diabetes in pregnancy by shabnam naz

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Diabetes mellitus in pregnancy:

Diabetes mellitus in pregnancy Dr Shabnam Naz Assistant professor Obgyn Smbbmu larkana


OBJECTIVES Definition of diabetes mellitus Pathophysiology of diabetes Risk factors Types of diabetes Effects of diabetes on pregnancy and fetus Screening and diagnosis Medical management of diabetes Obstetrical management of diabetes mellitus

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Eberts Papyrus Ancient China Other ancient cultures Celso( I b.c ) Areteo of Capodocia(II b.c ) 1696 Thomas Willis(1766) A Brief History Frequent and abundant elimination of urine . ”sweet urine” Thirst disease Excessive hunger Polyuria, Polydipsia Diabetes(unquenchable thirst) Evidence of Inheritance Presence of sugar ( Mellitus =Sugar)

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Langerhans(Berlin, 1869) Is lets Bonting & Best(Canada) Pa ncreatic extract Sanger(1960) Insulin Molecule

Diabetes mellitus:

Diabetes mellitus It is metabolic syndrome which is characterized by hyperglycemia due to deficiency or resistance of insulin

Classification :

Classification Type 1 Type 2 GDM: any degree of glucose intolerance, with onset or first recognition during pregnancy 2-12% in various studies 17% in Indian studies

White classification:

White classification A - Asymptomatic but abnormal GTT B -onset age >20 years or duration <10 years no vascular complications C - onset 10-19 years or duration 10-19 years no vascular complications D - onset <10 years or duration>20 years with vascular complications e.g.; retinopathy or leg artery calcification F - nephropathy R - proliferative retinopathy H -diabetes with heart disease T - diabetes required renal transplant


PREVALENCE Diabetes is most common medical condition encounterd in pregnancy 0.5% and 5% pregnanccies being complicated by diabetes Diabetes is 1.2%in reproductive age women Non pregnant pregnant Type1 - 10% Type1 -73% Type 11 -90% Type11 —27%

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Report of a WHO Study Group. Geneva: World Health Organization; (%)of diabetes In (20-79)years 2011. No. 844.

Diabetes and fertility :

Diabetes and fertility Delayed menarche in Type 1 Menstrual abnormalities Premature Ovarian Failure PCOD

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Genetic Origin Intervene in lesser or greater degree Environmental Factors Immunological Factors Viral Infections Hereditary Factors Identical twin Both parents diabetic One of the parents diabetic and the non diabetic parent with a relative of the 1 st order diabetic or a brother with a diabetic child. Extrinsic Factors Obesity Stress Pregnancy Infections Trauma


POTENTIAL RISK FACTORS suggestive of DIABETES Family history of diabetes mellitus in one first-degree or two second- degree relatives. Poor obstetric history (specifically death of a macrosomic baby, especially with evidence of fetal pancreatic beta cell hyperplasia) unexplained still birth Older women GDM in previous pregnancies Presence of significant glycosuria Polyhydramnios Macrosomic infant in the current pregnancy

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PREGNANCY : A DIABETOGENIC EVENT Langerhans Islets The woman is transformed from a physiological point of view by: Nutritional demands by the fetus Metabolic changes in the mother Placenta as a site of exchange and it’s hormonal effects: Insulin -Progesterone Glucagon -Estrogen Somatotropic Hormone Cortisol Adrenalin Thyroxine Placental lactogen

Pre gestational Diabetes: Types 1 and 2:

Pre gestational Diabetes: Types 1 and 2

Type 1 diabetes:

Type 1 diabetes juvenile onset autoimmune disease destruction of islets of cells Present in child hood and adulthood Insulin deficiency Genetic components and association with HLA-DR3,and HLA-DR4. No association with obesity Baby of affected mother 2%risk of DM Both parents diabetic risk of DM 30%

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Primary Pancreatic Beta-Cell Hyperplasia

Type 2 diabetes:

Type 2 diabetes maturity onset Disease of peripheral insulin resistance usually after 40 yrs but often occur in younger(25years) in south Asian and afro-caribbean Associated with BMI (direct proportional) Type 1 and 2 both have risk of microvascular and macro vascular complications. Higher risk of affected offspring than type1 15% affected offspring if either parent affected 75% affected offspring if both parents affected.

