library London. Riddle M. Rosenstock J. Gerich J. 2003 The insulin Glargine 2004 study investigators The treatto-target trial: Randomized addition of glargine to human NPH insulin to oral therapy in type diabetes patients. Diabetes Care 26 3080–3086. Ridker P. 2012 What works and in whom A simple easily applied evidence-based approach to guidelines for statin therapy. Circulation Cardiovascular Quality Outcomes 5 592–593. Rosak C. Mertes G. 2012 Critical evaluation of the role of Acarbose in the treatment of diabetes: Patient considerations. Diabetes Metabolic Syndrome Obesity: Targets and Therapy 3 357–367. Rosenstock J. Schwartz S. Clark C. et al. 2001 Basal insulin therapy in type 2 diabetes: 28-week comparison of insulin Glargine HOE 901 versus NPH insulin. Diabetes Care 24 631–636. Rossi S. ed. 2007 Australian Medicines Handbook. Australian Medicines Handbook Pty Ltd Adelaide. Roter D. Hall J. Mersica R. et al. 1998 Effectiveness of interventions to improve patient compliance: A meta-analysis. Medical Care 36 1138–1161. Rutherford E. Wright E. Hussain Z. Colagiuri R. on behalf of the DAWN Committee 2004 DAWN: Diabetes Attitudes Wishes and Needs. The Australian Experience. NovoNordisk Australasia Sydney. Salpeter S. Greyber E. Pasternak G. Salpeter E. 2006 Risk of fatal and non-fatal lactic acidosis with Metformin use in Type 2 diabetes mellitus. Cochrane Database of Systematic Reviews www. Cochrane Library London. Scottish Intercollegiate Guideline Network SIGN 2010 Management of Type 2 diabetes: A national Guideline. SIGN Edinburgh. Shah B. Hux J. Laupacis A. et al. 2005 Clinical Inertia in Response to Inadequate Glycemic Control. Diabetes Care 28 3 600–606. Shenfield G. 2001 Drug interactions with oral hypoglycaemic agents. Australian Prescriber 24 4 83–84. Shrank W. Libeman J. Fischer M. et al. 2011 Are caregivers adherent to their own medicines Journal of the American Pharmacists Association 51 41 492–498. Simons L. 2002 Test CK before starting on statins. Medical Observer 30th August 5. Skyler J. Cefalu W. Kourides I. et al. 2001 Efficacy of inhaled human insulin in Type 1 diabetes mellitus. Lancet 357 331–335. Standl E. Erbach M. Schnell O. 2012 What should be the antihypertensive drug of choice in diabetic patients and should we avoid drugs that increase glucose levels Pros and cons. Diabetes Metabolism Research Reviews 28 Suppl 2 50–66. Strowig S. Aviles-Santa L. Raskin P. 2004 Improved glycaemic control without weight gain using triple therapy in Type 2 diabetes. Diabetes Care 27 1577–1583. Sullivan D. 2008 Raising HDL cholesterol in diabetes. Diabetes Management Journal 22 16. Sumner J. Barber C. Williams V. 2000 What do people with Type 1 diabetes know about hypoglycaemia Practical Diabetes International 17 6 187–190. Tan Y. 2006 Initiating insulin in patients with Type 2 diabetes. Diabetes Management Journal 14 28–29. Tay M. Messersmith R. Lange D. 2001 What do people on insulin therapy remember about safety advice Journal of Diabetes Nursing 5 6 188–191. Ting R. 2006 Metformin use increases vitamin B12 deficiency in patients with diabetes. Archives of Internal Medicine 166 1975–1079. Tung A. 2011 The mystery of guideline non-compliance: Why don’t doctors do the right thing Anaesthesiology 503 3–10. Turner R. Cull C. Frighi V. Holman R. 1999 Control with diet sulphonylurea Metformin or insulin in patients with Type 2 diabetes mellitus: Progressive requirement for multiple therapies UKPDS 49. Journal American Medical Association 281 2005–2012. United Kingdom Prospective Diabetes Study UKPDS 33 1998 Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with Type 2 diabetes. 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Medicines Management 159 Wang F. Surh J. Kaur M. 2012 Insulin Degludec as an ultralong-acting basal insulin one a day: A systematic review. Diabetes Metabolism and Obesity Targets and Therapy 5 191–204. Whaley J. Reilly T. Poucher S. et al. 2012 Targeting the kidney and glucose excretion with Dopagliflozin: Preclinical and clinical evidence for SGLT2 inhibition as a new option for treatment of Type 2 diabetes mellitus. Diabetes Metabolic Syndrome and Obesity: Targets and Therapy 5 135–138. Willi C. Bodenmann P. Ghali W. Faris P. Cornuz J. 2007 Active smoking and the risk of Type 2 diabetes: A systematic review and meta-analysis. Journal of the American Medical Association 298 2654–2664. Williams G. Pickup J. 1992 Handbook of Diabetes. Blackwell Science Oxford. Williams P. 1993 Adverse effects of exogenous insulin: Clinical features management and prevention. Drug Safety 8 427–444. Wright J. Randall O. Miller E. et al. for the African-American Study of Kidney Disease and Hypertension 2006 Differing effects of antihypertensive drugs on the incidence of diabetes mellitus among patients with hypertensive kidney disease. Archives of Internal Medicine 166 797–805. Woloshin S. Schwartz L. 2007 The effectiveness of a primer to help people understand risk. Annals of Internal Medicine 146 256–265. Worthington B. 2003 The nurses’ role in patient-centred medicines management. Professional Nurse 19 3 142–144. Yki-Jarvinen H. Ryysky L. Nikkila K. et al. 1999 Comparison of bedtime regimens in patients with Type 2 diabetes mellitus: A randomized controlled trial. Archives of Internal Medicine 130 389–296. Yki-Jarvinen H. Juurinen L. Alvarsson M. et al. 2007 Initiate insulin by aggressive titration and educate INITIATE. Diabetes Care 30 1364–1369. Zadelaar S. Kleemann R. Verschuren L. et al. 2007 Mouse Models for Atherosclerosis and Pharmaceutical Modifiers Arteriosclerosis Thrombosis Vascular Biology DOI:10.1161/ATVBAHA.107.142570.

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Chapter 6 Hypoglycaemia Cure Diabetes in 21 Days Key points • Hypoglycaemia is one of the most common short-term complications of diabetes treatment with insulin and some oral glucose-lowering medicines. • The brain depends on a constant supply of glucose because it is unable to synthesise or store glucose. Severe hypoglycaemia is associated with cognitive impairment that affects the person’s ability to self-manage the hypoglycaemia and function normally during a hypoglycaemia and has longer term effects on various aspects of cognotion. • Hypoglycaemia symptoms are often atypical especially in older people who usually present with predominantly neurogenic symptoms. • The glucagons response diminishes with longer duration of diabetes in both Type 1 and Type 2 diabetes but can be lost early in the course of diabetes in Type 1. • Self-treated hypoglycaemia is associated with clinically significant effects on well-being and functioning. • Hypoglycaemia is the most feared side effect of insulin especially in the presence of hypoglycaemic unawareness. Rationale Hypoglycaemia can be prevented by proactive self-care including regular blood glucose monitoring appropriate nursing care and recognising impending hypoglycaemia and managing it appropriately. The prevalence of hypoglycaemia is increasing due to the focus on achieving blood glucose levels as close to normal as possible and initiating insulin early in people with Type 2 diabetes. Hypoglycaemia can be a barrier to optimal control and is an independent cause of excess morbidity and increased costs Brod

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Hypoglycaemia 161 Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. Barnett 2012. People who have hypoglycaemia appear to be more affected by diabetes than people who do not have hypoglycaemia and often report lower general health Lundkvist et al. 2005. Introduction Hypoglycaemia is the most common and the most serious adverse event associated with insulin use. The prevalence of hypoglycaemia has increased since the results of the Diabetes Control and Complications Trial DCCT in people with Type 1 diabetes DCCT Trial Group 1997 and DCCT/EDICT 2003 and the United Kingdom Prospective Diabetes Study UKPDS UKPDS 1998 in Type 2 diabetes demonstrated that keeping blood glucose in the normal range reduced the risk of long-term diabetes complications. The blood glucose target range and HbA1c indicators of ‘good glycaemiac’ control are now as close as possible to the normal ranges which increases the risk of and frequency of hypoglycaemia. Severe hypoglycaemia was three times more frequent in the intensive insulin treatment group compared to conventional treatment in the DCCT 61 events per 100 people. Hypoglycaemia was more common in men than women and in adolescents than adults. The risk of severe hypoglycaemia was one in three and the risk of coma one in ten DCCT 1991. Concern about hypoglycaemia was thought to contribute to the difficulty achieving glycaemic targets. Likewise Pramming et al. 1991 reported mild hypoglycaemia was 1.8 episodes per patient per week and 1.4 episodes of severe hypoglycaemia per patient per year. The increased rate of hypoglycaemia is largely due to the focus on achieving normoglycaemia by intensifying management in both Type 1 and Type 2 and transferring people with Type 2 diabetes onto insulin sooner since the results of these studies were released. In early reports from the UKPDS major hypoglycaemia occurred between 0.4 and 2.3 of insulin-treated patients per year compared with 0.4 of those treated with diet or sulphonylureas UKPDS. Later studies also show the frequency and severity of hypoglycaemia in people with Type 2 diabetes is lower than Type 1 Yki- Jarvinen et al. 1999. Wright et al. 2006 recorded self-reported hypoglycaemia rates and graded severity as transient 1 temporarily incapacitated 2 requiring assistance 3 requiring medical attention 4 in various treatment groups who remained on their prescribed therapy for six years from diagnosis as part of the UKPDS. Grades 1 and 2 occurred in 0.8 in the diet and 1.7 in the Metformin groups per year and 0.1 and 0.3 respectively for grades 2–4 per year. Rates for those on sulphonylureas were 7.9 and 1.2 21.2 and 3.65 on basal insulin and 32 and 5.5 on basal and pre-meal insulin. Younger people 45 years women those with HbA1c 7 and islet autoantibodypositive people were twice as likely to report hypoglycaemia. Wright et al. claimed the low rates of hypoglycaemia in Type 2 diabetes was unlikely to have a major negative impact on people’s ability to achieve glycaemic targets. Approximately 30 of people initially recruited were lost from the study possibly due to intensifying treatment to achieve optimal glycaemic control thus the numbers of people in each treatment group was small and the overall hypoglycaemia rate was low. Not surprisingly hypoglycaemia risk was greater in people on insulin with poorer control but lower doses of insulin were associated with a 35 lower rate of hypoglycaemia. Older people 65 were not included in the study thus their risk and ability to recognise hypoglycaemia is unclear from the study but subsequent research suggests they are at high risk and often unable to recognise or treat hypoglycaemia Chapter 12. A number of researchers suggest the rate of mild and severe hypoglycaemia is lower in insulin-treated Type 2 diabetes than in Type 1. However hypoglycaemia risk increases once insulin is commenced and with increasing duration of diabetes Henderson et al. 2003 and the loss of counter-regulatory hormone function in Type 2 diabetes of longer duration parallels progressive beta cell loss and increases the risk of hypoglycaemia Amiel et al. 2008 Unger 2012. Hypoglycaemic unawareness is uncommon in Type 2 diabetes but when present it is associated with a higher incidence of severe hypoglycaemia. Hypoglycaemic unawareness in adolescents with Type 1 diabetes is influenced by duration of diabetes but can occur early after the diagnosis Johnston et al. 2012. The DARTS study in Scotland suggests the hypoglycaemia rate in people with Type 2 diabetes on insulin is the same as those with Type 1 Leese et al. 2003 and that insulin treatment is a predictor of hypoglycaemia in people with Type 2 diabetes Donnelly et al. 2005 and is particularly high in people treated with insulin for long periods of time Unger 2012. Significantly hypoglycaemia is likely to become more prevalent in people with Type 2 diabetes given the increasing prevalence of Type 2 diabetes and the trend to early initiation of insulin in Type 2 diabetes.

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162 Care of People with Diabetes The cost of treating hypoglycaemia is higher for people with Type 2 than Type 1 diabetes Farmer et al. 2012. Farmer collected retrospective data over 12 months 2009–2010 from the South Central Ambulance Service National Health Service Trust in the UK to estimate the incidence of severe hypoglycaemia requiring ambulance assistance. Farmer et al.’s findings suggest ambulance services manage a high prevalence of hypoglycaemia in younger than older age groups: 2.1 over age 15 and 7.5 in the 15–35-year age group. The prevalence was 1.9 in people over 65 years. They concluded that despite the higher hypoglycaemia rates in young adults the absolute number of incidents was higher in older people. The authors acknowledged that ambulance services may not attend all cases of severe hypoglycaemia thus the study may underestimate the incidence of severe hypoglycaemia. The rate of severe hypoglycaemia is higher in young children: 0.49 in children 6 years compared to 0.16 in children 6 Davis et al. 1997. Daneman et al. 1989 reported 31 of children n 311 mean age 11.6 and mean duration of diabetes 4.6 years had at least one coma or convulsion since diagnosis. Other researchers report rates ranging from 6.8 to 12. In contrast Nordfeldt Ludvigsson 1997 stated that the incidence of hypoglycaemic coma did not increase when HbA1c improved from 8.1 to 6.9 but episodes of severe hypoglycaemia increased from 1.01 to 1.26 per patient per year. Early recognition and treatment of hypoglycaemia in young children is essential because their brains are vulnerable to hypoglycaemia which may cause permanent cognitive deficits Tattersall 1999. Practice point People’s perceptions of and beliefs about hypoglycaemia differ significantly from clinical definitions and those of health professionals. People with diabetes use different language and explanatory models to explain hypogylycaemia and its severity. It is essential to understand people’s perceptions of hypoglycaemia to help them develop suitable hypoglycaemia prevention/management strategies. The counter-regulatory response Normal glucose homeostasis was discussed in Chapter 1. Counter-regulatory hormones especially glucagon the catecholamines growth hormone and cortisol are released when the blood glucose falls below the normal range to maintain the blood glucose level and ensure a constant supply of energy to the brain. Glucagon and the catecholamines stimulate gluconeogenesis and reduce glucose utilisation. The severity and duration of hypoglycaemia determines the magnitude of the counter-regulatory response and begins as the blood glucose falls to 3.5–3.7 mmol/L before cognitive function is impaired around 3.0 mmol/L Heller Macdonald 1996. The counter-regulatory hormones are largely responsible for the signs and symptoms of hypoglycaemia through activating the autonomic nervous system. Several researchers have compiled lists of hypoglycaemic symptoms and most diabetes-related text books and chapters list the signs and symptoms of diabetes. Recognising the signs enables early treatment to be initiated. Significantly symptoms are specific to the individual and are interpreted differently from health professionals. For example people report symptoms differently if they are asked to indicate the relevance of each symptom to themselves Tattersall 1999 p. 57 Unger 2012. In the author’s experience some people think ‘a hypo means you go into a coma’ and do not associate mild symptoms with hypoglycaemia other people and their relatives associate trembling vagueness and aggressive behaviour as ‘having a fit’ which suggests some information included in hypoglycaemia education programmes may not be appropriate to everybody and that hypoglycaemia education should be individualised taking account of the person’s hypoglycaemia risk profile. Worryingly a US national survey n 2530 found many people reported they are not informed about hypoglycaemia risk factors and often experience hypoglycaemia in their daily lives while they are working and driving Moghissi 2011. When the blood glucose is 3.0 mmol/L fine motor coordination mental speed and concentration and some memory functions become impaired. Reaction times are slower especially when the individual needs to make decisions do mental arithmetic and short-term verbal memory and working memory are impaired Sommerfield et al. 2003. McAuley et al. 2001 also demonstrated significant impairment of attentional ability during hypoglycaemia but found fluid intelligence problem-solving ability was not impaired. Thus many everyday tasks appear to be impaired during hypoglycaemic events including the individual’s ability to manage the hypoglycaemic episode.

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Hypoglycaemia 163 Factors associated with increased cognitive deficits include male gender hypoglycaemic unawareness Type 1 diabetes and high IQ. These findings have implications for effective hypoglycaemia self-management and safety. For example people drive slowly swerve more steer inappropriately spend more time driving off the road and position the car badly on the road when the blood glucose is 2.6 mmol/L Chapter 10. The counter-regulatory response to recurrent hypoglycaemia may be blunted in subsequent hypoglycaemia and the individual may not recognise hypoglycaemia signs and symptoms. Often people do not recall severe hypoglycaemic episodes. Results from continuous glucose monitoring systems CSII suggest people taking four insulin injections per day have at least one blood glucose level 2.8 mmol/L of varying duration per day which may not cause symptoms Thorsteinsson et al. 1986. The hypoglycaemia frequency and severity is affected by a number of factors including the number of injections per day the type of insulin and variations in food absorption within individuals and among injection sites. Emotions are also affected and mood changes in the three basic mood types: energetic arousal feel active tense arousal feel anxious and hedonic state feel happy occur during or in anticipation of hypoglycaemia. Many people with diabetes fear hypoglycaemia which can lead them to inappropriately lower their insulin doses to reduce the risk of hypoglycaemia see Chapter 15. Thus the effects of hypoglycaemia are complex and multifactorial. Education and strategies to prevent/manage hypoglycaemia should be individualised and accompany changes in medication management and include family and significant others. Definition of hypoglycaemia Hypoglycaemia is defined in various ways using different parameters by various organisations and many differ in the threshold set for hypoglycaemia which range form 3.9 to 3 mmol/L. The 2012 American Diabetes Association ADA 2013 Standards of Medical Care in Diabetes defined hypoglycaemia as a fasting blood glucose 3.9 mmol/L which is higher than the threshold often used in clinical trials. However The ADA set the threshold at a higher level because the aim of treatment is to avoid hypoglycaemia. Thus hypoglycaemia is often defined biochemically as blood glucose below a specific level. It is also defined according to severity as: • Mild: symptomatic where the individual is able to self-treat. The symptoms are often vague and may not be related to the actual blood glucose level. The most commonly reported initial symptoms that closely reflect the actual blood glucose level are trembling sweating tiredness difficulty concentrating and hunger. • Severe: symptomas associated with neuroglycopaenia where help is required to treat the episode. People do not always remember a severe hypoglycaemic episode because of retrograde amnesia or denial. Severe hypoglycaemia can occur without coma. • Profound: associated with coma and sometimes convulsions Tattersall 1999 pp. 55–87. In addition a grading system is sometimes used especially in research as follows: • Grade 1 – mild: the person recognises and self-treats. • Grade 2 – moderate: the person requires assistance but oral treatment normalises the blood glucose. • Grade 3 – severe: the person is semiconscious and requires assistance and glucagon or IV glucose may be needed. None of the definitions appear to state the important fact that hypoglycaemia occurs in people with diabetes treated with insulin or oral glucose-lowering medicines GLMs. Hypoglycaemia can occur as a consequence of rare endocrine conditions such as insulinoma but concomitant insulinoma and diabetes is rare. Significantly part of the diagnostic process for suspected insulinoma includes screening for surreptitious insulin of GLM use. Practice points 1 People with diabetes managed on diet alone do not usually have hypoglycaemia and do not require treatment of low blood glucose levels. 2 People treated with insulin are at the greatest risk of hypoglycaemia.

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164 Care of People with Diabetes 3 Hypoglycaemia is the most significant side effect of insulin including the newer insulin analogues. Although hypoglycaemia is lower with insulin analogues particularly nocturnal hypoglycaemia in clinical trials ‘real world’ data is lacking Brod Barnett 2012. In addition to insulin and/or GLM treatment age gender and associated medical conditions such as liver disease cerebrovascular disease autonomic neuropathy and the rate at which the blood glucose falls influences the development and recognition of Table 6.1 Signs and symptoms of hypoglycaemia. These symptoms are so common that they are used in the Edinburgh Hypoglycaemia Scale Deary 1993. Symptoms are different in young children and older people and may vary between episodes in the same individual. Some people may not experience any of the symptoms listed therefore it is important for people to learn to recognise their own hypoglycaemic cues. Sympathetic or adrenergic a Neuroglycopaenic b Weakness Headache Pale skin Tiredness Sweating Hypothermia Tachycardia Visual disturbances Palpitations Difficulty concentrating Shaking Difficulty speaking Tremor Confusion Nervousness or feeling anxious Amnesia Irritability Seizures Tingling of the mouth and fingers Coma Hunger Inappropriate behaviour a Caused by increased activity of the autonomic nervous system triggered by a rapid fall in blood glucose. Also referred to as sympathetic and sympathomedullary. b Caused by decreased activity of the central nervous system because of very low blood glucose. Psychomotor function deteriorates. Some people appear withdrawn others become restless and irritable. They may refuse treatment. Recovery can be slow or rarely the person may die if they do not have help. Nausea and vomiting may occur but are unusual. hypoglycaemic symptoms. In general a rapid fall in blood glucose results in the development of the classic symptoms of hypoglycaemia described in Table 6.1. The classic presentation is more likely to occur in insulin-treated patients. The onset of hypoglycaemia is usually slower with sulphonylureas especially in older people and hypoglycaemia can be prolonged and recur for 24 hours despite treatment. Mortality rates between 4 and 10 are reported and permanent neurological damage is present in 5 of those who survive Salas Caro2002. Long-acting sulphonylureas increase the risk because of their long duration of action active meta bolites and the reduced ability to mount a counter- regulatory response that occurs with increasing duration of diabetes and increasing age. Presenting symptoms may be neuroglycopaenic often confusion dizziness and altered behaviour rather than sympathetic and the hypoglycaemia can be mistaken for stroke transient ischaemia or early dementia and lead to unnecessary investigations and delayed treatment Dunning 2005 Sinclair 2006. Risk factors for hypoglycaemia in older people include: • Treatment with sulphonylureas or insulin especially long-acting agents although long-acting insulin analogues have significantly lower risk hypoglycaemia can still occur with such analogues see Chapters 5 and 12. • Recent discharge from hospital especially if the GLM was changed in hospital and documentation and/or discharge planning is inadequate and the person lives alone. • Erratic eating or malnutrition. • Renal or liver disease.

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Hypoglycaemia 165 • Excess alcohol consumption. • Inadequate knowledge of the signs and symptoms of hypoglycaemia people with diabetes their carers and health professionals. • Inability to self-treat the hypoglycaemia for example due to confusion delirium or concomitant geriatric syndromes. • On multiple medicines. • Using glucose-lowering conventional and complementary medicines together. Many recent management guidelines recommend individualising diabetes management including blood glucose and HbA1c targets to ensure patient safety Del Prato et al. 2010. Recognising hypoglycaemia Some or all of the signs and symptoms listed in Table 6.1 can be present. A number of factors affect the individual’s ability to recognise hypoglycaemia as indicated. In addition some commonly consumed substances such as caffeine which can increase the intensity of the symptoms and alcohol which clouds judgement can make it difficult for people to recognise hypoglycaemia. Symptoms are more varied in children than adults and between hypoglycaemic episodes in the same child and they have more difficulty recognising the symptoms. Young children may become naughty aggressive complain of abdominal pain feeling ‘awful’ yawning daydreaming and warm to the touch Ross et al. 1998. As indicated older people with Type 2 diabetes commonly present with neurological symptoms. Many emergency departments now have a policy of testing the blood glucose in all unconscious patients to detect hypoglycamia. Gonder-Frederick et al. 1997 described a number of factors that affect the individual’s ability to detect and treat hypoglycaemia including: • The blood glucose level. • Usual metabolic control. • Recent hypoglycaemia. • Chronic hypoglycaemia which can occur ‘acutely’ in older people as a result of repeated unrecognised hypoglycaemia or as a result of hypoglycaemic unawareness see Chapter 8. • Counter-regulatory response and amount of adrenaline secreted. The counter-regulatory response especially glucagon release diminishes over time in Type 1 diabetes. • Medications such as beta blockers can mask the sympathetic warning signs and caffeine can cause trembling and sweating that can be mistaken for hypoglycaemia. Smoking confers a 2.6 times greater risk of severe hypoglycaemia in Type 1 diabetes Klein .2007 as well as contributing to the long-term complications of diabetes and other diseases. • Distractions such as concentrating on work when anxious and stressed which also activates the autonomic nervous system ‘fight or flight’ response. • Knowledge such as not recognising the symptoms. • Hypoglycaemic unawareness or impaired mental function which inhibits appropriate management. • Cognitive impairment. Other research shows older people especially those living alone young children who depend on their parents McCrimmon et al. 1995 adolescents DCCT 1997 those Table 6.2 The counter-regulatory hormonal response to hypoglycaemia. Hormone Action Glucagon Increases glucose output from liver and muscle glycogenolysis Adrenaline and noradrenaline Enhances glycogenolysis in liver and muscle Enhances gluconeogenesis Reduces insulin secretion Causes many of the signs and symptoms of hypoglycaemia autonomic response see Table 6.1

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166 Care of People with Diabetes Cortisol Mobilises the substrates for gluconeogenesis Growth hormone Acts with cortisol and adrenaline to inhibit peripheral glucose utilisation determined to achieve strict glycaemic control lower social class Muhlhauser et al. 1998 and pregnant women with Type 1 diabetes experience more hypoglycaemia. For example 45 of pregnant women with Type 1 diabetes experience severe hypoglycaemia during pregnancy particularly in the first trimester and 3–5 mild hypoglycaemic events per patient-week especially in the presence of previous severe hypoglycaemia and impaired or hypoglycaemia unawareness Ringholm Nielsen 2008. Counter-regulatory hormonal response to hypoglycaemia The brain requires 120–140 g glucose per day to function normally and has limited capacity to manufacture its own glucose. Therefore it depends on adequate levels of circulating blood glucose. When the blood glucose falls below normal the body releases hormones to counteract the effects of hypoglycaemia. This is known as the counterregulatory response. Glycogen stores are liberated and new glucose is formed in the liver from precursors for example fatty acids and protein. The hormones released are shown in Table 6.2 along with their resultant action the net result being an increase in blood glucose. Causes of hypoglycaemia Although hypoglycaemia is associated with insulin and GLM use the relationship among these agents and food intake exercise and a range of other contributory factors is not straightforward. Some episodes can be explained by altered awareness or mismatch between food intake and/or food absorption and insulin. It should be noted that serum insulin levels and glucose clearance following insulin injections varies in the same individual even when the same dose is injected at the same time dose and approximate site each day Galloway Chance 1994 even with modern purified insulins Del Prato et al. 2010. Exercise is also a contributing factor in many cases but the effect of exercise is also difficult to predict and depends on exercise intensity and duration planned or spontaneous time of the day previous food intake when it occurred in relation to insulin/ GLM dose and the insulin injection site. For example absorption is enhanced if exercise commences immediately after injecting insulin but not if exercise commences 35 minutes after injecting. As indicated sulphonylureas cause hypoglycaemia but less often than insulin however when sulphonylurea-induced hypoglycaemia does occur it causes significant morbidity and mortality may be prolonged and may accompany or precipitate a stroke or myocardial infarction. Interactions with other medicines including complementary medicines should be considered especially in the setting of compromised renal function see Chapters 8 and 19. Alcohol may be a contributing factor. Frequent hypoglycaemia might indicate changing renal function and insulin doses may need to be reduced. GLMs may be contraindicated. Lowered appetite and nausea accompanying renal disease may contribute to hypoglycaemia risk. If no reasonable common contributing factor can be identified less common causes such as endocrine disorders gastroparesis and coeliac disease should be considered Chapter 10. Psychological factors also need to be considered see Chapter 15. However a specific reason for the episode cannot always be found which makes prevention difficult:the number of hypoglycaemic events where a cause cannot be identified ranges between 19 and 38. Various authors attribute hypoglycaemia to ‘patient non-compliance’ such as manipulating insulin doses reducing intake or omitting meals. While these behaviours do occur especially in adolescents Chapter 13 health professionals need to understand the reason for the behaviour rather than attaching a label to the individual. They need to appreciate the complexity of achieving diabetes balance and the frustration it causes many people with diabetes and the fear associated

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Hypoglycaemia 167 with hyppoglycaemia Jones 2011 Bernard et al. 2012 . The view that achieving blood glucose balance is an equation where : insulin/GLMs+ appropriate diet +appropriate exercise target glucose levels is simplistic and ignores significant individual factors not included in the equation. Preventing and managing hypoglycaemia Preventing hypoglycaemia is challenging and may be impossible to achieve. It is possible to help people understand hypoglycaemia and recognise their unique symptoms and signs and limit the severity and frequency of hypoglycaemia. Key management strategies include: • Undertaking a personalsied hypoglycaemia risk profile especially with vulnerable people such as older people children those with recurrent severe hypoglycaemia those with hypoglycaemic unawareness those with cognitive impairment those with renal and liver disease and people who consume excess alcohol. The assessment should include helping people identify situations that increase the risk of hypoglycaemia. In hospital settings people at high risk of hypoglycaemia include those on insulin infusions. • Using the information to determine safe blood glucose and HbA1c targets for the individual. • Appreciating the emotional and psychological components of hypoglycaemia and the associated fear and impacts on self-care. These aspects should be part of an individualised comprehensive assessment when people commence insulin and at regular intervals especially when the person experiences an hypoglycaemic event. • Appropriate prescribing and medicine reviews and dose adjustment. • Including medicine reviews in annual complication screening programmes. • Educating the person about insulin action hypoglycaemia symptoms and food intake and exercise in relation to insulin action and managing hypoglycaemic episodes. The education might include insulin dose adjustment and carbohydrate counting especially for people using insulin pumps and those on basal bolus regimens. Regular education revision is advisable. • Regular blood glucose-self-monitoring and using the information to tailor food exercise and medicine doses. • Wearing appropriate identification and carrying hypogycaemic treatment at all times. • Using new technologies such as blood glucose meters and algorithms embedded in insulin pumps and glucose sensor systems that can be programmed to identify high and low blood glucose. Systems are available that suspend insulin for two hours when hypoglycaemia is detected. Continuous glucose monitoring can be used as part of a risk assessment and a range of mobile phone apps are available to help people manage their diabetes. • Having back up and support systems in place if the individual is unable to manage the hypoglycaemic episode themselves. • Helping people with hypoglycaemia unawreness recognise changed body signs of hypoglycaemia including structured programmes such as BGATT Cox et al. 2001. Hypoglycaemic unawareness The ability to recognise hypogycaemia warning signs is essential to prevention of severe hypoglycaemia and associated risk of injury falls and coma. People’s experience of hypoglycaemia varies considerably from each other and between hypoglycaemic episodes Speight 2011. Hypoglycaemic unawareness may encompass reduced intensityof the symptoms and/or a change in the type of symptoms the individual experiences Speight 2011. Hypoglycaemic unawareness means people no longer recognise the early autonomic hypoglycaemic signs and do not recognise hypoglycaemia thus they do not treat it and are at risk of severe hypoglycaemia and coma. Recurrent episodes of hypoglycaemia reduce the counter-regulatory response associated symptoms and cognitive responses which affects the individual’s ability to recognise and treat the episode. People with both Type 1 and Type 2 diabetes have compromised counter-regulatory response and a cycle of recurrent hypoglycaemia where each episode

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168 Care of People with Diabetes becomes increasingly severe may develop. If counter-regulation is compromised endogenous insulin secretion is not inhibited. Significantly glucagon release in response to hypoglycaemia is impaired soon after diagnosis of diabetes and becomes progressively defective in people with diabetes. Adrenaline release is also reduced which ultimately contributes to hypoglycaemic unawareness DCCT Research Trial Group 1991 Unger 2012. Hypoglycaemic unawareness may develop when the usual blood glucose is in the low/normal range and people may begin to recognise the symptoms again if the blood glucose targets are raised. Chronic hypoglycaemic unawareness develops with long duration of diabetes usually as a result of autonomic neuropathy and diminished counterregulatory response. Both acute and chronic hypoglycaemic unawareness can be aggravated by medicines such as beta blockers alcohol and stimulants such as caffeine. Hypoglycaemic unawareness increases the risk of severe and profound hypoglycaemia and is one criterion for islet cell transplants. Prevalence of hypoglycaemic unawareness Determining the prevalence of hypoglycaemic unawareness is difficult because experts use different definitions and assessment methods. An estimated 19.5–25 of adults with Type 1 diabetes have hypoglycaemic unawareness and are older than people who recognise hypoglycaemic symptoms Geddes et al. 2008. Rates for people with Type 2 diabetes are more difficult to determine because fewer data are available but increasing age and duration of diabetes contribute to hypoglycaemic unawareness which may be present in 8 of people with Type 2 diabetes Speight 2011. However hypoglycaemic unawareness in people with Type 2 diabetes could be under-recognised and under-reported. Indicators that chronic hypoglycaemia might be present in older people especially those on GLMs include confusion changes in cognition personality changes and disordered behaviour and must be distinguished from other less easily reversible causes of these signs. Accurately monitoring the blood glucose levels is important to detect chronic hypoglycaemia and CGMS can be useful. Management consists of revising the care plan and checking: • That carbohydrate intake is adequate and evenly distributed. • The individual is able to accurately prepare and administer their insulin. • Whether any new medications or complementary therapies were commenced and reviewing the individual’s medication self-management practices. • Teeth/dentures to ensure there is no infection or mouth ulcers and that false teeth fit and are worn • Presence of diabetic complications or comorbidities that can affect self-care ability. • Knowledge which might mean relatives and friends need information about managing hypoglycaemia including how and when to use. People may benefit from education programmes such as BGATT see this book Chapter 16 and some regain the ability to recognise hypoglycaemia or new body cues after a period free from hypoglycaemia. Several methods are used to assess hypoglycaemic unawareness and include careful questioning when hypoglycaemic unawareness is suspected for example changed hypoglycaemic symptoms over time combined with appropriate use of the individuals blood glucose monitoring pattern and serial HbA1c levels frequent presentations to emergency for hypoglycaemia and continuous blood glucose monitoring CGM. Clinical trial methods include the: • Clarke method assesses people’s threshold for and symptomatic response to hypoglycaemia but is limited by out-dated definition of severe hypoglycaemia and lack of consensus about the glycaemic thresholds for hypoglycaemic severity. • Gold Method is a single item measure of hypoglycaemic unawareness and is the most frequently used method but it is limited by the difficulty of interpreting scores between 1 awareness and 4 unawareness. • Pederson-Bjergaad method could overestimate the prevalence of hypoglycaemic unawareness. • Functional neuroimaging to measure regional brain metabolism which is a proxy measure of neuronal activation during hypoglycaemic episodes Dunn et al. 2007. • Hypoglycaemicia Awareness Questionnaire HYPOA-Q is a new tool that consists of 18 items that assess a range of issues related to hypoglycaemic unawareness. In future the HYPOA-Q could enable earlier diagnosis and evaluation of hypoglycaemic unawareness and proactive management and might be the most clinically relevant measure. Nocturnal hypoglycaemia

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Hypoglycaemia 169 Nocturnal hypogycaemia is defined as blood glucose 3.3 mmol/L occurring during the night and mainly occurs in Type 1 diabetes usually as a consequence of relative insulin excess and impaired glucose production overnight. Increased insulin sensitivity overnight plays a role. More than 80 of people treated with insulin experience nocturnal hypoglycaemia 40 of these episodes are severe and are associated with significant morbidity and rarely death. CGSM suggests the prevalence of nocturnal hypoglycaemia is 10–56 lasts for 6 hours the time of the lowest level nadir depends on the insulin type and regimen Raju et al. 2006. Raju et al. 2006 did not find differences in mean nocturnal blood glucose or mean nadir using CGSM to compare four insulin regimens in people with Type 1 diabetes with HbA 1c 7.1 but detected high rates of under- and overestimation of the glucose level. Pramming et al. 1985 tried to identify predictors of early morning hypoglycaemia. They suggested if the blood glucose was 6 mmol/L at 11 p.m. there was an 80 chance of nocturnal hypoglycaemia compared to 12 risk if the blood glucose was 5 mmol/L. Other researchers report similar predictive blood glucose levels but the likelihood of nocturnal hypoglycaemia increases if multiple injections are used compared to CSII Whincup Milner 1987 Bendtson et al. 1988. Vervoort et al. 1996 found the bedtime blood glucose level predicted hypoglycaemia in the early part of the night but not hypoglycaemia occurring in the early morning and that a fasting blood glucose before breakfast 5.5 mmol/L indicated early morning hypoglycaemia. However the only risk factor Cooperberg et al. 2008 identified in a study to determine the amount of glucose needed to prevent exercise-induced hypoglycaemia was frequent exercise. In Young et al.’s study nocturnal hypoglycaemia occurred on both exercise and sedentary nights. Blood glucose 7.2 mmol/L at 9 p.m. predicted overnight hypoglycaemia on sedentary days. Exercise has multiple effects on fuel utilisation and mobilisation. Initially in the first 5–10 minutes muscle glycogen is the primary fuel source followed by circulating glucose and then fuel derived from gluconeogenesis and fatty acid oxidation Silverstein 2008. When the counter- regulatory response is abnormal people are unable to effectively mobilise glucose stores for gluconeogenesis. In many cases the individual does not recognise the signs of nocturnal hypoglycaemia and does not wake up. Repeated episodes of nocturnal hypoglycaemia reduce the counterregulatory response to hypoglycaemia. Undetected autonomic dysfunction and nocturnal hypoglycaemia can increase the risk of fatal cardiac ventricular dysrrhythmias ‘dead in bed’ syndrome. Indicators of nocturnal hypoglycaemia • Night sweats. • Nightmares or vivid dreams. • Unaccustomed snoring. • Morning lethargy or chronic fatigue. • Headaches or ‘hung over’ feeling. • Mood change particularly depression. • High blood glucose before breakfast Somogyi effect. • Morning ketouria. • Relatives notice unusual behavior such as snoring or ‘sleep walking.’ Factors that contribute to nocturnal hypoglycaemia include preceding physical activity that may have occurred many hours previously insufficient carbohydrate in meals excess insulin as a result of these factors enhanced sensitivity to insulin and/or inappropriate insulin dose and alcohol consumption. The Somogyi effect refers to pre-breakfast hyperglycaemia following an overnight hypoglycaemic episode. If any of the above symptoms occur the blood glucose should be measured at 2 to 3 a.m. over several nights to establish whether nocturnal hypoglycaemia is occurring. The insulin is then adjusted accordingly by decreasing the morning long-acting dose for those on a daily insulin the afternoon long-acting dose for those on BD insulin or the pre-evening meal or bedtime dose for basal bolus regimes. Clinical observations

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170 Care of People with Diabetes 1 Sometimes the evening short-acting insulin rather than the intermediate or long-acting insulin causes nocturnal hypoglycaemia depending on the time the insulin was administered. 2 Rapid-acting insulins have a shorter duration of action and are less likely to cause nocturnal hypoglycaemia. 3 Stress and illness are usually associated with hyperglycaemia however they can induce hypoglycaemia in some people with Type 1 diabetes. Practice point The Somogyi effect should be distinguished from another condition that results in morning hyperglycaemia the ‘dawn phenomenon’. The dawn phenomenon refers to a situation where insulin requirements and blood glucose concentration increase between 5 a.m. and 8 a.m. which occurs in up to 75 of people with diabetes. Treatment consists of increasing the insulin dose. Many other hormones have a normal physiological rise in the early morning for example testosterone which causes early morning erections. Managing nocturnal hypoglycaemia Not surprisingly people with diabetes and their relatives are very fearful of hypoglycaemia at any time but particularly at night and careful explanations about the possible causes and suggestions of ways to prevent nocturnal hypoglycaemia are essential. Families/significant others need to know how to manage the hypoglycaemia by maintaining the person’s airway and calling an ambulance. If they have glucagon at home they should give the injection. Various methods have been used to prevent nocturnal hypoglycaemia these include providing carbohydrate snacks at bedtime although there is no real evidence to support the practice Allen Frier 2003 or demonstrate efficacy Raju et al. 2006 and adjusting the insulin regimen. The long-acting insulin analogues with their more predictable action profile are associated with significantly lower rates of nocturnal hypoglycaemia. Helping the individual and their family/carers recognise cues to hypoglycaemia through hypoglycaemia training programmes such as HYATT and BGATT may be effective Cox et al. 2004. CGSM may provide important clues to assist in such training. More recently antihypoglycaemic agents such as ß2-adrenergic agonists Terbutaline were trialled and a significant reduction in the frequency and severity of nocturnal hypoglycaemia was demonstrated Raju et al. 2006. The morning blood glucose was significantly higher after Terbutaline and the pulse rate was elevated. Acarbose with a carbohydrate bedtime snack also reduced the mean blood glucose nadir but did not prevent nocturnal hypoglycaemia. Relative hypoglycaemia People who are accustomed to high blood glucose levels for long periods of time may experience the symptoms of hypoglycaemia when blood glucose control improves and blood glucose levels normalise. In general it is not necessary to treat the symptoms once the blood glucose is recorded but reassurance support and education are necessary until the person adapts to the new blood glucose range. Medicine interactions Some commonly prescribed medicines can interact with sulphonylureas and increase the possibility of hypoglycaemia see Table 6.3. Practice points

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Hypoglycaemia 171 • Consider whether the person is using complementary medicines such as herbs supplements and other complementary therapies CAM such as massage and relaxation therapies. These therapies can exert hypoglycaemic effects themselves interact with conventional medicines or cause liver or renal damage that alters the pharmacokinetics and pharmacodynamics of medicines and predisposes the person to hypoglycaemia or indirectly affect the blood glucose by reducing stress see Chapter 19. • People with diabetes are high CAM users. Table 6.3 Commonly prescribed medicines that can increase the hypoglycaemic effect of sulphonylurea medicines. Medicines Means of potentiation Sulphonamides Salicylates Warfarin Clofibrate Phenylbutazone Displaces sulphonylureas from protein binding sites Coumarin derivatives Chloramphenicol Phenylbutazone Inhibits/decreases hepatic metabolism of the sulphonylurea Probenecid Salicylates Tuberculostatics Tetracyclines Delays urinary excretion of the sulphonylurea MAO inhibitors Increases action by an unknown mechanism Objectives of care In hospital settings staff need to be alert to the possibility of hypoglycaemia in all patients on insulin or GLMs and should hypoglycaemia occur to: 1 Supply quick-acting carbohydrate to immediately raise blood glucose levels if the person is conscious and able to eat. 2 Maintain blood glucose levels within the acceptable range of 4–8 mmol/L most of the time for most people but the range may vary in specific situations such as surgical procedures. 3 Ascertain the cause of the hypoglycaemic episode. 4 Limit further episodes of hypoglycaemia. 5 Allay fear and anxiety including that of relatives. 6 Prevent trauma occurring as a result of hypoglycaemia for example falls. 7 Assess the individual’s knowledge about managing hypoglycaemia and educate or refer to a diabetes educator if necessary. In particular people should be assisted to recognise their personal risk of hypoglycaemia and learn to recognise their individual ‘hypo symptoms’ rather then being provided with a list of textbook signs and symptoms. 8 Consider including an alert in the individual’s medical record if they are at high risk of hypoglycaemia. 9 Consider safety issues related to hypoglycaemia such as falls and associated fractures in older people and plan care and organise the environment to reduce such risks. Johnston et al. 2012 examined hypoglycaemic events and fall- related fractures in people with Type 2 diabetes over 65 years over two consecutive 12-month periods. They also collected data about the presence other falls risk factors such as vascular disease medicines including TZDs. Johnston et al. found hypoglycaemia was independently associated with increased risk of falls-related fractucres. Common fractures included hip spine pelvis leg and upper arm. The findings suggest hypoglycaemia should be included on falls risk assessment tools when the individual has GLM-treated diabetes Dunning 2005 .

