diabetes.ppt

DIABETES MELLITUS – ANAESTHETIC CONSIDERATIONS: 

DIABETES MELLITUS – ANAESTHETIC CONSIDERATIONS Dr.J.Rajesh

INTRODUCTION: 

INTRODUCTION Diabetes Mellitus is a chronic disorder of carbohydrate, fat and protein metabolism due to deficiency of insulin secretion or insulin resistance or combination of both Characterized by chronic hyperglycemia, with or without glycosuria, hyperlipidemia and tendency to cause end organ damage

CLASSIFICATION: 

CLASSIFICATION Type 1A - Immune mediated Type 1B - Idiopathic Type 2 - Insulin resistance with relative insulin deficiency Type 3 - a) Genetic defects of β cell function b) Genetic defects in insulin action c) Diseases of exocrine pancreas d) Endocrinopathies e) Drug/ chemical induced f) Infection induced g) Uncommon syndromic associations Type 4 – Gestational Diabetes

DIFFERENCES: 

DIFFERENCES TYPE 1 Age at onset usually < 30yrs Lean body habitus Insulin forms initial therapy Associated with propensity of DKA, risk for autoimmune diseases, thyroid or adrenal insufficiency, prenicious anemia Auto antibodies present TYPE 2 Usually > 30 yrs 80% sufferers are obese Insulin is not required initially Prone to develop hyperosmolar state Associated with other conditions – Hypertension, Cardiovascular disease, Dyslipidemias

RISK FACTORS FOR TYPE 2 DM: 

RISK FACTORS FOR TYPE 2 DM Race or ethnicity Family history Habitual physical inactivity Obesity ( BMI > 25kg/sq.m ) History of vascular disease History of gestational diabetes HDL cholesterol ≤ 35mg% or triglycerides ≥ 126mg%

PATHOPHYSIOLOGY: 

PATHOPHYSIOLOGY Type 1 → Auto immune destruction of beta cells Type 2 → Derangement of insulin secretion, insulin resistance, decrease in peripheral utilization of glucose due to receptor abnormality Target organ damage → sorbitol accumulation, lipid abnormality, non enzymatic glycolisation of proteins

METABOLIC ABNORMALITIES: 

METABOLIC ABNORMALITIES Hyperglycemia – glycogenolysis, gluconeogenesis, decreased skeletal muscle uptake of glucose Increased free fatty acids – Lipolysis Increased serum ketones Increased serum triglycerides Decreased protein synthesis Osmotic diuresis - Dehydration

REVISED DIAGNOSTIC CRITERIA: 

REVISED DIAGNOSTIC CRITERIA DM is defined by any of the following 3 criteria either unequivocally, or on two separate days Symptoms + casual glucose level of ≥200 mg/dl Fasting plasma glucose level of ≥126mg/dl (normal value <100mg/dl) Glucose concentration of ≥200mg/dl 2 hours after oral ingestion of 75g glucose (normal value <140mg/dl)

PRE DIABETIC STATES: 

PRE DIABETIC STATES Impaired fasting glucose - Fasting blood glucose level 100mg/dl to 125mg/dl Impaired glucose tolerance – Glucose concentration 140mg/dl to 199mg/dl

GLYCOSYLATED Hb (HbA1c): 

GLYCOSYLATED Hb (HbA1c) Utilized for assessment of glycaemic control in a known diabetic patient not for diagnosis Index of risk of diabetic complications Reflects state of glycaemia in preceding 8 to 12 weeks A rise of 1% in HbA1c corresponds to an approximate average increase of 2mmol/l in blood glucose

HbA1c: 

HbA1c Normal value - ≤ 7.5% of total Hb HbA1c >9% - development of osmotic diuresis HbA1c >12 – 15% - on verge of DKA HbA1c consistently >8% - Microvascular complications more likely

HbA1c: 

HbA1c Problems Anaemia, pregnancy, uremia, haemoglobinopathies

GLYCATED SERUM PROTEINS (FRUCTOSAMINE ) : 

GLYCATED SERUM PROTEINS (FRUCTOSAMINE ) Shorter half life, indicates glycaemic control over preceding 2 weeks Useful only in diabetic pregnancy Normal value – 1.5 – 2.4 mmol/l

DRUG THERAPY: 

DRUG THERAPY Oral agents Drugs that increase insulin secretion – sulfonylureas and nonsulfonylureas Drugs that increase sensitivity to insulin – biguanides and thiazolidinediones Drugs that decrease glucose absorption – alpha glucosidase inhibitors or fat absorption – intestinal lipase inhibitors