Physiologic changes of glucose metabolism in pregnancy:

Physiologic changes of glucose metabolism in pregnancy Altered carbohydate metabolism in pregnancy Hyperplasia of pancreatic islets

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Doubling insulin production due to hyperplasia b/w 1 st and 3 rd trimester Insulin sensitivity increased initially in 1 st trimester due to placental production of anti-insulin hormones : hPL, cortisol , and glucagon FBS  Postprandial glucose ↑ ↑ Insulin production ↑ ↑ 2 folds in N women Insulin requirements ↑ ↑ in diabetic women

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Progressive insulin resistance as gestation advanced Increase glucose uptake of fetus Increase peripheral uptake Increase glycogensis Reduced hepatic gluconeogensis  renal threshold for glucose  glycosuria

Sign and symptoms :

Sign and symptoms Polyuria , Polyphagia,Polydipsia Easy fatigability Blurring of vision UTI Candidiasis

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EFFECT OF PREGNANCY ON PRE-EXISTING DM Increase requirement for insulin doses Nephropathy , autonomic neuropathy may deteriorate Progress in diabetic retinopathy (2X) Hypoglycemia Diabetic ketoacidosis

Diabetes and pregnancy:

Diabetes and pregnancy Placental structure and function is affected Early IUGR as high BG inhibits trophoblast proliferation Hypertension, renal disease more frequent High glycogen content in placenta

Diabetes and embryogenesis:

Diabetes and embryogenesis Early fetal loss due to apoptosis of blastocyst, modulated by regulatory gene Bax, which is stimulated by high BG Malformation rate 3X higher [4-10%] High BG reduces total cell mass and number of blastocysts, esp in inner cell layer Cardiac 4x Anencephaly 5x Spina bifida 3x Caudal regression syn 212x Arthrogryposis 28x Cleft lip/palate 1.5x Ureteric duplication 23x Renal agenesis 5x Pseudohermaphroditism 11x Anorectal atresia 4x

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INCREASE RISK OF CONGENITAL ABNORMALITIES sacral agenesis, congenital heart disease, neural tube defects Hba1c level Risk normal not increased <8% 5% >10% 25 %

Stillbirths in diabetes:

Stillbirths in diabetes Fetal hypoxia as O 2 is diverted to non-visceral tissues, acidosis Hypokalemia Placental dysfunction Hypoglycemia Oxidative stress Impaired O 2 delivery to foetus as GHb has higher O 2 affinity

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Effects of DM on pregnancy toxemia Preterm labor Infections Urinary Vaginal Wound infection Vascular Retina Renal Acidosis Coma Hydramnios

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Effects of DM on fetus: Embryo Fetus Newborn Abortions Malformations Growth alterations MACROSOMIA IUGR Dystocia Perinatal asphyxia Unexplained iud Metabolic alterations Hypoglycemia Hyocalemia Hyperbilirubinemia Policythemia Jaundice,birth trauma Alterations of maturity Respiratory distress syndrome

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Maternal Hyperglycemia (Placenta) Fetal hyperglycemia Fetal pancreatic hyperplasia Fetal Hyperinsulinemia Delivery Fetal macrosomia Neonatal hypoglycemia Reduced surfactant Polycythemia

Who Should Be Screened:

Who Should Be Screened BMI>25kg/m 2 Women over 25 GDM in previous pregnancy Women with a family history of DM Previous large macrocosmic baby Previous still birth Asian ,white ethnic origin More then 9 babies 31

Value of Screening During the Current Pregnancy :

Value of Screening During the Current Pregnancy Increased screening, identification and treatment can decrease the morbidity and mortality of GDM: Decreased macrosomia, cesarean birth and birth trauma due to a > 4000g infant Decreased neonatal hypoglycemia, hypocalcaemia, hyperbilirubinemia, polycythemia Identify women at future risk for diabetes and those with insulin resistance 32

Screening and Diagnosis of DM:

Screening and Diagnosis of DM Urine testing at each antenatal visit. Timed blood glucose at booking &28 wks or glycosuria is 1+ or more. OGCT OGTT Hba1c Fructose amine

Screening for GDM:

Screening for GDM 1 hr GCT 140 mg % 75 g GTT 2 h: 155 mg % 100 g GTT 1 h: 180 mg % 2 h: 155 mg % 3 h: 140 mg % All venous samples. Normal meals x 3 days No smoking Patient seated 8 – 14 hrs fasting 50 gm glucose Any time of day No regards to meals

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WHO Diabetes criteria – Interpretation of Oral Glucose Tolerance Test:

WHO Diabetes criteria – Interpretation of Oral Glucose Tolerance Test Glucose levels NORMAL Impaired Fasting Glycaemia Impaired Glucose Tolerance Diabetes Mellitus (I.F.G.) (I.G.T.) (D.M.) Venous Plasma Fasting 2 hrs Fasting 2 hrs Fasting 2 hrs Fasting 2 hrs (mmol/l) < 6.1 < 7.8 ≥6.1 & <7.0 <7.8 < 7.0 ≥ 7.8 ≥ 7.0 ≥11.1 (mg/dl) < 110 < 140 ≥110 & <126 <140 < 126 ≥ 140 ≥ 126 ≥ 200

Management of diabetes in pregnancy:

Management of diabetes in pregnancy PRE CONCEPTION COUNSELLING Multidisciplinary approach Optimizing glycaemic control –Aim for HbA 1C 6.1 or less Discuss hypoglycemia Review diet and weight loss Discuss complication of pregnancy Folic acid supplementation Review renal function and blood pressure Retinal assessment Review other medications e.g. ACE inhibitors,statins,smoking cessation

Medical management…..DIAET CONTROL:

Medical management …..DIAET CONTROL Diet Exercise Insulin DIET High carbohydrate, High fibers, Low fat diet

Exercise during pregnancy :

Exercise during pregnancy Upper limb exercises Avoid resistance exercises Walking + swimming+ Breathing exercises + Avoid jogging Pelvic floor exercises

Oral hypoglycemic drugs :

Oral hypoglycemic drugs Oral hypoglycemic often used in type 2 DM, except sulphonylurea and biguanides (metformin) little data available for there safety in pregnancy. Can cross the placenta and can lead to fetal hypoglycemia Can be used as alternate to insulin in type 2 and GDM when self administration difficult due to education or other reasons.

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If preprandial blood glucose levels are greaten than 6 mmol (108 mg %) than patient should be kept on insulin treatment Blood glucose should be measured 4 times a day. Begin insulin with a single long acting injections at bed time Pre breakfast levels should be between 4 & 6 mmol. If more than 6 mmol add three short acting insulin injection. Human insulin is preferred. Monthly glycosylated haemoglobin (HBA1c) or fortnightly glycosylated plasma protein. INSULIN THERAPY

Types of insulin :

Types of insulin Type Examples Onset Peak Duration Rapid acting Lispro 15 min 30-90 min 5 hours Aspart (nova rapid) - - - Glulisine ( apidra - - - Short acting Regular 30 min 2-4 hours 4-8 hours Inter mediate acting NPH ( isophane ) lenate 2-6 hours 4-14 hours 14-20 hours Long acting Ultralenate 6-14 hours Small (or none) 10-16 hours 20-24 hours Glargine 1-2 hours none 24 hours Detemir - - -

Subcutaneous Insulin Therapy:

Subcutaneous Insulin Therapy “Regular” insulin = Humalog, Novalog

Insulin Analogues:

Insulin Analogues 1 . rapid-acting insulin analogs ( lispro ) Cat B concerns about teratogenesis , antibodies formation, growth-promoting properties majority of evidence showed that it does not cross placenta, and has no adverse maternal or fetal effects Long acting insulin analogs ( glargin ) Cat c not well studied

antenatal Management :

antenatal Management Multidisciplinary team . Pregnant diabetic women should ideally be seen in joint diabetic antenatal clinic by obstetrician, diabetologist specialist nurse & a dietitian. Dating scan for viability and gestational age

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SCREENING FOR DIABETIC COMPLICATION microvascular macro vascular Ratinopathy Maculopathy Renal disease Neuropathy CAD

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SCREENING FOR NON DIABETIC CO-MORBIDITIES Auto immune t hyroiditis,Obesity\ Assesment and optimization of glycemic control - RBS less then 9.1 mmol/L - Hb A1c less the 5.8% Advice how to cope with hypoglycemia Proper diet control Insulin regemen

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Patients Month: year: Insulin (s) A: B: Date Time of Test Blood glucose Insulin dose A B Sign Comments here Hypos (time) Urine glucose ketones Sunday PB PC PL PT PS BT Monday PB PC PL PT PS BT OBSTETRIC DIABETIC RECORD


OBSTETRIC MANAGEMENT Antenatal visits should be every 2 week until 32 – 34 weeks and then weekly there after as frequent changes in insulin dosage are required especially in the third trimester. CRL as soon as possible. BPD at 16 weeks.

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Blood for screening of NTD & down syndrome at 16 weeks. Detailed ultrasound at 19 – 20 weeks to exclude fetal anomalies. Serial measurements of fetal head & abdominal circumference. Management of obstetrical complications, like PH, PE, PTL.

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TIME OF DELIVERY Ideally at 38 – 39 weeks. If prior to term (37 weeks) give Dexamethsone with I.V insulin. Delivery after 40 weeks can cause IUD birth trauma & shoulder dystocia due to macrosomia . .

mode of delivery :

mode of delivery Spontaneous vaginal delivery is a primary goal. Elective caesarean section for fetal malpresentation or fetal weight > 4.5 kg. Labour should not be prolonged > 12 hours. Antibiotic should be given prophylactically to avoid wound infection

Post natal care:

Post natal care Breast feeding reduces insulin requirement upto 25 %. POP is safe no effect on sugar levels COCs can be taken Progesotgens injection may cause insulin resistance but not contraindication. IUCd’s can also be used. Better sterilization, if family completed. OGTT between 6 weeks & 3 months after delivery

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