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172 Care of People with Diabetes Treatment Rapid treatment is important to prevent mild hypoglycaemia progressing to severe hypoglycaemia and limit the potential adverse risks associated with severe episodes. The following management refers to people in hospital but can be applied in other settings. Mild hypoglycaemia Test and record the blood glucose level. Provide 10–15 g of carbohydrate as quick-acting glucose or other high glycaemic index carbohydrate to raise the blood glucose immediately for example: 3 level teaspoons sugar in 1/2 cup water or 1/2 regular sugary/soft drink not low calorie joule or proprietary glucose preparation such as glucose gels/tablets or person’s usual hypoglycaemia treatment for example jelly beans. Traditional treatment advice is to follow the initial glucose treatment with long- acting carbohydrate to maintain blood glucose until the next meal. However the extra carbohydrate may not always be necessery if the hypoglycaemia is due to rapid-acting insulins with short duration of action. The person’s experience and clinical judgement are important determinants of the need for extra carbohydrate but remember many people over treat hypoglycaemia. If follow up carbohydrate is required provide: 1 /2 sandwich or 2 to 4 dry biscuits unsweetened or 1 piece of fruit. Check blood glucose in one hour and then as necessary. The next dose of insulin or GLM is not usually withheld following a mild hypoglycaemic episode. However if hypoglycaemia occurs frequently the management regimen might need to be adjusted for example extra carbohydrate in the diet reduced medication dose. Severe hypoglycaemia with impaired conscious state Note: Do not give anything by mouth if the person is unconscious. Confused patients often spit fluids out or refuse to swallow. Gels are preferable and can be smeared onto the buccal mucosa but the dose may not be sufficient to reverse the hypoglycaemia. 1 Place the person on their side. 2 Clear airway. 3 Notify the doctor in hospital settings or call an ambulance. 4 Test the blood glucose level and confirm with the laboratory i.e. urgent glucose. 5 Give IM glucagons. Instructions for glucagon administration are shown at the end of the chapter. Prepare an IV tray containing 50 dextrose. Fifty per cent glucose should be given into an antecubital vein because injection into hand veins often results in extravasation and thrombophlebitis. Ten per cent glucose is recommended for children to reduce the risk of hyperosmolality. Dose: adult 20–30 mL 50 glucose child 2–5 mL/kg bolus 10 glucose then 0.1 mL/kg/minute until the child regains consciousness. Consciousness usually returns within five minutes Therapeutic Guidelines TG 2004. 6 Monitor blood glucose 1–2 hourly until blood glucose level is stable above 5 mmol/L and then revert to the usual testing regimen. 7 Give complex carbohydrate low glycaemic index food to maintain the blood glucose level when consciousness returns. The patient may still be confused and may need to be reminded to chew and swallow. The patient should be monitored for at least 36 hours. Ascertain the time and dose for the next insulin injection/OHA dose. Provide education counselling and support to the individual and their family/carers. Prolonged hypoglycaemia

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Hypoglycaemia 173 Recovery from hypoglycaemia can be prolonged if the episode is severe prolonged and/or associated with coma and/or seizures. Other causes of impaired consciousness should be considered such as stroke and insulin overdose. Insulin overdose should be excluded when high doses of IV glucose are needed to maintain the blood glucose 5 mmol/L. Hypoglycaemia related to long-acting sulphonylureas is a medical emergency and the person should be managed in hospital. Prolonged infusion of 10 IV and 1–2 hourly blood glucose monitoring is often necessary. Some experts recommend using 50 mg of subcutaneous octreotide 8 hourly for three doses TG 2004. In some cases a brain scan will be indicated and if cerebral oedema is present IV mannitol is administered. Shorr et al. 1996 suggested the crude rate of prolonged hypoglycaemia associated with longacting sulphonylureas is 16.6 per 1000 person years compared to 1.9 in secondgeneration agents. However long-acting sulphonylureas are no longer used in most countries. Significantly recent discharge from hospital is a significant predictor of serious medicine-associated hypoglycaemia in older people days 1–30 especially the very old frail those on more than 5 medicines Shorr et al. 1997. Recovery should be rapid. If recovery does not occur in 10–15 minutes exclude other causes of unconsciousness. 1 Record episode and blood glucose level on the appropriate chart/s and in patient’s medical record. Consider whether an ‘alert sticker’ should be included in their medical record. 2 Monitor progress/recovery from the episode. 3 Look for the cause of hypoglycaemia for example meal delayed or missed inadequate intake of carbohydrate unaccustomed activity excessive medication medication/medication medication/herb or herb/herb interactions. 4 Reassure the patient and relatives. 5 Ensure patient has an understanding of causes and management of hypoglycaemia refer to diabetes nurse specialist/diabetes educator . 6 See Chapter 12 for information about managing hypoglycaemia in older people. Patients most at risk of hypoglycaemia A number of factors significantly increase the risk of hypoglycaemia. These include: • Those taking insulin or GLM especially long-acting formulations and intensive insulin therapy see Chapter 12. However the long-acting insulin analogues have lower hypoglycaemia risk than the other long-acting and biphasic insulins. • Medicine doses not adjusted for changes such as weight loss increased activity following acute illness and when reducing oral corticosteroid doses. • Beginning an exercise/diet regimen or prolonged aerobic exercise. Hypoglycaemia can occur many hours after exercise often during the night. Unaccustomed activity such as rehabilitation programmes should be considered ‘exercise’. • People on insulin achieving blood glucose within the normal range. • History of hypoglycaemia. • People with an irregular lifestyle and irregular meal and exercise patterns and when carbohydrate content of the meal is low. • Eating disorders. • Young children. It is difficult to predict their activity levels and food intake and the presenting signs may be difficult to distinguish from other causes such as tiredness and misbehaving. It is important to support and educate the family. • Adolescents possibly because of their erratic eating patterns and experimentation with alcohol and striving for ‘good control’. • Older people especially those who live alone. • Insulin-treated pregnant women and newborn babies of women with GDM or on insulin. • Those with renal or hepatic disease. Severe hypoglycaemia is independently associated with microalbuminuria in people with Type 2 diabetes Jae-Seung et al. 2013. • Those with long-standing diabetes who may have autonomic neuropathy are at risk of hypoglycaemic unawareness and effects on the gastrointestinal tract that may delay gastric emptying and food absorption. • People with brittle diabetes Chapter 10. • People fasting for a procedure/surgery or religious reasons for example Ramadan and Buddhist Lent.

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174 Care of People with Diabetes • People with diarrhoea and vomiting where food absorption is impaired. Hypoglycaemia may impair gastric emptying Russo et al. 2005. • Those with an impaired conscious state. • Those sedated or on narcotic infusions. • Endocrine diseases such as insulinoma hypothyroidism and hypoadrenalism. • Alcohol may also cause hypoglycaemia particularly if food is not eaten at the same time. The hypoglycaemia can occur hours after consuming alcohol. • People taking a lot of medications and/or complementary medicines especially those that lower blood glucose. • Social class where people may not be able to afford appropriate food or hypoglycaemia treatment and prevention. Practice points 1 The signs of alcohol intoxication can make hypoglycaemia difficult to recognise. Alcohol impairs cognitive function and reduces the ability to recognise and effectively treat hypoglycaemia. Self-care and diet are often inadequate. In addition chronic alcohol abuse leads to malnutrition and limited glucose stores to mount an effective counter-regulatory response. 2 People with chronic alcohol addiction are very difficult to manage because OHAs are often contraindicated and insulin puts them at high risk of hypoglycaemia. Psychological effects of hypoglycaemia Hypoglycaemia is feared and hated by many people with diabetes and the effects are often under-rated by health professionals. The importance of recognising and accepting these concerns cannot be overemphasised. Hypoglycaemia has profound effects on people’s quality of life social activities for example driving and work and they fear brain damage and death from hypoglycaemia. It is not unusual for people to deliberately run their blood glucose levels high to avoid hypoglycaemia Dunning 1994 see Chapter 15. They can then be termed ‘non-compliant’ and placed in a conflict situation. Commonly expressed concerns about hypoglycaemia are: • loss of control of the situation • reminder that they have diabetes • losing face and making a fool of themselves • blood glucose rising too high after treatment • sustaining brain damage however the DCCT and EDIC studies did not show a relationship between hypoglycaemia and declining cognitive function DCCT Trial Group/ EDICT 1993. The DCCT is not relevant to older people. Hershey et al. 2005 found impaired spatial long-term memory performance and repeated episodes of severe hypoglycaemia particularly when the hypoglycaemia commenced before five years of age. Severe repeated hypoglycaemia has also been associated with a lower volume of grey matter in the left superior temporal region of the brain which is associated with episodic memory in young people with Type 1 diabetes Perantie et al. 2007. • recovery can take days following serious hypoglycaemia and leave residual headache and tiredness • death. Hypoglycaemia can affect the individual’s confidence in their ability to cope. Support and understanding and exploring all of the issues physical mental and social that affect coping is an important part of management. Clinical observation Pet dogs sometimes recognise their owner’s hypoglycaemia and alert them in time for them to be able to treat the hypoglycaemia or rouse another family member.

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Hypoglycaemia 175 Consequences of hypoglycaemia There are a number of physical sequels to hypoglycaemia in addition to the psychological consequences that include: • Neurological impairment. Two main areas of the brain function are affected: cognitive ability most commonly hippocampal functions such as memory and affective ability which affects mood and anxiety level. Blood glucose 1 mmol/L is referred to as neurogycopaenia and usually results in coma loss of consciousness seizures and death or permanent brain damage Mc Nay Cotero 2010. Less profound hypoglycaemia blood glucose 2 mmol/L can interfere with the individual’s ability to perform usual activities and lead to irritability drowsiness vision changes difficulty speaking and confusion Unger Parkin 2011. These neurological changes are particularly dangerous in older people and contribute to or accelerate dementia. Zhang et al. 2010 suggested that the risk of dementia attributable to hypoglycaemia is 2.9 per year. However the longer term neurological effects are controversial. Interestingly Dunn et al. 2007 suggested that although hypoglycaemia is distressing it might also be weakly rewarding because the brain regional networks serving hedonic responses are relatively unaffected in hypoglycaemic people. Amiel one of the coauthors used the term ‘hypo junkies’ in a presentation in Melbourne to refer to a very small group of people who derived pleasure from hypoglycaemia. • Cardiovascular outcomes. Symptomatic mild and severe hypoglycaemia is associated with increased cardiovascular events hospital admissions from all causes and mortality from all causes Pai-Feng et al. 2012. Likewise Zoungas 2010 found a significant increase in risk of major macrovascular events hazard ratio HR 2.88 95 confidence interval CI microvascular events HR1.81 95 CI 1.19–2.74 death from macrovascular events HR 2.68 95 CI 1.72–4.19 and death from any causeHR 2.69 95 CI 1.97–3.67 p all 0.001 associated with severe hypoglycaemia. The presence of macroalbuminuria predicts severe hypoglycaemia Jae-Seung et al. 2013. • Non-vascular outcomes are also affected Zoungas 2010. Associations between severe hypoglycaemia and outcomes such as respiratory digestive and skin conditions. • Falls and fall-related fractures Johnston et al. 2012 which compromise self-care mobility increase anxiety and could mean admission to an aged care facility. Guidelines for administering glucagon Glucagon is a hormone produced by the alpha cells of the pancreas. Glucagon stimulates glycogenolysis and hepatic glucose output. Glucagon is available in a single dose pack containing one vial of glucagon hydrochloride powder 1 mg and a glass syringe prefilled with sterile water for injection. Indication Glucagon is used to treat severe hypoglycaemia in people with diabetes treated with insulin or GLMs primarily people who are unable to take glucose orally for whom oral glucose is ineffective who are unconscious or uncooperative or having a seizure. Glucagon can be administered by relatives. Instructions for use 1 Individual patients must be assessed to determine the appropriate dose and route of administration. Glucagon is given according to body weight and muscle bulk intramuscularly or subcutaneously. The buttock is the ideal injection site. 2 The intravenous route may be the preferred route in hospital in profound hypoglycaemia to ensure rapid absorption and reversal of the hypoglycaemia. DCCT data suggest unconscious patients recover within 6 minutes of the glucagon injection. Glucagon may be ineffective in people with low glycogen stores such as thin frail older people and those with liver disease including alcoholics. 3 Check the expiry date. Do not reconstitute the glucagon until just before it is administered prepare and administer. Glucagon should be used soon after reconstitution. Do not use if reconstituted solution is not clear and colourless. 4 Follow the instructions in the package to prepare the injection and the medical order for the dose. 5 Record the time and route of administration the dose and the patient’s response. Dosage

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176 Care of People with Diabetes • Adults and children of weight 25 kg full dose 1 mg. • Children of weight 25 kg half dose 0.5 mg. Practice points 1 A second dose of Glucagon can be given however repeated injections can cause nausea making subsequent food intake difficult thus repeat dosing is not recommended. 2 If recovery does not occur within 10–15 minutes IV glucose might be required. Slow recovery could indicate limited glucose stores but other causes of unconsciousness should be considered. 3 Glucagon may be contraindicated where glycogen stores are low for example in fasting states chronic hypoglycaemia chronic adrenal insufficiency and malnutrition where the individual is unable to mount an effective counterregulatory response. Adverse reactions Adverse reactions are rare. Occasionally transient nausea occurs that can make it difficult to consume sufficient oral carbohydrate which is necessary to avoid the blood glucose dropping again. Vomiting occurs occasionally usually only after a second dose. Glucagon is a peptide so theoretically hypersensitivity is possible and is more likely in atopic patients. In reality hypersensitivity is rare. Clinical observations • Hypothermia can prolong recovery from hypoglycaemia especially in the elderly in winter. Management of the hypothermia as well as the hypoglycaemia is usually required. • Hypothermia represents a poor prognosis. References Accord Study Group 2008 Effects of intensive glucose lowering in Type 2 diabetes. New England Journal of Medicine 358 24 2545–2559. Allen K. Frier B. 2003 Nocturnal hypoglycaemia: Clinical manifestations and therapeutic strategies towards prevention. Endocrine Practice 9 530–543. American Diabetes Association 2013 Standards of Medical Care in Diabetes – 2013. Diabetes Care January 2013 36: S4-S10 DOI: 10.2337/dc 13-S004. Amiel S. Dixon T. Mann R. Jameson K. 2008 Hypogycaemia in Type 2 diabetes. Diabetic Medicine 25 3 245–254. Bernard K. Cavan D. Ziegler R. et al. 2012 The ticking time bomb: Fear of hypoglycaemia and its impact on diabetes control: Baseline results from ABACUS. Poster presented at the European Association for the Study of Diabetes Berlin. Bendtson I. Kverneland A. Pramming S. Binder C. 1998 Incidence of nocturnal hypoglycaemia in insulin-dependent diabetic patients on intensive therapy. Acta Medica Scandinavica 223 543–548. Brod M. Barnett A. 2012 Impact of self-treated hypoglycaemia in Type 2 diabetes: A multinational survey in patients and physicians. Current Medical Research and Opinion 28 12 1947–1958. Cooperberg B Breckenridge S Arbelaez A et al. 2008 Terbutaline and the prevention of nocturnal hypoglycemia in type 1 diabetes. Diabetes Care 31 2271–2272. Cox D. Clarke W. Gonder-Frederick L. et al. 1985 Accuracy of perceiving blood glucose in IDDM. Diabetes Care 8 529–536. Cox D. Gonder-Frederick W. 2001 Blood glucose awareness training BGAT 3 long term benefits. Diabetes Care 24 4 637–642. Cox D. Kovatchev B. Koev D. 2004 Hypoglycaemia anticipation awareness training HYATT reduces occurrences of severe hypoglycaemia among adults with Type 1 diabetes. International Journal Behavioural Medicine 11 212–218. Davis E. Keating B. Byrne G. Russell M. Jones T. 1997 Hypoglycaemic incidence and clinical predictors in a large population based sample of children and adolescents with IDDM Diabetes Care 20 22–25. Daneman T. Frank M. Perlman K. Tamm J. Ehrlich R. 1989 Severe hypoglycaemia in children with insulin dependent diabetes: Frequency and predisposing factors. Journal of Paediatrics 115 681–685. Deary I. 1993 Effects of hypoglycaemia on cognitive function in Hypoglycaemia and Diabetes: Clinical and Pyysiological Aspects eds B. Frier and B. Fisher Edward Arnold London pp. 80–92.

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Hypoglycaemia 177 Del Prato S. LaSalle J. Mattheai S. Bailey C. 2010 Tailoring treatment to the individual in Type 2 diabetes practical guidance from the Global Partnership for Effective Diabetes Management. International Journal of Clinical Practice 64 3 295–304. DCCT Diabetes Control and Complication Trial Research Group 1991 Epidemiology of severe hypoglycaemia in the Diabetes Control and Complications Trial. American Journal of Medicine 90 450–459. DCCT Diabetes Control and Complication Trial Research Group 1997 Hypoglycaemia in the Diabetes Control and Complications Trial. Diabetes 46 271–286. Diabetes Control and ComplicationsTrial DCCT/Epidemiology of Diabetes Interventions and Complications Research Group DCCT 1993 The effect of intensivetreatment of diabetes on the development and progression of long-term complications in insulin dependent diabetes mellitus. New England Journal Medicine 329 977–986. Diabetes Control and ComplicationsTrial DCCT/Epidemiology of Diabetes Interventions and Complications Research Group 2003. Intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. New England Journal Medicine 348 2294–2903. Dunn J. Cranston I. Marsden P. Amiel S. Reed L. 2007 Attenuation of amydgala and frontal cortical responses to low blood glucose concentration in asymptomatic hypoglycaemia in Type 1 diabetes: A new player in hypoglycaemic unawareness. Diabetes 36 2706–2773. Dunning P. 1994 Having diabetes: Young adult perspectives. The Diabetes Educator 21 1 58–65. Dunning T. 2005 Managing Diabetes in Older People. Wiley Blackwell Chichester. Donnelly L. Morris A. Frier D. 2005 Frequency and predictors of hypoglycaemia in Type 1 diabetes and insulin treated Type 2 diabetes: A population based study. Diabetic Medicine 22 6 749–755. Farmer A Brockbank K Keech M et al. 2012 Incidence and costs of severe hypoglycaemia requiring attendance by the emergency medical services in South Central England. Diabetic Medicine Mar 21. DOI: 10.1111/j.1464-5491.2012.03657.x. Galloway J. Chance R. 1994 Improving insulin therapy: Achievements and challenges. Hormone and Metabolic Research 26 591–598. Geddes J. Schopman J. Zammitt M. Frier B. 2008 Prevalence of impaired awareness of hypoglycaemia in adults with Type 1 diabetes. Diabetic Medicine 24 4 501–504. Gonder-Frederick L. Cox D. Driesen N. Ryan C. Clarke W. 1994 Individual differences in neurobehavioural disruption during mild to moderate hypoglycaemia in adults with IDDM. Diabetes 43 1407–1312. Henderson J. Allen K. Deary I. Frie H. 2003 Hypoglycaemia in insulin-treated Type 2 diabetes: Frequency symptoms and impaired awareness. Diabetic Medicine 20 12 1016–1021.The measurement of cognitive function during acute hypoglycaemia: experimental limitations and their effect on the study of hypoglycaemia unawareness. Heller S. Macdonald I. 1996 Diabetic Medicine 13 7 607–15. Hepburn D. 1993 Symptoms of hypoglycaemia in Hypoglycaemia and Diabetes: Clinical and Physiological Aspects eds B. Frier and B. Fisher Edward Arnold London pp. 93–103. Hershey T. Perantie D. Warren S. 2005 Frequency and timing of severe hypoglycaemia affects spatial memory in children with Type 1 diabetes. Diabetes Care 28 2372–2377. Jae-Seung Y Sun-Hye K Sun-Hee K 2013 resence of Macroalbuminuria Predicts Severe Hypoglycemia in Patients With Type 2 Diabetes Mellitus: A 10-year follow-up study. Diabetes Care December 17 2012 DOI: 10.2337/dc 12-1408. Jones T. 2011 Strategies for preventing hypoglycaemia in intensively managed Type 1 diabetes patients. Diabetes Management 37 30–34. Jones T. Porter P. Sherwin R. 1998 Decreased epinephrine responses to hypoglycaemia during sleep. New England Journal of Medicine 338 1657–1662. Johnston S. Conner C. Aagren M. Ruiz K. Bouchard J. 2012 Association between hypoglycaemic events and fall-related fractures in Medicare-covered patients with Type 2 diabetes. Diabetes Obesity and Metabolism 14 634–643. Klein R. 2007 Smoking is linked to hypoglycaemia in Type 1 diabetes. Diabetes Care 30 1437–1441. Laing S. Swerdlow A. Slater S. 1999 The British Diabetic Cohort Study 1. All-cause mortality in patients with insulin-treated diabetes mellitus. Diabetic Medicine 16 459–465. Leese G. Wang J. Broomhall J. 2003 Frequency of severe hypoglycaemia requiring emergency treatment in Type 1 and Type 2 diabetes: A population based study of health service resource use. Diabetes Care 26 4 1176–1180. Lundkvist J. Bolinder C. Johnson L. 2005 The economic and quality of life impact of hypoglycaemia. European Journal of Health Economics 6 197–202. McAuley V. Deary I. Ferguson S. Frier B. 2001 Acute hypoglycaemia in humans causes attentional dysfunction while nonverbal intelligence is preserved. Diabetes Care 24 1745–1750. McCrimmon R. Gold A. Deary I. Kelnar C. Frier B. 1995 Symptoms of hypoglycaemia in children with IDDM. Diabetes Care 18 851–861. McNay E. Cotero V. 2010 Mini-review: Impact of recurrent hypoglycaemia on cognitive and brain function. Physiology Behaviour 100 3 234–238. Muhlhauser I. Overmann H. Bender R. Bott U. Berger M. 1998 Risk factors of severe hypoglycaemia in adult patients with Type 1 diabetes – A prospective population based study. Diabetologia 14 1274–1282. Morris A. DARTS/MEMO Collaboration 2003 Frequency of severe hypoglycaemia requiring emergency treatment in Type 1 and Type 2 diabetes: A population-based study of health service resource use. Diabetes Care 26 1176–1180. Moghissi E. 2011 Patients with diabetes lack knowledge about hypoglycaemia. Presented at the 20 th Annual Meting and Clinical Congress of the American Association of Clinical Endocrinologists San Diego California. National Health and Medical Research Council 1991 Hypoglycaemia and Diabetes. Australian Government Printers Canberra. Nordfeldt S. Ludvigsson J. 1997 Severe hypoglycaemia in children with IDDM. A prospective study 1992–1994. Diabetes Care 20 497– 503.

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178 Care of People with Diabetes Pai-Feng H. Shih-Hsien S. Hao-Min C. et al. 2012 Association of clinical symptomatic hypoglycaemia with cardiovascular events and total mortality in Type 2 diabetes mellitus: A nationwide populationbased study. Diabetes Care DOI: 10.2337/dc12-0916. Perantie D. Wu J. Koller J. 2007 Regional brain volume differences associated with hyperglycaemia and severe hypoglycaemia in youth with Type 1 diabetes. Diabetes Care 30 2331–2337. Pramming S. Thorsteinsson B. Ronn B. Binder C. 1985 Nocturnal hypoglycaemia in patients receiving conventional treatment with insulin. British Medical Journal 291 376–379. Pramming S. Thorsteinsson B. Bendtson I. Binder C. 1991 Symptomatic hypoglycaemia in 411 Type 1 diabetic patients. Diabetic Medicine 8 217–222. Raju B. Arbelaez A. Breckenridge S. Cryer P. 2006 Nocturnal hypoglycaemia in Type 1 diabetes: An assessment of preventative bedtime treatments. Journal Clinical Endocrinology and Metabolism 91 2087–2092. Ringholm N. Nielsen L. 2008 Hypoglycaemia most common in early pregnancy in women with Type 1 diabetes. Diabetes Care 31 9–14. Ross L. McCrimmon R. Frier B. Kelnar C. Deary I. 1998 Hypoglycaemic symptoms reported by children with Type 1 diabetes mellitus and by their parents. Diabetic Medicine 15 836–843. Russo A. Stevens J. Chen R. et al. 2005 Insulin-induced hypoglycaemia accelerates gastric emptying of solids and liquids in long standing Type 1 diabetes. Journal of Clinical Endocrinology and Metabolism 90 4489–4495. Salas M. Caro J. 2002 Are hypoglycaemia and other adverse effects similar among sulphonylureas Adverse Drug Reactions Toxicology Review 21 205–217. Silverstein J. 2008 The lows of exercise: Another piece of the puzzle. International Diabetes Monitor 20 1 44–46. Shorr R. Daugherty W. Griffin M. 1996 Individual sulfonylureas and serious hypoglycaemia in older people. Journal of the American Geriatric Society 44 7 751–755. Shorr R. Ray W. Daugherty J. Griffin M. 1997 Incidence and risk factors for serious hypoglycaemia in older persons using insulin or sulphonylureas. Archives of Internal Medicine 157 15 1681–1686. Sinclair A. 2006 Special considerations in older adults with diabetes: Meeting the challenge. Diabetes Spectrum 19 229–233. Sommerfield A. Deary I. McAuley V. Frier B. 2003 Short-term delayed and working memory are impaired during hypoglycaemia in individuals with Type 1 diabetes. Diabetes Care 26 390–396. Speight J. 2011 Assessing impaired awareness of hypoglycaemia. Diabetes Management 34 36–37. Siafarikas A. Johnston R. Bulsara M. et al. 2012 Early loss of the glucagons response to hypoglycaemia in adolescents with Type 1 diabetes. Diabetes Care 35 1757–1762. Tattersall R. 1999 Frequency causes and treatment of hypoglycemia in Frier B. and Fisher B. eds Hypoglycemia in Clinical Diabetes Wiley Chichester UK pp. 55–87. Therapeutic Guidelines TG 2004 Hypoglycaemia. htm accessed December 2007. Thorsteinsson B. Pramming S. Lauritzen T. Binder C. 1986 Frequency of daytime biochemical hypoglycaemia in insulin-treated diabetic patients: Relation to daily median blood glucose concentrations. Diabetic Medicine 3 147–151. UKPDS 1998 Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with Type 2 diabetes UKPDS 33. Lancet 352 837–853 correction Lancet 1999 354 602. Unger J. 2012 Uncovering undetected hypoglycaemic events. Diabetes Metabolic Syndrome and Obesity 5 57–74. Unger J. Parkin C. 2011 Hypoglycaemia in insulin-treated diabetes: A case for increased vigilance. Postgraduate Medical Journal 123 4 81–91. Vervoort G. Goldschmodt H. van Doorn L. 1996 Nocturnal blood glucose profiles in patients with Type 1 diabetes on multiple 4 daily insulin injection regimens. Diabetic Medicine 13 794–799. Veneman T. Mitrakou A. Mokan M. Cryer P. Gerich J. 1993 Induction of hypoglycaemia unawareness in asymptomatic nocturnal hypoglycaemia. Diabetes 42 1233–1237. Whincup G. Milner R. 1987 Prediction and management of nocturnal hypoglycaemia in diabetes. Archives of Diseases in Childhood 62 4 333–337. Wright A. Cull C. Macleod K. Holman R. 2006 Hypoglycaemia in Type 2 diabetic patients randomized to and maintained on monotherapy with diet sulphonylurea Metformin or insulin for six years from diagnosis. UKPDS 73. Journal of Diabetes Complications 20 395–401. Yki-Jarvinen H. Ryysy L. Nikkila K. et al. 1999 Comparison of bedtime insulin regimens in patients with Type 2 diabetes mellitus. A randomised controlled trial. Archives of Internal Medicine 130 399–396. Yogev Y. Chen R. Ben-Haroush A. 2003 Continuous glucose monitoring for the evaluation of gravid women with Type 1 diabetes mellitus. Obstetrics and Gynaecology 101 633–638. Zhang Y. Wieffer H. Modha R. et al. 2010The burden of hypoglycaemia in Type 2 diabetes: A systematic review of patient and economic perspectives. Journal of Clinical Outcomes Management 17 12 547–557. Zoungas S. 2010 Severe hypoglycaemia and risks of vascular events and death. Results in Diabetes 3 1 3.

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Chapter 7 Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA Hyperosmolar Hyperglycaemic States HHS and Lactic Acidosis Cure Diabetes in 21 Days Key points • Acute illness most commonly causes hyperglycaemia and less commonly hypoglycaemia. • Untreated hyperglycaemia can precipitate ketoacidosis and hyperosmolar states which are serious short-term complications of diabetes even if they are managed competently. • Meticulous attention to detail and proactive insulin use reduces morbidity and mortality. • Monitor hydration status closely especially in children and older people. • Gradually lower the blood glucose level to avoid hypoglycaemia. • Monitor ketone clearance in blood. • Consider whether infection could be an underlying cause but note the white cell count is often elevated in hyperglycaemic states and may not indicate infection. • Hyperglycaemia-related abnormalities favour thrombosis inflammatory changes and impair ischaemic preconditioning which is a protective mechanism and predisposes the individual to cardiac events and the formation of superoxide anion oxidative stress that cause tissue damage. • Hyperglycaemia is associated with cerebral neuronal damage possibly due to elevated tissue acidosis and lactate levels that occur in hyperglycaemia. • Insulin is the most effective way to manage hyperglycaemia-induced abnormalities and reduce the associated complications. • Educate the person with diabetes and their family about how to manage future intercurrent illnesses. • Consider psychological and social issues especially if there are repeated admissions for DKA.

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180 Care of People with Diabetes Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. Rationale This chapter primarily concerns managing hyperglycaemia associated with illnesses in hospital settings but preventative self-care is included. Hyperglycaemia DKA and HHS are preventable short-term complications of diabetes. When hyperglycaemia does occur effective proactive management can reduce the progression to DKA or HHHS and limit the attendant metabolic derangements should these conditions occur. Hyperglycaemia induces a range of metabolic abnormalities that predispose the individual to cardiovascular cerebrovascular and cognitive complications and other adverse events. People with well-controlled diabetes do not usually experience higher rates of intercurrent illness than non- diabetics. However those with persistent hyperglycaemia may have lower immunity delayed wound healing and are at increased risk of infections including infections including infections caused by organisms that are not normally pathogenic such as tuberculosis and have a poorer response to antibiotics Australasian Paediatric Endocrine Group APEG 2005 Australian Diabetes Society ADS 2012. Infection is the most common cause of DKA and HHS. Thus optimal blood glucose targets and the most appropriate method to achieve the target for people in hospital need to be decided. Maintaining the blood glucose range between 5 and 10 mmol/L is appropriate for most patients ADS 2012 including those on corticosteroid medicines Chapter 10 Clement et al. 2004. However a number of factors affect clinical decisions and where possible decisions should be made with the individual concerned and their relatives and carers or according to their advanced care plan ACP Chapter 18. Key factors that affect clinical decisions are: • duration and acuity of the presenting problem • risks associated with hyperglycaemia and/or ketosis • duration of diabetes: long standing diabetes or new diagnosis • presence of existing diabetes complications and/or other comorbidities • nutritional status • medicine regimen and risk of hypoglycaemia and consequent adverse events Chapter 6 • life expectancy • available resources and expertise Ismail-Beigi et al. 2011. Prevention: proactively managing intercurrent illness Prevention strategies consist of educating the person with diabetes and their family about how to prevent intercurrent illness or proactively manage intercurrent illnesses to limit the metabolic consequences. Illness prevention/management strategies should be individualised and based on a thorough physical psychological and social assessment using a risk management and quality use of medicines QUM approach Chapter 5. General health care should be considered as well as diabetes-related issues and encompass risk screening for breast and other forms of cancer such as bowel and prostate disease and preventative vaccinations in children adults and older people. Illness prevention education should encompass: • Proactive health care such as identifying key illness risk times for example colds and flu during winter having an individualised documented plan for managing illness and a kit containing essential equipment and information such as ketone test strips and relative’s and health professional’s telephone numbers. • Recognising and managing the signs and symptoms of DKA and HHS which includes the importance of monitoring blood glucose and ketones and using the information to adjust glucose-lowering medicine GLM doses or to seek medical advice and how to maintain fluid intake. • How to adjust insulin/GLMs and dietary intake to control blood glucose levels. • When to seek assistance. In addition health professionals should regularly reassess the individual’s illness selfcare capability including:

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 181 • Knowledge according to the factors outlined in the preceding list. • Physical ability to manage such as mobility sight manual dexterity and other activities of daily living bearing in mind these may all be compromised by hyperglycaemia. This is an important aspect of long-term complication screening programmes. Groups likely to need assistance are children pregnant women frail older people who live alone people with disabilities those who are acutely ill and those who are depressed. The most effective management strategy for these people may be to seek health professional advice quickly. • Psychosocial factors such as mental health and coping skills cognitive function and available support from family or other carers considering the carer’s state of health and coping ability especially older people. • Preventative health care strategies such as vaccinations mammograms prostate checks bowel screening usual metabolic control and their sick day management plan and kit. Annual influenza and pneumococcal vaccinations are recommended for people with diabetes COPD and cardiovascular disease including children with these conditions National Asthma Council 2005. Mortality increases by 5–15 in people with diabetes during influenza epidemics especially those with cardiovascular and renal complications Smith Poland 2004. The increased risk may be due to older age cardiovascular disease or to the diabetes itself due to the impaired immune function due to DKA/HHS Diepersloot et al. 1990. Kornum 2007 suggested that Type 2 diabetes predicted mortality associated with pneumonia and further hyperglycaemia on admission 11 mmol/L in people with diabetes and 6 mmol/L in non-diabetics predicts pneumonia-related mortality. • Observational data suggest influenza vaccination prior to and during an influenza epidemic reduces the associated hospital admissions and mortality in people with diabetes Wang et al. 2004. Thus all people with diabetes aged 6 months and older should receive annual influenza vaccination unless contraindicated. Contraindications include allergy/anaphylactic reaction to eggs and/or the vaccine intercurrent illness with fever 38 °C. • Regular medicine reviews including complementary and over-the-counter medicines. In particular assessing the continued need for diabetogenic medicines such as atypical antipsychotic medications glucocorticoids and thiazide diuretics. If these medicines are necessary and there are no alternatives the lowest effective dose should be used for the shortest possible time. • Early recognition of new presentations of diabetes. • Good access to competent medical and nursing care and ongoing education. • Good knowledge on the part of people with diabetes and health professionals. • Good communication/therapeutic relationship between the person with diabetes and their health professionals Munro et al. 1973: this is an old reference but it is still pertinent in the light of the frequent presentations to hospital with hyperglycaemiaassociated conditions. • Psychological screening should be incorporated into routine complication assessment programmes Ciechanowski et al. 2000 Dunning 2001. Self-care during illness People with Type 1 diabetes are at greatest risk of DKA but DKA can occur in seriously ill people with Type 2 diabetes and HHS is associated with significant morbidity and mortality. A suggested plan for monitoring blood glucose and ketones is shown in Table 7.1 International Society for Paediatric and Adolescent Diabetes ISPAD 2000 Kitabchi et al. 2006 American Diabetes Association 2002 Laffel et al. 2005 Australian Diabetes Educators Association ADEA 2006 Dunning 2007. In the early stages of the illness people may be able to be managed at home if they are capable of performing self-care have support and can telephone their doctor at least every 1–2 hours. Admission to hospital is advised in the following situations: • children especially younger than 2 years • persistent vomiting and/or bile-stained vomitus • persistent diarrhoea • blood glucose persistently ≤ 4 mmol/L or 15 mmol/L and ketones present • severe localised abdominal pain • hyperventilation Kussmaul’s respirations • dehydration • coexisting serious illness • impaired conscious state

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182 Care of People with Diabetes • the individual parent or care providers are unable to cope. Hyperglycaemia Hyperglycaemia refers to an elevated blood glucose level 10 mmol/L due to a relative or absolute insulin deficiency. The symptoms of hyperglycaemia usually occur when the blood glucose is persistently above 15 mmol/L. The cause of the hyperglycaemia should be sought in people with an established diagnosis of diabetes and corrected to avoid the development of diabetic ketoacidosis DKA or HHS. Hyperglycaemia DKA and HHS are often referred to as short-term complications of diabetes. DKA develops relatively quickly. HHS is often insidious and usually evolves over several days to weeks. Hyperglycaemia disrupts multiple organ systems and needs to be treated to reduce the morbidity and mortality associated with the illness and its metabolic consequences American Association of Clinical Endocrinologists AACE 2011 ADS 2012 Inzucchi et al. 2012. Fluid resuscitation corrects dehydration improves microcirculation and reduces tissue damage during acute sepsis which helps correct hyperglycaemia but increased insulin doses and/or dose frequency or rescue insulin therapy in Type 2 diabetes is usually required. Many researchers have demonstrated that hyperglycaemia is associated with adverse outcomes in hospitalised people both people with diabetes and non-diabetics and that controlling the blood glucose improves outcomes Abourzik et al. 2004 Clement et al. 2004 ACE Taskforce 2006 ACE/ADA Taskforce 2006 Inzucchi et al. 2012. However higher rates of hypoglycaemia are associated with stringent control of blood glucose below 5 mmol/L and hypoglyacaemia especially severe hypoglycaemia is associated with significant adverse events Unger 2011 Chapter 6. There is still debate about whether continuous IV insulin infusion is the safest way to manage hyperglycaemia in hospital despite the well described benefits in people with and without diabetes van den Berghe et al. 2001 AACE 2011. Intensive insulin therapy protects renal function in critically ill patients and reduces the incidence of oliguria and the need for renal replacement therapy in surgical patients and improves lipid and endothelial profile Schetz 2008. Table 7.1 Self-management advice for managing blood glucose ketones and fluid during illness. These recommendations should be tailored to the individual’s self-care capabilities available assistance and their physical condition. Ketosis can develop rapidly in people using insulin pumps. The underlying cause needs to be ascertained and treated. Type 1 Type 2 Blood glucose BG Monitor 2 hourly Monitor ketones 2 hourly if 15 mmol on two consecutive occasions in a 2–6 hour period Monitor 2 hourly If 15 mmol on two consecutive occasions in an 8–12 hour period increase monitoring frequency to 2–4 hourly QID testing may be adequate in people Blood ketones managed with diet and exercise 1 mmol/L 1–1.4 mmol/L: 1.5 mmol/L: 1 mmol/L 1–1.4 mmol/L 1.5 mmol/L 1 mmol/L 1 –1.4 mmol/L 5 mol/L BG 4–15 mmol/L recheck in 2 hours BG 8 mmol/L extra sweet fluids: 8 mmol/L extra 5 insulin BG 8 mmol/L extra sweet fluids: 8 mmol/L extra 5–10 insulin BG 15–22 mmol/L 5 extra insulin 10 extra insulin 15–20 extra insulin and hospitalise if ketones persist BG 22 mmol/L 10 extra insulin 15 extra insulin 20 extra insulin and hospitalise if ketones persist Follow the same test procedure as described for Type 1 diabetes Ketones are less common in Type 2 diabetes but do occur in serious illness such as septicaemia and myocardial infarction

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 183 Medicines Give supplemental doses of quick/rapid acting insulin 2–4 hourly GLMs Consider ceasing Metformin Increase sulphonylurea dose unless on maximal doses or on a slow release preparation when insulin is preferred 1 GLM and insulin Supplemental doses of quick/rapid-acting insulin Insulin treated Supplemental doses of quick/rapid-acting insulin Refer to hospital Unable to maintain fluid intake Blood glucose and ketones not falling despite supplemental insulin Unable to self-care and no support available Condition deteriorating Unable to maintain fluid intake Blood glucose and ketones not falling despite supplemental insulin Unable to self-care and no support available Condition deteriorating Fluids BG 4 mmol/L usual meals and extra sweet fluids if tolerated 10–12 mmol/L and able to tolerate food 150 ml easily digested fluid every 1–2 hours for example soup fruit juice ice cream BG 12 mmol/L and unable to tolerate food 100– 300 ml low calorie fluids every hour for example gastrolyte low calorie soft drink mineral water water Unable to tolerate fluids at any BG level refer to hospital BG 4 mmol/L usual meals and extra sweet fluids if tolerated 10–12 mmol/L and able to tolerate food 150 ml easily digested fluid every 1–2 hours for example soup fruit juice ice cream BG 12 mmol and unable to tolerate food 100–300 ml low calorie fluids every hour for example gastrolyte low calorie soft drink mineral water water Unable to tolerate fluids at any BG level refer to hospital a If the person has no experience of insulin they will need reassurance and a careful explanation about why insulin is needed. If they are not able to manage or do not have assistance and home nursing is not available they may need to be managed in hospital. Laboratory or capillary blood glucose tests are used to monitor blood glucose during hospitalisation. Capillary tests are undertaken more frequently than laboratory tests except in intensive care situations and may give better insight into the blood glucose pattern Cook et al. 2007. The trend of the blood glucose pattern over time up or down is important information on which to base management decisions including about medicines. Quality management organisations in the US are currently developing hospital outcome measures for managing hyperglycaemia in hospitalised patients Joint Commission on Accreditation of Healthcare Organisations 2006. Despite the evidence that insulin requirements increase during illness insulin doses are often reduced even in the presence of significant hyperglycaemia because health professionals are concerned about causing hypoglycaemia whereas the factors contributing to hypoglycaemia are only rarely investigated and addressed Cook et al. 2007. Coughlin 2012 suggested that hospitals need to focus on patients’ views of their hospital experience which should be measured using appropriate tools rather than the ubiquitous ‘patient satisfaction’ questionnaires. Diabetic ketoacidosis DKA Diabetic ketoacidosis is a life-threatening complication of diabetes. In the absence of sufficient insulin glucose is unable to enter the cells and accumulates in the blood. Insulin deficiency leads to catecholamine release lipolysis and the mobilisation of free fatty acids and subsequently the formation of ketone bodies B-hydroxybutyrate acetoacetate and acetone resulting in metabolic acidosis ADA 2002. Protein catabolism also occurs and forms the substrate for gluconeogenesis which further increases the blood glucose. At the same time glucose utilisation in tissues is impaired. DKA usually only occurs in people with Type 1 diabetes but can occur in people with Type 2 people in the presence of severe infections or metabolic stress. The mortality rate in expert centres is 5 but is higher at the extremes of age and if coma and/or hypotension are present Chiasson et al. 2003. Diabetic ketoacidosis is characterised by hyperglycaemia osmotic diuresis metabolic acidosis glycosuria ketonuria and dehydration. The definition by laboratory results is blood glucose 17 mmol/L ketonaemia ketone bodies 3 mmol/L acidosis pH 7.30 and bicarbonate 15 mEq/L. The signs symptoms of and precipitating factors for DKA are shown in Table 7.2 and Figure 7.1 outlines the physiology and the signs and symptoms that occur as a result of impaired glucose utilisation and the biochemical manifestations found on blood testing.