SULFONYLUREAS: 

SULFONYLUREAS Decreases glucose levels by stimulating insulin secretion from pancreatic β -cells Binds to sulfonylurea receptors on β cells → closure of ATP- dependent K – channel → membrane depolarization, opening of voltage gated calcium channel → increased intracellular calcium → insulin secretion

SULFONYLUREAS: 

SULFONYLUREAS Long half life – associated with prolonged (up to 72 hours) hypoglycemia during fasting Metabolished in liver, excreted by kidneys – Renal or hepatic failure can accentuate hypoglycemia Inhibit ischemic preconditioning – myocardial protection E.g – Glyburide, glipizide, glimepiride, chlorpropamide, tolbutamide

NONSULFONYLUREAS: 

NONSULFONYLUREAS Binds to sulfonylurea receptors on β cells but at different site Shorter duration of action, peak activity within 30 to 60 minutes, elimination half lives of approximately 1 hour Can be safely continued until cessation of regular meals and restarted on return to oral feeding E.g. – Repaglinide, nateglinide, mitiglinide

BIGUANIDES: 

BIGUANIDES Metformin decreases hepatic glucose production and increases peripheral glucose disposal Excreted unmodified by kidneys Most significant side effect is lactic acidosis Metformin has to be stopped for major surgeries

ABSORPTION INHIBITORS: 

ABSORPTION INHIBITORS Acarbose, miglitol - α glucosidase inhibitors Orlistat – gastric & pancreatic lipase inhibitor Slows carbohydrate, fat absorption ; lowers postprandial glucose levels Hypoglycemia due to added drugs needs oral glucose or dextrose Has no effect during fasting, can be continued until the start of preoperative fast

THIAZOLIDINEDIONES: 

THIAZOLIDINEDIONES Reduces lipolysis, circulating free fatty acid levels and TNF - α , increases adeponectin Has beneficial effect on lipid profile, antihypertensive effect, antiatherosclerotic effect Side effects – fluid retention, edema – peripheral & pulmonary, dilutional anaemia, CCF Slow acting, takes 6 to 12 weeks for peak effect Half life – 3 to 4 hours Stopping or continuing peri operatively is not conclusive

FUTURE DRUGS: 

FUTURE DRUGS Glucagon like peptide-1 (GLP -1) analogs – liraglutide, exenatide Augments insulin secretion, inhibits glucagon secretion, delays gastric emptying and possibly induces pancreatic β cell proliferation Inhibitors of GLP1 degradation – in trial

INSULIN: 

INSULIN Short acting – Lispro, Aspart, Regular Intermediate acting – NPH, Lente Long acting – Ultralente, Glargine Combinations of above

METABOLIC ACTIONS OF INSULIN: 

METABOLIC ACTIONS OF INSULIN Increases Carbohydrate metabolism Glucose transport Glucose phosphorylation Glycogenesis Glycolysis Lipid metabolism Triglyceride synthesis Fatty acid synthesis (liver) Protein metabolism Amino acid transport Protein synthesis Decreases Glycogenolysis Gluconeogenesis Lipolysis Ketogenesis Fatty acid oxidation (liver) Protein degradation

EFFECT OF HYPERGLYCEMIA: 

EFFECT OF HYPERGLYCEMIA Impairs host response to infection Impairs neutrophil action Have pro inflammatory effect Worsens neurological outcome Postoperative cardiac events aggrevated

PRE ANAESTHETIC EVALUATION: 

PRE ANAESTHETIC EVALUATION Age Duration of DM Method used for blood glucose control Previous hospitalization Symptoms of end organ damage Autonomic dysfunction Previous anesthetic exposure Documentation of neuropathy

BS CONTROL ASSESMENT: 

CONTROL FBS PPBS HbA1c% Excellent <110 <120 <8 Good <120 <150 8 - 10 Fair <140 <180 10 - 12 Poor >140 >180 >12 BS CONTROL ASSESMENT

PRE MEDICATION: 

PRE MEDICATION Surgery should be preferably scheduled as first case Minimize dose of sedatives as pre medicatives Advice prokinetics for those with gastroparesis

INVESTIGATIONS: 

INVESTIGATIONS Routine haemogram Blood sugar – fasting, postprandial Urine – sugar, albumin, ketones Chest X ray, ECG BUN, Creatinine, Electrolytes Ophthalmic examination X ray cervical spine ABG

ANAESTHETIC GOALS: 