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184 Care of People with Diabetes Late signs of severe DKA The initial signs and symptoms of DKA polyuria polydipsia lethargy and Kussmaul’s respirations are compensatory mechanisms to overcome the acidosis. If treatment is delayed the body eventually decompensates. Signs of decompensation late signs include : • peripheral vasodilation with warm dry skin • hypothermia • hypoxia and reduced conscious state • oliguria Table 7.2 Early signs symptoms and precipitating factors of diabetic ketoacidosis DKA. Symptoms and signs Precipitating factors Thirst Polyuria Fatigue Weight loss Nausea and vomiting Abdominal pain Muscle cramps Tachycardia Kussmaul’s respirations early sign 1 Newly diagnosed Type 1 5–30 2 Omission of insulin therapy/GLMs 33 3 Inappropriate insulin/GLM dose reduction. DKA has also been associated with inaccurate use of insulin delivery devices after changing devices in both older people and adolescents Bhardwaj Metcalfe2006. 4 Eating disorders 5 Severe emotional distress either directly or by insulin manipulation 6 Relative insulin deficiency due to: 7 Insulin pump failure 8 Severe morning sickness during pregnancy a Acute illness: Infection 10–20 of cases Myocardial infarction Trauma burns Cerebrovascular accident Surgical procedures b Endocrine disorders rare: Hyperthyroidism Pheochromocytoma Acromegaly Cushing’s disease c Medications: Glucocorticoids Thiazide diuretics Sympathomimetic agents Alcohol Illicit drugs Brittle diabetes: life-disrupting blood glucose lability associated with frequent admission to hospital Benbow et al. 2001 Chapter 10 • slow respiratory rate and absence of Kussmaul’s respirations • bradycardia. The signs and symptoms can be masked by intercurrent illness. For example pneumonia can cause tachyapnoea dry mouth and dehydration abdominal pain and vomiting are symptoms of gastrointestinal disease likewise abdominal pain is usual in appendicitis and in labour. Polyuria and polydipsia can be difficult to detect in toddlers not yet toilet trained bedwetters and incontinent older people. Unexplained bedwetting in these groups needs to be investigated and DKA considered when the onset of incontinence and bedwetting is sudden. Hypothermia as a result of peripheral vasodilation can mask fever due to underlying infection and is associated with poor prognosis.

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 185 Differential diagnosis • Starvation ketosis which can be determined by taking a careful clinical history of the presentation. • Alcoholic ketosis where the blood glucose is usually only mildly elevated or low. The implications of the metabolic and physiological changes associated with DKA are shown in Table 7.3. the development of diabetic ketoacidosis DKA. Assessment The following factors should be established: • whether the person has known diabetes • usual insulin/GLM dose dose interval and type/s of insulin/GM • the time the last dose was taken and dose administered • presence of fever which can be a sign of myocardial infarction as well as infection • duration of the deteriorating control/illness • remedial action taken by the patient sick day self-care • whether the person has taken any other medications complementary medicines alcohol or illegal drugs • conscious state. A thorough physical assessment should be undertaken and blood taken to: • Establish the severity of the DKA: glucose urea and electrolytes pH and blood gases degree of ketonaemia. If severe acidosis is present pH 7.1 and the blood glucose is

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186 Care of People with Diabetes not significantly elevated alcohol aspirin overdose or lactic acidosis need to be excluded especially in older people. Ketones in the presence of low blood glucose can indicate starvation malnutrition or cachexia. • Assess the cause: full blood count cardiac enzymes blood cultures ECG chest X-ray urine culture. Table 7.3 The metabolic consequences of diabetic ketoacidosis and associated risks. Many of these changes increase the risk of falls in older people. Metabolic consequences of ketoacidosis Associated risk Metabolic acidosis Nausea and vomiting Cardiac arrest Coagulopathies Increased white cell count which may not be a sign of infection. The white cell function is changed in hyperglycaemic states. Hyperlipidaemia Thrombosis/embolism Substrate for ketone formation if insulin is not replaced Haemoconcentration and coagulation changes Myocardial infarction stroke thrombosis Dehydration Volume depletion Renal hypoperfusion Can cause acute tubular necrosis Gastric stasis Inhalation of vomitus aspiration pneumonia Delayed absorption of food and fluids given via the oral route Abdominal discomfort Hyperkalaemia but overall deficit in total potassium due to loss in osmotic diuresis. Cardiac arrhythmias Hyperglycaemia which is exacerbated by glycogenolysis and gluconeogenesis Plasma hyperosmolality Cellular dehydration Osmotic diuresis Compromised immune function leading to infection and delayed wound healing also thrombosis low mood vision changes Glycosuria Hyponatraemia and ketonaemia which contributes to sodium potassium and chlorine loss Hyponatraemia is common but if sodium is 120 mmol/L may indicate hypertriglyceridaemia Abdominal pain Unnecessary surgery inappropriate pain relief causing further respiratory distress missed labour Death Aims of treatment of DKA Treatment aims to: 1 Correct: • Dehydration • electrolyte imbalance • ketoacidosis • hyperglycaemia by slowly reducing the blood glucose to 7–10 mmol/L. Hyperglycaemia relative insulin deficiency or both predispose people with and without diabetes to complications such as severe infection polyneuropathy multiorgan failure and death van den Bergh et al. 2001 Clement et al. 2004. 2 Reverse shock. 3 Ascertain the cause of DKA and treat appropriately. 4 Prevent complications of treatment. 5 Educate/re-educate the patient and their family/carers.

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 187 Objectives of nursing care To support the medical team to: 1 Restore normal hydration euglycaemia and metabolism. 2 Prevent complications of DKA including complications occurring as a result of management. 3 Pay meticulous attention to detail. 4 Document progress of recovery e.g. blood glucose levels medicines administered vital signs. 5 Re-educate/educate the patient and their family/carers about the management of illness at home or general diabetes education if the person is newly diagnosed. Patient education about managing diabetes during illness can be found in this chapter. 6 Ensure follow-up care is arranged after discharge in particular: review of diabetes knowledge nutritional assessment and physical and psychological assessment. Preparing the unit to receive the patient Assemble: 1 Oxygen and suction tested to ensure they are in working order. 2 Intravenous trolley IV containing: • dressing tray and antiseptic solution • local anaesthetic • selection of intravenous cannulae • IV fluids: normal saline SPPS dextrose/saline • IV giving sets burette • IMED pump or syringe pump • clear short- or rapid-acting insulin preferably administered as an IV infusion • blood gas syringe • blood culture bottles. 3 Cot sides and IV pole. 4 Blood glucose testing equipment cleaned calibrated. 5 Blood ketone testing equipment. 6 Appropriate charts: • fluid balance • blood glucose monitoring • medication • conscious state. 7 Urinary catheterisation equipment. 8 Nasogastric tubes may or may not be used. Some experts recommend passing a nasogastric tube to prevent gastric dilatation and aspiration. 9 Initial care in the intensive care unit is preferable for moderate to severe ketoacidosis. If the patient is admitted to the intensive care unit central venous pressures continuous blood gas and electrocardiogram monitoring is usually performed. Practice point Rapid-acting insulin and quickly promotes transport of glucose into the cells. Intravenous administration is preferred because absorption is more predictable than by the subcutaneous route. Nursing care/observations The nursing management of DKA involves traditional nursing actions as well as monitoring the response to medical therapy. Initial patient care

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188 Care of People with Diabetes Initial patient care is often given in the intensive care unit. The procedure is: • Maintain the airway. • Nurse the patient on their side even if the patient is conscious because gastric stasis and inhalation of vomitus is a possible and preventable complication of DKA. • Ensure strict aseptic technique. Nursing observations 1–2 hourly 1 Observe ‘nil orally’. Provide pressure care especially in older people. 2 Provide mouth care to protect oral mucous membranes and relieve the discomfort of a dry mouth. 3 Administer IV fluid according to the treatment sheet usually initially isotonic saline until the blood glucose is 12 mmol/L then 10 dextrose. However the first litre of saline may be 0.45 in the presence of hypernatraemia sodium 150 mmol/L. 4 Administer insulin according to the treatment sheet it is usually given via an insulin infusion and the dose adjusted according to blood glucose tests see Chapter 7. Intensive insulin therapy maintains the blood glucose within a narrow range and thereby reduces the morbidity and mortality associated with critical illness van den Berghe et al. 2001. In some cases rapid- or short-acting insulin is given intramuscularly usually in remote areas where ICU units are not available. 5 Replace serum potassium. If the initial biochemical result is 5.0 mmol/L potassium is not required initially. It should be added to the second or third litres of IV fluid or when levels fall to 4.5 mmol/L depending on expected potassium loss for example from vomiting. Initially potassium levels should be monitored on an hourly basis. 6 There is general agreement that bicarbonate replacement is not required if the pH is 7.0. There is no consensus about pH 7.0. Some experts state that bicarbonate should be given to minimise respiratory decompensation. Others believe bicarbonate automatically corrects as the acidosis resolves with fluid and insulin Hamblin 1995. Some experts use bicarbonate if the pH is 7.1 if the patient presents with a cardiac arrest or cardiac arrest is imminent. 7 Estimate blood glucose levels 1–2 hourly and confirm biochemically in the early stages. 8 Observe strict fluid balance. Record second hourly subtotals of input/output from admission. Urine output should be 30 mL per hour measured hourly in a calibrated collecting device. Report a urine output of 30 mL per hour. Measure specific gravity SG. Be aware that some creatinine assays cross react with ketones and creatinine may not reflect renal function in DKA. • Heavy glycosuria invalidates SG readings. • Record fluid loss for example vomitus. 9 Monitor central venous pressure. 10 Monitor conscious state. In children with DKA the level of consciousness initially is significantly associated with pH as well as age but not blood glucose or sodium levels Edge et al. 2006. Therefore cerebral function in DKA is related to the severity of the acidosis in children even when cerebral oedema is not present. Cerebral oedema is a serious complication of DKA and has a high morbidity rate in children and older people. If coma is prolonged heparin might be indicated to prevent thrombosis and pulmonary embolism. 11 Record pulse respiration and blood pressure. Fever associated with DKA indicates sepsis. But it should be noted that an elevated white cell count can be due to metabolic abnormalities and does not necessarily indicate the presence of infection. 12 Administer oxygen via face mask or nasal catheter. 13 Monitor and report all laboratory results electrolytes and blood gases. 14 Report any deterioration of condition immediately. 15 Physiotherapy may be helpful to prevent pneumonia and emboli due to venous stasis and to provide passive mobilisation. 16 Administer other medications as ordered potassium calciparine broad-spectrum antibiotics to treat underlying infections Mannitol to reduce cerebral oedema. 17 Reposition and provide skin care to avoid pressure areas and/or venous stasis.

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 189 Subsequent care As the patient’s condition improves: • Review the frequency of blood glucose testing decreasing to 4-hourly including the night time. • Allow a light diet and ensure the patient is eating and drinking before the IV is removed. • Administer subcutaneous insulin before the IV is removed. Often the infusion is turned off before a meal but the IV line left in situ until the person can eat and drink normally and the blood glucose level is stable within the normal range. • Continue to monitor temperature pulse and respiration every 4 hours. • Provide support and comfort for the patient. • Establish the duration of deteriorating control and identify any precipitating factor such as infection. Plan for: • Medical follow-up appointment after discharge. • Nutrition review. • Education/re-education about appropriate management for days when the patient is unwell see Chapter 16. • Review medication dosage especially insulin. DKA can occur as a result of incorrect use of insulin delivery devices which highlights the importance of checking insulin administration technique particularly given hospital staff do not consider incorrect technique as a potential cause Bhardwaj Metcalfe 2006. • Consider psychological review. For example sexual assault is an uncommon but important cause of DKA and should be considered when repeated admissions occur. This is a difficult area to assess and should be undertaken by people with the appropriate skills and with consideration of the legal implications and the effect on the individual and their family. Practice points • Psychiatric consultation should be considered if a patient repeatedly presents in DKA. Eating disorders complicate 20 of recurrent cases of DKA Polonsky et al. 1994. • People especially young women reduce their insulin doses to avoid weight gain and hypoglycaemia. Reducing or stopping insulin is also a form of risk taking and rebellion at having diabetes Dunning et al. 1994. Brittle diabetes and hyperglycaemia Brittle diabetes is difficult to understand and manage for people with diabetes and their carers and health professionals. Brittle diabetes most commonly occurs between 15 and 30 years of age and often leads to frequent hospital admissions for DKA or hypoglycaemia. However brittle diabetes also occurs in older people. Criteria for brittle diabetes in older people are 60 years treated with insulin experiencing unstable blood glucose associated with frequent often prolonged admissions to hospital Gill et al. 1996 Benbow et al. 2001. In the older group women are more likely to present with brittle diabetes than men but the preponderance of women may reflect the proportion of older men and women in the population. There does not appear to be consistent underlying causative factors but cognitive behavioural factors appear to play a role Benbow et al. 2001 . See also Chapter 10. Complications that can occur as a result of DKA Most complications of DKA are due to complications of treatment and most are avoidable: 1 hypoglycaemia due to over-zealous treatment 2 inhalation of vomitus causing aspiration pneumonia 3 hypokalaemia which may lead to cardiac arrhythmias 4 cerebral oedema is rare and can be fatal. It occurs in 0.7–10 of children especially on the first presentation of diabetes and any morbidity that occurs is permanent Rosenbloom 1990

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190 Care of People with Diabetes 5 myocardial infarction 6 deep venous thrombosis 7 adult respiratory distress syndrome. Be extra vigilant with: 1 Older people especially those with established vascular and coronary disease. Risks include myocardial infarction and deep venous thrombosis. 2 Children are at increased risk of cerebral oedema which has a high mortality rate in this group of patients. Euglycaemic DKA Munro et al. originally documented euglycaemic DKA in 1973 Munro et al.1973. Euglycaemic DKA refers to ketoacidosis in the setting of near normal blood glucose levels. Euglycaemia indicates that the blood glucose level and development of DKA do not necessarily correlate. De Child 2001 postulated that heavy glycosuria triggered by counter-regulatory hormone activity or reduced hepatic glucose production could result in lower than expected blood glucose levels. Although euglycaemic DKA is a rare condition it highlights the importance of monitoring serum ketones and blood gases and using low-dose IV insulin infusions in all people with diabetes during illness. Ketosis without hyperglycaemia occasionally occurs postoperatively in the presence of repeated vomiting. Rehydration with dextrose/saline and controlling the vomiting are required to restore depleted hepatic glycogen stores. Hyperosmolar Hyperglycaemic States HHS is a serious metabolic disturbance characterised by a marked increase in serum osmolality the absence of ketones hyperglycaemia usually 40 mmol/L and extreme dehydration caused by a concomitant illness often infection that leads to inadequate fluid intake. It most commonly occurs in people with Type 2 diabetes usually in older people 65 however HHS has been reported in a 9-month-old baby toddlers Goldman 1979 Sagarin et al. 2005 and children Kershaw et al. 2005. People with Type 2 diabetes usually secrete enough endogenous insulin to prevent lipolysis and ketoacidosis Kitabchi et al. 1994 but not sufficient to prevent hyperglycaemia and hepatic glucose output. HHS has a higher mortality rate than DKA an estimated 10–20 although mortality rates as high as 58 are reported. The severity of the metabolic derangements especially delay establishing the diagnosis inadequate treatment and the degree of dehydration contribute to the high mortality rate Hemphill Schraga 2012. In addition the hyperosmolality may limit ketogenesis and the level of free fatty acids available for ketogenesis Sagarin et al. 2005. Type 2 diabetes is associated with progressive beta cell loss so the risk of DKA and HHS may be higher with long duration of Type 2 diabetes or people with LADA see Chapter 1. Approximately one third of cases occur in people with no previous diagnosis of diabetes. Dehydration is usually severe. The patient is often confused and focal and general neurological signs are usually present however despite the name coma is rare occurring in 10 of cases Sagarin et al. 2005 Hemphill Schraga 2012. Once HHS develops it can be difficult to differentiate it from the precipitating illness Hemphill Schraga 2012. Practice point People with Type 2 diabetes usually still have sufficient endogenous insulin production to prevent the formation of ketones. HHS occurs in 17.5 cases per 1 000 000 in the US and has a mortality rate of 10–20 with a slightly higher prevalence in women Sagarin et al. 2005. The onset is associated with severe stress such as acute febrile illnesses

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 191 including infection for example pneumonia and UTI extensive burns myocardial infarction stroke and/or reduced fluid intake. People in aged care facilities are at the highest risk of HHS because they are often unaware of thirst and are not always offered fluids in hot weather. However the cause is not identifiable in many people. Other precipitating factors include an acute illness that increases the counter-regulatory hormone response in the setting of insulin deficiency such as: • stroke • intracranial haemorrhage • silent myocardial infarct which should be considered in all presentations of HHS until it is excluded • pulmonary embolism • underlying congestive heart failure and/or renal disease although hyperosmolality can trigger rhabdomyolysis and cause acute renal failure • surgery especially cardiac surgery some endocrine conditions such as Cushings syndrome • some medications such as diuretics for example IV diazoxide and furosemide in the surgical setting corticosteroids atypical antipsychotice beta blockers Histamine2 blockers immunosuppressant agents • dialysis • parenteral nutrition solutions that contain dextrose • IV fluids that contain dextrose • non-adherence with GLMs and other diabetes self-care. There is a high mortality rate associated with HHS. The mortality rate has decreased since the 1960s but is still 10– 20 ADA 2002 Sagarin et al. 2005. Presenting signs and symptoms HHS usually develops over days to weeks. People may complain of thirst polyuria or increased incontinence or new onset of incontinence in people with dementia weight loss primarily due to fluid loss and lethargy. Oral hydration may be compromised by lack of thirst dementia vomiting and mobility deficits. A thorough physical examination should be carried out to detect sources of infection and include eyes ears nose throat and teeth and gums pneumonia UTI skin meningitis pelvic infection and triggers such as CCF and acute respiratory distress syndrome. HHS is the initial presentation in 30–40 of presentations Kitabchi et al. 2006. • Neurological signs such as drowsiness and lethargy delirium seizures visual disturbances hemiparesis diminished reflexes unsteady gait and sensory deficits. • Dehydration indicated by: reduced skin turgor sunken eyes and dry mouth. • Tachycardia is an early sign hypotension is a late sign and indicates profound dehydration. Tachycardia could also indicate thyrotoxicosis. • Tachypnoea as a consequence of respiratory compensation for the metabolic acidosis. • Hypoxaemia which may compound the effects of dehydration on mental function. • Signs of infection such as enlarged lymph nodes. Warm moist skin is an early indication of infection whereas cool dry skin indicates late sepsis. • Vision changes and other sensory and speech deficits. • Focal or generalized seizures. Specific investigations depend on the results of the physical assessment. Laboratory investigations include blood glucose ketones electrolytes renal function BUN and creatinine which can be elevated due to the dehydration osmolality ≥320 mOsm/kg creatine phosphokinase CPK blood cultures coagulation studies arterial blood gases pH is usually 7.30 bicarbonate ≥15 mEq/L and urine cultures. Other investigations such as ECG cardiac enzymes and troponins lumbar puncture and CSF studies chest X-ray head and abdominal CT and HbA1c as an indication of preceding metabolic control may be useful to plan future management Kitabchi et al. 2006. The nursing care and objectives are similar to those for DKA but extra vigilance and close monitoring is needed because of the age of most people presenting with HHS.

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192 Care of People with Diabetes • Record strict fluid balance. • IV fluid rate. Central venous access may be used. In some cases a Swan-Ganz catheter is inserted to monitor intravascular volume. There is usually a large fluid deficit 10 L. Replacement: in the first 2 hours 1–2 L isotonic saline but the rate depends on the degree of dehydration if severe a higher volume may be indicated lower volumes may be used if there is no urine output. Half normal saline is used once the blood pressure and urine output are normalised and stable. • An arterial line may be inserted in ICU settings to monitor blood gases. • Blood glucose may fall with rehydration alone over the first 1–3 hours but usually insulin is indicated to correct the hyperglycaemia and is usually given as an IV insulin infusion adjusted according to the blood glucose level tested 1–2 hourly. • ECG. • Urine output. A urinary catheter may be indicated to accurately measure output and obtain a clean urine specimen to detect infection but can introduce infection. • Neurological observations. • Manage the airway. • Maintain skin integrity including the feet. Compromised peripheral circulation and peripheral neuropathy increases the risk of foot ulcers which are slow to heal and increase length of stay and the risk of amputation. Nursing on air mattresses may be indicated. • Observe for deep venous thrombosis or embolism. • Administer medications as indicated which might include antibiotics which might be administered IV. Subsequent care as for DKA. Education may be more difficult initially because of the mental confusion associated with HHS and the age of these patients. Ensuring that the family/caregivers understand how to care for the patient and ensuring follow-up education occurs in 2–3 weeks is important. Figure 7.2 outlines the factors involved in the development of hyperosmolar coma. There are similarities with DKA and some important differences. Ketone production is absent or minimal because the patient is usually producing enough endogenous insulin to allow the ketone bodies to be metabolised and utilised. The degree of dehydration is often greater in HONK and the serum and urine osmolality is increased. Lactic acidosis Lactic acidosis is another uncommon condition that sometimes occurs in people with diabetes. Lactic acidosis occurs in 0.06 cases per 1000 patient years usually those with predisposing factors Pillans 1998. Lactate is a product of anaerobic glucose metabolism. Disordered lactate metabolism frequently occurs in critically ill people who are at risk of multiorgan failure and the mortality rate is 70 if the serum lactate remains 2 mmol/L for 24 hours Nicks 2006. Lactate is primarily cleared from the blood by the liver kidneys and skeletal muscles. Lactic acidosis is defined as metabolic acidosis associated with serum lactate 5 mmol/L. It occurs due to either an increase in hydrogen ions or reduction in bicarbonate with increased acid production loss of alkali and reduced renal clearance of acids. Lactic acidosis should be considered during acute illness in patients with vasoconstriction hypotension and with underlying diseases associated with poor tissue perfusion and hypoxia such as: • recent myocardial infarction • cardiac failure and cardiogenic shock • pulmonary disease • cirrhosis • sepsis • renal impairment • medicines and toxins such as isoniazid salicylates beta-adrenergic agents alcohol and biguanides especially in older people with hypoxic diseases and/or dehydration • surgery

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 193 • inborn errors of metabolism such as fructose 1 6-diphosphatase deficiency. Figure 7.2 An outline of the development of hyperosmolar Hyperglycaemic States HHS. Excess lactate is produced in ischaemic skeletal muscle and to a lesser extent in the intestine and erythrocytes and accumulates due to a fall in lactate consumption in the liver which overwhelms the buffering system Nicks 2006. Lactate levels correlate with tissue hypoperfusion and mortality and the duration and degree of lactic acidosis predicts morbidity and mortality. Lactate 4 mmol/L for 24 hours carries an 11 mortality rate in critically ill patients. After 48 hours only 14 survive. Signs and symptoms • signs that the cardiovascular system is compromised for example cyanosis cold extremities tachycardia hypotension dyspnea • lethargy confusion stupor • dry mucous membranes. Biochemistry shows an anion gap lactate 4–5 mmol/L normal 1 mmol/L low pH usually 7.1 but only moderate if any ketones and mildly elevated blood glucose usually 20 mmol/L. Lactic acidosis should be managed in ICU settings. Lactic acidosis associated with Metformin Ninety per cent of metformin is excreted unchanged via the kidneys and the half-life is prolonged and renal clearance reduced in patients with renal impairment where creatinine clearance is reduced. Renal impairment may develop

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194 Care of People with Diabetes slowly as a complication of diabetes or acutely. Metformin is contraindicated when the creatinine 0.16 mmol/L hepatic disease and conditions associated with hypoxia Pillans 1998. Some experts suggest 0.15 mmol/L Nesbit et al. 2004 and that age muscle mass and protein turnover influence the creatinine clearance rate. Although Metformin-associated lactic acidosis is rare it remains the most frequently reported cause of medicine-associated mortality Pillans 1998. It may present as respiratory failure and shock cardiac arrhythmias hypothermia and hypoglycaemia Cohen 2008. In Australia 48 cases of metformin-induced lactic acidosis were reported to the Australian Adverse Drug Reactions Advisory Committee ADRAC between 1985 and 2001 ADRAC 2001. Thirty-five had known risk factors for lactic acidosis. An average of six Metformin-related adverse events are reported to ADRAC per year. Nisbet et al. 2004 calculated the prevalence of lactic acidosis in Australia to be 1 in 30 000 based on 200 000 metformin prescriptions per year and the reported adverse event rate. They caution that the actual rate may be higher due to under-reporting. In the US 204 of 263 patients admitted to hospital were taking Metformin 27 had at least one contraindication and Metformin was continued in 41 of these despite the contraindication Calabrese Turner 2002. Emslie- Smith et al. 2001 identified contraindications to Metformin in 24.5 of 1847 of people taking the medicine. Regular physical assessment to identify patients at risk of lactic acidosis including monitoring renal function structured medication reviews adhering to Metformin prescribing guidelines and reporting medicine adverse events are important aspects of care. Management Management consists of: • IV fluid replacement with normal saline to maintain the circulating volume and tissue perfusion • Oxygen therapy • Bicarbonate given early to correct the acidosis and should be administered slowly to avoid causing metabolic alkalosis and ventilatory failure. Thiamine 50–100 mg IV followed by 50 mg orally for 1–2 weeks in some cases where thiamine deficiency is likely such as malnourished older people and alcoholics. • IV insulin at a rate of 10–12 units/hour in dextrose solution • Monitoring renal and cardiac status • The mental status should be monitored as well as monitoring the physical status • Withdrawing precipitating medicines or toxins which might include haemodialysis in some cases • Antibiotics if sepsis is present • Medication review and discontinuing medication or reducing the dose if contraindications exist. Metformin is the medicine of choice in overweight Type 2 patients but doses 500 mg per day should be used with caution in older people with renal liver and cardiac disease or other hypoxic diseases Nisbet et al. 2004. References Abourzik N Vora C Verma P. 2004 Inpatient diabetology: the new frontier. Journal General Internal Medicine 19: 466-471 American College of Endocrinology and American Diabetes Association ACE ADA 2006 Consensus statement on inpatient diabetes and glycemic control Ace/ada task force on inpatient diabetes Endocrine Practice 12 4:458–468. American Diabetes Association ADA 2002 Hyperglycaemic Crisis in Patients with Diabetes Mellitus. American Diabetes Association USA. American Association of Clinical Endocrinologists AACE 2011 Medical guidelines for clinical practice for developing a diabetes mellitus comprehensive care plan. Endocrine Practice 17 Suppl 2:1–53. Australian Diabetes Educators Association ADEA 2006 Guidelines for Sick Day Management for People with Diabetes. ADEA Canberra. Australian Diabetes Society ADS 2012 Guidelines for routine glucose control in hospital ADS Canberra ADSGuidelinesforRoutineGlucoseControlinHospitalFinal2012_000.pdf accessed November 2012. Australian Drug Reactions Bulletin ADRAC 2001 Incidence of lactic acidosis between 1985–2001. ADRA 20 1 accessed December 2007.

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Hyperglycaemia Acute Illness Diabetic Ketoacidosis DKA 195 Australian Paediatric Endocrien Group APEG 2005 The Australian Clinical Practice Guidelines on the Management of Type 1 Diabetes in Children and Adolescents http// accessed January 2013 Benbow S. Walsh A. Gill G. 2001 Brittle diabetes in the elderly. Journal of the Royal Society of Medicine 94 578–580. van den Berghe M. Wouters P. Weekers F. et al. 2001 Intensive insulin in critically ill patients. New England Journal of Medicine 345 1359–1367. Bhardwaj V. Metcalfe N. 2006 Diabetic ketoacidosis after changing insulin pens: Check technique to avoid complications. British Medical Journal 332 1259–1260. Brunkhurst F. 2008 Intensive insulin therapy Pentastarch may be harmful for patients with severe sepsis. New England Journal of Medicine 358 125–139. Calabrese A. Turner R. 2002 Evaluation of prescribing practices: Risk of lactic acidosis with Metformin therapy. Archives of Internal Medicine 162 434–437. Chiasson J. Josse R Gomis. et al. 2002STOP-NIDDM Trial Research Group. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM Trial Lancet 359: 2072–2077 Ciechanowski P. Katon W. Russo J. 2000 Depression and diabetes. Impact of depressive symptoms on adherence function and costs. Archives of Internal Medicine 160 3278–3285. Clement S Braithwaite S Magee M et al. 2004 Management of diabetes and hyperglycaemia in Hospitals. Diabetes Care 27 2 553– 591. Cohen Z. 2008 Lactic acidosis. American Thoracic Society. care-cases/ accessed 9 February 2008. Cook C. Castro J. Schmidt R. et al. 2007 Journal of Hospital Medicine 2 4 203–211. Coughlin C. 2012 An ethnographic study of main events during hospitalization: Perceptions of nurses and patients. Journal of Clinical Nursing DOI: 10.111/j.1365-2702.2012.04083.x. De P. Child D. 2001 Euglycaemic ketoacidosis – Is it on the rise Practical Diabetes International 18 7 239–240. Diepersloot R. Bouter K. Hoekstra J. 1990 Influenza infection and diabetes mellitus. Case for annual vaccination. Diabetes Care 13 876–882. Dunning P. Ward G. Rantzau C. 1994 Effect of alcohol swabbing on capillary blood glucose measurements. Practical Diabetes 11 4 251–254. Dunning T. 2001 Depression and diabetes summary and comment. International Diabetes Monitor 13 5 9–11. Dunning T. 2007 Diabetes: Managing sick days a patient-centred approach. General Practice Continuing Education Conference Proceedings. Exhibition Centre Royal Australian College of General Practitioners RACGP Melbourne. Edge J. Roy Y. Bergomi A. et al. 2006 Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood glucose concentration. Pediatric Diabetes 7 11. Emslie-Smith A. Boyle D. Evans J. 2001 Contraindications to Metformin therapy in patients with Type 2 diabetes – A population based study of adherence to prescribing guidelines. Diabetic Medicine 18 483–488. Gill G. Lucas S. Kent L. 1996 Prevalence and characteristics of brittle diabetes in Britain. Quarterly Journal of Medicine 89 839– 843. Goldman S. 1979 Hyperglycaemic hyperosmolar coma in a 9-month-old child. Archives of Paediatrics and Adolescent Medicine 133 2 30. Hamblin S. 1995 Diabetic ketoacidosis. Australian Diabetes Educator’s Association Journal Spring 17. Hemphill R. Schraga E. 2012 Hyperosmolar Hyperglycaemic State article/1914705 accessed October 2012. Inzucchi S. Bergenstal R. Buse al. 2012 Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position Statement of the American Diabetes Association ADA and the European Association fo the Study of Diabetes EASD Diabetologia DOI: 10.1007 / s00125-012-2534-0. Ismail-Beigi F. Moghissi A. Tiktin M. et al. 2011 Individualising glycaemic targets in Type 2 diabetes mellitus: Implications of recent clinical trials. Annals of Internal Medicine 54 554–559. Joint Commission on Accreditation of Health Care Organisations 2006…/joint-commission-on-accreditation-of- healthcare-organizations-jcaho.aspx -accessed January 2013 Kershaw M. Newton T. Barrett T. Berry K. Kirk J. 2005 Childhood diabetes presenting with hyperosmolar dehydration but without ketoacidosis. Diabetic Medicine 22 5 645–647. Kitabchi A. Fisher J. Murphy M. Rumbak M. 1994 Diabetic ketoacidosis and the hyperglycaemic hyperosmolar nonketotic state in Joslin’s Diabetes Mellitus eds C. Kahn G. Weir Lea Febiger Philadelphia pp. 738–770. Kitabchi A. Umpierrez G. Murphy M. Kreisberg R. 2006 Hyperglycaemic crises in adult patients with diabetes: A consensus statement from the American Diabetes Association. Diabetes Care 29 12 2739–2748. Kornum J. 2007 Type 2 diabetes linked to higher pneumonia-related mortality. Diabetes Care 30 2251–2257. Laffel L Wentzell K Loughlin C et al. 2005: Sick day management using blood 3-hydroxybutyrate 3-OHB compared with urine ketone monitoring reduces hospital Diabetes Care 28:1277–1281. Malone M. Gennis V. Goodwin J. 1992 Characteristics of diabetic ketoacidosis in older versus younger adults. Journal of the American Geriatric Society 40 1100–1104. Munro J. Campbell I. McCuish A. Duncan L. 1973 Euglycaemic ketoacidosis. British Medical Journal 2: 578–580. National Asthma Council Australia 2005 Roles of Influenza and Pneumococcal Vaccinations in Subgroups with Asthma COPD Diabetes or Heart Disease. CSL Pharmaceuticals Canberra. Nicks B. 2006 Lactic acidosis. E medicine accessed January 2008. Nisbet J. Sturtevant M. Prins J. 2004 Metformin serious adverse effects. Medical Journal of Australia 180 2 53–54.

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196 Care of People with Diabetes Pillans P. 1998 Metformin and fatal lactic acidosis. Center for Adverse Reactions Monitoring CARM accessed January 2008. Polonsky W. Anderson B. Lohrer P. et al. 1994 Insulin omission in women with IDDM. Diabetes Care 17 1178–1185. Rosenbloom A. 1990 Intracerebral crises during treatment of diabetic ketoacidosis. Diabetes Care 13 22–33. Sagarin M. McAfee A. Sachter J. et al. 2005 Hyperosmolar Hyperglycaemic Coma. E medicine accessed January 2008. Schetz M. 2008 Intensive insulin therapy may protect renal function in critically ill patients. Journal of the American Society of Nephrologists Online January 30 accessed January 2008. Shulman R. Finney J. O’sullivan C. Glynne P. Greene R. 2007 Tight glycaemic control: A prospective observational study of computerized decision-supported intensive insulin therapy. Critical Care 11 4 R75 DOI:10.1186/cc5964. Smith S. Poland G. 2004 American Diabetes Association: Influenza and pneumococcal immunisation in diabetes. Diabetes Care 27 Suppl. 1 S111–S113. Unger R Cherrington A 2011 Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover Journal of Clinical Investigation 122 1:4-12. Unger J. 2012 Uncovering undetected hypoglycaemic events. DiabetesMetabolic Syndrome Obesity Targets and Therapy 5 57–74. Wang C. Wang S. Lai C. 2004 Reducing major cause-specific hospitalization rates and shortening hospital stays after influenza vaccination. Clinical Infectious Diseases 39 1322–1332.

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Chapter 8 Long-Term Complications of Diabetes To Cure Diabetes Permanently Click Here Key points • Diabetes is associated with devastating long-term complications that are psychologically physically and financially costly to the person with diabetes. • Diabetes complications cause a great deal of morbidity and represent a significant cost to the health system. • Maintaining euglycaemia reduces the likelihood of complications developing however in Type 2 diabetes complications are often present at diagnosis and/or trigger the diagnosis. • People with diabetes especially older people often require assistance to perform diabetes self-care and other activities of daily living as a consequence of complications. • People with diabetes worry about developing complications and the worry and/or actuality of complications affects their emotional well-being and can lead to depression. • People with diabetes often have other comorbidities in addition to diabetes complications which increases the risk of less than best practice care frequent hospitalisations and polypharmacy. • Proactive preventative complication screening and assessment is essential and should encompass assessing the individual’ risk profile to plan holistic personalised care. • Focusing on improving the individual’s self-care skills and detecting and managing diabetes-related distress and improving the patient-health professional relationship and communication is as essential as the medical aspect of care. Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning.

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198 Care of People with Diabetes © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. Introduction The physical long-term complications of diabetes are generally classified as: • Macrovascular disease: cardiovascular disease cerebrovascular disease and peripheral vascular disease. These are common in Type 2 diabetes and are often present at diagnosis. Type 2 diabetes is often preceded by the metabolic syndrome which confers a high level of cardiovascular risk. Significantly myocardial infarction is often ‘silent’ and sudden. • Microvascular disease: nephropathy and retinopathy. These are a major concern in both Type 1 and Type 2 diabetes. Type 2 diabetes-related nephropathy is one of most common reasons for commencing dialysis. • Neuropathy: peripheral which predominantly affects the feet and legs and autonomic which can lead to gastroparesis erectile dysfunction ED and hypoglycaemic unawareness. These conditions are inter-related and often occur concomitantly. For example ED has vascular and nerve components. In the long term in the presence of persistent hyperglycaemia diabetes can affect almost all body systems and is associated with a number of other disease processes especially Type 2 diabetes where there is an association between obesity some cancers and sleep apnoea. Diabetes is also associated with a range of musculoskeletal diseases osteoporosis depression and dementia although the causal links are not clear in all cases Chapter 10. The presence of other concomitant and agerelated diseases such as arthritis contribute to reduced quality of life and depression and inhibit self-care thus psychological issues are also complications of diabetes. The simultaneous occurrence of two or more chronic conditions multimorbidity Bayliss et al. 2008 increases the risk that the individual will not receive best practice care will be hospitalised more frequently and for longer length of stay use a greater range of health services at increased cost and be prescribed more medicines polypharmacy Taylor et al. 2010. Prevalence estimates for multimorbidity range from 35 to 80 Fortin et al. 2005 Nagel et al. 2008 Britt et al. 2008 although the prevalence is difficult to determine because different data collection methods and definitions are used and many studies focus on older people. The prevalence of multimorbidity increases with age but it is also an issue in younger age groups: more than 40 of people 60 years have several comorbidities Taylor et al. 2010. Multimorbidity often coexists with smoking and obesity which increase the risk the person will develop more morbidities. Multimorbidites affect self-care and can represent a significant carer burden for relatives. Thus a multifactorial approach to managing diabetes complications and other concomitant morbidities is needed and encompasses regular systematic individualised risk assessment processes effective selfcare optimising physical and mental health and diabetes education to prevent/reduce the morbidity and mortality and reduce the health costs associated with diabetes. Pathophysiology of diabetes complications The pathophysiology of diabetes complications is complex but glycaemic control is the most important determinant of optimal mitochondrial function and therefore longterm diabetic complications Brownlee 2000. Changes in mitochondrial function result in oxidative stress and play a key role in the development and progression of both micro and macrovascular complications associated with diabetes. Thus maintaining normoglycaemia to preserve normal oxidative mitochondrial function is needed to delay or prevent the progression of complications Forbes Cooper 2007. Increases in HbA1c from normal to 9.5 confer a 10-fold increased risk of microvascular disease. The relationship between macrovascular disease and hyperglycaemia is not as clear for example only a twofold increase in macrovascular disease risk at the same HbA1c was noted in the UKPDS UKPDS 1998. This finding might be partly explained by the fact that free fatty acids can also be utilised as fuel for oxidative processes in the mitochrondria. Hyperglycaemia initiates a cascade of pathological changes that underlie diabetes complications. Glucose is the major source of fuel for energy production by oxidative phosphorylation. Hyperglycaemia has significant effects on metabolic pathways concerned with generating cellular energy especially in the mitochondria. Most cells have the

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Long-Term Complications of Diabetes 199 capacity to reduce glucose transport across the plasma membrane into the cytosol to maintain glucose homeostasis in the presence of hyperglycaemia. However some cells are not able to adapt and reduce glucose transport sufficiently to prevent intercellular changes in glucose concentration. Cells are at particular risk include capillary endothelial cells in the retina mesangial cells in renal glomeruli and neuronal and Schwann cells in peripheral nerves Forbes Cooper 2007. An increasing body of research suggests that reactive oxygen species ROS initiate the development of diabetic complications Nishikawa et al. 2000. ROS are generated by damaged or dysfunctional mitochondria. The antioxidant chain is a complex pathway involving the metabolism of oxygen and the transfer of electrons from glucose and other fuels through the respiratory chain via a complex series of reactions. When excess fuel enters the respiratory chain the mitochondrial membrane potential is overwhelmed and leaks electrons to oxygen to form superoxide Nishikawa et al. 2000. However despite the increasing evidence that ROS plays a role in the pathogenesis of diabetes complications the exact mechanisms are still being determined. Maintaining optimal mitochondrial function appears to be important to reduce the progression of diabetes complications. More recent research suggests preventing glucose variability might also be important Weber Schnell 2009 Wen et al. 2012 Picconne et al. 2012. The role of antioxidant agents in managing diabetes complications and reducing oxidative damage is controversial although is widely promoted by complementary practitioners. Folic acid has been shown to reduce oxidative damage in Type 2 diabetes Lazalde-Ramos et al. 2012. Likewise Coenzyme Q10 CQ-10 is essential for all energy-dependent processes in the heart consequently the heart is very sensitive to CQ-10 deficiencies Kumar et al. 2009. CQ-10 is often deficient in diabetes and cardiac disease. CQ-10 is available in foods such as beef poultry and broccoli fish oils and peanuts but dietary intake is inadequate to achieve optimal CQ-10 levels in the blood. Supplements reduce the progression of atherosclerosis proinflammatory cytokines and blood viscosity Kumar et al. 2009. Hyperglycaemia contributes to cell death thickened basement membranes in blood vessels stiffened vessels and reduces the functionality and structure of resistance vessels proximal vessels before the blood flows into the capillaries. Calcium-regulated potassium channels are disrupted which affects smooth muscle cell contraction which contributes to hypertension. As a result both under-perfusion and over-perfusion occur. The myogenic response is lost so the resistance vessels no longer have the capacity to cope with the increased blood flow. Increased basement membrane dysfunction and reduced nerve fibre density is apparent in impaired glucose tolerance. Micro- and macrovascular and endothelial cell damage and reduced lumenal size also occur. Brownlee 2000 suggested that no ‘unifying hypothesis’ links the four main hypotheses proposed to explain the pathogenesis of diabetic complications shown below but suggested either redox changes in the polyol pathway or hyperglycaemia-induced formation of ROS might account for all the underlying biochemical changes. 1 Formation of advanced glycation endproducts AGE. Products of glucose metabolism from glycolysis and the tricarboxylic acid cycle initiate protein glycosylation more rapidly than glucose. The protein–glucose complex is broken down by proteosomes or form AGE that become cross-linked and resistant to proteosome activity. Tissues become stiffened and function is compromised. AGE formation may be due to the effects of glucose metabolites rather then glucose itself Wells-Knecht et al. 1995 Dantas et al. 2012. The interaction of AGEs with their receptor RAGE triggers a variety of cellular signaling processes that mediate gene expression and enhance the release of proinflammatory molecules and oxidative stress Farmer Kennedy. 2009. 2 Activation of protein kinase C PKC isoforms. Hyperglycaemia stimulates diacylglycerol the lipid second messenger which activates isoforms of PKC and alters gene and protein expression in organs prone to complications. Inhibiting PKC prevents renal and retinal damage in animal models and a number of clinical trials are in progress involving ruboxisataurin Forbes Cooper 2007. 3 Increased flux through the polyol pathway. In the polyol pathway glucose is converted into sorbitol via aldose reductase and subsequently oxidised to fructose which eventually contributes to the mitochondrial respiratory chain. Intracellular hyperglycaemia results in increased production of sorbitol and reduces the level of other important enzymes involved in detoxifying toxic aldehydes such as glutathione and adenine dinucleotide phosphate and compounds oxidative stress. Sorbitol does not cross cell membranes and causes osmotic stress. Inhibiting aldose reductase delays or prevents diabetes complications especially neuropathy Kaiser et al. 1993. To date aldose reductase inhibitor medications have been disappointing despite improvements in nerve physiology and nerve fibre density largely due to poor tissue penetration and side effects Hotta et al. 2001.