ANAESTHETIC GOALS Mimic normal metabolism Avoid hypoglycemia Prevent excessive hyperglycemia, ketoacidosis, electrolyte disturbances

GUIDELINES: 

GUIDELINES Decrease the stress response to surgery Smooth induction with minimal sympathetic stimulation Anticipate difficult intubation Prevention of aspiration Avoid sympathetic stimulation Muscle relaxant dose to be reduced Careful positioning

Slide 31: 

Patient condition Patient on diet control Patient on OHA Patient on insulin Patient with uncontrolled DM Surgery Elective or Emergency Minor or Major

ON DIET CONTROL: 

ON DIET CONTROL Elective surgery Major or Minor → treat as normal patient Emergency surgery Major or Minor → Insulin SOS Observe capillary blood sugar every hourly

ON OHA: 

ON OHA Elective Minor surgery → omit morning dose of OHA M ajor surgery → omit OHA, convert to insulin Emergency Check status and decide Minor → confirm last dose of OHA Major → BS monitoring, Insulin as sliding scale

ON INSULIN: 

ON INSULIN Elective Minor surgery → omit morning dose of insulin M ajor surgery → convert to plain insulin Emergency Check last dose of insulin to avoid hypoglycemia Dextrose with insulin infusion

UNCONTROLLED DM: 

UNCONTROLLED DM Elective Control blood sugar pre operatively Emergency Minor surgery → Low dose insulin + BS monitoring Major surgery → Insulin infusion

INSULIN REGIMES: 

INSULIN REGIMES

Slide 37: 

No Insulin, No Glucose Widely used for Type 1 DM undergoing short procedures Insulin and glucose to be restarted in post op. period as early as possible Partial morning dose s.c with dextrose infusion Not a satisfactory technique

Slide 38: 

GIK Regime (Alberti and Thomas regimen) Pre operative stabilisation with soluble insulin Insulin is omitted on day of surgery GIK infusion to be started as – 500ml 0f 10%glucose with 10U soluble insulin and 1gm of kcl – 100ml/hr Blood glucose is measured every 2 – 3 hours and immediate before induction

Slide 39: 

BS < 90mg/dl → bag changed with 5U insulin BS >180mg/dl → bag changed with 15U insulin Kcl supplementation according to serum potassium Revert to subcutaneous dosing when oral intake is resumed

Slide 40: 

Alberti regime (modified) Initial solution – 500ml 10% glucose with 10 mmol Kcl with 15U insulin – 100ml/hr BS measurement every 2 hours BS <117mg/dl → 10U insulin BS 117 - 200mg/dl →15U insulin BS >200mg/dl → 20U insulin Problems – frequent change, hyponatremia

Slide 41: 

Tight control regimen Check BS day before surgery Start 5% dextrose 50ml/hr Infusion- 50U of regular insulin in 250ml of 0.9%NS (in piggyback infusion pump) → flush 60ml Check BS every 4 hours Infusion rate – BS/150U/hr ( in case of patient on steroids reduce insulin to 100U)

Slide 42: 

Day of surgery → check BS IVF – NS+ electrolytes in separate IV line BS every 1-2hrs → infusion – BS/150U/hr Maintain BS between 100 – 200mg/dl BS <50mg/dl → stop infusion, rush 25ml 0f 50% dextrose Reassess after 30 min

Slide 43: 

Non tight control regimen Nil oral overnight in previous day of surgery Keep orange juice ready Day of surgery at 6am → start 5%dextrose – 125ml/hr Half of regular dose of insulin to be given subcutaneously Continue same IVF intra operatively After surgery check BS

Slide 44: 

Hirsh regimen 500ml NS + 50U regular insulin (1U/hr = 10ml/hr) Infusion to be initiated as 0.5-1U/hr Measure BS every 1-2 hrs If BS <80mg/dl → stop infusion for 30 min administer 25ml of 50% dextrose remeasure BS in 30min 80 – 120mg/dl→ decrease infusion rate by 0.3U/hr 120 – 180mg/dl→no change 180 – 220mg/dl→ increase infusion rate by 0.3U/hr >220mg/dl→ increase infusion rate by 0.5U/hr Provide glucose (5-10g/hr) and potassium (2-4meq/l)

COMPLICATIONS OF DIABETES: 

COMPLICATIONS OF DIABETES

ACUTE COMPLICATIONS: 

ACUTE COMPLICATIONS Diabetic ketoacidosis (DKA) Hyperglycemic hyperosmolar state (HHS)

CHRONIC COMPLICATIONS: 