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200 Care of People with Diabetes 4 Increased flux through the hexosamine pathway. When intracellular glucose is high the normal glucose-6- phosphate metabolic cascade is disrupted and a series of moieties are produced that bind to transcription factors and increase the synthesis of some proteins such as transforming growth factor-b1 and plasminogen activator inhibitor type 1 both of which have adverse effects on blood vessels Du et al. 2000. The role of the hexosamine pathway in the pathogenesis of diabetic complications is still evolving. CARDIOVASCULAR DISEASE AND DIABETES Key points • Cardiovascular disease is a leading cause of death in people with diabetes. • Excess mortality from cardiovascular disease is evident in all age groups but especially in young people with Type 1 diabetes. • People with diabetes and no heart disease need to be treated as if they have heart disease especially people with Type 2 diabetes. • Chest pain may be atypical in people with diabetes and may present as weakness fatigue hyperglycaemia or congestive cardiac failure CCF. • Women with diabetes have a higher relative risk of death from cardiovascular disease than men but the absolute risk is lower. • Primary prevention by managing dyslipidaemia hypertension and hyperglycaemia is imperative to lower the risk of heart disease and stroke. • Smoking increases micro- and macrovascular damage. Smoking cessation is imperative. • Depression is common in people with diabetes and cardiac disease. • Transient ischaemic attacks TIA may indicate impending stroke. Rationale Diabetes is a significant risk factor for cardiovascular disease for example coronary heart disease cardiomyopathy peripheral vascular disease and stroke Australian Institute of Health and Welfare AIHW 2007 Dantas et al. 2012. Cardiovascular disease contributes to 54 of all male deaths and 59 of all female deaths in Australia AIHW 2011 and is a major cause of hospital admissions and mortality in people with diabetes. It is often associated with other vascular disease and depression. Complex metabolic abnormalities are present and the need for surgical intervention is high. Autonomic neuropathy can give rise to atypical presentations of cardiovascular disease and heart attack and lead to delayed treatment. The major clinical manifestations of cardiovascular disease involve: • the heart and coronary circulation • the brain and cerebral circulation • the lower limbs: peripheral vascular disease. Cardiac disease is a common complication of diabetes and carries a higher mortality rate than for people without diabetes. The World Health Organization WHO 2003 estimated 16.7 million people die from cardiovascular disease each year. Cardiac disease accounts for 50 of deaths in Type 2 diabetes Standl Schnell 2000 Huang et al. 2001 and half of these people die before they reach hospital. The mortality rate has not been reduced despite new therapeutic measures and preventative health programmes. Myocardial infarction may be a diabetes risk equivalent in non-diabetics. Diabetes often occurs within 3.5 years of an infarct particularly in older people those with a high BMI hypertension and smokers. The risk is lower in people consuming a Mediterranean diet and those on lipid-lowering medicines Mozaffarian 2007. There is an association among increasing age duration of diabetes the presence of other complications and mortality. Cardiac disease is associated with diffuse atherosclerosis coexisting cardiomyopathy autonomic neuropathy hyperglycaemia and hyperlipidaemia the metabolic consequences being hypercoagulability elevated catecholamines and insulin resistance. Atherosclerosis is more frequent and more severe in people with diabetes. It occurs at a younger age than in people without diabetes and is more prevalent in women especially after menopause.

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Long-Term Complications of Diabetes 201 Female sex hormones especially oestrogen has many haemodynamic vascular and metabolic effects which are associated with cardiovascular protection in women Dantas et al. 2012. The protective effects of oestrogen include: • Influencing the metabolism of lipoproteins. • Controlling blood pressure. • Reducing formation of atheromatous plaques. • Increasing NO bioavailability. • Regulating the production of endothelium-derived relaxing factors and endotheliumderived hyperpolarizing factors which affect vascular relaxation and resistance. Oestrogen also has an effect on vascular constrictor factors. • Suppressing vascular inflammation by down regulating proinflammatory molecules including cytokines and adhesion molecules. • Regulating energy balance fat distribution and insulin sensitivity which is largely lost after the menopause. Oestrogen replacement therapy in postmenopausal women has beneficial effects on diabetes and cardiovascular risk Margolis et al. 2004 but the benefits must be weighed against the risks for each individual woman. A number of clinical trials and guidelines emphasise the importance of reducing lipids blood pressure and blood glucose to reduce the risk of cardiovascular disease Hansson et al. 1998 UKPDS 1998 NICE 2009 SIGN 2010 ADA 2013. Hypertension leads to thicker less elastic blood vessel walls and increases the strain on the heart. There is a linear relationship between the diastolic blood pressure and the eventual outcome of Type 2 diabetes. Reducing the blood pressure below 90 mmHg significantly improves the outcome UKPDS 1998. Subtle changes occur in the heart as a result of ischaemia-induced remodelling and the effects of hyperglycaemia on the endothelium of large blood vessels that predispose the individual to heart failure Standl Schnell 2000. Heart muscle metabolism is critically dependent on glucose during ischaemia and heart muscle performance is improved in the presence of insulin which stimulates glucose uptake which support the use of IV insulin in acute myocardial infarction Malmberg et al. 1995. However impaired heart performance is multifactorial and blood pressure lipids and prothrombin imbalance all play a part. Table 8.1 outlines some of the diabetes-specific abnormalities linked to the development of cardiovascular disease. Myocardial infarction is ‘silent’ in 32 of people with diabetes which leads to delay in seeking medical attention and may be a factor in the increased mortality rate. ‘Silent’ infarct means that the classic pain across the chest down the arm and into the jaw is absent. Only mild discomfort often mistaken for heartburn may be present. The atypical nature of the chest pain may make it difficult for people to accept that they have had a heart attack. Risk factor modification may not be seen as essential. The person may present with hypertension heart failure cardiogenic shock or in older people with diabetes ketoacidosis or hyperosmolar states. Diabetes may be diagnosed at the time an infarct occurs or during cardiac surgery. Emotional stress and the associated catecholamine response leads to increased blood glucose levels in 5 of patients admitted to coronary care units CCU. The blood glucose may normalise during convalescence however counselling about diabetes and its management is important especially if other diabetes risk factors are present. Tact and sympathy are necessary when informing the patient about the diagnosis of diabetes in these situations. Women with cardiovascular disease have poorer outcomes than men regardless of other comorbidities and management Davidson et al. 2011. As discussed earlier low female sex hormone levels after menopause especially oestrogen may play a role in cardiovascular disease in women. Atrial fibrillation in women confers a greater risk of stroke than in men and anticoagulation therapy is associated with a higher risk of bleeding problems Davidson et al. 2011 Medicines and cardiovascular disease Many types of medicines may be needed to prevent and/or manage cardiovascular disease Chapter 5. The choice of medicines depends on the clinical indications patient factors such as cardiovascular risk contraindications/precautions risk of medicine interactions availability and cost. Generally management targets address hypertension hyperglycaemia coagulopathies and hyperlipidaemia. Most modern guidelines recommend individualising targets and commonly recommend: • Blood pressure 130/80 mm Hg including in people with albuminuria.

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202 Care of People with Diabetes • LDL cholesterol 2 mmol/L. Table 8.1 Some diabetes-specific cardiovascular abnormalities that predispose an individual to heart disease. Abnormality Relevance to cardiovascular disease Insulin resistance Increases cardiovascular mortality Chronic hyperglycaemia Every 1 11 mmol/mol increase in HbA1c is associated with a 15 in crease in hazard of all-cause mortality 25 for cardiovascular mortality and 17 fatal coronary heart disease Zhang et al. 2012 In the UKPDS each 1 11 mmol/mol reduction in HbA 1c was associated with a 21 lower risk of diabetes-related death and 14 lower risk of MI over 10 years Contributes to microvascular disease Microvascular disease with microalbuminuria May be detected earlier than macrovascular disease and often occurs concomitantly with macrovascular disease Affects nutrient and oxygen exchange Nephropathy frequently in association with retinopathy Nephropathy doubles the risk cardiac disease in people with Type 1 diabetes Lehto et al. 1999 but it is not clear whether reducing microalbuminuria reduces cardiovascular risk Autonomic neuropathy Postural hypotension Abnormal cardiovascular reflexes Loss of sinus rhythm Resting sinus tachycardia Painless myocardial ischaemia and infarction ‘silent MI’ Delayed recognition and treatment Increased anaesthetic risk Increased risk in critical care situations Sudden death Endothelial damage in basement membrane or outer lining of large blood vessels Weak vessel walls stiffened vessels contributing to hypertension Impaired blood flow Reduced tissue oxygenation and nourishment Hypertension Thickening of blood vessel walls Increased strain on the heart Risk of cardiovascular disease increases progressively with increasing systolic blood pressure Each 10 mm Hg reduction in systolic blood pressure is associated with 15 reduction in risk of cardiovascular death over 10 years Hyperlipidaemia Obesity predisposes the individual to insulin resistance dyslipidaemia and high circulating free fatty acids FFA but does not appear to be an independent risk factor for cardiovascular disease Ethnicity needs to be considered when determining obesity Increased LDL cholesterol or total cholesterol is an independent risk factor for cardiovascular death Type 2 diabetes is associated with high triglycerides low HDL and small dense LDL A 1 mmol/L reduction in LDL represents a 21 reduction in risk Hypertriglyceridaemia is an independent marker of increased cardiovascular risk in Type 2 diabetes Increased lipolysis as FFA are liberated from adipose tissue Increased mediators of vascular function such as angiotensinogen adiponectin IL-6 prostaglandins and TNF∂ Adiponectin and adipocyte-derived protein Associated with metabolic derangements including type 2 diabetes via their role in glucose regulation and catabolism of fatty acids Adiponectin levels correlate with the development of insulin resistance progression of Type 2 diabetes and hypertension. High adiponectin is related to higher all-cause mortality after controlling for other confounders Singer et al. 2012 • HbA1c:  Diabetes short duration and no cardiovascular risk 6 42 mmol/mol

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Long-Term Complications of Diabetes 203  Lifestyle management with or without Metformin 6.5 48 mmol/mol  Requiring any glucose lowering medicine besides Metformin or insulin 7 53 mmol/mol  Requiring insulin 7 53 mmol/mol  Diabetes of long duration and/or presence of cardiovascular disease because these people do not benefit from tight blood glucose control 7 53 mol Mol Accord Study Group 2011  If the person has severe hypoglycaemia or hypoglycaemic unawareness and older people 8 64 mmol/mol National Prescribing Service NPS 2012. The Accord Study Group 2011 found that tight blood glucose control 6 42 mmol/mol resulted in 10 extra deaths per 1000 people over 3.5 years. Likewise severe hypoglycaemia is associated with increased morbidity and mortality Chapter 6. It is also associated with long duration of diabetes and microalbuminuria Yun et al. 2012. These significant adverse events highlight the importance of determining individual risk for cardiovascular disease and the risks associated with treatment. Estimating cardiovascular risk in people with diabetes is complicated: currently available risk calculators such as the Framingham and UKPDS risk calculator are inaccurate in people with diabetes Coleman et al. 2007 and people should be informed that the risk calculation is only an estimate of their actual risk NICE 2009. However the likelihood of error is reduced if the person has several cardiovascular risk factors NICE 2009. Risk calculators can underestimate risk in South Asian Maori Pacific Islanders and Middle Eastern peoples NPS 2012. In addition to medicines stopping smoking a healthy diet and regular exercise and effective self-care are essential to achieving optimal control. Sedentary time is associated with increased risk of Type 2 diabetes 112 increased relative risk RR cardiovascular disease 90 RR and all cause mortality 40 RR NPS 2012 Wilmot et al. 2012. Sedentary time includes occupational sitting and watching TV. Medicines may be required to manage cardiovascular risk or treat cardiovascular disease. Medicine commonly used to manage cardiovascular disease include: • Antithrombotic medicines to prevent thromboembolism generally and during coronary procedures and surgery prevent stroke in patients with atrial fibrillation prevent thromboembolism in patients with prosthetic heart valves and treat acute MI. Types of medicines include Vitamin K antagonists warfarin heparin enoxaparin platelet aggregation inhibitors aspirin and thrombolytic enzymes alteplase. These medicines require frequent monitoring and interact with many other medicines including complementary medicines CAM. The benefits of low dose aspirin 75–150 mg/day outweigh the risks in adults with diabetes and existing cardiovascular disease. However evidence for the benefits for people without existing cardiovascular disease including people with diabetes is weak NPS 2012. Thus aspirin is not recommended for primary prevention SIGN 2010. The risk of major bleeds and macular degeneration are significant. Consequently the NPS the National Vascular Disease Prevention Alliance Guidelines and SIGN 2010 do not recommend routine use of low dose aspirin in people without existing cardiovascular disease. NICE 2009 recommends offering 75 mg aspirin/day to anybody with blood pressure 145/90 mmHg and the American Diabetes Association ADA 2012 recommends people with 10-year cardiovascular disease risk 10 should take 75 mg aspirin/day. ADA does not advocate using aspirin for people whose cardiovascular risk is 5 and that clinical judgement should be used for people whose 10 year risk is 5–10. • Cardiac medicines to treat arrhythmias cardiac glycosides such as digoxin heart failure antiarrythmics such as amiodarone relieve cardiac symptoms such as angina vasodilators such as isorbide treat high and low blood pressure cardiogenic shock and MI cardiac stimulants such as adrenaline. • Antihypertensive agents often used as primary prevention to reduce the risk of microvascular disease. These include low dose diuretics as first-line treatment frusemide peripheral vasodilators oxpentifylline calcium channel blockers amlodipine. Antihypertensive therapy is usually selected according to the comorbidities present to achieve blood pressure 130/80 in people with cardiovascular disease. The first-line medicine for people with diabetes and hypertension is an ACEI or an ARB the most appropriate choice in an older person following a MI is a calcium channel blocker to reduce the risk of stroke however most people require several antihypertensive medicines European Society of Hypertension 2007. • Beta blocking agents Atenolol Metorpolol Propanolol which can be used with a diuretic and an ACE inhibitor. Beta blockers confer benefit in the medium- to long-term but can cause decompensation and worsen heart failure and hypotension in the short term. They should be started at a low dose and gradually increased. Contraindications include asthma heart block and symptomatic hypotension.

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204 Care of People with Diabetes • Medicines acting on the renin–angiotensin system such as ACEI which are first-line treatment in heart failure left ventricular dysfunction following MI and diabetes in the presence of microalbuminuria Ramipril angiotensin 11 antagonists Irbesartin which are used if the person cannot tolerate ACE. For example ACE inhibitors are associated with a three times higher rate of cough. SIGN 2010 recommends ACEI be considered in people with all New York Heart Association NYHA functional classes of heart failure due to left ventricular systolic dysfunction. • Lipid-lowering agents such as HMG-CoA reductase inhibitors statins e.g. Atorvastatin which reduces LDL cholesterol fibrates which are first choice if triglycerides are elevated nicotinic acid which lowers both cholesterol and triglycerides but is not tolerated very well Australian Medicines Handbook 2006. However there is not enough evidence to recommend fibrates Ezetimibe or nicotinic acid for primary prevention SIGN 2010. • Glucose-lowering medicines are discussed in Chapter 5. However these medicines are not always prescribed optimally. For example antithrombotic medicines ACE inhibitors ACE and beta blocker combinations and antihypertensive agents are under-utilised National Institute of Clinical Studies 2005. Patient non-adherence with many medicines is high and is a significant limiting factor in achieving optimal outcomes. Complementary medicines CAM Recently WS 1442 a formula of Crateaegus monogyna hawthorn was shown to increase intracellular calcium concentration contractile force action potential and the refractory period improve coronary blood flow and reduce preload and after load Pittler et al. 2008. Animal studies have also demonstrated a smaller area of infarction after induced MI using Crateaegus monogyna. These findings suggest WS 1442 might have a place in managing cardiovascular disease but that place is not yet defined. Coenzyme Q10 CQ-10 lowers systolic and diastolic blood pressure and reduces inflammation. Individuals with mild-to-moderate hypertension and cardiac disease might benefit from CQ-10 supplements Rosenfeldt et al. 2007 but like W1442 its place is under-researched. CQ-10 is an antioxidant and is present in LDL-c where it reduces the potential for LDL-c to be oxidised and become atherogenic. Some experts suggested CQ-10 might be a useful addition to statins to reduce myotoxicity. However while it may have a place at present there is no recommendation to use CQ-10 in people taking statins Barenholtz Kohlhaas 2006. If people do elect to use CQ-10 the effects on their conventional medicines need to be monitored. Other complementary therapies such as massage meditation and Tai Chi can help reduce stress improve quality of life and manage pain but should be used within a Quality Use of Medicine framework Chapter 19. Other management considerations Hyperglycaemia is common in MI and there is an association between initial blood glucose level and outcomes including mortality even if the blood glucose is only mildly elevated ADS 2012. However hyperglycaemia is also associated with adverse outcomes Chapter 6. Various guidelines suggest different blood glucose targets in acute MI generally the aims should be blood glucose 10 mmol/L and IV infusions are recommended when resources permit ADS 2012. The International Diabetes federation IDF 2011 suggested a two-hour postprandial blood glucose 7.8 mmol/L is a stronger predictor of cardiovascular events than fasting blood glucose and recommended monitoring postprandial blood glucose and to aim for 7.5 mmol/L. Patients with an acute cardiovascular event are usually cared for in CCUs but patients in other wards and in the community may develop cardiovascular problems including silent MI. A longer stay in CCU may be indicated for people with diabetes because 35 of patients die often in the second week after the infarct Karlson et al. 1993. People with diabetes and unstable angina MI without ST elevation or STEMI have a higher mortality risk within one year of the onset of acute coronary syndrome than non-diabetics Donahoe et al. 2007.

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Long-Term Complications of Diabetes 205 Silent MI may be relatively common in common critical care settings the diagnosis can be difficult to establish and the MI is often missed due to analgesia controlling chest pain intubation sedation and coma Lim et al. 2008. Lim et al. 2008 suggested screening for elevated troponin levels in critically ill patients and performing an ECG could reduce mortality and that elevated troponins might be predicative of mortality. Although more research is needed these findings might be particularly relevant to people with diabetes where the risk of cardiovascular disease is likely to be high. Short- and long-term morbidity and mortality can be improved by IV insulin/ glucose infusion followed by multidose subcutaneous insulin injections Malmberg et al. 1995. Acute myocardial infarction causes a rapid increase in catecholamines cortisol and glucagon. Insulin levels fall in the ischaemic myocardium and tissue sensitivity to insulin falls and impairs glucose utilisation by cardiac muscle. Free fatty acids are mobilised as fuel substrates and potentiate ischaemic injury by direct toxicity or by increasing the demand for oxygen and inhibiting glucose oxidation. IV insulin during acute episodes and subcutaneous insulin for three months after the infarct may restore platelet function correct lipoprotein imbalance reduce plasminogen activator inhibitor-1 activity and improve metabolism in non-infarcted areas of the heart. The need for invasive procedures depends on the severity at presentation and the results of relevant investigations. Pfisterer 2004 showed that invasive treatment provided short-term symptomatic relief reduced the rate of revascularisation and hospitalisation and less frequent use of antianginal medicines compared to medicine treatment. In the longer term both strategies were effective in older patients with angina. Mortality risk factors included age 80 years prior heart failure left ventricular ejection 45 and the presence of two or more comorbidities. Mental health and cardiovascular disease Anxiety is common among people with cardiac disease and can have serious consequences for self-care and long- term outcomes if it is not recognised and managed to prevent depression. However anxiety can be life-saving if it prompts the person to seek help early Moser 2007. Significantly depression is an independent risk factor for cardiovascular disease and its prognosis. Both depression and heart disease are associated with social isolation and lack of social support Bunker et al. 2003. These factors need to be considered when estimating cardiovascular risk. Several trials have investigated the cardiovascular benefit of treating depression. These include ENRICH cognitive behaviour therapy and SSRI medicines which is difficult to interpret but which showed no significant difference between treatment and usual care. SADHART SSRI showed improvements in mild-to-moderate depression but no significant differences in cardiac events. The results of CREATE SSRI Citalopram and interpersonal psychotherapy are not yet available but suggest depression improves but HbA1c does not significantly improve Reddy 2008. The effects on mental health may change for example Gudjhar Dunning 2003 found that people with diabetes were most concerned about the implications of the MI immediately after the event and less concerned about the impact of diabetes on their long-term physical health mental health and quality of life. Patient generated qualityof- life tools were used. As people recovered and realised they would survive about four months after the MI concern about the MI began to diminish and pre-MI worry about diabetes and its complications re-emerged. Depression may increase cardiovascular risk and vice versa via several mechanisms: • Risk behaviours such as inadequate diet and inactivity smoking and non-compliance with medicines. • Effects on autonomic function by enhancing sympathetic nervous system activity and heart rate variability. • Consequence model: inflammatory processes with sub-chronic elevation of cytokines activate the stress response and inhibit serotonin. MI might also induce physical changes in the brain that are mediated by the inflammatory response and cause depression. • Coincidence model: autonomic dysregulation decreased heart rate variability and increased risk of ventricular arrhythmias changes in platelets inflammation and changes in endothelial function some of which might be linked to dietary factors. For example increasing omega-3 fatty acids improves cardiac function Lesperance Frasure-Smith 2007. Objectives of care in hospital

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206 Care of People with Diabetes Nursing care should be planned to avoid constantly disturbing the patient and allow adequate rest and sleep. The objectives of care are to: • treat the acute attack according to medical orders guidelines and standard protocols • stabilise cardiac status and relieve symptoms • prevent extension of the cardiac abnormality and limit further episodes • retain independence as far as possible • achieve and maintain euglycaemia but prevent hypoglycaemic events thus blood glucose monitoring is important • provide psychological support • prevent complications while in hospital • counsel about risk factor modification • educate/re-educate about diabetes. Nursing responsibilities 1 To be aware that myocardial infarction can present atypically in people with diabetes and may present as CCF syncope vomiting abdominal pain and fatigue that improves with rest. An ECG should be performed urgently if any of these symptoms are present. A high resting heart rate is associated with mortality in people with diabetes. Sanchis 2007 developed a risk assessment process for patients without an increase in troponins or ST deviation that was able to identify patients with a similar prognosis to patients with elevated troponins and ST depression that might be useful in people with diabetes. 2 To provide psychological educational and physical care. 3 To monitor blood glucose 2–4 hourly depending on stability and route of insulin administration. 4 To provide adequate pain relief and to control vomiting which contribute to/exacerbate high blood glucose levels. 5 To deliver care according to the medical orders for the specific cardiac abnormality. 6 To administer insulin: • Many patients on GLMs are changed to insulin during the acute phase to improve blood glucose control. • Insulin is usually administered via an infusion at least for the first 48 hours. Only clear insulin is used. Insulin infusions are discussed in Chapter 7. The patient should be eating and drinking normally before the infusion is removed and a dose of subcutaneous insulin given to prevent hyperglycaemia developing. Some endocrinologist/cardiologist teams have adopted Malmberg et al.’s recommendations the so-called DIGAMI protocol or some variation of it which usually involves commencing an IV insulin infusion for people with diabetes presenting with MI from the time of presentation in the emergency room. IV insulin is usually continued for 24 hours after which time subcutaneous insulin is commenced and maintained for three months. The aim of the IV insulin is to normalise glucose utilisation in the myocardium achieve normoglycaemia and reduce morbidity and mortality. 7 Other medications: GLMs should be stopped while the patient is having IV insulin to reduce the risk of hypoglycaemia. Thiazide diuretics can: • Increase blood glucose levels. • Cause hypokalaemia. • Beta blockers reduce mortality by 30. Ace inhibitors improve blood pressure and cardiac remodelling and stabilise the rate of progression of renal disease. There is a close association between cardiac and renal disease in diabetes. Non-cardiac-specific beta-blocking agents may mask the signs of hypoglycaemia. Patients who are normally on oral GLMs will require support and education about the use of insulin. It should be explained that insulin is being given to increase the glucose available to the myocardium and decrease free fatty acids in the blood. Units where IV insulin infusions are used often discharge the patient on subcutaneous insulin which is continued for three months then reassessed the individual’s medicine needs are reassessed. 8 Physical status: • Monitor fluid balance and maintain accurate documentation to help assess kidney function.

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Long-Term Complications of Diabetes 207 • Monitor blood pressure lying and standing. Some antihypertensive medications can cause orthostatic hypotension. Counsel the patient to change position gradually especially on getting out of bed or out of a chair. Postural hypotension is a risk factor for falls especially in older people. • Monitor ECG. • Observe for weakness fatigue CCF or unexplained hyperglycaemia which could indicate another infarct or extension of the original infarct. • Provide appropriate skin care to prevent dryness and pressure areas. 9 Investigative procedures: • Monitor serum electrolytes cardiac enzymes blood gases and potassium levels. Report abnormalities to the doctor promptly. Fluctuating potassium levels can cause or exacerbate cardiac arrhythmias. • Prevent hypoglycaemia by carefully monitoring the blood glucose and carbohydrate intake. • Prepare the individual for investigative procedures appropriately and inform them what to expect Chapter 9. 10 Thrombolytics are beneficial to reduce plaque. Low-dose aspirin reduces emboli and reduces the risk of cardiac disease and stroke in people with existing cardiovascular disease see the previous section. 11 If relevant consider end-of-life care Chapter 18 and support the family to cope with the crisis. In many cases metabolic control prior to the MI was suboptimal and insulin therapy indicated for some time before the infarct occurred. Some OHAs are contraindicated if cardiac renal and/or liver disease is present see Chapter 5. Practice points 1 The person may not recognise the signs of hypoglycaemia if: • Autonomic neuropathy is present. • Non-selective beta-blocking agents are used. 2 Neuroglycopenic signs of hypoglycaemia confusion slurred speech or behaviour change may predominate. Alternatively these signs may indicate a cardiovascular event. Medical tests/procedures see Chapter 9 1 The eyes should be assessed before thrombolytic medications are commenced. If proliferative retinopathy is present bleeding into the back of the eye may occur requiring urgent treatment. 2 Diagnostic procedures that require the use of contrast dyes for example angiograms have been associated with renal complications. Ensure adequate hydration before and after procedures and monitor urine output especially in older people and people with renal disease. 3 There is a high prevalence of cardiovascular disease in people with renal disease Levin 2000. Rehabilitation Structured rehabilitation after an acute cardiovascular event and heart failure improves long-term outcomes reduces social isolation and improves function and quality of life. 1 Encourage activity within tolerance limits. Refer for physiotherapy/occupational therapy. 2 Encourage independence. 3 Counsel about resumption of normal activity including sexual intercourse after discharge home. 4 Explain restrictions on driving after cardiac surgery. 5 Ensure diabetes education/re-education is available. Refer to diabetes nurse specialist/ diabetes educator dietitian and physiotherapist. Education should include the need to protect kidney function and also address the risk factors involved in the development of cardiac disease. Particular areas of concern are: • recognise hypoglycaemia

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208 Care of People with Diabetes • correct insulin technique • correct blood glucose monitoring technique • possible indicators of further cardiac problems • dietary assessment and advice • risk factor modification 6 explain the need for multi-medicine therapy and the importance of adhering to the medicine regimen 7 monitor to detect anxiety and depression and treat early. Modifying risk factors associated with the development of cardiac disease Current cardiovascular management guidelines focus on reducing global cardiovascular risk which requires a proactive approach and attention to multiple risk factors taking age into account: cardiovascular risk which can be stratified and individualised to enable personalised teaching using tools such as the QRISK and ASSIGN in the UK and the Framingham algorithm which is sex-specific and is based on the presence of hypertension dyslipidaemia and smoking. The Systematic Coronary Risk Evaluation SCORE based on cholesterol blood pressure and age was developed for European countries Zannad 2008. Note the discussion about the limitations of risk scores in a previous section of this chapter. Significantly research suggests that doctors do not adequately assess cardiovascular risk and this contributes to patients not achieving management targets Bohm 2008 Mulnier 2012. Other researchers found general practitioners overestimate the risk of diabetes complications but the impact on patient care and service utilisation or outcomes was not reported Haussler et al. 2007. People with diabetes require both information and support to manage diabetes and reduce the risk of adverse health outcomes. Personalised information is more effective than generalised information. Management targets are described in this chapter and Chapter 2. As indicated in Chapter 16 helping people determine their cardiovascular age could be a useful way to help people understand their cardiovascular risk and help them adhere to their risk reduction strategies. Key messages are to: • Stop smoking. • Avoid high calorie foods and high fat intake especially trans fats to achieve sensible weight reduction. Include omega-3 fatty acids in the diet. Reduce salt intake. Suitable diets are described in Chapter 4 and include the DASH and Mediter ranean diets. • Limit alcohol intake. • Maintain a healthy weight range suitable to age and developmental stage. In particular reduce abdominal obesity. • Increase regular exercise/activities. • Achieve acceptable blood glucose levels. • Reduce blood lipids. If this is not achieved by diet and exercise lipid-lowering agents are needed see Chapter 5. High LDL-c low HDL-c and mixed hyperlipidaemia significantly increase the risk of developing cardiovascular disease Hansel 2004. • Reduce blood pressure by appropriate diet exercise and stopping smoking. Optimal blood pressure control is important and people are often prescribed three or more antihypertensive agents. The choice of medication is individualised and includes reducing blood glucose as part of a comprehensive cardiovascular risk management plan Lowe 2002. Hypertension is also a risk factor for poorer performance on verbal and concept formation tests in Type 2 diabetes Elias et al. 1997 which has implications for self-care and activities of daily living. • Manage hypertension and monitor the day-night dip. A blunted day-night dip is associated with a blunted morning BP surge and vice versa. A blunted morning BP surge could be an independent predictor of cardiovascular events Verdecchia et al. 2012. • Secondary prevention programmes such as cardiac rehabilitation are important to help individuals regain the best possible functioning. • Manage stress. Long-term stress is associated with increased risk of cardiovascular disease in both men and women and a high level of trait anger in middle aged men with hypertension is associated with increased risk of hypertension progression to a cardiovascular event Player et al. 2007.

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Long-Term Complications of Diabetes 209 • Seek treatment for depression. • People with known cardiac disease should have a written action to plan to follow if they experience chest pain. They should know early management is important and not to delay presenting to hospital. The plan might include using short-acting nitrate medicines resting taking aspirin if they are not already prescribed this medicine calling an ambulance notifying their doctor and wearing medic alert information. Telephone coaching Telephone coaching for people with coronary heart disease and suboptimal lipid levels improves adherence to medication therapy and dietary advice. It contributes to an improved lipid profile and could be an important aspect of cardiac rehabilitation programmes Vale et al. 2003. The COACH protocol is currently under investigation in a general practice setting with practice nurses providing coaching with support from the COACH investigators Young et al. 2007. Cerebrovascular disease The incidence of stroke associated with diabetes is high and mortality following a stroke is higher in people with diabetes than non-diabetics. The brain is supplied with blood by four main arteries: two carotids and two vertebral arteries. The clinical consequences of cerebrovascular disease depend on the vessels or combination of vessels involved. Transient ischaemic attacks TIAs arise when the blood supply to a part of the brain is temporarily interrupted without permanent damage. Recovery from a TIA usually occurs within 24 hours. If TIAs occur frequently they can indicate impending stroke. Small repeated strokes that cause progressive brain damage can lead to multi-infarct dementia which is common in diabetes. Signs of multi-infarct dementia include: • gradual memory loss • diminished intellectual capacity • loss of motor function • incontinence. Strokes are classified as thrombotic or haemorrhagic and occur when a major vessel is blocked. They frequently cause permanent damage requiring prolonged rehabilitation and often significantly reduced self-care potential and quality of life. In these cases diabetes management should be discussed with the family or carers who will be responsible for assisting the person with diabetes. The risk factors for cerebrovascular disease are similar to those for cardiovascular disease. High BMI 25 kg/m 2 and systolic hypertension increase risk of death after a stroke among men Chen 2008. However there appear to be some significant differences between men and women. Women may have worse outcomes after acute stroke than men if they do not receive thrombolytic therapy and women are more likely to benefit from thrombolytic therapy than men Lutsep 2008. Likewise healthy women over age 65 benefit from alternate day aspirin 100 mg to prevent stroke but aspirin has not been shown to prevent strokes in healthy men Ridker et al. 2005. However the NPS SIGN. NICE and ADA guidelines regarding aspirin use should be considered. There are also gender differences in response to treatment and outcome following acute stroke. Women with carotid artery stenosis have a lower risk of recurrent stroke than men and receive less benefit from surgical treatment of moderate carotid artery stenosis than men Alamowitch et al. 2005. Women with intracranial stenosis are at higher risk of recurrent stroke than men Williams et al. 2007. Poor sleep quality is linked to increased risk of vascular events including stroke and daytime sleepiness could be an independent risk factor for stroke conferring a 4.5-fold increased risk Boden-Albala 2008 Chapter 10. Signs and symptoms • A careful history will elicit failing mental function. • Carotid bruits are usually present and can be evaluated using Doppler studies. • Angiography is required in symptomatic cases. Management

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210 Care of People with Diabetes There is limited evidence concerning managing stroke in people with diabetes. The preventative measures outlined for cardiovascular disease apply to cerebrovascular disease. Acute stroke is managed the way as for people without diabetes but hyperglycaemia and hyoglycaemia should be avoided Blood glucose monitoring will aid decisions about titrating GLM medicine doses and the dose regimen. Carotid endarterectomy is indicated if the carotid arteries are significantly narrowed. Low-dose aspirin may be beneficial considering the risks and benefits. Management in a stroke unit improves outcomes and optimal collaboration among care providers in the emergency department and stroke unit is essential. Nursing responsibilities include care during investigative procedures see Chapter 9. Rehabilitation focuses on returning the person to optimal functioning and independence within their capabilities. Observational data suggests there is an association between blood glucose in the first 24- hours and mortality and infarct size. ADS 2012 recommends maintaining blood glucose 10 mmol/L and avoiding hypoglycaemia 5 mmol/L. Middleton et al. 2011 developed a treatment protocol Fever Hyperglycaemia Swallowing FeSS for managing stroke in the first 72 hours following an acute stroke. The protocol involves: • Monitoring and documenting fever every 4 hours and treating fever 37.5 with paracetamol IV rectally or orally unless contraindicated. • Monitoring venous blood glucose on admission and capillary glucose every 1–6 hours. • Commencing an IV saline infusion and deliver for 6 hours when blood glucose is between 8 and 11 mmol/L in people with diabetes or 8 and 16 mmol/L in people without diabetes. • Commencing an IV insulin infusion if the blood glucose is 11 mmol/L in people with diabetes and if the blood glucose is 16 mmol/L in non-diabetics. • Screening for dysphagia and clearly documenting the findings in the person’s medical record. Middleton et al. developed an education program to train nurses to undertake dysphagia screening. Speech therapists usually undertake such assessments. People who were managed using the FeSS protocl had better outcomes after discharge. Middleton et al. like other stroke researchers used a combination of strategies and it is difficult to separate the different contribution of the IV insulin infusion. The combination may be the important element. However ADS 2012 choose not to include the FeSS study in their review when developing guidelines for managing hyperglycaemia in hospital. Other important assessments after the acute phase include functional ability and mental health as well as social support and whether the home environment requires modification. Rehabilitation programmes can help people improve physical functioning and independence. Driving assessment needs to be undertaken following a stroke and assessed regularly see Chapter 10. DIABETES AND EYE DISEASE Key points • Encourage independence. People with visual loss are capable of caring for themselves if they are provided with appropriate sight aids and information. However vision impairment has a profound impact on an individual’s ability to learn diabetes self-care tasks and on their psychological well-being. • Becoming blind is a significant fear for people with diabetes. • Maintain a safe environment. • Orient patient to the environment and staff. • Explain procedures carefully fully recognising that the person is probably not a visual learner. • Return belongings to the same place. • Use appropriate teaching style to the individual’s learning style. Rationale

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Long-Term Complications of Diabetes 211 Retinopathy is a significant complication of diabetes. Prevention and early identification of people at risk are essential. Nurses need to be aware of the impact of visual loss on the self-care and psychological well-being of people with diabetes and their role in preventative care. Other vision changes occur in people with diabetes in addition to diabetic retinopathy for example macular degeneration is common in older people. Age-related macular degeneration might be related to elevated levels of high-sensitivity CRP. Cataracts and glaucoma are common in people with diabetes but also occur in non-diabetics. Introduction Vision impairment and blindness are significant complications of diabetes. Blindness occurs in 50–60 people/100 000 people with diabetes Cormack et al. 2001. Most people with diabetes do not have sight-threatening retinopathy but if they have macular oedema and/or proliferative retinopathy it must be treated to reduce the progression to vision impairment. Screening programmes have enabled early identification and treatment of early retinal changes and reduced the progression to sight-threatening retinopathy. The specific cellular mechanisms that lead to reduced visual acuity have not been defined. Antonetti et al. 2006 proposed a combined nerve and vascular mechanism that causes loss of neurons which compromises neurotransmission and altered structure and function of retinal cells types. Macular cysts could scatter light and reduce the quality of the image and/or visual function could decline as a result of fluid accumulation in the retina. The neurons are susceptible to circulating amino acids antibodies and/or inflammatory cells that reach the retina through leaking capillaries. The vascular leakage can affect vision even when macular oedema is not present Antonetti et al. 2006. Kim et al. 2012 found an association between 15-anhydroglucitol 15-AG a marker of postprandial hyperglycaemia and diabetic retinopathy especially in people with ‘moderate’ glucose control but not albuminuria. The authors suggested 15-AG could be used as a marker to target people at risk of retinopathy. There is also evidence that cognitive ability declines over time in people with diabetes and may be linked to complications such as proliferative retinopathy Ryan et al. 2003. Key changes in the eye include: • Maculopathy: macular oedema and macular ischaemia. The macular may be distorted or elevated or vitreous haemorrhages may occur and distort the ocular media Antonetti et al. 2006. • Retinopathy: stages of retinopathy have been described based on a system of photographic grading that requires comparison with a standard set of photographs showing different features and stages of retinopathy DRS 1981 EDTRS 1991. • Generalised ocular oedema. • Lens opacity: cataract. • Papillopathy: optic disc swelling that occurs in Type 1 diabetes. Some degree of retinopathy occurs in almost all people with Type 1 diabetes after 20 years duration of diabetes and 70 of people with Type 2 diabetes DRS 1981 DCCT 1993. Retinopathy occurs as a result of microvascular disease that manifests as increased capillary permeability and closure of the retinal capillaries which causes vascular leakage retinal oedema and accumulation of lipids that is seen as hard exudates in the retina and retinal ischaemia. Risk factors for retinopathy The factors that lead to an increased risk of retinopathy are similar to the risk factors for other complications and include: • long duration of diabetes • poor metabolic control • renal disease with microalbuminuria and proteinuria • hyperlipidaemia especially hypertriglyceridaemia which contribute to macular exudates and oedema • low haematocrit

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212 Care of People with Diabetes • pregnancy in people with diagnosed diabetes. Pregnancy may exacerbate existing retinopathy see Chapter 14 but it does not usually develop in women with gestational diabetes • smoking although the effect of smoking on the development and progression of retinopathy is unclear • hypertension. People with diabetic eye disease are at greater risk of developing other diabetes-related complications unless they are screened regularly take appropriate preventative action and treatment is commenced early. Vision impairment from non-diabetic causes can coexist with diabetes. People with diabetes also have an increased incidence of glaucoma and cataracts and there is an increasing correlation with age-related macular degeneration. Many of the underlying causes that lead to macular degeneration are also associated with diabetes see Table 8.2 which depicts risk factors for age-related macular degeneration Lim 2006. Many of these risk factors are similar to the risk factors for diabetic retinopathy and the same risk reduction strategies apply to both conditions. The table shows modifiable and nonmodifiable factors. Sun exposure and iris and hair colour do not appear to be associated with AMD Khan et al. 2006. Table 8.2 Risk factors for age-related macular degeneration Data from Lim 2006. Modifiable factors Non-modifiable factors Cigarette smoking the risk increases with long duration of smoking Increasing age: for both exudative and non-exudative AMD 1 Diet high in fats especially monounsaturated and polyunsaturated fats. Linoleic acid increases the risk for advanced AMD Omega-3 fatty acids are associated with lower risk High GI 2 food is related to the development of retinal pigmentation abnormalities Chui et al. 2006. Emerging research suggests a diet rich in fruit and vegetables especially carotenoids may help prevent AMD. Vitamins C and E and zinc van Leeuwen et al. 2005 Ethnicity. AMD is more prevalent in Whites. Especially for the components of late AMD increased retinal pigmentation and retinal pigment epithelial depigmentationCataracts and glaucoma are more common in Blacks High BMI 3 . The risk of developing AMD increases with increasing BMI and geographic atrophy could be associated with high BMI low education and antacid use Clemons et al. 2005 Hypertension is associated with exudative AMD but not non-exudative AMD Hypercholesteraemia is also associated with exudative AMD Inflammation. Recent studies suggest C-reactive protein is associated with intermediate and advanced AMD Seddon et al. 2004 Genetic inheritance AMD: age-related macular degeneration. GI: glycaemic index. BMI: body mass index. Poor vision can be a significant disadvantage during diabetes education and general living because most diabetic and general health information contains essential visual components . Practice points 1 The shape of the lens changes with changes in blood glucose concentrations leading to refractive changes and blurred vision. This usually corrects as the blood glucose is normalised but may take some time if the blood glucose has been high for a long time.