CHRONIC COMPLICATIONS Microvascular Eye disease Retinopathy Macular edema Neuropathy Sensory and motor ( mono and polyneuropathy) Autonomic Nephropathy

Slide 48: 

Macrovascular Coronary artery disease Peripheral vascular disease Cerebrovascular disease Other Gastrointestinal - gastroparesis Genitourinary – sexual dysfunction, uropathy Dermatological, infectious Cataract, Glaucoma

ATHEROSCELORITIC VASCULAR DISEASE: 

ATHEROSCELORITIC VASCULAR DISEASE Hyperglycemia → endothelial injury, coagulation changes Coronaries – Coronary Arterial Disease, Cardiomyopathy, Hypertension,Silent MI Cerebral – Cerebrovascular accidents, TIA, Peripheral Vascular Disease

MICROANGIOPATHIES: 

MICROANGIOPATHIES Kidneys – Glomerulosclerosis, tubular nephritis, pyelonephritis, ARF, CRF Nerves – thickening of schwann cellmembrane and segmental demyelination causing distal symmetric polyneuropathy (glove and stocking anaesthesia)

AUTONOMIC DYSFUNCTION: 

AUTONOMIC DYSFUNCTION Orthostatic hypotension Resting tachycardia Sinus arrhythmias Gastroparesis – risk of aspiration Nocturnal diarrhoea Asymptomatic hypoglycaemia Impotence Urinary retention Sudden death syndrome

MISCELLANEOUS: 

MISCELLANEOUS Bones – charcot’s joints, osteopathies, atlanto axial joint involvement Stiff joint syndrome – Prayer sign Pupils – spastic miosis Skin – waxy, neurogenic ulcers, scleroderma DKA, HHS

DIABETIC KETOACIDOSIS: 

DIABETIC KETOACIDOSIS

INITIAL EVALUATION: 

INITIAL EVALUATION History and physical examination Lab tests → ABG, CBC, DC, urine analysis, blood glucose, BUN, creatinine, electrolytes ECG CXR, culture as needed Start IVF – 1L of 0.9%NS/ hr initially (15 – 20 ml/kg/hr)

DIAGNOSTIC CRITERIA: 

DIAGNOSTIC CRITERIA Blood glucose level >250mg/dl Arterial pH <7.3 Sodium bicarbonate <15 meq/l Moderate ketonuria, ketonemia

IV FLUIDS: 

IV FLUIDS Determine hydration state Hypovolemic shock → 0.9%NS 1L/hr Cardiogenic shock→ haemodynamic monitoring Mild hypotension → evaluate corrected Sr.Na+ level → administer 0.45% or 0.9% NS 7-14ml/kg/hr accordingly

INSULIN: 

INSULIN Regular insulin bolus 0.15U/kg ↓ Regular insulin infusion 0.1U/kg/hr ↓ Target fall in BS is 50-70mg/dl, if fails double the infusion till the target reaches ↓ When BS reaches 250mg/dl change to 5% dextrose with 0.45% saline

Slide 58: 

Continue insulin infusion at rate of 0.05-0.1U/kg/hr or 10Us.c every 2 hrs Keep glucose level 150-200mg/dl

POTASSIUM: 

POTASSIUM K + <3.3meq/L → Hold insulin; give potassium 40meq/l K + ≥5.5meq/l → check K + every 2 hrs K + >3.3 <5.5meq/l → add 20-30meq/l of K + in each litre of IV fluid Keep K +level at 4-5meq/l

AFTER RESOLUTION : 

AFTER RESOLUTION Check electrolytes every 2-4hrs Check BS every 4 hrs Treat precipitating causes Sliding scale regular insulin s.c in 5U increments of every 50mg/dl above 150mg/dl to maximum of 20U

HYPERGLYCEMIC HYPEROSMOLAR STATE : 

HYPERGLYCEMIC HYPEROSMOLAR STATE

LAB FINDING: 

LAB FINDING Hyperglycemia – BS >600mg/dl Plasma osmolality >320mosm/l Absence of ketonemia ABG - pH> 7.3 ; Bicarb>20meq/l Renal azotemia Lactic acidosis

TREATMENT: 

TREATMENT Fluid replacement Insulin Electrolyte correction Treat precipitating factors – stress, infections, alcohol etc.

CONCLUSION: 

CONCLUSION Diabetes mellitus is an extremely common condition with co morbidity Complications are related to end organ damage Side effects of OHA should always be remembered Intra operative poor control of blood sugar affects post operative outcome

THANK YOU: 

THANK YOU