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Long-Term Complications of Diabetes 213 2 Vision can worsen in the short term when blood glucose control begins to improve for example when commencing insulin and during pregnancy. 3 The temporary vision disturbance creates significant stress for the person with diabetes and a careful explanation is needed. Eye problems associated with diabetes 1 One-third of people with diabetes have retinopathy as a result of microvascular disease. The incidence is related to the duration of diabetes. Sixty per cent of people with diabetes and duration of more than 15 years have some degree of retinopathy especially women. Up to 30 people with Type 2 diabetes have retinopathy at diagnosis 4–8 is sight-threatening. There is increasing evidence that ACE inhibitors can reduce the risk of microvascular disease see Chapter 5. 2 People can have severe eye damage without being aware of it. Vision is not always affected and there is usually no pain or discomfort. 3 Cataracts are more common in people with diabetes. 4 Maculopathy is the most common cause of visual loss in people with diabetes. 5 Sudden loss of vision is normally an emergency. It may be due to: • vitreous haemorrhage • retinal detachment • retinal artery occlusion. Reassurance avoidance of stress and sudden movement and urgent ophthalmological assessment are required. 6 Prevention and early detection are important aspects in the management of visual impairment. It involves: • Good blood glucose control can slow the rate of progression in Type 1 diabetes DCCT 1993. • Regular eye examinations commencing at diagnosis in Type 2 and from age 12 in Type 1. Screening should be undertaken annually if retinopathy is present of every two years it there is no retinopathy SIGN 2010. • Using an ophthalmoscope opportunistically during regular appointments. • 7-field stereoscopic photography with the pupils dilated to investigate macula oedema and proliferative retiopathy • Retinal photography or slit lamp biomicroscopy • Confocal microscopy is increasingly being applied to diabetes complication screening especially to detect eye changes and neuropathy. Confocal microscopy enables greater contrast to be achieved and three- dimensional images to be created that show great detail. The technique uses a spatial pinhole to eliminate out of focus light and flare. It enables faster diagnosis is non-invasive and painless. • Fluorescein angiography is still sometimes used. 7 Laser treatment is very effective in preventing further visual loss. Vitrectomy if there is evidence of persistent vitreous haemorrhage. Cataract extraction should not be delayed when indicated. Advanced cataracts need to be removed or stabilised prior to surgery and reviewed closely in the postoperative period SIGN 2010. 8 Medicines include intravitreal Triamcinolone which reduces retinal thickness in the short term and improves visual acuity but may not have long-term benefits. Small studies suggest Simvaststin reduces oedema and improves visual acuity Sen et al. 2002 and Atorvastation reduced the severity of hard exudates after laser treatment in people with Type 2 diabetes and high lipids Gupta et al.2004. Although there is some befefits using antivascular endothelia growth factor VEGF in combination with laser therapy there is insufficient evidence recommend using VEGF routinely SIGN 2010. Clinical observation Eye drops occasionally cause pain and increased pressure in the eye some hours after they were instilled. If this occurs the patient should be advised to call the doctor. Resources for people with visual impairment

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214 Care of People with Diabetes People with significant visual loss often require assistance to perform blood glucose monitoring and to administer their own insulin. It is important to encourage independence as far as possible. Careful assessment is important and should include assessment of the home situation. Vision Australia and the Royal National Institute for the Blind in the UK and similar organisations in other countries offer a variety of services for people who have degrees of visual loss. These services include: • assessing the home situation to determine whether modifications are necessary to ensure safety at home • low vision clinics • talking library and books in Braille • training on how to cope in the community with deteriorating vision. • Guide dogs. It takes time to train a dog to guide a blind person and time for a person to learn to work with a guide dog usually through a harness and for the person to recognise tactile and sound clues to complement their knowledge of the environment. Several factors can affect the individual’s ability to work with a guide dog including loss of sensitivity in hands or feet hypoglycaemia which affects concentration and sometimes behaviour Stanway 2012. Interestingly dogs can perform more than one kind of medical assistance and actually enjoy the extra work medical detection dogs. For example they can be trained to become familiar with chemical markers associated with diabetes and can detect hypoglycaemia and fetch the person’s hypo kit or alert another person. A recent report in the author’s local newspaper described a how a blue heeler dog which was deaf was learning to recognise sign language. Other help includes: • Services such as pensions which may be available from the government. • A range of diabetes products are available that can help vision impaired people remain independent see next section. The community nurses and home-based services play a major role in maintaining vision-impaired people in their own homes especially when they are older. Aids for people with low vision Various magnifying devices are available to help people continue to care for themselves. They can be obtained from diabetes associations and some pharmacies specialising in diabetes products. Other aids include: 1 Insulin administration: • Instaject devices clicking insulin pens • chest magnifying glass available from some opticians Magniguide – fits both 50 and 100 unit syringes and enlarges the markings • location tray for drawing up insulin if syringes are used. 2 Blood glucose monitoring: • strip guides for accurate placement of the blood on to the strips • talking blood glucose meters blood pressure monitors and talking weight scales • meters with large result display areas. 3 Medications: • dosette boxes which can be prefilled with the correct medication Nursing care of visually impaired patients Aims of care • To encourage independence as far as possible. • To ensure the environment is safe when the patient is mobile. People confined to bed 1 Introduce yourself and address the patient by name so the patient is aware that you are talking to them.

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Long-Term Complications of Diabetes 215 2 Ascertain how much the patient is able to see. Few people are totally blind. Assess whether the blood glucose fluctuates at certain times. High and low levels can interfere with clear vision. Plan education to avoid these times and determine measures that can avoid such fluctuations for example appropriate timing of meals and medications. Dexterity and cognitive function may also be impaired especially in the elderly and hamper diabetes education. Visual impairment increases the risk of falls in elderly patients see Chapter 12. 3 Some people prefer a corner bed because it makes location easier avoids confusion with equipment belonging to other patients and enables greater ease in setting up personal belongings. 4 Introduce the patient to other people in their ward or close by. 5 If you move the patient’s belongings they must be returned to the same place. 6 Explain all procedures carefully and fully before commencing. An injection when you can’t see it and don’t expect it can be very unnerving. 7 If eye bandages are required make sure the ears and other sensory organs are not covered as well. 8 Consider extra adjustable lighting for those patients with useful residual vision. 9 Mark the person’s medication with large print labels or use a dosette. 10 A radio talking clock talking watch Braille watch or a large figured watch helps the patient keep orientated to time and place. 11 Indicate when you are leaving the room and concluding a conversation. People who are mobile 1 A central point like the person’s bed helps them orient around the room. 2 When orientating a person to a new area walk with them until they become familiar with the route. 3 Keep obstacles trolleys etc. clear of pathways where possible. Meal times 1 Describe the menu and let the person make a choice. 2 Ensure the person knows their meal has been delivered. 3 Ask ‘Do you need assistance with your meal’ rather than say ‘I will cut your meat for you.’ 4 Colour contrast is important for some patients. A white plate on a red tray-cloth may assist with location of place setting. When the person has a guide dog provide water in hot weather bur remember the dog is doing a job. Ask the owner’s permission before patting the dog or offering treats which can distract the dog and confuse it. DIABETES AND RENAL DISEASE Key points • Diabetes is the most common cause of renal disease. • Measuring microalbuminuria is a useful method of detecting abnormal renal function. Microalbuminuria indicates early renal disease and predicts cardiovascular disease in people with diabetes. • Microalbuminuria predicts severe hypoglycaemia in people with Type 2 diabetes. • Hypertension is an early indicator of renal disease. • There is a strong association between retinopathy and renal disease. Women with diabetes have greater prevalence of advanced kidney disease than men with diabetes especially among older people. • People with diabetes and nephropathy are at increased risk of cardiovascular disease. Introduction Diabetic nephropathy is a significant microvascular complication of diabetes and diabetes is the second most common cause of end-stage renal disease in Australia and the UK ANZDATA 2000 Department of Health 2001. There is a similar initial disease progression in both Type 1 and Type 2 diabetes. Eventually microalbuminuria

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216 Care of People with Diabetes occurs in up to 20 of people with Type 1 diabetes and in a similar percentage of people with Type 2. Some cultural groups are at significant risk for example Aboriginal and Torres Strait Islander Peoples and Afro-Caribbeans. Stages of chronic kidney disease Kidney disease is progressive unless it can be prevented and is usually classified according to the following stages: GFR ml/min/1.73 m 2 1 Kidney damage with normal glomerular filtration rate GFR 90 2 Kidney damage with mild reduction in GFR 3 Moderately reduced GFR: 60 – 89 a. 3A 45 – 59 b. 3B 30-44 4 Severe reduced GFR 15 – 29 5 End stage renal failure 15 Proteinuria must be present to diagnose stages 1 and 2. People on dialysis are classified as stage 5D and people with a functioning renal transplant are denoted by the suffix ‘T.” Proteinuria is an important marker for cardiovascular disease in Type 2 diabetes. Prediction equations that improve the inverse correlation between serum creatinine and GFR have been developed and take account of variables that affect the relationship for example: • Cockcroft-Gault equation which estimates creatinine clearance which encompasses age gender weight and creatinine. • Four variable formula used in the Modification of Diet in Renal Disease MDRD study which encompasses age gender and ethnicity. Risk factors for renal disease There is a strong link between hypertension and the progression of renal disease. The risk of end-stage renal failure increases as the diastolic blood pressure increases to 90–120 mmHg . Other risk factors include: • Smoking which represents a significant and dose-dependent risk. • Hyperglycaemia predialysis control is an independent predictor of the outcome in people with Type 2 diabetes on haemodialysis Wu et al. 1997. The Diabetes Control and Complications Trial DCCT demonstrated that good control of blood glucose delayed the rate and progression of microvascular disease including renal disease DCCT 1993. • The presence of microalbuminuria and proteinuria are independent risk factors for the development and progression of renal disease in people with diabetes Keane 2001. People with diabetes are at risk of renal disease if they have any of the following. The more of these factors present the greater the risk:  A urine albumin excretion rate in the upper range of normal 20–30 mg/day.  Systolic blood pressure 130 mmHg.  HbA1c 9. Preventing and managing hyperglycaemia reduces the development of renal disease.  Total cholesterol 5.2 mmol/L Sheldon et al. 2002. Duration of diabetes exceeding 5 years Kerr 2008. Treatment includes minimising proteinuria using ACEIs and ARBs often in combination. Hyperkalaemia is a risk when ACEI and ARBs are combined but may not be significant.  Tests for microalbuminuria include timed urine collections 12- or 24-hour collections usually on an outpatient basis but compliance is poor. The spot albumin– creatinine urine test which corrects the albumin level for the urine concentration is the optimal screening test for early renal disease. A level 3.5 mg/mmol most likely indicates early renal disease Kerr 2008. However alternative causes of proteinuria such as nephrosclerosis and hypertensive renal disease should be considered: The estimated GFR eGFR which approximates the GFR rate and is based primarily on serum creatinine as well as age and gender gives a reasonable approximation of

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Long-Term Complications of Diabetes 217 the GFR Kerr 2008. However renal function declines with age by approximately one mL/min/year after age 25. Thus approximately 60 of people over age 65 will have an eGR in the normal range 60–90 mL/min.  Hypertension which is a risk factor for cardiovascular disease and kidney disease and the risk is continuous and independent of other cardiovascular risk factors Committee on the Prevention Detection Evaluation and Treatment of High Blood Pressure: Chobanian et al. 2003. Most people with advanced renal disease develop hypertension. If not controlled hypertension can accelerate the rate of decline in renal function. If the cycle from hypertension to renal impairment can be halted fewer people would require dialysisNurko 2004. Thus good blood pressure control is important and is the single most effective measure to slow the progression of renal disease. The Australian and New Zealand Society of Nephrology and Diabetes recommend that everybody with diabetes and microalbuminuria or nephropathy should be treated with an ACE- inhibitor and recommend a target blood pressure of 130/85 in people over 50 years and 120/70–75 in people younger than 50 years. The Guidelines also advise that multiple antihypertensive agents might be needed. • presence of retinopathy Gilbert et al. 1998 • long duration of diabetes • male gender although a recent study suggests women are more at risk of diabetes-related renal disease than men with diabetes especially in the older age group Yu et al. 2012. • increasing age. However people with Type 2 diabetes often have microalbuminuria at diagnosis which is consistent with the fact that impaired glucose tolerance or diabetes is often present for many years before it is diagnosed. Thus screening should begin at diagnosis in Type 2 diabetes. Microalbuminuria is rarely present in Type 1 diabetes at diagnosis so screening usually begins at 5 years duration of diabetes. However people with LADA may present differently and screening might need to be commenced earlier in these patients. Practice points 1 False-positive results can occur after heavy exercise or if the person has an UTI. 2 Women with diabetes may develop proteinuria during pregnancy and the cause should be investigated to ensure the protein is not an early sign or preeclampsia especially if they also present with hypertension. 3 If a person develops heavy proteinuria in a short period of time other cause should be investigated. 4 Serum creatinine alone is a poor indicator of renal status in older people. Underweight and overweight are risk factors for misclassifying the degree of renal dysfunction Giannelli et al. 2007. Renal failure Early referral to a nephrologist is imperative to improve the long-term outcomes especially when dialysis or transplantation may be needed. However collaboration with diabetes and other relevant experts must still occur. Late referral is associated with higher morbidity and mortality rates in people on dialysis even when they survive the first year on dialysis Cass et al. 2002. Nephrologists can advise about managing issues associated with renal failures such as: • Calcium and phosphate abnormalities • Calcific medial stenosis which contributes to cardiovascular disease. Phosphate binders might be prescribed to manage the problem if the phosphate is 1.6 mmol/L. • Managing anaemia which might include erythropoietin as well as iron vitamin B12. • Preparing the person for dialysis. Renal failure often requiring dialysis occurs in 25 of people diagnosed with diabetes before the age of 30. The presence of mild renal disease increases the risk of cardiovascular disease even with only small elevations of urinary protein but the relationship is not clear. The presence of other cardiovascular risk factors increases the risk and endothelial cell dysfunction may play a part. Angiotensin converting enzyme ACE inhibitors have been shown to delay or stabilise the rate of progression of renal disease and to decrease cardiac events Keane 2001 Kerr 2008.

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218 Care of People with Diabetes The development of renal problems is insidious and frank proteinuria may not be present for 7–10 years after the onset of renal disease. Microalbuminuria on the other hand is detectable up to 5–10 years before protein is found in the urine. Regular urine collections to screen for microalbuminuria are still used in some places controlling blood glucose and blood pressure the use of ACE inhibitors Type 1 and angiotensin receptor blockers Type 2 and avoiding nephrotoxic agents can attenuate renal and cardiac disease Gilbert Kelly 2001. ACE inhibitors have been shown to be more effective than other antihypertensive agents in reducing the time- related increase in urinary albumin excretion and plasma creatinine in Type 2 diabetes and in people with other cardiovascular risk factors heart failure and myocardial infarction Ravid et al. 1993. Likewise the HOPE and MICRO-HOPE studies demonstrated that ACE inhibitors reduced cardiovascular events and overt nephropathy whether or not microalbuminuria was present HOPE 2000. An ARB can be used in people with Type 1 diabetes do not tolerate ACE and people with Type 2 should be treated with ACE and/or ARB SIGN 2010. However ACE and ARBs are more effective in Caucasians than Blacks of African descent and the benefits need to be assessed in these people. Great care should be taken if IV contrast media are required for diagnostic purposes see Chapter 9. Contrast- induced nephropathy CIN is defined as renal dysfunction following any investigative procedure where radi-opaque contrast media were used Rudnick et al. 2006. Most episodes of CIN do not cause oliguria but result in a rise in serum creatinine 2 days after the procedure which usually returns to pre-procedure levels within a week. CIN occurs in 7–15 of patients and up to 50 in high risk groups such as people with diabetes with a mortality rate of 14 Rudnick et al. 2006. Risk factors for CIN are: • pre-existing renal disease • increasing age • congestive heart failure • hypotension • using large volumes of contrast media • the type of contrast media used • presence of anaemia • diabetes. In addition to diabetes per se people with diabetes are likely to have greater than two other risk factors for CIN which puts them in a very high-risk group. A rise in serum creatinine by 25 is an indicator of CIN but the inaccuracy of creatinine in various states has been outlined. Therefore eGFR may be a better marker. The Australian Adverse Drug Reactions Bulletin 2008 issued a warning about using gadolinium-containing contrast agents in people with renal impairment because of the risk of nephrogenic systemic fibrosis NSF. The incidence of NSF may vary between the different gadolinium agents available. Renal function should be assessed in all patients before using gadolinium especially if they are in a high-risk category and the risks and benefits of using gadolinium carefully considered. Using as low a volume of contrast media as possible and ensuring the person is well hydrated are important preventative measures Meschi et al. 2006. However recent research suggests IV sodium bicarbonate administered seven hours before procedures involving radio contrast media reduces the incidence of CIN from 15 to 2 Briguori 2007. Research is currently underway to determine whether oral sodium bicarbonate will be effective. Renal function can decline in critically ill patients especially people with diabetes and is associated with high morbidity and mortality Schetz et al. 2008. For example hyperglycaemia and insulin resistance are common in critically ill patients with and without diabetes. Associations between interoperative hyperglycaemia during cardiac surgery cardiac catherisation total parenteral nutrition and acute kidney injury have been noted. Intensive insulin therapy in these settings is renoprotective. The incidence of oligouria and the need for renal replacement therapies dialysis is reduced Schetz et al. 2008. The authors suggested insulin improves the lipid profile and reduces nitric oxide levels and oxidative damage as well as controlling hyperglycaemia. Over 50 of patients on GLMs with significant renal disease require insulin therapy. Insulin requirements often reduce in people already on insulin because insulin like many other medicines is degraded and excreted by the kidney. Kidney damage can delay degradation and excretion of many medicines and prolong their half-life increasing the risk of unwanted side effects and medicine interactions. The medicine/s dose or dose interval may need to be altered.

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Long-Term Complications of Diabetes 219 The American Society of Nephrology 2012 released new recommendations to avoid unnecessary testing and reduce costs as part of the ‘Choosing Wisely’ campaign. The recommendations are not specific for diabetes and stress the need for close collaboration between the patient and their doctors and the following key recommendations: • Avoid cancer screening in people receiving dialysis who have limited life expectancy unless they have signs and symptoms of cancer. • Do not administer erthropoiesis-stimulating medicines if the person had haemoglobin 10 g/dl unless they have symptoms of anaemia. • Avoid nonsteroidal anti-inflammatory agents in people with hypertension heart failure or chronic kidney disease from all causes including diabetes. • Avoid placing peripherally inserted central catheters in people with stages 3–5 renal disease without consulting a nephrologist. • Avoid initiating chronic dialysis without discussing all the issues with the person concerned and their carers and other health professionals. Renal disease and anaemia Anaemia occurs as a consequence of chronic renal insufficiency. Renal anaemia occurs earlier in people with diabetes than in people without diabetes. It is more severe and is associated with other factors such as erythrocyte abnormalities and increased osmotic stress that are associated with decreased erythropoietin production Bosman et al. 2001 Ritz 2001. As renal function declines the anaemia becomes more marked. Anaemia is associated with fatigue decreased quality of life depression left ventricular hypertrophy decreased exercise capacity malaise and malnutrition. Annual testing is recommended on people with renal disease stages 3–5. Anaemia is treated with recombinant human erythropoietin rhEPO in conjunction with intravenous iron. Clinical observation To date there has been little if any focus on monitoring haemoglobin Hb as part of routine biochemical monitoring or diabetes complication screening in patients with renal impairment. Dunning et al. 2012 demonstrated Hb can be determined in point of care testing at the same time as blood glucose tests are performed provided staff are trained to use the equipment. Diet and renal disease Improving nutritional status can delay end-stage renal failure Chan 2001 2008. Nutritional needs are individual and depend on the stage and type of renal disease. The aim is to maintain homeostasis and electrolyte balance decrease uraemic symptoms and regularly reassess dietary requirements to ensure changing needs are addressed National Kidney Foundation 2002. The nutritional goals for people with renal disease need to be individualised and assessed regularly to ensure they are appropriate for the degree of renal damage. The goals focus on: • Maintaining a desirable body weight body composition and nutritional status and prevent protein loss Protein Energy Wasting. • Control accumulation of uraemic toxins. • Control uraemic symptoms and its consequences such as nausea. • Manage blood glucose and lipids. • Maintain fluid and electrolyte balance which may involve fluid restriction. • Manage comorbidities such as blood glucose reducing salt intake or omitting salt hypertension maintaining calcium phosphate and vitamin D balance bone disease and hyperparathyroidism calcific medial arteriosclerosis reducing lipids cardiovascular disease maintaining iron folate and vitamin B12 anaemia.

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220 Care of People with Diabetes • Improve graft survival if the person receives a transplant. Specific goals apply to the stages of CK: • Stages 1–4: the predialysis stages: the aim is to slow the progression of renal disease and preserve remaining renal function. • Stage 5 end stage renal disease: conservative management control symptoms and provide nutritional support. Stage 5 on dialysis: replace dialysis nutrient losses which include protein and water-soluble vitamins. • Stage 5 transplant: manage side effects of immunosuppressant medicines manage. Monitor dietary needs Chan 2012. Conversations about management options preparing for end-of-life care and preparing advanced care directive may be appropriate in any of these stages but especially stage 5. The diet generally comprises: • 15–20 of protein in daily intake but low protein diet 0.6 g/kg/day might be required to slow the declining eGFR. 0.8 g/kg/day is recommended to alleviate uraemic symptoms. Protein requirements increase once dialysis is implemented. Protein sources should supply all the essential vitamins and minerals. • Carbohydrates should contribute 50–60 of the total daily energy. When protein requirements change in advanced renal disease extra carbohydrates are sometimes needed. • Fat intake should be about 30 of daily total energy and where possible should come from unsaturated fat but the proportion may increase in advanced kidney disease. Mono- and polyunsaturated fats are preferred. People on dialysis and those who have a renal transplant require a low fat diet. • Vitamin and mineral supplements may be required especially when dialysis commences for example iron and water-soluble vitamins e.g. B12 and C as well as vitamin D. Protein and energy malnutrition are common and need to be corrected to prevent catabolism lipid metabolism and anaemia. Sodium restriction is often recommended but salt substitutes should not be used because they are usually high in potassium and can increase the serum potassium usually already elevated in renal disease. Anorexia is often a feature of renal disease and food smells can further reduce appetite and predispose the patient to malnutrition. Small frequent meals may be more appealing. Malnutrition has implications for the individual’s immune status and phagocyte function and increases the risk of infection Churchill 1996. Referral to a dietitian is essential. Malnutrition is prevalent in haemodialysis patients and has a high mortality rate Lopes et al. 2007. Lack of appetite is a significant predictor of malnutrition and is related to inflammation and may link protein-energy malnutrition in these patients. However appetite varies and is often lower on haemodialysis days. This predisposes the person to hypoglycaemia in the short term and malnutrition in the long term. Lopes et al. 2007 suggested asking people with diabetes on haemodialysis about their appetite in the past four weeks or asking them to keep a food and appetite diary for 3–4 days is helpful. The Kidney Disease Quality of Life-Short Form KDQOL-SF Hays et al. 1994 includes questions about appetite. Depression the presence of several coexisting comorbidites cachexia using oral medicines being older and women on haemodialysis are particularly at risk of malnutrition. As anorexia increases markers of malnutrition decreases serum albumin creatinine nPCR and BMI Lopes et al. 2007 see also Chapters 4 and 12. Renal disease and older people Older people with renal disease are at increased risk of adverse medicine events. A wide range of medicines are used in older people and some may need dose adjustments especially digoxin ACE inhibitors narcotics antimicrobials and GLMs Howes 2001. Longacting agents are contraindicated because of the risk of hypoglycaemia see Chapters 5 and 6. Medicine therapy needs to be closely monitored along with monitoring renal function and nutritional status and non-medicine alternatives used where possible. Practice points

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Long-Term Complications of Diabetes 221 1 Lower rates of creatinine are produced by older people and creatinine clearance rates can be misleading especially in people with low muscle mass. 2 Renal disease is an important cause of medicine toxicity in older people necessitating a hospital admission. Kidney biopsy See Chapter 9. Extra care is required for people with renal disease undergoing renal biopsy. A pressure dressing should be applied to the site and the patient should lie supine after the procedure for six hours. The blood pressure should be monitored and fluids encouraged to maintain urine output unless fluid is restricted. Activity should be reduced for two weeks. Renal dialysis Dialysis can be used in the management of diabetic kidney disease. Dialysis is a filtering process which removes excess fluid and accumulated waste products from the blood. It may be required on a temporary basis or for extended periods of time. Some patients may eventually receive a kidney transplant. Several forms of dialysis are in use. Haemodialysis Blood is pumped through an artificial membrane then returned to the circulation. Good venous access is required and special training in management. Haemodialysis is usually administered three times per week. A recent Canadian study suggests frequent nocturnal haemodialysis six times per week is associated with improved left ventricular mass fewer antihypertensive agents improved mineral metabolism and improvements in some aspects of quality of life Culleton 2007. Hypotension is common when haemodialysis therapy is first commenced. Management consists of: • An appropriate haemodialysis prescription. • Minimising interdialytic fluid gains by setting limits on fluid intake. • Elevating the foot of the bed. • Differentiating between disequilibrium syndrome and hypoglycaemia. • Advising the patient to sit on the edge of the bed or chair to allow the blood pressure to stabilise before standing Terrill 2002. • Maintaining good glycaemic control. Significantly 50 of people with diabetes on haemodialysis have HbA 1c 7 especially those with long duration of diabetes microvascular disease and on insulin Iliescu 2007. These findings probably reflect advanced diabetes and may not be due to haemodialysis. However given the amount of glucose in dialysate it is imperative that HbA1c be as close to normal as possible without causing excess hypoglycaemia to reduce the risk of infection and other complications. Iliescu 2007 suggested it may not be possible to achieve good control with medicines and suggested insulin pumps might be a useful strategy. Significantly poor glycaemic control is linked to lower survival rates in patients on haemodialysis Oomichi et al. 2007. Strict aseptic technique and careful patient education are essential when managing dialysis therapies. Patients with CKD are susceptible to infections due to abnormal immune function which is likely to be worse in people with diabetes and hyperglycaemia where neurophil function is abnormal and malignancies Choudhury Luna-Salazar 2008. Mucocutaneous barriers are often disrupted secondary to skin excoriation from pruritis xerosi and sweat gland atrophy. Common bacterial infections include Staphylococcus species Escherichia coli Klebsiella and Mycobacterium tuberculosis. Viral infections are also common. Strict aseptic technique and careful patient education are essential when managing dialysis therapies. Peritoneal dialysis

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222 Care of People with Diabetes The filtering occurs across the peritoneum. This form of dialysis is an excellent method of treating kidney failure in people with and without diabetes. The uraemia hypertension and blood glucose can be well controlled without increasing the risk of infection if aseptic techniques are adhered to. However infection is a significant risk and is often the reason people change to haemodialysis. Continuous ambulatory peritoneal dialysis CAPD CAPD is a form of peritoneal dialysis in which dialysate is continually present in the abdominal cavity. The fluid is drained and replaced 4–5 times each day or overnight if the patient is on automated peritoneal dialysis APD. The person can be managed at home which has psychological advantages once the care of equipment is understood and the person is metabolically stable. CAPD can also be used postoperatively to control uraemia related to acute tubular necrosis or early transplant rejection. Insulin added to the dialysate bags achieves smoother blood glucose control because the insulin is delivered directly into the portal circulation and is absorbed in the dwell phase which is closer to the way insulin is normally secreted after a glucose load. However it also has disadvantages and is an infection risk and is not always recommended. The usual insulin dose may need to be increased because of glucose absorption from the dialysate fluid and to account for insulin binding to the plastic of the dialysate bags and tubing if it is added to the dialyslate bag. The continuous supply of glucose and lactate in the dialysate fluid are calorie-rich energy sources and can lead to weight gain and hyperglycaemia. The art is to calculate insulin requirements to avoid hyperinsulinaemia which carries its own complication risks. Glucose-free solutions such as Nutrimeal and glucose polymers may help reduce complications associated with high insulin and glucose levels Rutecki Whittier 1993. Insulin is usually administered subcutaneously if the person is on APD. Many renal dialysis units do not advocate adding insulin to dialysate bags due to the increased risk of infection. Priorities of dialysis treatment 1 remove waste products and excess fluids from the blood urea and creatinine 2 to provide adequate nutrition and safe serum electrolytes and to prevent acidosis 3 patient comfort 4 to prevent complications of treatment 5 to provide information and support to the patient 6 to ensure privacy. Objectives of care The individual’s ability to carry out self-care tasks needs to be assessed early when considering renal replacement therapies. Changed joint structure due to oedema and tissue glycosylation e.g. carpel tunnel syndrome can limit the fine motor skills required to manage CAPD. Visual impairment due to retinopathy frequently accompanies renal disease and if present can limit self-care abilities. 1 To assess the patient carefully in relation to: • knowledge of diabetes • preventative healthcare practices • ability to use aseptic technique • usual diabetic control • presence of other diabetic complications • support available family relatives • motivation for self-care • uraemic state. 2 To ensure thorough instruction about administration of dialysate and intraperitoneal medication insulin. 3 To ensure a regular meal pattern with appropriate carbohydrate in relation to dialysate fluid.

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Long-Term Complications of Diabetes 223 4 To maintain skin integrity by ensuring technique is aseptic especially in relation to catheter exit site and skin care. 5 To monitor urea creatinine and electrolytes carefully. 6 To provide psychological support. 7 To encourage simple appropriate exercise. 8 To ensure adequate dental care and regular dental assessments. Poor oral health causes chronic inflammation and is a site of infection. Untreated uraemia is associated with stomatitis and patients on dialysis are prone to gingivitis and peridontitis. Prophylactic antibiotics for dental procedure may be advisable Choudhury Luna-Salazar 2008. 9 To prevent pain and discomfort especially associated with the weight of the dialysate. 10 To ensure the patient reports illness or high temperatures immediately. 11 Monitor for infections and advise people to have preventative vaccines such as influenza and pneumococcal vaccination and an annual screen for tuberculosis. Regular screening for nasal staphylococcal infections certain types of malignancy may also be indicated for example renal cell carcinoma prostate cancer breast and cervical cancer. Nursing responsibilities 1 Meticulous skin care. 2 Inspect catheter exit site daily report any redness swelling pain or discharge. 3 Monitor fluid balance carefully: • measure all drainage • maintain progressive total of input and output • report a positive balance of more than 1 litre: the aim generally is to achieve a negative balance to maintain the dry weight. 4 Monitor blood glucose. 5 Monitor temperature pulse and respiration and report abnormalities. 6 Monitor nutritional status – intake and biochemistry results. 7 Weigh daily to monitor fluid intake and nutritional status. 8 Ensure patency of tubes and monitor colour of outflow. Report if: • cloudy • faecal contamination • very little outflow tube blocked. 9 Report lethargy and malaise that can be due to uraemia or high blood glucose levels. 10 Warm dialysate before the addition of prescribed drugs and before administration to decrease the possibility of abdominal cramps. 11 Oral fluid intake may be restricted – provide mouth care and ice to suck. 12 Assess self-care potential: • blood glucose testing • adding medication to bags • aseptic technique • psychological ability to cope. 13 Protect the kidney during routine tests and procedures by avoiding dehydration and infection Chapter 9. Commencing CAPD in patients on insulin A 24-hour blood glucose profile is often undertaken prior to commencing intraperitoneal insulin to assess the degree of glycaemia and calculate insulin requirements. The glucose profile should be carried out following catheter implantation with the patient stabilised on a CAPD regimen. One method consists of: 1 Obtaining venous access for drawing blood samples. 2 Obtaining hourly blood glucose levels for 24 hours.

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224 Care of People with Diabetes 3 Sending at each bag change: • 10 mL new dianeal fluid for glucose analysis • 10 mL drained dianeal fluid for glucose and insulin analysis to the appropriate laboratory. One protocol for administering insulin to people with diabetes on CAPD based on four bag changes each day is: 1 Calculate usual daily requirement of insulin and double it. 2 Divide this amount between the four bag changes. 3 The overnight bag should contain half the daytime dose. Some centres only administer 10 of the total daily dose at night. Example usual total insulin units 60 units multiply this amount by 2 120 units divide 120 units by 4 exchanges 30 units 3 daily exchanges 30 units/bag overnight exchange 15 units/bag Adjustments for the dextrose concentration of the dialysate may be necessary. Intraperitoneal insulin requirements are usually one-third higher than the amount needed before CAPD. Practice point Many renal units no longer recommend adding insulin to dialysis bags because of the risk of infection. Subcutaneous insulin via an insulin pump using a basal bolous regimen could be an effective way of administering insulin to people receiving dialysis providing absorption was affected and the individual has the knowledge and skills to manage the insulin pump. Educating the patient about CAPD The patient should be instructed to: 1 Not have a shower or bath for the first 5 days after the catheter is inserted. 2 Always carefully wash hands prior to changing the bags. 3 Wear loose fitting clothes over exit site. 4 Examine feet daily for signs of bruising blisters cuts or swelling. 5 Wear gloves when gardening or using caustic cleaners. 6 Avoid hot water bottles and electric blankets because sensory neuropathy can diminish pain perception and result in burns. 7 Avoid constrictive stockings or wearing new shoes for a long period of time. 8 Wash cuts or scratches immediately with soap and water and apply a mild antiseptic e.g. betadine ointment. Any wound that does not improve within 24–36 hours or shows signs of infection redness pain tenderness must be reported promptly. 9 Bag exchanges should be carried out 4–6 hours apart. The person may be on APD having overnight exchanges. 10 Only short-acting clear insulin must be used in bags. 11 Adjust insulin doses according to diet activity and blood glucose levels and at the physician’s discretion. 12 Accurately monitor blood glucose 4-hourly. A blood glucose meter may be required. 13 Provide written information.

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Long-Term Complications of Diabetes 225 Immediate help should be sought if any of the following occur: • decreased appetite • bad breath/taste in mouth • muscle cramps • generalised itch • nausea and vomiting especially in the morning • decreased urine output • signs of urinary infection such as burning or scalding. Supportive care Some people especially older people may require supportive care if they are not suitable for or choose not to have dialysis or a renal transplant. Supportive care is generally conservative Moustakas et al. 2012. Although some experts differentiate supportive care from palliative care they have similar goals and encompass shared decisionmaking promoting autonomy optimal functioning within the person’s capabilities maintaining quality of life and comfort. End of life care should be part of shared decision-making and documented in an Advanced Care Plan Chapter 18. Renal disease and herbal medicine see also Chapter 19 People with end-stage renal failure often try complementary therapies to alleviate the unpleasant symptoms of their disease. Some therapies for example aromatherapy to reduce stress and maintain skin condition or counselling for depression are beneficial and usually safe. Herbal medicines are popular with the general public but they may not be appropriate for people with renal disease Myhre 2000. The kidneys play a key role in eliminating medicines and herbal products from the system. Some of these medicines and herbs can cause kidney damage that may be irreversible and put already compromised renal function at great risk. In addition some herbal products particularly those used in traditional Chinese medicine TCM are often contaminated with drugs heavy metals and other potentially nephrotoxic products Ko 1998. Frequently these contaminants are not recorded in the list of ingredients in the product. As well as the direct effect of the herbs on the kidney the intended action of particular herbs can complicate conventional treatment. An herb Taxus celebica used in TCM to treat diabetes contains a potentially harmful flavonoid and has been associated with acute renal failure and other vascular and hepatic effects Ernst 1998. Kidney damage can be present with few specific overt renal symptoms therefore it is vital that kidney and liver function is closely monitored in people taking herbs especially if kidney function is already compromised by diabetes. Potentially adverse renal effects include: • electrolyte imbalances for example Aloe barbedensis • fluid imbalances for example liquorice root • hypokalaemia for example Aloe Senna • kidney damage for example Aristolochia. In addition herbal and conventional medicine interactions may occur see Chapter 19. Practice points 1 Nurses must know when their renal patients are taking herbal medicines so that their kidney function can be closely monitored. People should be asked about the use of complementary therapies periodically. 2 Conventional medicines can also cause significant renal damage and dose adjustments may be needed or alternative medicines used for example NSAID statins OHA.

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226 Care of People with Diabetes PERIPHERAL AND AUTONOMIC NEUROPATHY Key points • Lower limb problems represent a significant physical psychological social and economic burden for people with diabetes and the health system. • Forty to seventy per cent of lower limb amputations occur in people with diabetes. • Peripheral neuropathy vascular disease infection foot deformity and inappropriate footwear predispose people to foot disease. • Screening for foot disease and preventative self-care practices is essential. • Foot complications are common in older people. • A multidisciplinary team approach and good communication are essential to optimal management. • Many subgroups of neuropathy occur including mononeuropathy peripheral and autonomic neuropathy. The two most common forms are discussed in this chapter are: peripheral and autonomic neuropathy. Introduction Peripheral neuropathy is present in 20 of people with Type 1 diabetes after 20 years duration of diabetes and is already present at diagnosis in 10 of people with Type 2 at diagnosis and 50 by 20 years duration of diabetes. Peripheral neuropathy leads to inability to sense pressure and pain in the feet dry skin reduced joint mobility bony deformity and problems with balance which increases the risk of falling. Common foot deformities associated with diabetes are claw toes hammer toes hallus valgus haalus rigidus callus flattened or high foot arches Charcot’s feet and amputation sites. These changes mean the normal cushioning that protects the feet during usual activities are deficient and the foot is at high risk of injury. Foot ulcers occur in 25 of people with diabetes: 25 develop an infection 20 –60 of ulcers involve bone osteomyelitis and 34 present with a recurrent ulcer/ year. Careful assessment consideration of the causative factors and managing the existing problems can limit further exacerbation of diabetic foot disease. Appropriate nursing care can prevent foot problems occurring as a result of hospitalisation or placement in an aged care facility. Diabetic foot disease is a common cause of hospital admissions and is associated with long length of stay: 59 longer than for non-foot admissions and significant morbidity and mortality. Significantly foot ulcers also occur during hospital admissions. Diabetic foot disease is a heterogeneous disease entity defined as a group of syndromes that lead to tissue breakdown. Infection neuropathy and ischaemia are usually present and increase the risk of infection Apelqvist Larsson 2000. Foot disease and its management have an adverse impact on the well-being and quality of life of people with diabetes Brod 1998. The disease itself and some management practices for example non-weight-bearing regimes restrict physical activity and social interaction and often result in non-adherence. Foot care self-care and foot care in hospital is an extremely important aspect of the nursing care of people with diabetes in any setting. Significantly preventative foot care is often neglected in acute care settings. The combination of mechanical factors and vascular and nerve damage as a complication of diabetes leads to an increased risk of ulceration infection and amputation. In older people these factors increase the risk of falling. An estimated 40 of people with diabetes have peripheral neuropathy but it occurs in up to 50 of older people Boulton 2005 and 20 of hospital admissions are for foot-related problems. Not surprisingly peripheral neuropathy is associated with significantly impaired quality of life and effects on energy pain mobility and sleep Papas et al. 2103. Forty to seventy per cent of lower limb amputations occur in people with diabetes and most begin with an ulcer. The amputation rate can be reduced by preventative foot care. The spectrum of diabetic foot disease varies globally depending on socioeconomic circumstances but the basic underlying pathophysiology is the same Bakker 2000. Charcot’s deformity is a severe form of diabetic foot disease that is often missed through misdiagnosis in the early stages and delay in appropriate management. The possibility of Charcot’s deformity should be considered in any person with long-standing diabetes neuropathy and foot disease.

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Long-Term Complications of Diabetes 227 Vascular changes People with diabetes and peripheral vascular disease are predisposed to atherosclerosis which is exacerbated by chronic hyperglycaemia endothelial damage nonenzymatic tissue glycosylation and polyneuropathy. These conditions impair vascular remodelling. The risk increases when the individual smokes has hypertension and hypelipidaemia. 1 Macrovascular major vessel disease may lead to: • intermittent claudication and rest pain • poor circulation to the lower limbs which leads to malnutrition tissue hypoxia and delayed healing if any trauma occurs in this area. The injured tissue is prone to infection and gangrene can result. 2 Microvascular small vessel disease leads to thickening of capillary basement membranes poor blood supply to the skin and tissue hypoxia predisposing the feet to infection and slow healing. Infection Foot infections are a common and serious problem in people with diabetes. They are prone to infections and non- healing wounds. Foot infection occurs as a result of skin ulceration or deep penetrating injuries for example standing on a drawing pin. These injuries can go unnoticed for days because the person does not feel pain if they have peripheral neuropathy. They act as a portal for infection that can involve tissues at all levels and foot structures including bone. The diagnosis of an infected wound is based on clinical signs. These include purulent discharge or two or more of erythemia swelling local heat and pain. These signs may also indicate the presence of Charcot’s foot rather than infection and alkaline phosphatase ESR X-ray and/or MRI may be indicated Papas et al 2013 samples should also be collected to determine what organisms are present in the wound. The samples need to be collected from deep within the wound after the wound has been debrided or biopsy samples from the base of the wound rather than superficial swabs. Acute infections are usually due to aerobic Gram-positive cocci such as Staphylococcus aureus or β-haemolytic streptococci especially if the individual has limited exposure to antibiotics previously. Chronic ulcers and deep infections are often due to Gramnegative bacilli and anaerobic organisms such as Escherichia coli Klebsiella Proteus Bacteroides and Peptostreptococcus with Staphylococcus aureus is also likely to be present sometimes as the only pathogen but usually in combination with other pathogens Lipsky Berendt 2000 Papas et al 2013. Charcot’s foot is a relatively common under-diagnosed condition that complicates management of the neuropathic foot and can lead to significant pain mobility deficits and amputation Piaggesi et al. 2005. Charcot’s foot is due to the progressive destruction of the bones and joints in neuropathic diabetic feet secondary to inflammation following trauma which is usually not recognised by the person with diabetes. Inflammation is followed by sclerosis which leads to changes in the bony architecture of the foot and reduces the capacity to reduce subsequent everyday stress such as walking. Reactivation of the inflammatory process increases bone reabsorption and increases the risk of further trauma. Higher rates of foot fractures and Charcot’s feet have been observed in patients following successful pancreas transplants and those on long-term corticosteroid therapy possibly because these medicines reduce bone resistance to minor trauma Jeffcoate et al. 2000. Regular assessment of bone densitometry may be indicated in people on long-term corticosteroids. Managing diabetic foot pathology requires a collaborative team approach and includes: • Admission to hospital for a thorough foot and clinical assessment including self-care ability bed rest administration of broad-spectrum antibiotics which needs to be continued after the acute phase resolves and surgical procedures if indicated. • Broad-spectrum antibiotics are usually commenced initially until the results of the wound swabs are known and may be given IV for severe infections. Antibiotic therapy may be required for 1–2 weeks and up to 6 weeks if osteomyelitis is present. The risk of the person developing antibiotic resistance must be considered and every effort made help them to prevent recurrent foot infections. The person should be asked whether they are allergic to penicillin before commencing antibiotic therapy. Flucloxacillin can be used for superficial infections and cellulitis if the person is not allergic to penicillin. Cephalexin can be used for minor infections and Clindamycin for severe infections. If the infection is deep Augmentin or a combination of ciprofloxacin and Clindamycin may be indicated.

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228 Care of People with Diabetes • X-ray although the classical finding of osteomyelitis are not usually seen on plain X-ray until 10–21 days after the onset of bone infection MRI bone scans to determine

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230 Care of People with Diabetes whether osteomyelitis is present and determine the extent of the soft-tissue injury. If it is a long course of antibiotics and/or amputation is indicated. Alkaline phosphatase 135U/L ESR 70 mm/hour and/or being able to feel bone when probing the base of the wound are suggestive of osteomyelitis. • Bone densitometry or ultrasound may be indicated. • Surgical débridement to clean the wound and appropriate dressings. Referral to the wound care nurse and/or infectious disease team may be warranted. • Revascularisation for example femoral/popliteal bypass or amputation if indicated. • Selection and application of appropriate wound dressings Edmonds et al. 2000 Harding et al. 2000. • Pressure off-loading to improve blood supply to the foot. Biomechanical measures such as total contact casts to relieve pressure in high-pressure ulcers and Charcot’s foot deformity. Casts enable the person to remain mobile thus improving their social and psychological wellbeing. Infection and subsequent oedema must be managed because they aggravate the pressure on muscles and can lead to muscle necrosis. In hospital settings high specification foam mattresses make a significant difference in preventing neuropathic foot ulcers. Prefabricated walkers are also used but must be correctly fitted. • Improving blood glucose control and diet to ensure optimal neutrophil functioning and nutrition to promote wound healing. • Dietetic assessment. • Counselling to stop smoking if relevant. • Rehabilitation including regular podiatric assessment. Footwear and orthotics may need to be modified. Practice points 1 Swabs need to be taken from deep in the ulcer cavity which can be painful and analgesia may be required. Superficial swabs often do not identify all the organisms present particularly anaerobes.

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Long-Term Complications of Diabetes 231 2 Hyperglycaemia inhibits wound healing. Thus people undergoing amputations and other surgical procedures are at high risk of post-operative infections. Good metabolic control optimal nutrition and aseptic technique reduce the risk. Diabetes-related peripheral neuropathy Diabetic neuropathy is defined as the presence of clinical or subclinical evidence of peripheral nerve damage which cannot be attributed to any other disease process Boulton et al. 1998. Neuropathy can affect the sensory nerves resulting in pain tingling pins and needles or numbness. These symptoms are often worse at night. The sensory loss results in insensitivity to pain cold heat touch and vibration. The patient may not detect trauma pressure areas sores blisters cuts and burns. Callous formation ulceration and bone involvement can occur. The motor nerves can also be affected resulting in weakness loss of muscle fibres and diminished reflexes. Both types of nerves can be affected at the same time. Medications may not be effective in the treatment of neuropathic pain but some commonly used medicines prescribed to manage the discomfort are shown in Table 8.3. Differentiating between the different types of nerve fibres involved allows a more targeted approach to pain management. Where unmyelinated C-fibres are affected characterised by burning dysthetic pain capsaicin or Clonidine may be effective. Where the alpha fibres are involved the pain is often deep and boring and insulin infusion lignocaine or gabapentin may be effective Vinik et al. 2000. Often both types of fibres are affected. Medicines under study include a-Lipoic acid an antioxidant that scavenges free radicals and has been shown to reduce pain when administered parenterally Ziegler et al. 2004. Preliminary studies suggest the protein kinase C inhibitor LY33531 improves allodynia and prickling pain Litchy et al. 2002. C-peptide has recently been shown to improve early neurological abnormalities in people with Type 1 diabetes with established clinical neuropathy Brismar et al. 2007. It is given subcutaneously QID and appears to be most effective when baseline neuropathy is mild. Aldose reductase inhibitors have been under study for many years with various degrees of success. Recent research suggests Epalrestat improves objective and subjective measures of peripheral neuropathy and might slow the progression of retinopathy Hotta 2006. Other pain management strategies Other non-medicine options with varying degrees of evidence to support their benefits include: • Physiotherapy and exercise such as Tai Chi to maintain muscle tone and strength. • Percutaneous nerve stimulation static magnetic field therapy low intensive laser therapy bodyflow technology and monochromatic infrared light. These techniques might improve peripheral circulation and reduce local oedema which reduces some of the local pressure and relieves local pain. • Acupuncture which has benefits up to six months Abusaisha et al. 1998. • Other non-medicine measures include improving blood glucose control stopping smoking reducing alcohol intake and eating a healthy diet. The autonomic nervous system may also be affected by diabetes. Autonomic nervous system involvement may lead to an absence of sweating which causes dry cracked skin and increases the risk of infection. Other effects of autonomic neuropathy include gastric stasis erectile dysfunction hypoglycaemic unawareness and incontinence. The small muscle wasting secondary to longstanding neuropathy can lead to abnormal foot shapes for example clawing of the toes making the purchase of well-fitting shoes difficult.

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232 Care of People with Diabetes Vascular disease neuropathy and infection are more likely to develop if there is longstanding hyperglycaemia which contributes to the accumulation of sorbitol through the polyol pathway leading to damage to the nerves and small blood vessels. Figure 8.1 illustrates the inter-related factors that lead to foot problems in people with diabetes. Table 8.4 lists changes in feet due to the normal ageing process. These factors should all be incorporated in the nursing assessment to ensure that appropriate foot care is part of the overall management of the patient. Nerve damage neuropathy Reduced sensation muscle weakness/atrophy abnormal foot shape High blood trauma glucose levels InfectionDeath of tissue Tisue hypoxia decreased nutrition Poor blood supply Smoking High blood pressure Inappropriate foot self-care Figure 8.1 Diagrammatic representation of the factors leading to foot problems in people with diabetes. Table 8.4 Changes in feet due to normal ageing. 1 Skin becomes thin fragile 2 Nails thick and often deformed 3 Blood supply is reduced 4 Nerve function often impaired 5 Muscle weakness and wasting 6 Arthritis may lead to pain and deformity Stages of peripheral neuropathy • Chronic and painful – improve metabolic control. • Acute and painful – analgesia. • Painless – education orthoses regular assessment. • Late complications Vinik et al. 2000. Risk factors for developing foot problems 1 Diabetes especially if blood glucose is continually high. 2 Smoking: people with chronic neuropathic pain are twice as likely to smoke as those with chronic nociceptive pain but this might not represent a causative effect Todd et al. 2008. Some studies suggest nicotine has a mild analgesic effect. 3 Obesity. 4 High blood pressure. 5 Cardiovascular disease. 6 Lack of or inadequate foot care which is likely to be multifactorial including inability to reach the feet and lack of knowledge.

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Long-Term Complications of Diabetes 233 7 Vision impairment. 8 Inappropriate footwear. 9 Delay in seeking help. 10 Previous foot problems and amputation. 11 Depression. These factors should be part of the nursing assessment. The more risk factors present the greater the likelihood of amputation Pecorara 1990. Routine assessment to detect neuropathy and associated foot changes should be part of regular health assessment in primary care. Objectives of care 1 To assess the individual’s risk of developing a foot ulcer by screening at least annually. The result of a structured foot examination can be entered into online screening tools such as the SCI-DC which automatically stratifies the risk and recommends a management plan. Risk stages and key factors entered into the SCI-DC are: • high risk: active ulcer infection ischaemia and/or gangrene • moderate risk: previous ulcer and/or amputation more than one risk factor such as reduced sensation callous • moderate risk: one risk factor such as peripheral vascular disease • high risk: no risk factors present. 2 Identify feet most at risk of trauma ulceration and infection in aged care rehabilitation and hospital settings by assessing vascular nerve and diabetic status: • Sensation using 10 g Semmes–Weinstein monofilaments 128 Hz tuning forks and disposable pin prickers Apelqvist and Larson 2000 recently a new non-invasive test that can be undertaken by the person with diabetes was developed and is said to have 87 sensitivity and 66 specificity Papas et al. 2013. The test the indicator plaster neuropad IPN can be performed in 10 minutes and might be a useful screening tool to incorporate into the individual’s foot self-care regimen. • Presence of vascular insufficiency by checking capillary return and the presence of foot and peripheral pulses Doppler ultrasound toe pressures and transcutaneous oxygen measurement are used in some centres. • Foot deformity. 3 To assess patient knowledge of foot care. 4 To reinforce appropriate preventative foot care. 5 To prevent trauma infection and pressure ulcers. 6 To treat any problem detected. 7 To refer to podiatry orthotics physiotherapy rehabilitation diabetes nurse specialist/diabetes educator or specialist foot clinic as necessary. 8 To control or eliminate any factors which predispose the patient to the risk of foot problems in hospital. 9 Risk of falls in the elderly see Chapter 12. 10 Pain management. Nursing responsibilities 1 Prevent neuropathic ulcers occurring in people with diabetes and peripheral neuropathy during a hospital admission. 2 To assess the feet carefully on admission. Assess self-care potential can the patient reach the feet see clearly. When assessing the feet obtain information about: a Past medical history: • glycaemic control • previous foot-related problems/deformities • smoking habits • nerve and vascular related risk factors • claudication rest pain • previous foot ulcer/amputation

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234 Care of People with Diabetes • alcohol intake. b Type of footwear socks shoes: • hygiene • activity level. c Social factors: • living alone • older. 3 When examining the feet: • Check both feet • check pulses dorsalis pedis posterior tibial • assess toenails: thick layered curved ingrowing toenails will need attention • note foot structure overlapping toes prominent metatarsal heads on the sole of the foot • check for callous cracks and fungal infections that can indicate inadequate foot care and poor hygiene. 4 Note also: • pallor on elevation of leg • capillary return normally 1–2 seconds • any discoloration of legs • hair loss on the feet. 5 To ensure appropriate foot hygiene: • wash in lukewarm water – use pH-neutral soap products that do not dry the skin especially in older people or people on steroid medications and those with atopic skin • check water temperature with wrist before putting the patient into a bath • dry thoroughly including between toes • apply cream to prevent dryness and cracks urea cream sorbelene. 6 Ensure Elastoplast/Band Aids bandages do not encircle toes as they can act like tourniquets and reduce the circulation which could result in gangrene. Apply elastic support stockings correctly. 7 Maintain a safe environment: • use a bed cradle • ensure shoes are worn if walking around the ward • strict bed rest may be necessary while the ulcer is healing • maintain aseptic technique. 8 Check feet daily and report any changes or the development of any callus abra sion or trauma. 9 Monitor blood glucose control. 10 Attend to dressings and administer antibiotics according to treatment order. Antibiotics are often given intravenously if foot infection is present. 11 Take the opportunity to ensure self-care knowledge is current and that complication screening has been attended to. Ensure preventative foot care education is provided to give the patient with diabetes: • an understanding of effects of diabetes on the feet • a knowledge of appropriate footwear • the ability to identify foot risk factors • an understanding of the principal effects of poor control continual hyperglycaemia on foot health • knowledge about the services available for assistance with their diabetes care and how to obtain advice about foot care • knowledge about appropriate foot care practices in particular that they must inspect their feet daily and seek help early if any problems are found • odour control can be an issue when infection and gangrene are present. Some wound dressings have an absorbent layer that eliminates odour by absorbing bacteria. Good foot hygiene helps reduce the odour. Classification of foot ulcers A number of ulcer classification systems are in existence and nurses are advised to follow the system in their place of employment. In 2002 an international working party was established to develop an international consensus foot ulcer classification system. Foot ulcers can be loosely classified as:

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Long-Term Complications of Diabetes 235 1 clean superficial ulcer 2 deep ulcer possibly infected but no bone involvement 3 deep ulcer tracking infection and bone involvement 4 localised gangrene and necrosis usually forefoot heel 5 extensive gangrene of foot. The depth and width of the ulcer should be recorded regularly a plastic template dated and filed in the patient’s history aids in the assessment of changes in ulcer size. The presence amount and type of exudate must be recorded. Clinical observation Aromatherapy essential oils on the surface of the secondary dressing can help reduce wound odour. They should not be applied directly to the wound. They can be used in a vapouriser for environmental fragrancing. Some essential oils can help improve mood. Wound management Dressings may be needed to absorb the exudate and protect the foot. No dressing is appropriate for all wound types. Surgical débridement amputation or an occlusive dressing may be required. It is important to keep the temperature at 37 °C the dressing moist and the pH acidic to promote healing. Choose a dressing that does not cause tissue damage when it is removed that is does not stick to the wound and Practice point Painting the area with a betadine or other skin antiseptic is of little value. Coloured antiseptics can obscure some of the signs of infection. protects the wound from infection. The moisture aids in pain relief decreases the healing time and gives a better cosmetic result. An acidic environment promotes granulation tissue. The management of ulcers in hospital and other specific foot problems are listed in Table 8.5. Diabetic foot ulcers heal slowly and bed rest is important. The patient may be otherwise well. Encourage independence with blood glucose testing and insulin administration. Refer for occupational therapy. The person may benefit from counselling if they are depressed. Careful discharge planning is imperative: • To ensure mobilisation and rehabilitation and that there is a safe environment at home. • Interim placement in an extended care facility may be necessary. • Assess the physical and social support available after discharge. Table 8.5 Managing of specific foot problems while the person is in hospital or community settings. Problem Treatment Burning paraesthesia aching Assess neuropathic status Encourage person to walk Maintain euglycaemia Appropriate analgesia Manage depression if present Pain Foot cradle sheepskin Analgesia

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236 Care of People with Diabetes Dry skin cracks Clean dry carefully apply moisturiser for example urea cream sorbelene A duromet can be used to evaluate skin hardness and identify areas of where plantar hyperkeratosis is likely to develop Plantar pressures which can indicate force and workload Claudication Medications as ordered Rest Elevate feet Cardiovascular assessment peripheral pulses ankle/brachial pressure index APBI transcutaneous oxygen tension Tcp O 2 Angiography Foot deformity Clinically evaluate and describe Estimate joint mobility Refer to podiatrist Physiotherapy Charcot’s deformity Orthotist Ulcers infection The presence of a lesion transforms an at-risk foot into an acute clinical emergency. Grade the ulcer for example University of Texas Staging System for Diabetic foot ulcers X-ray and MRI may be indicated to assess the depth Record the width and depth for example using a polyurethane sheet Refer to specific medical order Assess daily Make template to note change in size of ulcer Antibiotics Débridement amputation ABPI 0.9 normal 0.9–0.5 indicates peripheral vascular disease is present 0.5 indicates critical limb ischaemia. ABPI 1.3 usually indicates medial artery calcification Monckerberg sclerosis an indirect sign of autonomic neuropathy Piaggesi et al. 2005. TcpO 2 pressure 60 mmHg indicates local ischaemia 40 mmHg indicates critical ischaemia. Piaggesi et al. 2005. Practice point Orthopaedic patients with diabetes and foot or leg plasters should be encouraged not to scratch under the plaster especially if they have ‘at risk’ feet. Damage can occur and remain undetected until the plaster is removed. Wound management techniques under study Several new wound management products for hard-to-heal ulcers are under study: • platelet-derived growth factor applied topically to increase granulation • Hyaff • Dermagraft • Apilgraf • granulocyte-colony stimulating factor Edmonds et al. 2000. Hyperbaric oxygen may be beneficial in some serious ulcers. Oxygen is necessary for wound healing and hyperbaric oxygen can increase tissue oxygen levels and improves the killing power of phagocytes Bakker 2000. Rehabilitation Despite the best care amputations are required in 5–15 of people with diabetes presenting with a foot problem particularly in the presence of gangrene non-healing ulcers which may be associated with osteomyelitis and severe foot

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Long-Term Complications of Diabetes 237 infection. A rehabilitation process is necessary once the acute stage has settled. Below-knee amputations give a favourable result even if the popliteal pulses are diminished Steinberg 1991. The goals of rehabilitation are: • Appropriate stump care. In the early stages this may involve bandaging to reduce oedema. Circular bandages should be avoided because they tend to act like tourniquets and reduce the blood supply to the stump. Analgesia should be available. Later correctly fitting the stump into the socket of the prosthesis and regular inspection for the presence of infection or pressure areas. • Prevent muscle contracture with regular physiotherapy. • Help the person be as independent and active as possible. • Ambulation with a prosthesis or wheelchair depending on the individual assessment. However not all people with diabetes benefit from having a prosthesis people who have advanced neurological disease such as stroke Parkinson’s disease CCF obstructive pulmonary disease unstable angina knee and hip contractures may not be suitable for a prosthesis. These people often have limited ability to mobilise even before an amputation. High risk of gangrene or infection in the other limb may warrant delaying an amputation. • Early mobilisation in whatever capacity is usually desirable after amputation to reduce postoperative complications. The person will need to learn how to manage whatever mobilisation method is appropriate. • Care of the stump is important to prevent wound contractures. Practice points 1 Amputation should not always be seen as treatment failure. It can relieve pain enable the person to return home and enjoy an improved quality of life. Amputation is distressing for the person with diabetes and their family and careful explanation support and counselling are essential. The patient should be included in the decision-making process and make the final decision. Their social and psychological situation should be considered as well as their physical needs. 2 Amputation increases the risk of a second amputation. Autonomic neuropathy Key points • Often several organs are involved. • Signs and symptoms are often non-specific. • Autonomic neuropathy is often undiagnosed. • Postural hypotension is the most significant sign of autonomic neuropathy. • People with postural hypotension and nocturnal diarrhoea should be investigated for autonomic neuropathy. • The progression to autonomic neuropathy is related to poor metabolic control. • It is more common in people over 65 but it can occur in the first year after diagnosis. Introduction Autonomic neuropathy is a distressing condition for people with diabetes. It can cause erratic blood glucose readings. People are often accused of manipulating their food and/ or diabetic medications which causes stress and anxiety. The symptoms associated with the various manifestations of autonomic neuropathy can be uncomfortable painful and have an adverse impact on the individual’s quality of life. The autonomic nervous system plays an important role in the regulation of carbohydrate metabolism. Many processes are affected by autonomic neuropathy for example it both facilitates and inhibits insulin secretion.

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238 Care of People with Diabetes 1 Stimulates the right vagus nerve which innervates the pancreatic islet cells or the beta-adrenergic receptors in the islet cells stimulates insulin secretion. 2 Stimulates the alpha-adrenergic receptors in the islet cells decreases insulin secretion which is an essential aspect of blood glucose regulation and to maintaining glucose homeostasis. The autonomic nervous system also has a role in the conversion of glycogen into glucose in the liver where free fatty acids undergo further metabolism to ketones. Neurogenic stimulation of the hypo-pituitary axis results in cortisol secretion one of the counter-regulatory hormones that have a role in correcting hypoglycaemia. In stress situations especially prolonged stress hyperglycaemia results. Diabetes is the commonest cause of autonomic neuropathy but it also occurs in association with other diseases such as advanced Parkinson’s disease and Guillain–Barre syndrome. Autonomic neuropathy is a common under-diagnosed condition associated with a range of signs and symptoms depending on the specific nerves and organs affected Vinik et al. 2000 Aly Weston 2002. It has a slow onset and affects up to 30–40 of people with diabetes and although many people only have mild often subclinical features significant functional abnormalities can be present. Rarely in 5 of cases overt clinical features develop. Autonomic neuropathy can involve any system but commonly affects the heart GIT and genitourinary systems Spallone Menzinger 1997. The GIT is one of the most frequently affected systems but GIT problems not associated with autonomic neuropathy occur in 50 of the general population and are more common in people with diabetes Lock et al. 2000. Older people are at risk of having many neuropathic GIT changes but some GIT changes are age-related or associated with the use of vasoconstrictive drugs Aly Weston 2002. Delayed gastric emptying is present in 25–55 of people with Type 1 and 30 with Type 2 Wegener et al. 1990. Consequences of gastrointestinal autonomic neuropathy include early satiety abdominal distension reflux stomach spasm postprandial nausea vomiting altered medicine absorption and food absorption malnutrition and glucose variability. In addition it causes significant diabetes-related distress and reduces quality of life. Practice points 1 Autonomic neuropathy is physically uncomfortable and treatment options are limited. Where the GIT is involved frequent adjustment to the food and medication regimen is often needed. Blood glucose monitoring is important to allow such changes to be made appropriately. 2 Psychological distress is common. Support and understanding are important aspects of management. The commonly affected systems and associated clinical manifestations are shown in Table 8.6. Table 8.6 Organs commonly affected by diabetic autonomic neuropathy and the resultant clinical features. Affected organ Main clinical features Consequences Gastrointestinal tract gastroparesis Decreased peristalsis Abdominal distension and feeling of fullness Early satiety Postprandial nausea Vomiting undigested food Diarrhoea especially at night Depression Weight loss Erratic blood glucose control Stomach may not be empty even after fasting for example for procedures

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Long-Term Complications of Diabetes 239 Urinary tract Distended bladder Urine overflow Feeling of incomplete bladder emptying Stress incontinence Nocturia Vaginal mucous membrane excoriation in women Silent urinary tract infection Falls in elderly people Sleep disturbance Uncomfortable sexual intercourse Table 8.6 Continued. Affected organ Main clinical features Consequences Genitals Erectile dysfunction in men. Indeterminate if any effect in women Possibly vaginal dryness in older women Psychological sequelae including depression Negative impact on sexual health Cardiovascular system Blood pressure: Postural hypotension Loss of diurnal variation Dizziness when standing Resting tachycardia Reduced sympathetic tone Decreased beta-adrenergic responsiveness Silent myocardial infarction Stroke Falls Lower limbs Reduced sweating Reduced blood flow Reduced pain Redness Defective thermoregulation Foot ulcers and infection Sleep disturbance Brain Cognitive impairment Reduced self-care ability General Excessive sweating especially of the upper body resembling a hot flush and sometimes mistaken for hypoglycaemia Slow pupillary reaction Heat intolerance Trauma Depression Note: Many of these conditions predispose elderly people to falls see Chapter 12. Diagnosis and management Special tests are required to make a definitive diagnosis. The particular test depends on which organs are being tested for example gastric emptying times for the GIT Valsalva manoeuvre for the cardiovascular system and voiding cystourethrogram to determine the effects on the bladder. In many cases specific treatment is commenced on the basis of the clinical history and assessment. Management consists of: 1 Adopting preventative strategies early by: • improving blood glucose control and lipid levels • treating hypertension • regular complication screening • adequate self-care • being aware that antioxidants may have a role in preventing oxidative tissue damage and pre- and probiotics may have a role in maintaining normal gut flora and reducing inflammation although evidence specify to gastric autonomic neuropathy is limited Chapter 1. 2 Direction when present. Treatment is often by trial and error and is aimed at alleviating the unpleasant symptoms. Preventative measures should be continued. Treatment for specific autonomic neuropathic conditions consists of:

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240 Care of People with Diabetes a Gastrointestinal tract • Dietary management depends on the degree of malnutrition present and the symptoms. Frequent small light easily digested or fluid meals that are low in fat and fibre and contain a consistent proportion of carbohydrate place less burden on the gastrointestinal tract and reduce glucose variability Sadiya 2012. Large meals and fat delay gastric emptying and exacerbates the already slow gastric emptying time. It is imperative to ensure essential protein vitamins and minerals are consumed thus people with severe malnutrition might need supplements and/or enteral feeding Chapter 4. Consuming a liquid diet when the symptoms are worse sometimes helps. • Manage distress and depression. • GLM medicine dose usually need to be adjusted frequently thus a basal bolous or insulin pump provides the greatest flexibility • Stimulants such as caffeine alcohol and tobacco should be avoided. Likewise chewing gum increases air swallowing and contributes to bloating and foods that contain mint chocolate fat and caffeine lower oesophagal sphincter pressure. • Medications such as Metoclopramide and Cisapride may give some relief but should not be used continuously. • Antibiotics such as Tetracycline or Trimethoprim may be required to treat bacterial overgrowth that occurs as a consequence of gastric stasis. • Cholestyramine can be used to chelate bile salts which immobilise the gut. • Treating constipation nausea and vomiting as they occur. • Elevating the head of the bed to use gravity to assist gastric emptying. • Anecdotally gentle abdominal massage and compresses help reduce spasm and relieve bloating and constipation. • Jejunostomy is a last resort. b Cardiovascular system • Support garments such as stockings or a body stocking to support venous return and relieve stress on the heart. They should be put on while the person is lying down. • Managing postural hypotension – finding a balance between increasing the pressure on standing and preventing hypertension when lying. Fludrocortisone or Midodrine can be used. Medications should be reviewed to exclude drugs that precipitate postural hypotension. c Genitourinary • Urinary catheterisation and self-catheterisation. Sometimes parasympathomimetic drugs are also used. • Managing erectile dysfunction with drugs such as Sildenafil intracavernosal injections or mechanical and implanted devices and counselling see Chapter 17. d General measures • Adjusting insulin or OHAs and diet to cater for the erratic blood glucose profile. • Topical glycopyrrolate to alleviate gustatory sweating. • Stopping smoking. • Careful explanations about autonomic neuropathy and counselling to address the psychological consequences and treatment options. • Encouraging activity. Nursing care Nursing care is palliative and supportive in nature. Providing a safe environment and reducing the risk of falls is essential especially in older people to prevent trauma for example fractures. This could involve ensuring the home environment is safe before discharging patients. Nurses can have a role in the early identification of autonomic neuropathy by having a level of suspicion and taking a careful history. Important nursing responsibilities are:

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Long-Term Complications of Diabetes 241 1 The prevention early recognition and management of hypoglycaemia. 2 Taking care when moving the patient from a lying to a sitting position and from sitting to standing. Give them time for the blood pressure to adjust. Ensure their footwear will not contribute to the risk of falling. 3 Providing adequate foot care and appropriate advice to minimise the risk of ulcers including advice about footwear. 4 Arranging counselling if indicated. 5 Using aseptic technique. 6 Being alert to the possibility of silent pathology – myocardial infarction urinary tract infection. 7 Encouraging people to remain physically active within their individual limits. Physical activity aids many body systems and improves mental outlook. Clinical observation Gentle abdominal massage and warm compresses can help alleviate the discomfort of gastroparesis. Aromatherapy essential oils can be added to the compress. The abdomen is a vulnerable part of the body and this needs to be taken into consideration when offering an abdominal massage see Chapter 19. References Pathophysiology of diabetes complications Cardiovascular disease and diabetes American Diabetes Association ADA 2012 Standards of Medical care in diabetes 2012. Diabetes Care 35 Suppl 1 11–63. American Diabetes Association ADA 2013 Standards of Medical Care in Diabetes Diabetes Care + html accessed February 2013. Australian Diabetes Society ADS 2102 Guidelines for routine glucose control in hospital. ADS Canberra. AIHW 2011 Cardiovascular disease: Australian facts. AIHW Canberra. ACCORD Trial Study Group 2008 Intensive glucose control group of ACCORD Trial halted for excess deaths. National Heart Lung and Blood Institute. February 2008. ACCORD Study Group 2011 Long term effects of intensive glucose lowering on cardiovascular outcomes. New England Journal of Medicine 364 11–63. Alamowitch S. Eliasziw M. Barnett H. 2005 The risk and benefit of endarterectomy in women with symptomatic internal carotid artery disease. Stroke 36 27–31. Australian Institute Health and Welfare AIHW 2007 Medicines for Cardiovascular Health. AIHW Cardiovascular Series No. 27. AIHW Canberra. Australian Medicines Handbook 2006 Australian Medicines Handbook PTY Ltd Adelaide. Barenholtz H. Kohlhaas H. 2006 Considerations for supplementing with coenzyme Q10 during satin therapy. Annals of Pharmacotherapy 40 290–294. Bayliss E Edwards A Steiner J Main D. 2008 Processes of care desired by elderly patients with multimorbidities Family Practice 25 4 287–293. Boden-Albala B. 2008 Daytime sleepiness is an independent risk factor for stroke. Proceedings of the American Stroke Association International Stroke Conference. Abstract 94. New Orleans. Bohm M. 2008 Treating to protect: Current cardiovascular treatment approaches and remaining needs. Medscape Journal Medicine 10 Suppl. 3 1–13. Brownlee M. 2000 Mechanisms of Hyperglycaemic damage in diabetes in Atlas of Diabetes ed. R. Kahn Science Press London. Bruckert E. Hansel B. 2007 HDL-c is a powerful lipid predictor of cardiovascular disease. International Journal of Clinical Practice 61 11 1905–1913. Bunker S. Colquhoun D. Esler M. et al. 2003 ‘Stress’ and coronary heart disease: Psychosocial risk factors. Medical Journal of Australia 178 271–276. Chen Z. 2008 High BMI linked with stroke mortality in obese overweight men. Stroke Online January 31. accessed February 2008. Chiu C. Hubbard I. Armstrong J. 2006 Dietary glycaemic index and carbohydrate in relation to early age-related macular degeneration. American Journal of Nutrition 63 880–886. Coleman R. Stevens R. Retnakaran R. Holman R. 2007 Framingham SCORE and DECODE risk equations do not provide reliable cardiovascular risk estimates in type 2 diabetes. Diabetes Care 30 1292–1293. Cormack T. Grant B. Macdonald M. Steel J. Campbell I. 2001 Incidence of blindness due to diabetic eye disease in Fife 1990–9. British Journal of Ophthalmology 85 3 354–356.

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242 Care of People with Diabetes Dantas P. Fortes B. Catelli de Carvalho H. 2012 Vascular disease in diabetic women: Why do they miss the female protection Experimental Diabetes Research DOI: 10.1155/2012/570598 accessed September 2012. Davidson P. Mitchell J. DiGiacomo M. et al. 2011 Cardiovascular disease in women: Implications for improving cardiovascular health outcomes. Collegian 19 5–13. Donahoe S. Stewart G. McCabe C. et al. 2007 Diabetes mortality following acute coronary syndromes. Journal American Medical Association 298 7 765–775. Du X. Edelstein D. Rossetti L. 2000 Hyperglycaemia induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. Proceedings of the National Academy of Science USA 97 1222–1226. Elias P. Elias M. D’sgostino R. et al. 1997 NIDDM and blood pressure as risk factors for poor cognitive performance. The Framingham Study. 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Alford F. 2003 Metabolic and cardiac outcomes after acute myocardial infarction. Journal of Diabetes Nursing 7 6 208–212. Hansel B Giral P Nobecourt E. 2004. Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. Journal Clinical Endocrinology and Metabolism. 89 10 4963–4971. Hansson L. Zanchetti A. Carruthers S. et al. 1998 Effects of intensive blood pressure lowering and low dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment HOT randomised trial. Lancet 351 9118 1755–1762. Haussler B. Fischer G. Meyer S. Sturm D. 2007 Risk assessment in diabetes management: How do general practitioners estimate risks due to diabetes Quality and Safety in Health Care 16 208–212. Hotta N. Toyota T. 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Rodnbough R. 2004 Effect of oestrogen plus progestin on the incidence of diabetes in postmenopausal women: Results of the women’s health initiative hormone trial. Diabetologia 47 71175–1187. Middleton S. Ward J. Grimshaw M. et al. 2011 Implementation of evidence-based treatment protocols to manage fever hyperglycaemia and swallowing dysfunction in acute stroke QASC: A cluster randomized trial. The Lancet DOI: 10.1016/s0140-67361151485-2 accessed June 2012. Moser D. Kimble L. Alberts M. 2007. Reducing delay in seeking treatment by patients with acute coronary syndrome and stroke: a scientific statement from the American Heart Association Council on Cardiovascular Nursing and Stroke Council. Journal of Cardiovascular Nursing. 22 326–343. Mozaffarian D. 2007 Acute myocardial infarction: A prediabetes risk equivalent The Lancet 25 667–675. Mulnier H. 2012 Macrovascular disease and diabetes. Journal of Diabetes Nursing 16 8 307–313. Nakao N. Yoshimura A. Morita H. et al. 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Long-Term Complications of Diabetes 243 National Institute of Health and Clinical Excellence NICE 2008 Nice clinical guideline 66 The management of type 2 diabetes London NICE Nagel G. Peter R. Braig S. et al. 2008 The impact of education on risk factors and the occurrence of multimorbidity in the EPIC-Heidelberg cohort. BMC Public Health 8 384. DOI: 10.1186/1471-2458-8-384 Ning F. Tumilehto J. Pyorala K. Sodeberg S. 2011 Cardiovascular disease mortality in Europeans in relation to fasting and 3-h plasma glucose. Diabetes Care 33 2211–2216. Nishikawa T. Edelstein D. Du X. 2000 Normalising superoxide production blocks three pathways of hyperglycaemic damage. Nature 404 787–790. Pfisterer M. 2004 In elderly patients with chronic angina drugs offer outcomes equal to invasive treatment. Circulation on line accessed August 2007. Picconi F. Flaviani A. Malandruccio I. Giordani L. Frontoni S. 2012 Impact of glycaemic variability on cardiovascular outcomes beyond glycated haemoglobin. 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Journal of Human Hypertension 21 297–306. Sanchis J. 2007 Risk score useful in assessing chest pain with normal troponin levels. American Journal of Cardiology 99 797–801. Singer J. Palmas W. Teresi J. et al. 2012 Adiponectin and all-cause mortality in elderly people with type 2 diabetes. Diabetes Care DOI: 10.2337/dc11-2215 accessed August 2012. SIGN 2010 Management of Diabetes: A National Clinical Guideline. SIGN Edinburgh. Taylor A. Price K. Gill T. et al. 2010 Morbidity – not just an older person’s issue. Results from an Australian biomedical study. BMC Public Health 10 718. United Kingdom Prospective Study UKPDS Group 1998 Effect of intensive blood glucose control with metformin on complications in overweight patients with type 2 diabetes. Lancet 352 854–865. Wilmot E. Edwardson C. Achana F. et al. 2012 Sedentary time in adults and the association with diabetes cardiovascular disease and death: A systematic review and meta-analysis. Diabetologia DOI: 10.1007/s00125-012-2677-z accessed October 2012. Vale M. Jelinek M. Best J. et al. 2003 Coaching patients on achieving cardiovascular health COACH: A multicenter randomized trial in patients with coronary heart disease. Archives of Internal Medicine 163 2775–2783. Verdecchia P. Angeli F. Mazzotta G. Carofe M. 2012 Ambulatory blood pressure monitoring: Day-night dip and early-morning surge in blood pressure in hypertension. Hypertension 60 34–42. Wen Y. Hung L. Te L. et al. 2012 Variability in hemoglobin A1c predicts all-cause mortality in patients with type 2 diabetes. Journal of Diabetes and its Complications DOI: 1016/jdacomp.2012.03.029 accessed August 2012. Wells-Knecht K. Zyzak D. Litchfield J. 1995 Mechanism of autoxidative glycosylation: Identification of glyoxal and arabinose as intermediates in the autooxidative modification of proteins by glucose. Biochemistry 34 3702–3709. Williams J. Chimowitz M. Cotsonis G. Lunn M. Waddy S. 2007 WASID Investigators. Gender differences in outcomes among patients with symptomatic intracranial arterial stenosis. Stroke 38 2055–2062. WHO 2003 Cardiovascular Diseases CV fact sheet 317 updated March 2013 Geneva WHO www. accessed January 2013. Young D. Furler J. Vale M. et al. 2007 Patient engagement and coaching for health: The PEACH study – A cluster randomised controlled trial using the telephone to coach people with type 2 diabetes to engage with their GPs to improve diabetes care. BMC Family Practice 8 20 8–13. Zhang Y. Hu G. Yuan Z. Chen L. 2012 Glycosylated haemoglobin in relation to cardiovascular outcomes and death in patients with type 2 diabetes: A systematic review and meta-analysis. PloS One 2012 7 8: e42551. Zannad F. 2008 Cardiovascular high risk patients – Treat to protect but whom Medscape Journal of Medicine 10 Suppl. 2 1–11. Diabetes and eye disease Antonetti D. Barber A. Bronson S. et al. 2006 Diabetic retinopathy: Seeing beyond glucose-induced microvascular disease. 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244 Care of People with Diabetes Gupta A. Gupta V. Thapar S. Bhansali A. 2004 Lipid-lowering drug atorastatin as an adjunct in the management of diabetic macular oedema. American Journal of Ophthalmology 137 4 675–682. Khan J. Shahid H. Thurlby D. 2006 Age-related macular degeneration and sun exposure iris colour and skin sensitivity to sunlight. British Journal of Ophthalmology 90 29–32. van Leeuwen R. Boekhoorn S. Vingerling J. 2005 Dietary intake of antioxidants and risk of agerelated macular degeneration. Journal American Medical Association 294 3101–3107. Lim J. 2006 Risk factors for age-related macular degeneration. eMedicine. viewarticle/532642 1–5 accessed November 2007. Park H. Kim Y. Song S. Ahn H. 2012 Serum 15-anhydroglucitol is associated with diabetic retinopathy in type 2 diabetes. Diabetic Medicine 29 1184–1190. Ryan C. Geckle M. Orchard T. 2003 Cognitive efficiency declines over time in adults with Type 1 diabetes: Effect of micro- and macrovascular complications. Diabetologia DOI: 10.1007/soo125– 003-1128–2 940–948. Seddon J. Gensler G. Milton R. Klein M. Rifai N. 2004 Association between C-reactive protein and age-related macular degeneration. Journal American Medical Association 292 704–710. Sen K. Misra A. Kumar A. Pandey R. 2002 Simvastatin retards progression of retinopathy in diabetic patients with hypercholeserolaemia. Diabetes Research and Clinical Practice 56 1 1–11. SIGN 2010 Management of Diabetes: A National Guideline. SIGN Edinburgh. Stanway L. 2012 Multi-ability alert dogs for people with diabetes and visual impairment. Diabetes Voice 57 1 39–42. Diabetes and renal disease American Society of Nephrology ASN 2012 Kidney disease recommendations. Clinical Journal of the American Society Nephrology.…/2012/KN_2012_07_ jul.pdf - ANZDATA Registry 2000 Australian and New Zealand Dialysis Transplant Registry. Adelaide South Australia. Bosman D. Winkler A. Marsden J. MacDougall I. Watkins P. 2001 Anemia with erythropoietin deficiency occurs early in diabetic nephropathy. Diabetes Care 24 3 495–499. Briguori C. 2007 Renal insufficiency following contrast media administration trial REMEDIAL: A randomized comparison of 3 preventative strategies. Circulation 115 1211–1217. Cass A. Cunningham J. Arnold P. Snelling P. Wang Z. Hoy W. 2002 Delayed referral to a nephrologist: outcomes among patients who survive at least one year. Medical Journal of Australia 177 3 135–138. Chadban S. Lerino F. 2005 Welcome to the era of CKD and the eGFR. Medical Journal of Australia 183 3 117–118. Chan M. 2001 Nutritional management in progressive renal failure. Current Therapeutics 42 7 23–27. Chan M. 2008 Nutrition diabetes and chronic kidney disease. Diabetes Management Journal 25 6 – 7. Chan M. 2012 Nutrition diabetes and chronic kidney disease. Australian Diabetes Educator 15 3 18–23. Chobanian A. Bakris G. Black H. 2003 National Heart Lung and Blood Institute Joint National Committee on Prevention Detection Evaluation and Treatment of High Blood Pressure National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention Detection Evaluation and Treatment of High Blood Pressure: the JNC 7 report. Journal of the American Medical Association 289 2560–2572. Choudhury D. Luna-Salazar C. 2008 Preventive health care in chronic kidney disease and end stage renal failure. Clinical Practice Nephrology 4 4 3–16. Churchill D. 1996 Results and limitations of peritoneal dialysis in Replacement of Renal Function by Dialysis eds C. Jacobs C. Kjellstrand K. Koch F. Winchester. Kluwer Academic Publishers Boston. Culleton B. 2007 Frequent nocturnal hemodialysis may have better outcomes than conventional hemodialysis. Journal of the American Medical Association 298 1291–1299. DCCT Diabetes Control and Complications Trial Research Group 1993 Effects of intensive insulin therapy on the development and progression of long-term complications in IDDM. New England Journal of Medicine 329 977–986. Department of Health 2001 Diabetes National Service Framework: Standards for Diabetes Services. Department of Health London. Duncan H. Pittman S. Govil A. et al. 2007 Alternative medicine use in dialysis patients: Potential for good and bad. Nephrology and Clinical Practice 105 3 108–113. Dunning T. MacGinley R. Ward G. 2012 Is point of care testing for anaemia Hb and microalbumin feasible in people with type 2 diabetes attending diabetic outpatient clinics Renal Society of Australasia Journal 8 2 76–81. Ernst E. 1998 Harmless herbs A review of the recent literature. American Journal of Medicine 104 2 170–178. Giannelli S. Patel K. Windham G. Ferrucci F. Guralnik J. 2007 Magnitude of underascertainment of impaired kidney function in old normal serum creatine. Journal of the American Geriatric Society 55 6 816–823. Gilbert R. Akdeniz A. Jerums G. 1992 Semi-quantitative determination of microalbuminuria by urinary dipstick. Australian New Zealand Journal of Medicine 22 334–337. Gilbert R. Akdeniz A. Jerums G. 1997 Detection of microalbuminuria in diabetic patients by urinary dipstick. Diabetes Research in Clinical Practice 35 57–60. Gilbert R. Tsalamandris C. Allen T. Colville D. Jerums G. 1998 Early nephropathy predicts vision-threatening retinal disease in patients with Type I diabetes mellitus. Journal of the American Society of Nephrology 9 85–89. Hays R. Kallich J. Mapes D. Coons S. Carter W. 1994 Development of the kidney disease quality of life instrument KDQOL-SF. Quality of Life Research 3 329–338.

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Long-Term Complications of Diabetes 245 HOPE Heart Outcomes Prevention Evaluation Study Investigators 2000 Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: Results of the HOPE study and MICRO-HOPE substudy. Lancet 355 253–259. Howes L. 2001 Dosage alterations in the elderly: Importance of mild renal impairment. Current Therapeutics 42 7 33–35. Iliescu E. 2006 Glycaemic control often poor among hemodialysis patients. Diabetes Care 29 2247–2251. Keane W. 2001 Metabolic pathogenesis of cardiorenal disease. American Journal of Kidney Disease 38 6 1372–1375. Kerr P. 2008 Diabetic nephropathy: Who to refer and when. Diabetes Management Journal 25 4 – 5. Ko R. 1998 Adulterants in Asian patent medicines. New England Journal of Medicine 339 847. Lehto S. Ronnemaa T. Pyorala K. Laakso M. 1999 Poor glycaemic control predicts coronary heart disease events in patients with type 1 diabetes without nephropathy. Arteriosclerosis Thrombosis Vascular Biology 19 1014–1019. Levin S. Coburn J. Henderson W. Colwell J. Emanuele N. 2000 Effect of intensive glycaemic control on microalbuminuria in type 2 diabetes. Veterans Affairs Cooperative Study on Glycaemic Control and Complications in type 2 diabetes. Diabetes Care 23 910 1478– 1485. Lopes A. Elder S. Ginsberg N. et al. 2007 Lack of appetite in haemodialysis patients: Associations with patient characteristics indicators of nutritional status and outcomes in the international DOPPS. Nephrology Dialysis Transplant 22 12 3538–3546. Meschi M. Detrenis S. Musini S. Strada E. Savazzi G. 2006 Facts and fallacies concerning the prevention of contrast medium-induced nephropathy. Critical Care Medicine 34 8 2060–2068. Moustakas J. Bennett P. Nicholson J. Tranter S. 2012 The needs of older people with advanced chronic kidney disease choosing supportive care: A review. Renal Society of Australasia Journal 8 2 70–75. Myhre M. 2000 Herbal remedies nephropathies and renal disease. Nephrology Nursing Journal 27 5 473–480. National Kidney Foundation 2002 Clinical practice guidelines for nutrition in chronic renal failure. Kidney Outcome Quality Initiative American Journal of Kidney Disease 35 6 Supp. 2. Oomichi T. Emoto M. Tabata E. et al. 2007 Impact of glycemic control on survival of diabetic patients on chronic regular hemodialysis: A 7-year observational study. Diabetes Care 29 1496–1500. Oyibo S. Prichard G. Mclay L. et al. 2002 Blood glucose overestimation in diabetic patients on continuous ambulatory peritoneal dialysis for end-stage renal disease. Diabetic Medicine 19 693–696. Quellhorst E. 2002 Insulin therapy during peritoneal dialysis: Pros and cons of various forms of administration. Journal of the American Society of Nephrology 13 S92–S96. Ravid M. Savin H. Jutrin I. 1993 Long-term stabilising effect of angiotensin-converting enzyme on plasma creatinine and on proteinuria in normotensive Type II diabetic patients. Annals of Internal Medicine 118 577–581. Ritz E. 2001 Advances in nephrology: Success and lessons learnt from diabetes. Nephrology Dialysis Transplant 16 Suppl. 7 46–50. Rudnick M. Kesselheim A. Goldfarb S. 2006 Contrast-induced nephropathy: How it develops how to prevent it. Cleveland Clinic Journal of Medicine 73 1 75–87. Rutecki G. Whittier F. 1993 Intraperitoneal insulin in diabetic patients on peritoneal dialysis in Dialysis Therapy eds A. Nissenson R. Fine. Hanley Belfus Philadelphia. Schetz M. Vanhorebeck I. Wouters P. Wilmer A. van der Berghe G. 2008 Tight blood glucose control is renoprotective in critically ill patients. Journal American Society of Nephrology DOI:10.1681/asn2006101091. Terrill B. 2002 Renal Nursing: A Practical Approach. Ausmed Publications Melbourne. Wu M. Yu C. Yang C. 1997 Poor pre-dialysis glycaemic control is a predictor of mortality in Type II diabetic patients on maintenance haemodialysis. Nephrology Dialysis Transplant 12 2105–2110. Yu M. Rees-Lyles C. Bent-Shaw L. Young B. 2012 Risk factor age and sex differences in chronic kidney disease prevalence in a diabetic cohort: The Pathways Study. Nephrology 36 3 245–251. Peripheral and autonomic neuropathy Abusaisha B. Constanzi J. Boulton A. 1998 Acupuncture for treatment of chronic painful diabetic neuropathy: A long-term study. Diabetes Research Clinical Practice 39 115–121. Aly N. Weston P. 2002 Autonomic neuropathy in older people with diabetes. Journal of Diabetes Nursing 6 1 10–14. Apelqvist J. Larsson J. 2000 What is the most effective way to reduce incidence of amputation in the diabetic foot Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s75–s83. Apelqvist J. Bakker K. van Houtum W. Nabuurs-Franssen M. Schaper N. 2000 The international consensus and practical guidelines on the management and prevention of the diabetic foot. Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s84–s92. Bakker D. 2000 Hyperbaric oxygen therapy and the diabetic foot. Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s55–s58. Boulton A. 2000 The diabetic foot: A global view. Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s2–s 5. Boulton A. Jervell J. 1998 International guidelines for the management of diabetic peripheral neuropathy. Diabetic Medicine 15 6 508– 514. Boulton A. Gries F. Jervell J. 1998 Guidelines for the diagnosis and outpatient management of diabetic peripheral neuropathy. Diabetes Medicine 15 508–514. Brismar K. Johansson T. Lindström B. et al. 2007 C-Peptide replacement therapy and sensory nerve function in type 1 diabetic neuropathy Diabetes Care 30 1 71-6. Brod M. 1998 Quality of life issues in patients with diabetes and lower limb extremity ulcers: Patients and caregivers. 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246 Care of People with Diabetes DCCT 1993 The effect of intensive treatment of diabetes on the development and progression of longterm complications in insulin-dependent diabetes mellitus. New England Journal of Medicine 329 977–986. DRS 1981 Photocoagulation treatment of proliferative diabetic retinopathy: Clinical implications of DRS findings. DRS Report No. 8. Ophthalmology 88 583–600. Edmonds M. Bates M. Doxford M. Gough A. Foster A. 2000 New treatments in ulcer healing and wound infection. Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s51–s54. EDTRS 1991 Early photocoagulation for diabetic retinopathy: EDTRS Report No. 9. Ophthalmology 98 Suppl. 767–785. Foster A. Eaton C. McConville D. Edmonds M. 1994 Application of Op-cite film: A new effective treatment for painful diabetic neuropathy. Diabetic Medicine 11 768–772. Harding K. Jones V. Price P. 2000 Topical treatment: Which dressing to choose. Diabetes/ Metabolism Research and Reviews 16 Suppl. 1 s47–s50. Hemstreet B. Lapointe M. 2001 Evidence for the use of gabapentin in the treatment of diabetic peripheral neuropathy. Clinical Therapeutics 23 4 520–531. Hotta N. 2006 Epalrestat may delay progression and reduce symptoms of diabetic neuropathy. Diabetes Care 29 1538–1544. Huang E. Meigs J. Singer D. 2001 The effect of interventions to prevent cardiovascular disease in patients with Type 2 diabetes. American Medical Journal 11 8 663–642. International Diabetes Federation Consultative Section on Diabetes 2000 Diabetes Education for People who are Blind or Visually Impaired. Position Statement. International Diabetes Federation Brussells pp. 62–72. Karlson B. Herlitz J. Hjalmarson A. 1993 Prognosis of acute myocardial infarction in diabetic and non-diabetic patients. Diabetic Medicine 10 449–454. Larkins R. 1995 Aspirin: The effects are complex. Diabetic Communication 10 3 5–6. Lipsky B. Berendt A. 2000 Principles and practice of antibiotic therapy of diabetic foot infections. Diabetes/Metabolism Research and Reviews 16 Suppl. 1 s42–s46. Litchy W. Dyck P. Tesfaye S. for the MBBQ Study Group 2002 Diabetic peripheral neuropathy DPN assessed by neurological examination and composite scores is improved with LY333531 treatment. Diabetes 45 A197. Locke D. Ill G. Camileri M. 2000 Gastrointestinal symptoms among persons with diabetes in the community. Archives of Internal Medicine 160 2808–2816. Lowe J. 2002 Hypertension in diabetes. Australian Prescriber 25 1 8–10. Malmberg K. Ryden L. Efendic S. et al. 1995 Randomised trial of insulin–glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction DIGAMI study: Effects on mortality at 1 year. Journal of the American College of Cardiology 26 57–65. Papas N. Boulton A. Malik R. et al. 2013 A simple new non-invasive sweat indicator test for the diagnosis of diabetic neuropathy. Diabetic Medicine 30 525–534. Pecorara R. 1990 Pathways to diabetic limb amputation. Diabetes Care 13 5 513–530. Ponchilla S. Richardson K. Turner-Barry M. 1990 The effectiveness of six insulin measurement devices for blind persons. Journal of Visual Impairment and Blindness 84 364–370. Sadiya A. 2012 Nutritional therapy for the management of gastric paresis: A clinical review. Diabetes Metabolic Syndrome and Obesity Targets and Therapy 5 329–335. Semla T. Beizer J. Higbee M. 2002 eds. Geriatric Dosage Handbook. Hudson Ohio: Lexi-Company. Spallone V. Menzinger G. 1997 Autonomic neuropathy: Clinical and instrumental findings. Clinical Neuroscience 4 96 346–358. Standl E. Schnell O. 2000 A new look at the heart in diabetes: From ailing to failing. Diabetologia 43 1455–1469. Steinberg F. 1991 Rehabilitation after amputation. Diabetes Spectrum 4 1 5–9. Surwit R. Feinglos M. 1988 Stress and autonomic nervous system in Type 2 diabetes. A hypothesis. Diabetes Care 11 83–85. Sutton M. McGrath C. Brady L. Wood J. 2000 Diabetic foot care: Assessing the impact of foot care on the whole patient. Practical Diabetes International 17 5 365–372. Todd M. Welsh J. Key M. et al. 2008 Survey of Doppler use in lymphoedema practitioners in the UK. British Journal Community Nursing 13 4 S11–2 S14 S16–17. UKPDS Group 1998 Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with Type 2 diabetes UKPDS 33. Lancet 352 837–853. Vale M. Jelinek M. Best J. Santamaria J. 2002 Coaching patients with coronary heart disease to achieve cholesterol targets: A method to bridge the gap between evidence-based medicine and the ‘real world’ – randomized controlled trial. Journal of Clinical Epidemiology 55 245–252. Vinik A. Park T. Stansberry K. Henger P. 2000 Diabetic neuropathy. Diabetologia 43 957–973. Wegener M. Borsch G. Schaffsten J. Luerweg C. 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Chapter 9 Management During Surgical and Investigative Procedures To Cure Diabetes Permanently Click Here SURGICAL PROCEDURES Key points • Surgery induces the counter-regulatory response that can increase the blood glucose 6–8 times higher than normal in people with and without diabetes. Optimal control before during and after surgery reduces morbidity and mortality and length of stay. • Preventing hyperglycaemia reduces the risk of adverse outcomes in people with diabetes. • Morning procedures are desirable. • Insulin should never be omitted in people with Type 1 diabetes. • Complications should be stabilised before during and after surgery. • Cease oral glucose lowering medicines 24–36 hours before the procedure depending on the particular medicine and their duration of action but note some experts recommend continuing oral agents until the day of surgery if the blood glucose is high. • Ascertain whether the person is using any complementary therapies especially herbal medicines with a high risk of interacting with conventional medicines and/or causing bleeding. • An insulin-glucose infusion is the most effective way to manage hyperglycaemia in the operative period. Rationale Diabetes is associated with an increased need for surgical procedures and invasive investigations and higher morbidity than non-diabetics. Anaesthesia and surgery are associated with a complex metabolic and neuroendocrine response that involves the Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd.

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248 Care of People with Diabetes release of counter-regulatory hormones and glucagon leading to insulin resistance gluconeogenesis hyperglycaemia and neutrophil dysfunction which impairs wound healing. The stress response also occurs in people without diabetes but is more pronounced and difficult to manage in people with diabetes due to the underlying metabolic abnormalities. Advances in diabetes management surgical techniques anaesthetic medicines and intensive care medicine have significantly improved surgical outcomes for people with diabetes. Introduction People with diabetes undergo surgery for similar reasons to those without diabetes however because of the long-term complications of diabetes they are more likely to require: • cardiac procedures such as:  angioplasty or stents  bypass surgery • ulcer debridement amputations toes feet • eye surgery such as cataract removal repair retinal detachment vitrectory • carpal tunnel decompression. Surgical-induced stress results in endocrine metabolic and long-term effects that have implications for the management of people with diabetes undergoing surgery see Table 9.1. Stress induces hyperglycaemia which causes osmotic diuresis increased Table 9.1 Hormonal metabolic and long-term effects of surgery. Hormonal Metabolic Long-term effects if optimal blood glucose control is not achieved ↑ Secretion of a epinephrine norepinephrine ACTH cortisol and growth hormone ↑ secretion of insulin due to impaired beta cell responsiveness Insulin resistance Catabolic state and ↑ metabolic rate Hyperglycaemia Insulin resistance ↑ Glucose utilisation and glycogen storage ↑ Gluconeogenesis ↑ Protein catabolism and reduced amino acid and protein synthesis in skeletal muscle ↑ Lipolysis and formation of ketone bodies ↑ Storage of fatty acids in the liver Osmotic diuresis with electrolyte loss and compromised circulating volume ↑ Risk of cerebrovascular accident myocardial arrhythmias infarction electrolyte disorders ↑ Blood pressure and heart rate ↑ Peristalsis Loss of lean body mass – impaired wound healing ↑ resistance to infection Loss of adipose tissue Deficiency of essential amino acids vitamins minerals and essential fatty acids Surgical complications Longer length of stay a Norepinephrine is mostly augmented during surgery and epinephrine postoperatively. Stress stimulates glucagon secretion from the pancreatic alpha cells and together with growth hormone and cortisol potentiates the effects of norepinephrine and epinephrine. Cortisol increases gluconeogenesis. hepatic glucose output lipolysis and insulin resistance. Unless these metabolic abnormalities are controlled surgical stress increases the risk of DKA Hyperosmolar states HHS and lactic acidosis see Chapter 7 infection impaired wound

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Management During Surgical and Investigative Procedures 249 healing and cerebral ischaemia. The risk of HHS is high in procedures such as cardiac bypass surgery and has a high mortality rate Dagogo-Jack Alberti 2002. In addition anaesthesia and surgical stress as well as medicines induce gastrointestinal instability that can compound gastric autonomic neuropathy and lead to nausea vomiting and predispose the individual to dehydration and exacerbate fluid loss via osmotic diuresis and blood loss during surgery. As a result electrolyte changes particularly in potassium and magnesium increase the risk of cardiac arrhythmias ischaemic events and acute renal failure Dagogo-Jack Alberti 2002. The risk is particularly high in people with chronic hyperglycaemia HbA1c 8 existing diabetes complications older people and those who are obese all of which are associated with increased risk of interoperative and postoperative complications Dickersen 2003. Obesity is associated with functional risks in addition to the metabolic consequences of surgery that need to be considered when positioning the patient. The respiratory system is affected and functional residual capacity and expiratory reserve volume may be reduced possibly due to excess weight on the chest wall and/or displacement of the diaphragm. Severe obesity can lead to hypoventilation and obstructive sleep apnoea. These factors predispose the individual to aspiration pneumonia. Various cardiac changes increase the risk of heart failure and inadequate tissue oxygenation. In addition the risk of pressure ulcers is increased due to the weight and activity level is often compromised increasing the risk of venous stasis and emboli. The need for nutritional support may be overlooked in obese individuals and protein deprivation can develop because protein and carbohydrate are used as the main energy sources during surgery rather than fat. In addition energy expenditure is higher which impacts on wound healing Mirtallo 2008. Different types of surgery present specific risks as do the person’s age: the very young and older people are particularly at risk. The specific risks are summarised in Table 9.1. The blood glucose must be controlled to prevent DKA and HHS promote healing and reduce the risk of infection postoperatively. The target blood glucose range in the perioperative period is 5–10 mmol/L Australian Diabetes Society ADS 2012. Hyperglycaemia inhibits white cell function and increases coagulability Kirschner 1993. The magnitude of the metabolic/hormonal response depends on the severity and duration of the surgical procedure metabolic control before during and after surgery and the presence of complications such as sepsis acidosis hypotension and hypovolaemia Marks et al. 1998 ADS 2012. Significantly metabolic disturbances can be present in euglycaemic states De Child 2001. Surgery is often performed as a day procedure often without appropriate consideration of the effects of surgical and the related psychological stress on metabolic control. A multidisciplinary approach to planning is important. Children with diabetes undergoing surgical procedures Generally children with Type 1 and Type 2 diabetes needing general anaesthesia should be admitted to hospital and must receive insulin to prevent ketosis even if they are fasting and should be managed with a glucose infusion if they need to fast for more than two hours to prevent hypoglycaemia Betts et al. 2009. Blood glucose must be monitored hourly prior to and every 30 to 60 minutes during surgery to detect hypo- and hyperglycaemia. As in adults it is best to perform surgery when metabolic control is optimal and children should be first on the list if possible Betts et al. 2009. An IV insulin- glucose infusion should be commenced two hours prior to surgery. Older people with diabetes and surgical procedures The Geriatric Surgery Expert Panel of the American College of Surgeons recently released a comprehensive guideline for assessing older people prior to surgery Chow et al. 2012. The recommendations are not specific to people with diabetes but diabetesrelated information could be incorporated into the guidelines. In addition to conducting a thorough history and physical assessment the Expert Panel recommended assessing the individual’s: • Cognitive ability and capacity to understand the proposed surgery give informed consent. • Mental health: undertake a depression screen. • Risk of developing delirium postoperatively. • Alcohol tobacco and other substance use. • Functional status. • Falls history. • Frailty Index score.

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250 Care of People with Diabetes • Nutritional status. • Medicine regimen to determine whether the regimen may need to be adjusted and to assess the level of polypharmacy. Note information about insulin and other GLMs in this chapter and adherence to their medicine regimen. • Expectations of the surgery. • Social and family support. • Undertake appropriate investigations. These include renal function tests haemoglobin and serum albumin and in some cases white cell cont platelet count coagulation studies electrolytes and blood glucose and a urinalysis to detect UTI. Tests of physical and cognitive function are discussed in Chapter 12. Interestingly the guidelines do not mention CAM use but as indicated people with diabetes use CAM and many herbal medicines interact with conventional medicines and increase the risk of adverse events. Aims of management 1 To identify underlying problems that could compromise surgery and recovery by undertaking comprehensive presurgical assessment Dhatariya et al. 2012. 2 To achieve normal metabolism by supplying sufficient insulin to counterbalance the increase in stress hormones during fasting surgery and postoperatively and avoid the need for prolonged fasting. 3 To normalise metabolic control using regimens that minimise the possibility of errors and have the fewest adverse outcomes: target blood glucose range. 5–10 mmol/L and is best achieved with an insulin-glucose infusion ADS 2012. 4 To supply adequate carbohydrate to prevent catabolism hypoglycaemia and ketosis. 5 To ensure that the patient undergoes surgery in the best possible physical condition. 6 To prevent: • hypoglycaemia children 5 years are prone to hypoglycaemia during anaesthesia and surgery Kirschner 1993 • hyperglycaemia predisposing the patient to dehydration electrolyte imbalance ketoacidosis and hyperosmolar states • complications of surgery • electrolyte imbalance • worsening of pre-existing diabetic complications • infection. 7 To avoid undue psychological stress. Preoperative nursing care Good preoperative nursing care is important for both major and minor procedures. Preadmission clinics have an important role in identifying and managing preventable surgical risks. Sometimes people need to be admitted 2–3 days before major surgery to stabilise blood glucose levels and manage complications see Table 9.2. Many procedures only require a day admission. In all cases careful explanation about what is required and written instructions that are at a suitable language level and are culturally relevant are vital. The individual’s blood glucose profile needs to be reviewed and their diabetes regimen may need to be adjusted prior to surgery to achieve good metabolic control. Erratic control could indicate the presence of infection that should be treated prior to surgery. Alternatively it could indicate brittle diabetes that might require investigation because of the risk of hypoglycaemia and delayed gastric emptying depending on the underlying cause Chapter 10. If possible schedule for a morning procedure to avoid the need for prolonged fasting and counter-regulatory hormone release that leads to hyperglycaemia. Nursing actions 1 Confirm time and date of the operation and inform the patient.

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Management During Surgical and Investigative Procedures 251 2 Explain the procedure and postoperative care to the patient and/or family members if appropriate for example a child. Those patients on controlled GLMs may require insulin during surgery and immediately post-operatively. They should be aware of this possibility. Insulin during the operative period does not mean that diet- or tablet-controlled patients will remain on insulin when they recover from the procedure. People controlled by diet and exercise with good metabolic control HbA1c 6.5 may not require an IV insulin infusion for minor procedures but 1–2 hourly blood glucose monitoring is necessary ADS 2012. Diet-controlled people who become hyperglycaemic may require supplemental insulin peri- and/or postoperatively. If control is suboptimal and for procedures longer than one hour an IV insulin/dextrose infusion is advisable Dagogo-Jack Alberti 2002 Kwon et al. 2003. In fact Kwon et al. 2003 suggested ‘Perioperative glucose evaluation and insulin administration in patients with hyperglycaemia are important quality targets.’ It should be noted that suboptimal control is common in diet-treated individuals. 3 Ensure all documentation is completed: • consent form • medication chart • monitoring guidelines • chest X-ray and other X-rays • scans MRI magnetic resonance imaging • ECG. 4 GLMs: Sulphonylureas Metformin Repaglinide Acarbose TZDs and the incretins can be continued until the day of surgery to prevent preoperative hyperglycaemia ADS 2012. Chlorpropamide should be given 36 hours preoperatively because it is Table 9.2 Common complications of diabetes that can affect surgery and postoperative recovery. Many of these conditions may be documented in the person’s medical record and they may undergo regular complication assessment but health status can change rapidly especially older people. Therefore the current complication status should be assessed prior to surgery. Hyperglycaemia must be controlled. Complication Possible consequences Preoperative evaluation Cardiovascular Hypertension Ischaemic heart disease Cardiomyopathy Myocardial infarction which can be ‘silent’ and in the presence of autonomic neuropathy cause sudden tachycardia bradycardia and/ or postural hypotension Cerebrovascular disease Increased resting heart rate is associated with increased risk of death in older people Daytime sleepiness is associated with 4.5-fold increased risk of stroke and other vascular events Careful history and examination ECG Manage existing conditions such as heart failure Assess for silent cardiac disease autonomic neuropathy indicators include: shortness of breath palpitations ankle oedema tiredness and atypical chest pain Assess resting heart rate Ask about daytime sleepiness or assess formally for example using the Epworth Sleepiness Scale ESS Neuropathy Autonomic Peripheral Cardiac as above Inability to maintain body temperature during anaesthesia Pressure areas on feet and ulceration Foot infection Falls postoperatively Lying and standing blood pressure abnormal if decrease 30 mmHg Heart rate response on deep breathing abnormal if increase 10 beats/min Foot assessment assess for active and occult infection and signs of neuropathy Renal Nephropathy which may affect medication excretion Urinary tract infection UTI which may be silent and predispose to sepsis Acute renal failure and the need for dialysis UTI if catheterisation is needed Urine culture to detect UTI which should be treated with the relevant antibiotics Microalbuminuria and creatinine clearance eGFR Blood electrolytes correct potassium 5 mmol/L before surgery

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252 Care of People with Diabetes Respiratory Airway Obese people and smokers are prone to chest infections Obesity may be associated with reduced respiratory reserve and displacement of the diaphragm Reduced tissue oxygenation Soft tissue ligament and joint thickening that might involve the neck making it difficult to extend the neck and intubate and predispose the individual to neck injury and post operative pain Counsel to stop smoking Chest physiotherapy Chest X-ray Blood gases Nebulised oxygen pre- and postoperatively if indicated See test for musculoskeletal disease see page 341–342 Take extra care of the neck Gastrointestinal Autonomic neuropathy leading to gastric stasis delayed gastric emptying gastric reflux regurgitation and aspiration on anaesthesia induction Ileus May need to modify nutritional support if required postoperatively and given enterally Assess history of heartburn or reflux and whether the person sleeps in an upright position A H 2 antagonist and metclopramide might be indicated preoperatively Erratic food absorption can affect blood glucose levels Eyes Cataracts glaucoma and retinopathy can be exacerbated by sudden rise in blood pressure Assess retinopathy stage Neutrophil dysfunction Increased risk of infection Inability to mount an appropriate response to infection Check for possible foci of infection: including feet teeth and gums UTI Ensure optimal blood glucose control Optimise vascular function Table 9.2 Continued. Complication Possible consequences Preoperative evaluation Polypharmacy Risk of medicine interactions with anaesthetic agents and postoperative medicines Risk of lactic acidosis with Metformin Some medicines increase the risk of hyperglycaemia some hypoglycaemia Medicine review Ask about complementary medicines Give the person clear concise written instructions about how to manage their medicines preoperatively and postoperatively on discharge Musculoskeletal Difficulties with intubation and tube placement Falls risk Assess for example prayer sign Dupuytren’s contracture trigger finger Foot abnormality including Charcot’s foot Obesity Increased systemic vascular resistance leading to reduced tissue oxygenation and increased risk of lactic acidosis in people on Metformin especially if renal function is compromised and those with surgical wound infections Sleep apnoea and associated daytime sleepiness with associated risk of cardiovascular events Difficulty intubating the person Assumption that the person is well nourished when in fact nutritional deficiencies especially protein are common High prevalence of hypertriglyceridaemia Cardiovascular and respiratory effects which affect postoperative nutrition support if it is required Non-alcoholic fatty liver Risk of pressure ulcers Assess nutritional status Assess cardiovascular and respiratory status. Ask about daytime sleepiness or assess formally for example using the ESS Skin condition long acting however Chlorpropamide is rarely used nowadays and is no longer available in some countries e.g. Australia because of the significant hypoglycaemia risk. Metformin is

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Management During Surgical and Investigative Procedures 253 traditionally ceased 24 hours preoperatively but there is little evidence that ceasing Metformin or continuing Metformin in the perioperatic period increases the risk of hyperglycaemia. Metformin is associated with a risk of lactic acidosis although the risk is low however surgical procedures hypotension secondary to blood loss myocardial ischaemia sepsis and anaestheic agents can contribute to the development of lactic acidosis especially in people with renal impairment Chapter 7. Thus a careful clinical assessment of the risks and benefits of ceasing/continuing Metformin in individual patients is essential Insulin therapy must be initiated before the procedure in people with Type 1 diabetes. 5 Encourage patients who smoke to stop. 6 Assess: • Metabolic status: blood glucose control ketones in blood and urine hydration status nutritional status presence of anaemia diabetic symptoms. • Educational level and understanding of diabetes. • Family support available postoperatively. • Any known allergies or medicine reactions which should include asking about complementary therapies particularly herbal medicines because some herbs predispose the person to haemorrhage and/or interact with anaesthetic agents and should be stopped at least 7 days prior to surgery see Chapter 19. • Presence of diabetic complications and other comorbidities for example renal hepatic cardiac disease ECG for people 50 years to detect the risk of silent infarction is performed in some units presence of neuropathy. Patients with autonomic neuropathy pose special problems during anesthesia: gastroparesis delays gastric emptying and the stomach can be full despite fasting and increases the possibility of regurgitation and inhalation of vomitus or the vasoconstrictive response to reduced cardiac output may be absent and they may not recognise hypoglycaemia. • Current medication regimen. • Presence of infection check feet and be aware of silent infection such as UTI. • Self-care potential and available home support. Note: Complications should be managed before the operation where possible see Table 9.2. Major procedures Major surgery refers to procedures requiring anaesthesia and lasting longer than one hour Dagogo-Jack Alberti 2002. Day of the operation Premedication and routine preparation for the scheduled operative procedure should be performed according to the treatment sheet and standard protocols. Where insulin is required for example Type 1 diabetes major surgery and poor control an IV insulin infusion is the preferred method of delivering the insulin. The insulin dose should be balanced with adequate calories to prevent starvation ketosis for example saline/dextrose delivered at a rate that matches the insulin dose Alberti Gill 1997 see Chapter 5. Fluid replacement should be adequate to maintain intravascular volume normal saline/dextrose in water is the preferred solution for this purpose. Preoperative hyperglycaemia especially if polyuria is present can cause significant fluid deficits and intracellular dehydration. Clinical signs of dehydration are: • Thirst and a dry mouth: water loss 5 of body weight. • Capillary refill 2 seconds normal 2 seconds reduced skin turgor sunken eyes reduced urine output orthostatic hypotension fainting on standing low CVP/JVP: water loss 5–10 of body weight. • Unconscious or shock: water loss 10 of body weight French 2000. Morning procedure

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254 Care of People with Diabetes 1 Ensure oral medications were ceased on the operative day or earlier in specific circumstances. 2 Fast from 12 midnight. 3 Ascertain insulin regimen: commence insulin infusion. 4 Monitor blood glucose 1–2-hourly. If the individual an insulin pump they should continue their usual basal rate Joslin Diabetes Centre 2009. Afternoon procedure 1 Fast after an early light breakfast. 2 Ensure oral medications are ceased. 3 Ascertain insulin dose usually 1/2 to 1/3 of usual dose best given after IV dextrose has been commenced. 4 It is preferable for IV therapy to be commenced in the ward to: • prevent hyperglycaemia and dehydration • reduce the risk of hypoglycaemia. This will depend on the surgical and anaesthetic and usual hospital procedure. Some anaesthetists prefer to commence the infusion in theatre. It is preferable to insert the IV line in theatre in children unless blood glucose is 4 mmol/L Werther 1994. 5 Monitor blood glucose. Practice points • Sliding insulin scales are NOT appropriate to manage blood glucose postoperatively if they are used as the only method of managing uses blood glucose because it can lead to inadequate/inappropriate insulin administration and wide swing in the blood glucose levels. • Supplemental insulin doses given in addition to the individual’s medicine regimen is appropriate. Supplemental insulin is always short- or rapid-acting insulin and given before meals in addition to the insulin/GLM dose prescribed at that time. • A daily review of the individual’s blood glucose pattern and insulin requirements is essential to enable insulin doses to be calculated for the following day ADS 2012. • Persistent hyperglycaemia could indicate underlying infection or surgical or metabolic complications and severe pain. The anaesthetist is usually responsible for the intraoperative blood glucose monitoring. Interoperative blood glucose monitoring is essential to detect hypo-and hyperglycaemia. The anaesthetic masks the usual signs of hypoglycaemia. Precautions are needed to avoid regurgitation and aspiration cardiac arrhythmias and postural hypotension in young children and patients with autonomic neuropathy. Hypoglycaemia increases the risk of seizures. In all cases careful explanation about what to expect and how to prepare for the procedure to the patient and their family/carers is essential. The National Health Service in the UK released guidelines for managing people with diabetes in the perioperative period in 2012 Dhatariya et al. 2012. The guidelines describe seven stages of the surgical journey including referrals from primary care the surgical outpatient department preoperative assessment hospital admission surgery postoperative care and discharge. The guidelines highlight the value of insulin infusions and blood glucose monitoring during the operative process as well as the importance of patient education. The guidelines raise a number of areas of controversy such as whether high preoperative HbA1c is associated with worse outcomes using oral GLMS in the perioperative period and whether Metformin is associated with adverse events when radio contrast media are needed for investigative purposes. The guidelines highlight two key points: 1 Managing elective surgery in adults with diabetes should involve minimal fasting time e.g. only one missed meal and suggest that modifying the individual’s usual medicine regimen is preferable to intravenous insulin infusions. However this particular recommendation is not consistent with other experts who recommend insulin infusions during surgery. 2 A poor glycaemic control leads to worse outcomes and more adverse events and should be addressed before surgery. Postoperative nursing responsibilities

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Management During Surgical and Investigative Procedures 255 Immediate care 1 Monitor and record vital signs. 2 Monitor blood glucose and ketones initially 2-hourly. 3 Observe dressings for signs of haemorrhage or excess discharge. 4 Ensure drain tubes are patent and draining. 5 Maintain an accurate fluid balance. Document all information relating to input and output especially: Input Output IV fluid Drainage from wound Oral Vomitus EN and TPN Diarrhoea Urine 6 Maintain care of IV insulin infusion. 7 Ensure vomiting and pain are controlled. 8 Ensure psychological needs are addressed for example change in body image. 9 Ensure referral to appropriate allied health professional for example physiotherapist. 10 Insulin therapy is continued for people on oral GLMs until they are eating a normal diet and blood glucose levels are stabilised. Plans for ceasing the insulin infusion and commencing GLM should be in place and usually commenced two hours before the infusion is stopped Joslin Diabetes Centre 2009. 11 Provide pressure care including high-risk neuropathic feet. Ongoing care 1 Document all data accurately on the appropriate charts. 2 Prevent complications: • infection – aseptic dressing technique including IV sites • venous thrombosis – anti-embolic stockings physiotherapy early ambulation anticoagulants • hypo/hyperglycaemia • pressure ulcers. 3 Diabetes education instruct patient and their family/carers in wound care and medication management. 4 Rehabilitation. Antibiotics heparin and other medicines should be administered according to individual patient requirements and medical orders. Clinical observation People sometimes complain of a sore throat for 24 hours after a general anaesthetic. They need to be reassured that this is normal and resolves spontaneously but advised to seek medical advice if it persists. Minor procedures Minor surgery may be performed on an outpatient basis. The metabolic risks are still a consideration if the person is expected to fast for the procedure. Ensure the procedure is fully explained to the patient at the time the appointment is made. Give written instructions about how to manage insulin oral agents and other medications. Preoperative care is the same as for major surgery on the day of operation as regards: • managing diabetes medicines • complication screening and managing complications when they are present • morning procedure is preferred.

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256 Care of People with Diabetes Guidelines for informing patients about what they should do prior to surgical procedures Examples of instructions for people undergoing outpatient procedures can be found in Example Instruction Sheets 2 a and b see pages 298 and 299. Note: These are examples only and protocols in the nurse’s place of employment should be followed. Adjusting medications for investigations and day procedures is becoming more complex as the range of available insulin oral agents and other medicines increase and multiple insulin injections insulin pumps and combining insulin and oral agents is common practice. It is important to consider the individual’s blood glucose pattern the medication regimen they are on and the type of procedure they are having when advising them about preoperative medication self-care. Where people are on basal bolus regimes and scheduled for a morning procedure the bedtime insulin dose may need to be reduced and the morning dose omitted. If the procedure is scheduled for the afternoon the morning dose may be given and the lunchtime dose omitted. When people are on a combination of insulin and oral GLMs the oral GLMs are usually withheld on the day of the procedure and the morning dose of insulin may be withheld for morning procedures. A reduced dose of insulin will usually be given if the procedure is scheduled for the afternoon. Practice point Advice about medications should also include information about medications and complementary therapies the person may be taking besides insulin and oral glucose-lowering medicines. Morning procedure 1 Insulin may or may not be withheld in the morning on the day of the procedure depending on the type of diabetes and blood glucose range. 2 Test blood glucose and ketones if Type 1 before coming to hospital. 3 Fast from 12 midnight. 4 Some hospitals ask the individual to bring their insulin to hospital. 5 Advise the patient to have someone available to drive him or her home after the procedure. 6 Explain before discharge: a the risk of hypoglycaemia if not eating b what to take for pain relief c when to recommence OHAs/insulin d what and when to eat e any specific care for example wound dressings or care of a biopsy site. Afternoon procedure 7 Light breakfast e.g. tea and toast. 8 Fast after the breakfast. It may be necessary to explain what ‘fasting’ means. 9 Test blood glucose and ketones in Type 1 before coming to hospital. 10 Give insulin dose according to blood glucose test as ordered by the doctor. 11 Explain before discharge: a the risk of hypoglycaemia if not eating b what to take for pain relief c when to recommence OHAs/insulin d what and when to eat e any specific care for example wound dressings or care of a biopsy site. In both cases:

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Management During Surgical and Investigative Procedures 257 i Test blood glucose at the end of the procedure and before discharge and administer OHA or insulin dose. ii Ensure the patient has appropriate follow-up appointments with doctors and other relevant health professionals for example diabetes educator and dietitian. a ensure the patient has someone to accompany them home b allay concerns about the procedure c provide appropriate care according to the medical orders d inspect all wounds before discharge e it is not advisable to drive operate machinery or drink alcohol until the following day. Clinical observations It is important to ensure the patient and their family/carers understand what is meant by ‘fasting’ and ‘light breakfast’. People have stated that they will ‘come as fast as I can but I can only move slowly because of my hips’. Insulin pump therapy in patients undergoing surgery Insulin pumps or continuous subcutaneous insulin infusion CSII are becoming more common. The managing diabetes team in consultation with the patient the anaesthetist and surgical team should determine the best way to manage the person’s insulin needs during surgery. The patient must consent to continuing pump therapy in surgery. If the person does continue pump therapy during surgery a clearly visible identification tag should state the person is wearing a pump. The anaesthetist must have access to the pump during surgery and know how it operates and how to turn it off or disconnect it if necessary for example in persistent hypoglycaemia. Once euglycaemia is restored the pump therapy can be recommenced at a lower basal rate which may be temporary. Alternatively the pump can be recommenced at the same basal rate and the rate of the glucose infusion increased or the pump can be left off and an IV insulin infusion commenced Queensland Health 2012. If the decision is to continue to administer insulin using the pump then it is important to ensure the infusion site is secure and that the tubing cannot be inherently disconnected during transport to and from the operating room or surgery. If the surgery is of short duration the usual basal insulin rate can be continued and an IV infusion of 5 glucose administered according to the individual’s caloric requirement Betts et al. 2009. The usual morning insulin bolus is not given except to correct hyperglycaemia. Blood glucose must be monitored at least hourly pre- and postoperatively and every 30 minutes during surgery. If needed correction insulin doses can be administered via the pump. However if hyperglycaemia occurs it is important to ensure the pump is still functioning correctly the infusion tubing is patent and the needle has not been dislodged from the infusion site. If the pump is not functioning an IV insulin-glucose infusion may be required to prevent ketosis and hyperglycaemia which may compromise outcomes. A bolus does of insulin is usually administered when the person is ready to eat postoperatively. However managing an insulin pump requires a great deal of knowledge and skill and should not be used if the surgical team does not have the necessary knowledge skills and experience. Nassar et al. 2012 demonstrated inconsistent documentation of pump use and blood glucose monitoring throughout the perioperative period in 35 patients with insulin pumps who had surgical procedures in the US between 2006 and 2010. Likewise it was not clear whether the pump was functioning during most procedures. The authors recommended guidelines be developed. Their recommendation is interesting given least three such guidelines exist Betts et al. 2009 ISPAD ADS 2012 Queensland Health 2012. Emergency procedures Approximately 5 of people with diabetes will need emergency surgery at some stage of their lives. These may be for general surgical emergencies such as appendicitis or diabetes-specific such as acute foot ulcer. Abdominal pain in the presence of DKA may not be an abdominal emergency. However if the abdominal pain persists after the DKA is corrected

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258 Care of People with Diabetes an abdominal emergency should be considered. Likewise functional problems associated with gastroparesis gastroenteropathy and cyclical vomiting may be mistaken for a surgical emergency. Thus even in an emergency situation it is important to undertake a thorough assessment and medical history. The specific management will depend on the nature of the emergency. If possible the metabolic status should be stabilised before surgery is commenced. Many patients requiring emergency surgery have suboptimal control. The minimum requirements are: 1 Adequate hydration. IV access should be obtained and blood drawn for glucose ketones electrolytes pH and other tests as indicated by the presenting problem. 2 If possible surgery should be delayed until the underlying acid–base derangement is corrected if ketoacidosis DKA hyperosmolar or lactic acidosis is present. Dehydration is often severe in hyperosmolar states and the fluid volume needs to be replaced quickly taking care not to cause fluid overload or cerebral oedema. If the patient presents with an abdominal emergency ensure that it is not due to DKA before operating. Specific treatment depends on the: • Nature of the emergency. • Time of the last food intake and the presence of autonomic neuropathy/gastric stasis. • Time and type of the last insulin dose. • Blood glucose level which should be monitored hourly. • Presence of complications such as cardiac arrhythmias and renal disease. Postoperative care will depend on the reason for the emergency and will encompass the care outlined earlier in the chapter. Bariatric surgery Bariatric surgery a solution to obesity when other methods fail is becoming safer and more acceptable. A recent study demonstrated that laparoscopic adjustable gastric banding LAGB and conventional diabetes management had five times the diabetes remission rate than other methods in 60 obese people with Type 2 diabetes Dixon et al. 2008. Seventy three per cent achieved diabetes remission there was an average weight loss of 20 and average BMI fell from 36.6 to 29.5 and 80 achieved normoglycaemia. A recent report of a 15-year follow-up study involving 3000 Australians who had laparoscopic and adjustable banding surgery lost an average of 26 kg and maintained the weight loss for 10 years. O’srien 2006. There were no deaths in the Australian cohort but one in 20 people had the band removed in the follow up period. People who successfully lose weight after gastric banding are more likely to have improved insulin sensitivity reduced fasting blood glucose and HbA1c especially those with Type 2 diabetes and the lipid profile improves in people with Type 2 diabetes and those with impaired glucose tolerance Geloneze et al. 2001. However the risks and benefits need to be carefully considered on an individual basis. Diabetes Australia recommends gastric banding should be a last resort for very obese adults when lifestyle changes are unsuccessful. INVESTIGATIVE PROCEDURES Key points • Careful preparation and explanation to the patient and their family/carers. • Never omit insulin in Type 1 diabetes. • Radio-opaque contrast media may cause tubular necrosis in older people with diabetes so fluid balance must be monitored carefully. • Complementary therapies especially herbs and topical essential oils may need to be stopped temporarily.

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Management During Surgical and Investigative Procedures 259 Rationale Metabolic stress occurs to a lesser degree during investigative procedures than during surgical procedures but still occurs and needs to be managed appropriately to limit adverse outcomes. Clear written instructions about managing medications and any specific preparation required can improve the individual’s understanding and compliance with instructions. Management protocols for patients undergoing medical tests/procedures such as X-rays gastroscopy or laser therapy is not as intricate as those for ketoacidosis or major surgery. However vigilant nursing care is equally important to prevent excursions in blood glucose levels and consequent metabolic effects and psychological stress. Note: Morning procedures are preferred. The objectives of care 1 It is important to prevent hyperglycaemia during surgical procedures to improve outcomes. Hyperglycaemia and insulin therapy can affect the uptake of the radio isotope fluorine-18-fludrodeoxyglucose in the area to be investigated using Positron Emission Tomography PET scans. 2 To ensure correct preparation for the test. 3 To ensure the procedure has been explained to the patient. 4 To provide written instructions for the patient especially if the test is to be performed on an outpatient basis. These instructions should include what to do about their diabetes medications insulin and oral agents and any other medications they are taking and how to recognise and manage hypoglycaemia should it occur while they are fasting. They should also warn the person that it may not be safe for them to drive home depending on the procedure. Usually the doctor referring the person for a procedure should explain the procedure to the individual as part of the process for obtaining informed consent to undertake the procedure. Nurses have a duty of care to ensure instructions have been given and were followed. General nursing management 1 Be aware insulin pumps and continuous glucose monitoring devices should not be exposed to strong magnetic fields during X-rays MRIs and CT scans although they are designed to withstand common electromagnetic interference ADS 2012. 2 Insulin/oral hypoglycaemic agents: • insulin is never omitted in people withType 1 diabetes • if the patient needs to fast insulin doses should be adjusted accordingly • OHAs are usually withheld on the morning of the test • ensure written medical instructions are available including for after the procedure. 3 Aim for a morning procedure if fasting is required and avoid prolonged fasting that results in a catabolic state and counter-regulatory hormone release see Chapters 1 and 7. 4 Monitor blood glucose before and after the test and during the night 3 a.m. if fasting and in hospital. 5 Observe for signs of dehydration. Maintain fluid balance chart if: • fasting is prolonged • bowel preparations are required – some may lead to a fluid deficit especially in the setting of hyperglycaemia • an IV infusion is commenced • dehydration in older people may predispose them to kidney damage if a radioopaque contrast medium is used • An IV infusion may dilute some radio-opaque contrast media. The advice of the radiographer should be sought if IV therapy is necessary. Continue IV infusions and oral fluids after the procedure to wash out contrast medium. 6 Control nausea and vomiting and pain which can increase the blood glucose level. 7 Ensure the patient can eat and drink normally after the procedure to avoid hypoglycaemia. 8 Assess puncture sites e.g. angiography before discharge. 9 Recommence medications as per the medical order.

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260 Care of People with Diabetes 10 Counsel not to drive home if relevant. Bowel procedures for example colonoscopy 1 Iron aspirin and arthritis medications may need to be stopped one week before the procedure. Diabetes medications should be adjusted according to the procedures outlined for day procedures. Insulin doses may need to be reduced during the bowel preparation and people may only require long acting insulin. Oral medicines may not be absorbed because of the bowel preparation. 2 The day before the colonoscopy only clear fluids are permitted and some form of bowel preparation is usually required to clean out the bowel and allow a better view of the mucosa. Bowel preparations should be diluted in water because cordial can contribute to diarrhoea. Older people are at risk of dehydration and should be carefully monitored. Modern preparations are not absorbed and do not usually lead to significant electrolyte disturbances. 3 Fasting for at least 6 hours is usually necessary. 4 If diabetes is unstable or the individual is hyperglycaemic and the procedure is urgent admission to hospital and an IV insulin-glucose infusion during the procedure may be advisable ADS 2012. 5 Frequent blood glucose monitoring e.g. at least two hourly is important especially for people who have unstable or brittle diabetes. Eye procedures People with diabetes are more prone to visual impairment and blindness than the general population. The eye manifestations of diabetes can affect all ocular structures. The time of appearance rate of progression and severity of eye disease vary among individuals. However most patients have some evidence of damage after 25 years of diabetes and vision is threatened in 10 of people with diabetes. Retinopathy is symptomless and may remain undetected if an ophthalmologist or optician does not examine the eyes regularly. Retinal cameras are commonly used to assess the degree of retinopathy and do not require papillary dilation. Fluorescein angiography and retinal photography may aid in determining the severity of the disease. Management aims to conserve vision and laser therapy is often effective in this respect. Risk factors for eye disease include hypertension pregnancy nephropathy hyperlipidaemia and smoking see Chapter 8. Care of patient having fluorescein angiography Fluorescein angiography is usually an outpatient procedure. The reasons for the test and the procedure should be carefully explained to the patient. They should be aware that: • transient nausea may occur • the skin and urine may become yellow for 12–24 hours • drinking adequate amounts of fluid will help flush the dye out of the system • the dye is injected into a vein. Care of the patient having laser therapy photocoagulation ‘Laser’ is an acronym for light amplification stimulated emission of radiation. There are many types of laser. The ones that are used to treat diabetic patients are the argon krypton and diode lasers. The lasers absorb light which is converted into heat which coagulates the tissue. Laser therapy is frequently used to treat diabetic retinopathy and glaucoma. Goals of photocoagulation To maintain vision: • by allowing fluid exchange to occur and reducing fluid accumulation in the retina

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Management During Surgical and Investigative Procedures 261 • by photocoagulating the retina which is ischaemic and thereby causing new vessels that are prone to haemorrhage to regress. Laser therapy is usually performed on an outpatient basis. Fasting is not required and medication adjustment is unnecessary. Practice point Laser therapy may not increase vision but can prevent further loss of vision. Nursing responsibilities Ensure the purpose of laser therapy has been explained to the patient. Advise them to ask their doctor whether it is still safe to drive after the treatment – not just immediately after but generally. The majority can still drive safely but a driving assessment might be required. 1 Before the procedure the patient should know that: • the procedure is uncomfortable • the pupil of the eye will be dilated • anaesthetic drops may be used • the laser beam causes bright flashes of light • vision will be blurred for some time after the laser treatment • they should test their blood glucose before and after laser treatment • they should not drive home and that they may have tunnel vision after the procedure which can limit their visual field. The possible effects on driving should be explained see Chapter 10. 2 After the procedure the patient should know that: • sunglasses will protect the eye and help reduce discomfort • spots may be seen for 24–48 hours • there can be some discomfort for 2–3 weeks • headache may develop after the procedure • paracetamol may be taken to relieve pain • activities that increase intraocular pressure for example lifting heavy objects straining at stool should be avoided for 24–36 hours • night vision may be temporarily decreased • lateral vision may be permanently diminished this is known as ‘tunnel vision’. Practice point Aspirin is best avoided because of its anticoagulant effect. If new vessels are present due to retinopathy they can bleed and threaten sight. Other eye procedures include cataract operations. Practice point Blurred vision does not necessarily indicate serious eye disease. It can occur during both hypo- and hyperglycaemia. Vision often also becomes worse when diabetic control is improved for example after commencement of insulin therapy. Although this is distressing for the patient vision usually improves in 6–8 weeks. Prescriptions for glasses obtained in these circumstances may be inappropriate. Glasses are best obtained when the eyes settle down.

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262 Care of People with Diabetes The nursing care of people who are vision impaired is discussed in Chapter 14. Care of the patient having radio-contrast media injected Radio-contrast media are eliminated through the kidneys and can cause contrastinduced nephropathy that can result in lactic acidosis in people taking Metformin especially if the radio-contrast media is injected IV Klow et al. 2001. Metformininduced lactic acidosis following injection of radio-contrast media almost always occurs in people with pre- existing renal impairment. Thus the serum creatinine should be measured prior to the procedure. Most radiological services recommend withholding Metformin 24 hours prior and 48 hours after procedures requiring radiocontrast media. Fasting is often required before the procedure and the patient can become dehydrated especially if they are kept waiting for long periods and kidney complications can occur. Patients most at risk: • are over 50 years old • have established kidney disease • have had diabetes for more than 10 years • are hypertensive • have proteinuria • have an elevated serum creatinine but note the limitations of serum creatinine discussed in Chapter 3. Kidney problems caused by radio-contrast media may not produce symptoms. Reduced urine output following procedures requiring radio-contrast media may indicate kidney damage and should be investigated. Management 1 ensure appropriate preparation has been carried out 2 ensure the patient is well hydrated before the procedure intravenous therapy may be needed 3 maintain an accurate fluid balance chart 4 avoid delays in performing the procedure 5 monitor urine output after the procedure 6 assess serum creatinine and/or other kidney function tests after the procedure 7 maintain good metabolic control 8 encourage the patient to drink water to help flush out the contrast media. Complementary therapies and surgery and winvestigative procedures A version of the following information was published in the Australian Diabetes Educator 2008 see also Chapter 19. Fifty per cent of patients undergoing surgical and investigative procedures use complementary medicines CAM and other CAM. Women aged 40–60 years are high users and often use CAM on the advice of friends Tsen 2000 Norred 2000. Thus CAM use is an important consideration for people with diabetes having surgical and/or investigative procedures. Significantly despite the high rates of CAM usage most conventional practitioners do not ask about CAM use Braun 2006. CAM use can improve health outcomes of patients undergoing surgery: for example essential oil foot massage reduces stress and anxiety post CAGS Stevenson 1994 essential oils lower MRI-associated claustrophobia and stress acupuncture and peppermint or ginger tea reduce nausea a range of strategies relieve pain and improve sleep and CQ10 prior to cardiac surgery improves post-operative cardiac outcomes Rosenfeldt 2005. However there are also risks which need to be considered in the context of the particular surgery or investigation required and overall management plan. Bleeding is the most significant risk. Other risks include hypotension hypertension sedation and cardiac effects such as arrhythmias renal damage and electrolyte disturbances Norred 2000 2002. It is well documented that many conventional medicines need to be adjusted or ceased prior to surgery. Less information about managing CAM in surgical settings is available but a growing body of evidence suggests many CAM medicines may also need to be stopped or adjusted prior to surgery and some investigative procedures. The following general information applies to people already using CAM medicines and those considering using them before or after surgery. Conventional practitioners may be able to provide general advice regarding CAM use but people with diabetes should be advised to consult a qualified CAM medicine practitioner because many therapies should be used

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Management During Surgical and Investigative Procedures 263 under qualified supervision and for specific advice. Selfprescribing is not recommended in the surgical period because of the complex metabolic and neuroendocrine response to surgery. Preoperative phase People need written information about how to manage CAM medicines and conventional medicines in the operative period as well as any special preparation needed for the surgery or investigation. Conventional health professionals can provide such information if they are qualified to do so or refer the person to a qualified CAM practitioner. Such information should be provided in an appropriate format relevant to the individual’s health literacy level see Chapter 16. Great care is needed for major and high risk such as heart orthopaedic or neurosurgery if the person has renal or liver disease or is very young or elderly. The conventional medication list is unlikely to include CAM medicines or supplements although it should thus health professionals should discuss CAM use with people during all structured medicine reviews and preoperative health assessments. Some CAM medicines such as evening primrose oil bilberry cranberry fish oils ginger Gingko liquorice guarana willow bark meadowsweet and ginseng need to be stopped at least one week before surgery. St John’s Wort and supplements such as vitamin E should be stopped two weeks before surgery primarily because of the risk of bleeding. In addition medicines such as St John’s Wort need to be stopped gradually like conventional antidepressants. However when CAM medicines are the main form of treatment alternative management may be required to prevent the condition deteriorating and affecting the surgical outcome for example glucose-lowering herbal medicines. In addition to the bleeding risk some commonly used CAM medicines may/can interact with some anaesthetic agents and prolong their sedative effects some affect blood pressure and heart rate others cause changes in the major electrolytes potassium calcium and sodium levels in the blood. Grapefruit juice interferes with the action of some antibiotics such as cyclosporine which may be needed pre- or postoperatively. These problems do not occur in everybody who uses CAM in the same way that not everybody experiences adverse events associated with conventional treatments. It is sometimes difficult to predict who will or will not have problems. Some hospitals have policies and guidelines about using CAM and people who wish to continue using CAM in hospital should clarify such policies with the relevant hospital and surgeon before they are admitted. Most do not prescribe or supply CAM. In addition to managing CAM and conventional medicines achieving the best possible health status before surgery improves postoperative recovery. The preoperative assessment is an ideal time to revise the importance of eating a healthy balanced diet and exercise within the individual’s capability controlling blood glucose and lipids which will support immune system functioning and enhance wound healing. Most people should continue their usual physical activity unless it is contraindicated to maintain strength and flexibility. Stress management strategies such as meditation guided imagery essential oils administered in a massage or via an inhalation and music help reduce anxiety and fear about the surgery. Ginger capsules or tablets taken one hour before surgery reduces postoperative nausea Gupta Sharma 2001. The preoperative assessment is also an ideal time to discuss postoperative recovery including managing pain and promoting sleep. CAM may be a useful alternative to some conventional medicines provided a quality use of medicines framework is adopted see Chapter 5. For example valerian hops and lavender in a vapourised essential oil blend administered via massage or as herbal teas or medicines promote restful sleep and have a lower side effect profile than most conventional sedatives. Postoperative phase CAM users need information about whether and when it is safe to start using CAM again postoperatively considering any new conventional medicines that were prescribed for example anticoagulants which could influence the choice and/or dose of CAM medicines. Likewise some non-medicine CAM therapies might need to be used with care such as needle acupuncture and deep tissue massage because they can cause bruising and/or bleeding. A range of CAM strategies can be used to manage pain in the immediate postoperative phase as well as in the longer term is needed. Most are less likely to cause constipation and drowsiness than pethidine and morphine-based medicines. Alternatively if these medicines are the best method of managing pain high fibre CAM food/ medicines such as Aloe vera juice probiotics and psyllium can reduce constipation once oral feeding is permitted. Probiotics also increase bowel health and support natural bowel flora. Peppermint or ginger tea reduces mild-to-moderate nausea. Lymphatic drainage massage is very effective after some surgery to reduce swelling and relieve pain.

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264 Care of People with Diabetes Some CAM products promote wound healing for example Aloe vera Medihoney and calendula and could be used depending on the wound. Arnica ointment reduces bruising but should not be used on open wounds. Comfrey poultices are very effective at reducing local oedema and local pain but should not be used on open wounds or taken internally. Implications for nursing care • CAM has both risks and benefits for people with diabetes undergoing surgery and investigative procedures. • Not all the CAM therapies people use are medicines and not all CAM carry the same level of risk or confer equal benefits. • Adopting an holistic quality use of medicines QUM approach can optimise the benefits and reduce the risks. A key aspect of QUM is asking about and documenting CAM use. • People with diabetes who use CAM need written advice about how to manage their CAM during surgery and investigations. • People with diabetes and cardiac or renal disease and those on anticoagulants older people and children are at particular risk if they use some CAM medicines. References Alberti G. Gill G. 1997 The care of the diabetic patient during surgery in International Textbook of Diabetes Mellitus 2nd edn. eds G. Alberti R. DeFronzo H. Keen. Wiley Chichester pp. 1243–1253. Australian Diabetes Society ADS 2012 Peri-operative Diabetes Management Guidelines. ADS Canberra. Betts P. Brink S. Silink M. et al. 2009 Management of children and adolescents with diabetes requiring surgery. Paediatric Diabetes 10 Suppl 12 169–179. Braun L. 2006 Use of complementary medicines by surgical patients. Undetected and unsupervised in Proceedings of the Fourth Australasian Conference on Safety and Quality in Health Care Melbourne Chow W. Rosenthal R. Merkow R. Ko C. Esnaola N. 2012 Optimal Perioprative Assessment of the Geriatric Surgical Patient: A Best Practice Guideline From the American College of Surgeons National Surgical Quality Improvement Program and the American Geriatrics Society. http://dx.doi. org/10.1016/jamcollsurg.2012.06.017 accessed December 2012. Dagogo-Jack S. Alberti G. 2002 Management of diabetes mellitus in surgical patients. Diabetes Spectrum 15 44–48. De P. Child D. 2001 Euglycaemic ketoacidosis – Is it on the rise Practical Diabetes International 18 7 239–240. Dhatariya L. Levy N. Kilvert A. et al. 2012 NHS Diabetes guideline for the perioperative management of the adult patient with diabetes. Diabetic Medicine 29 420–433. Dickerson L Sack Y Hueston W. 2003 Glycaemic control in medical inpatients with type 2 diabetes receiving sliding scale insulin regimens versus routine diabetic medicines: a multicentre randomized control trial. Annals of Family Medicine 1 29–35. Dickerson R. 2004 Specialised nutrition support in the hospitalized obese patient. Nutrition in Clinical Practice 19 245–254. Dixon J. O’srien P. Playfair J. et al. 2008 Adjustable gastric banding and conventional therapy for Type 2 diabetes: A randomized contolled trial. Journal of the American Medical Association 299 3 316–323. French G. 2000 Clinical management of diabetes mellitus during anaesthesia and surgery. Update in Anaesthesia 11 13 1–6. Geloneze B. Tambascia M. Pareja J. Repetto E. Magna L. 2001 The insulin tolerance test in morbidly obese patients undergoing bariatric surgery. Obesity Research 9 763–769. Gill G. 1997 Surgery and diabetes in Textbook of Diabetes eds. G. Williams J. Pickup. Blackwell Science Oxford pp. 820–825. Gupta Y. Sharma M. 2001 Reversal of pyrogallol-induced gastric emptying in rats by ginger Zingber officinalis. Experimental Clinical Pharmacology 23 9 501–503. Joslin Diabetes Centre 2009 Guideline for inpatient management of surgical and ICU patients with diabetes pre peri and postoperative care. The Joslin Centre Boston USA. Kirschner R. 1993 Diabetes in paediatric ambulatory surgical patients. Journal of Post Anaesthesia Nursing 8 5 322–326. Klow N. Draganov B. Os I. 2001 Metformin and contrast media-increase risk of lactic acidosis Tidsskr Nor laegeforen 121 15 1829. Kwon S. Thompson R. Dellinger P. et al. 2003 Importance of perioperative glycaemic control in general surgery: A report from the surgical care and outcomes assessment program. Annals of Surgery 257 1 8–14. Marks J. Hirsch J. de Fronzo R. eds 1998 Current Management of Diabetes Mellitus. C.V. Mosby St Louis pp. 247–254. Mirtallo J. 2008 Nutrition support for the obese surgical patient. Medscape Pharmacist http://www. accessed February 2008. Nassar A. Boyle M. Seifert K. et al. 2012 Insulin pump therapy in patients with diabetes undergoing surgery. Endocrinology Practice 18 1 49–55. Norred C. 2000 Use of complementary and alternative medicines by surgical patients. Journal of the American Association of Nurse Anaesthetists 68 1 13–18. Norred C. 2002 Complementary and alternative medicine use by surgical patients. AORN 76 6 1013–1021. O’srien P. Dixon J. Laurie C. 2006. Treatment of mild to moderate obesity with laparoscopic adjustable gastric banding or an intensive medical program: A randomized trial. Annals of Internal Medicine 144 9:625-33. Queensland Health 2012 Inpatient guidelines: Insulin infusion pump management. Queensland Health Australia.

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Management During Surgical and Investigative Procedures 265 Rosenfeldt F. 2005 Coenzyme CQ-10 therapy before cardiac surgery improves mitochondrial function and in vitro contractility of myocardial tissue. Journal of Thoracic and Cardiovascular Surgery 129 25–32. Stevenson C. 1994 The psychophysiological effects of aromatherapy massage following cardiac surgery. Complementary Therapies in Medicine 2 1 27–35. Tsen I. 2000 Alternative medicine use in presurgical patients. Anaesthesiology 93 1 148–151. Werther G. 1994 Diabetes mellitus surgery. Royal Children’s Hospital Melbourne. http://www.rch. accessed February 2008. Zhuang U. et al. 2001 Do high glucose levels have differential effect on FDG uptake in inflammatory and malignant disorders Nuclear Medicine Communication 10 1123–1128. Example Instruction Sheet 2a: Instructions for people with diabetes on oral glucose-lowering medicines having procedures as outpatients under sedation of general anaesthesia Person’s Name: ….……………………………… UR….…………………………………........... Time Date of Appointment: ….………………………………….............................................. Where to go:………………………........................................................................................... IT IS IMPORTANT THAT YOU INFORM NURSING AND MEDICAL STAFF THAT YOU HAVE DIABETES Morning If your diabetes is controlled by diet and/or diabetes tablets and you are going to the operating theatre in the morning: • take nothing by mouth from midnight • test your blood glucose and bring your blood glucose record to the hospital with you • do not take your morning diabetes tablets. Afternoon If your diabetes is controlled by diet and/or diabetes tablets and you are going to the operating theatre in the afternoon: • have a light breakfast only coffee/tea 2 slices of toast with spread and nothing by mouth after that • test your blood glucose and bring your blood glucose record to the hospital with you • omit your morning diabetes tablets unless your doctor tells you to take them. If you have any questions: Contact: ….……………………………… Telephone: ….………………………................... Note: The inappropriate paragraph can be deleted or better still separate forms can be produced for morning and afternoon procedures. Example Instruction Sheet 2b: Instructions for people with diabetes on insulin having procedures as outpatients under sedation or general anaesthesia Patient’s Name: ….……………………………… UR: ….……………………………….................. Time Date of Appointment:….…………………………........................................................... where to go:……….……………………....... IT IS IMPORTANT THAT YOU INFORM NURSING AND MEDICAL STAFF THAT YOU HAVE DIABETES Morning If your diabetes is controlled by insulin and you are going to the operating theatre in the morning: • take nothing by mouth from midnight • test your blood glucose and bring your blood glucose record to the hospital with you • omit your morning insulin. OR Take units of insulin. Afternoon

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266 Care of People with Diabetes If your diabetes is controlled by insulin and you are going to the operating theatre in the afternoon: • have a light breakfast only coffee/tea 2 slices of toast with spread and nothing by mouth after that • test your blood glucose and bring your blood glucose record to the hospital with you • take ………………………………… units of insulin. If you have any questions: Contact:….……………………………… Telephone: ….………………………………........... Note: The inappropriate paragraph can be deleted or better still separate forms can be produced for morning and afternoon procedures.

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Chapter 10 Conditions Associated with Diabetes To Cure Diabetes Permanently Click Here Key points • Some of the conditions described in this chapter are rare others occur more often. • Many are overlooked in the focus on achieving metabolic targets. • Diabetes may be overlooked when managing conditions such as TB and HIV/ AIDs. • Most conditions could be identified as part of routine diabetes assessment and preventative screening programmes. • The concomitant presence of one or more of these conditions may influence diabetes management choices health outcomes diabetes self-care capability and mental health. Introduction This chapter outlines some conditions that are associated with diabetes. They are often managed in specialised services and some are very rare. A basic knowledge about these conditions can alert nurses to the possibility that they could be present allow appropriate nursing care plans to be formulated and facilitate early referral for expert advice which ultimately improves the health and well being of the individual. The conditions covered in this chapter are: • enteral and parenteral nutrition • diabetes and cancer • smoking and alcohol addiction • brittle diabetes • Illegal drug use • oral health • liver disease

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268 Care of People with Diabetes Care of People with Diabetes: A Manual of Nursing Practice Fourth Edition. Trisha Dunning. © 2014 John Wiley Sons Ltd. Published 2014 by John Wiley Sons Ltd. • breast mastopathy • coeliac disease • cystic fibrosis-related diabetes • sleep disturbance • tuberculosis • HIV/aids • hearing deficits • musculoskeletal disorders • corticosteroid and antipsychotic medications • diabetes and driving • fasting for religious observances. ENTERAL AND PARENTERAL NUTRITION Practice points • The policies and procedures of relevant health service facilities and countries should be followed when caring for people with central lines PEG tubes and nasogastric tubes. • Enteral and parenteral nutrition is used to supply nutritional requirements in special circumstances such as malnourished patients admitted with a debilitating disease and where there is a risk of increasing the malnourishment for example fasting states and palliative care. Malnourishment leads to increased mortality and morbidity thus increasing length of stay in hospital especially in older people Chapters 4 12 Middleton et al. 2001. Malnourishment can also affect medicine choices. Often the patient is extremely ill or has undergone major gastrointestinal head or neck surgery or has gastroparesis diabeticorum a diabetes complication that leads to delayed gastric emptying and can result in hypoglycaemia due to delayed food absorption bloating and abdominal pain. Alternatively hyperglycaemia can occur. Gastroparesis is very distressing for the individual. Aims of therapy 1 Reduce anxiety associated with the condition requiring enteral therapy and the procedure by involving the individual in management decisions explaining the process and why enteral feeing is necessary. In some cases family members/carers will need to be included in the education. Ample time should be allowed to enable people’s concerns to be addressed. 2 Prevent sepsis. 3 Maintain an acceptable blood glucose range 4–8 mmol/L except in frail older people when 6–8 mmol/L might be appropriate. 4 Maintain normal urea electrolytes liver function tests and blood gas levels. 5 Supply adequate nutrition in terms of protein fat and carbohydrate to support normal body functions and promote growth and repair. 6 Achieve positive nitrogen balance. 7 Prevent complications of therapy. 8 The long-term aim of enteral/parenteral feeding is the return of the patient to oral feeding. However if life expectancy is reduced and/or in older people it may be permanent Chapters 4 and 12. In such cases decisions about when to discontinue the feeding should be made proactively perhaps documented in an advanced care

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Conditions Associated with Diabetes 269 plan Dunning et al. 2012. Blood glucose monitoring and reviewing the diabetes management regimen including medicines is essential when oral feeding resumes Australian Diabetes Society ADS 2012. It may also be necessary to consider the balance of bacteria in the gut and the role these organisms play in altering dietary and metabolic processes. Specific ‘good bacteria’ appear to play a role in reducing systemic inflammatory processes. They also appear to play a role in fasting hyperglycaemia obesity steatosis insulin resistance and hyperinsulinaemia as well as in the secretion of gastrointestinal hormones such as the incretins see Chapter 1. Prebiotics and probiotics could be beneficial to gut and overall health but more research is required. Complications of enteral nutrition 1 Mechanical problems such as aspiration poor gastric emptying and reflux can occur especially if the person has altered mental status and/or a suppressed gag reflex. 2 Metabolic consequences include hyperglycaemia and hypernatraemia depending on the feed used the supplements added to the feed and when a high feeding rate is used. Hyperglycaemia in people receiving enteral nutrition is associated with increased risk of cardiac complications infection sepsis and acute renal failure. Significantly people with mean blood glucose 9.1 mmol/L have a 10-fold greater risk of death than people with mean blood glucose 6.9 mmol/L independent of age gender and presence of diabetes complications Australian Diabetes Society ADS 2912 Feeding into the small bowel rather than the stomach minimises metabolic disturbance. People who cannot indicate that they are thirsty and who have altered mental status particularly older people are at risk of these metabolic consequences. Hypoglycaemia can occur if food is not absorbed the calorie load is reduced and if there are blockages in the feeding tubes. Medicine interactions can also contribute to hyper and hypoglycaemia see Chapters 5 and 19. 3 Gastrointestinal problems the most common is diarrhoea which is usually osmotic in nature. Gastroparesis may be present. Routes of administration Enteral feeds The enteral route supplies nutrients and fluids when the oral route is inadequate or obstructed. Feeds are administered via a nasogastric duodenal jejunal or gastrostomy tube. Enteral feeding is preferred over parenteral feeding when the gut is functioning normally and oral feeds do not meet the patient’s nutritional requirements McClave et al. 1999. Nasogastric tubes may be used in the short term. Nasogastric feeds have a significant risk of pulmonary aspiration. The tubes are easily removed by confused patients and cause irritation to the nasal mucosa and external nares that can be uncomfortable and is an infection risk in immunocompromised patients and people with hyperglycaemia. Duodenal and jejunal tubes do not carry the same risk of pulmonary aspiration but the feeds can contribute to gastric intolerance and bloating especially in the presence of gastroparesis see Chapter 8. Gastroscopy tubes are used in the long term when the stomach is not affected by the primary disease which may preclude their use in people with established autonomic neuropathy that involves the gastrointestinal tract. The tubes can be inserted through a surgical incision and the creation of a stoma. More commonly percutaneous endoscopic techniques PEG are used Thomas 2001. Inserting a PEG tube involves making an artificial tract between the stomach and the abdominal wall through which a tube is inserted. The tube can be a balloon tube or a button type that is more discrete and lies flat to the skin. An extension tube is inserted into the gastroscopy tube during feeding. Gastrostomy PEG feeds Feeds can usually be undertaken 12–24 hours after the tube is inserted but can be given as early as 4–6 hours after tube insertion in special circumstances. The initial feed may be water and or dextrose saline depending on the patient’s condition.

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270 Care of People with Diabetes Mode of administration 1 Bolus instillation: may result in distension and delayed gastric emptying. Aspiration can occur. Diarrhoea may be a complication. This method is not suitable for people with diabetes who have autonomic neuropathy especially gastroparesis. 2 Continuous infusion: via gravity infusion or pump. This can lead to hyperinsulinaemia in Type 2 diabetes because glucose-mediated insulin production occurs. The effect on blood glucose can be minimised by using formulas with a low glycaemic index. Administering insulin via the IV route enables the caloric input to be balanced with the insulin requirements but is not suitable for long-term use or in some clinical settings. The strength of the feeds should be increased gradually to prevent a sudden overwhelming glucose load in the bloodstream. An IV insulin infusion is an ideal method to control blood glucose levels. Blood glucose monitoring is essential to gauge the impact of the feed on blood glucose and appropriately titrate medication doses. The feeds usually contain protein fat and carbohydrate. The carbohydrate is in the form of dextrose either 25 or 40 and extra insulin may be needed to account for the glucose load. A balance must be achieved between caloric requirements and blood glucose levels. Patients who are controlled by GLMs usually need insulin while on enteral feeding. Parenteral feeds Refers to administering nutrients and fluids by routes other than the alimentary canal that is intravenously via a peripheral or central line. Mode of administration Parenteral supplements are either partial or total. 1 Peripheral: used after gastrointestinal surgery and in malabsorption states. Peripheral access is usually reserved for people in whom central access is difficult or sometimes as a supplement to oral/enteral feeds. It is not suitable if a high dextrose supplement is needed because dextrose irritates the veins causing considerable discomfort. It can cause significant tissue damage if extravasation occurs. 2 Central: supplies maximum nutrition in the form of protein carbohydrate fats trace elements vitamins and electrolytes. For example in patients with cancer or burns larger volumes can be given than via the peripheral route. In addition it provides long-term access because silastic catheters can be left in situ indefinitely. If patients are at risk of sepsis the site of the central line is rotated weekly using strict aseptic technique. Central lines enable the patient to remain mobile which aids digestion and reduces the risk of pressure ulcers. Choice of formula The particular formula selected depends on the nutritional requirements and absorptive capacity of the patient. It is usual to begin with half strength formula and gradually increase to full strength as tolerated. The aim is to supply adequate: • fluid • protein • carbohydrate • vitamins and minerals • essential fatty acids • sodium spread evenly over the 24 hours • preserve/enhance gut health.

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Conditions Associated with Diabetes 271 Generally feeds low in carbohydrate/dextrose and high in monosaturated fatty acids are preferred for people with diabetes ADS 2012. Nutritional requirements can vary from week-to-week thus careful monitoring is essential to ensure the formula is adjusted proactively and appropriately. Diabetes medication insulin or oral agents are adjusted according to the pattern that emerges in the blood glucose profile. The dose depends on the feeds used as well as other prescribed medicines and the person’s condition. Generally the insulin/OHA doses are calculated according to the caloric intake. There is very little good quality research into the effects of glucose lowering medicines on blood glucose in people receiving enteral/parental nutrition. Nursing responsibilities Care of nasogastric tubes 1 Explain purpose of tube to patient. 2 Check position of the tube regularly to ensure it is in the stomach to prevent pulmonary aspiration. 3 Confirm the position of the tube with an X-ray. 4 Change the position of the tube in the nose daily to avoid pressure areas. 5 Flush regularly to ensure the tube remains patent. 6 Check residual gastric volumes regularly to avoid gastric distension and reduce the possibility of aspiration especially if gastroparesis is present. Care of PEG tubes The same care required for nasogastric tubes applies. Additional care: 1 Monitor gastric aspirates at least daily. 2 Elevate the head of the bed where there is a risk of pulmonary aspiration. 3 Weigh the patient to ensure the desired weight outcome is achieved. 4 Monitor nutritional status see Chapter 4. 5 Manage nausea and vomiting if they occur because they increase the risk of aspiration represent fluid loss and are uncomfortable for the patient. Record the amount and type of any vomitus. Antinausea medication may be required. Warm herbal teas such as chamomile peppermint or ginger may be helpful non-medicine alternatives if oral intake is permitted. 6 If the PEG tube blocks it can sometimes be cleared with a fizzy soft drink but local protocol should be followed because fizzy drinks can lead to electrolyte imbalances if they are used frequently. 7 Ensure there is adequate fluid in the feeds to avoid dehydration and the consequent risk of hyperosmolar states see Chapter 7 Thomas 2001. Care of IV and central lines 1 Dress the insertion site regularly using strict aseptic technique according to usual protocols. 2 Check position of the central line with a chest X-ray. 3 Maintain strict aseptic technique. 4 Maintain patency usually by intermittently installing heparinised saline weekly or when line is changed. 5 Patients should be supine when the central catheter is disconnected and IV giving sets should be carefully primed to minimise the risk of air embolism. 6 Check catheter for signs of occlusion e.g. resistance to infusion or difficulty withdrawing a blood sample. Reposition the patient: if the occlusion is still present consult the doctor. 7 Observe exit site for any tenderness redness or swelling. If bleeding occurs around the suture or exit site apply pressure and notify the doctor. 8 Monitor the patient for signs of infection for example fever. Note that elevated white cell count may not be a sign of infection in people with diabetes if hyperglycaemia is present.

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272 Care of People with Diabetes General nursing care 1 Ensure the person is referred to a dietitian. 2 Maintain an accurate fluid balance chart including loss from stomas drain tubes vomitus and diarrhoea. 3 Monitor serum albumin urea and electrolytes to determine nutritional requirements nitrogen balance and energy requirements. 4 Weigh regularly weekly at the same time using the same scales with the person wearing similar clothing to ensure energy balance and sufficient calories are supplied. Excess calories leads to weight gain and hyperglycaemia. Insufficient calories lead to weight loss and increase the risk of hypoglycaemia. 5 Monitor blood glucose regularly 4–6-hourly initially. If elevated be aware of possibility of a hyperosmolar event see Chapter 7. If stable less frequent monitoring might be appropriate. 6 Record temperature pulse and respiration and report if elevated 38 °C or if any respiratory distress occurs. 7 Check the label including the date and appearance of all infusions before they are administered. 8 Medications are given separately from the formula check with the pharmacist which medicines can be added to the formula. Follow pump instructions and local guidelines carefully. Be very careful with look-alike and sound-alike medicines. Insulin therapy should include regular basal insulin intermediate or long-acting and prandial correctional doses if needed. If the blood glucose is unstable and intravenous insulin infusion might be indicated ADS 2012. Sliding insulin scales are not recommended and increase the risk of hypoglycaemia ADS 2102. However prandial correction doses might be used see Medicines Chapter 5. Not all oral medicines can be crushed: it is essential to check before crushing medicines for oral administration via enteral tubes or orally. 9 Skin fold thickness and mid-arm muscle circumference measurement can also be useful to ascertain weight loss/gain. 10 Skin care around tube insertion sites and stoma care for gastrostomy tubes to prevent infection. Care when recommencing oral feeds 1 Monitor blood glucose very carefully. Long-acting insulin is often commenced when oral feeds are resumed so there is a risk of hypoglycaemia. Only rapid or short-acting insulin can be given intravenously. 2 Monitor and control nausea or vomiting and describe vomitus. 3 Maintain accurate fluid balance chart usually 2-hourly subtotals. DIABETES AND CANCER Diabetes especially Type 2 has been linked to various forms of cancer but the relationship is not straightforward. There appears to be an increased risk of cancer of the pancreas liver and endometrium and endometrial cancer also appears to be associated with diabetes and obesity Wideroff et al. 1997. Diabetes may be an early sign of pancreatic cancer la Vecchia et al. 1994. A recent study demonstrated a significant increased risk for all cancers at moderately elevated HbA1c levels 6−6.9 with a small increased risk at high levels 7 Travier et al. 2007. These findings support the hypothesis that abnormal glucose metabolism is associated with an increased risk of some cancers but may not explain the mechanism or causal relationship. Other cancers such as lung cancer do not appear to be associated with an increased risk in people with diabetes and the evidence for an association with kidney cancer and non-Hodgkin’s lymphoma is inconclusive. Few researchers have explored the association between Type 1 diabetes and cancer Giovannuci et al. 2010. Interestingly diabetes appears to be associated with lower risk of prostate cancer and the risk of pancreatic cancer appears to be restricted to people with diabetes that precedes the diagnosis of pancreatic cancer by at least 5 years. Researchers have also suggested that diabetes is an independent predictor of death from colon pancreas liver and bladder cancer and breast cancer in men and women Coughlin et al. 2004. Verlato et al. 2003 reported increased risk of death from breast cancer in women with Type 2 diabetes compared with non-diabetics and suggested that controlling weight reduced the mortality rate. Likewise median survival time is shorter Bloomgarden 2001.

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Conditions Associated with Diabetes 273 Common risk factors for cancer and diabetes appear to be ageing gender obesity physical inactivity diet excess alcohol consumption and smoking. Ethnicity and genetics also appear to play a role but the relationship is not straightforward. Likewise the inter-related effect of hyperinsulinaemia hyperglycaemia inflammation and insulin- like growth factors IGF in carcinogenesis is unclear. There is limited evidence that specific glucose-lowering medicines cause cancer. Reported associations for an association between cancer and thiazolidinediones sulphonylureas incretins and insulin glargine may be confounded by factors such as the effects of other cancer risks and cancer not being a primary end point. More research is needed into these issues Giovannuci et al. 2010. However early evidence suggests Metformin is associated with lower cancer risk and research is continuing to clarify the association. Management People with diabetes should be encouraged to participate in appropriate cancer screening programmes the same as non-diabetics e.g. mammograms bowel screens and prostate checks event though prostate cancer may not be associated with diabetes if it occurs glycaemic control is likely to be affected and it is a common and devastating cancer. A healthy well-balanced diet low in fat and alcohol and regular exercise are important preventative strategies as well as part of diabetes and cancer management plans. Cancer management is the same for people with diabetes as for people without diabetes however some extra considerations apply. Cancer cells trap amino acids for their own use limiting the protein available for normal body functions which sets the scene for weight loss especially where the appetite is poor and the senses of smell and taste are diminished. Malabsorption nausea and vomiting and radiation treatment further exacerbate weight loss. While weight loss may confer many health benefits it is often excessive in cancer and causes malnutrition which reduces immunity and affects normal cellular functioning and wound healing. Glucose enters cancer cells down a concentration gradient rather than through insulin-mediated entry and metabolism favours lactate production. Lactate is transported to the liver increasing gluconeogenesis. Hypoalbuminaemia also occurs. For the person with diabetes lactate production can contribute to hyperglycaemia and reduce insulin production with consequent effects on blood glucose control. Hyperglycaemia is associated with higher infection rates and the risk is significantly increased in immunocompromised patients and those on corticosteroid medications. In addition hyperglycaemia-associated symptoms cause discomfort Dunning et al. 2011 Savage et al. 2012 Diabetes UK 2012. Diabetes management should be considered in relation to the prognosis and the cancer therapy. Preventing the long-term complications of diabetes may be irrelevant if the prognosis is poor but controlling hyperglycaemia has benefits for comfort quality of life and functioning during the dying process Quinn et al. 2006 Dunning et al. 2012 Diabetes UK 2012. However many people have existing diabetes complications such as renal and cardiac disease that need to be managed to promote comfort and quality of life see Chapter 18. For example the chemotherapeutic agent cisplatin causes renal insufficiency and can exacerbate existing renal disease cisplatin paclitaxel and vincristine might exacerbate neuropathy. Side effects from chemotherapeutic agents are usually permanent. Where the prognosis is good improving the complication status as much as possible and controlling blood glucose and lipids may help minimise the impact of chemotherapy. Specific treatment depends on the type of cancer the patient has. Diagnosis of some types of cancer such as endocrine tumours can involve prolonged fasting and radiological imaging and/or other radiological procedures. The appropriate care should be given in these circumstances see Chapter 9. Corticosteroid therapy is frequently used in cancer treatment and can precipitate diabetes in people without diabetes especially if diabetes risk factors are present and cause hyperglycaemia in people with diabetes. Corticosteroids may be required for a prolonged time or given in large doses for a short period. Therefore blood glucose needs to be monitored regularly in patients on corticosteroid medications which are discussed later in this chapter. Objectives of care Primary prevention People with chronic diseases such as diabetes often do not receive usual preventative health strategies such as cancer screening Psarakis 2006. For example Lipscombe et al. 2005 found Canadia