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DIABETES IN PREGNANCY. BY DR. SHUMAILA ZIA. DIABETES IN PREGNANCY. INCIDENCE -- 3—4/1000 pregnancy. CARBOHYDRATE METABOLISM DURING PREGNANCY:. Increased tissue resistance to insulin. Normally glucose level stays constant b/w 4-4.5 mmol/l except after meals.
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DIABETES IN PREGNANCY BY DR. SHUMAILA ZIA
DIABETES IN PREGNANCY INCIDENCE -- 3—4/1000 pregnancy.
CARBOHYDRATE METABOLISM DURING PREGNANCY: • Increased tissue resistance to insulin. • Normally glucose level stays constant b/w 4-4.5 mmol/l except after meals. • With increasing insulin resistance, homeostasis can only be maintained by doubling insulin secretion from the end of 1st to 3rd trimester b/c insulin resistance increases with gestation. • Exact etiology unknown, most probably b/c of increased production of preg. associated hormones or free cortisol, like HPL (Human placental lactogen) most important.
INFLUENCE OF PREGNANCY ON CHO MET. • Increased insulin resistance –increased production of insulin by pancreas (hyperplasia/ hypertrophy) • Adequate insulin production may become inadequate to meet increased demand during pregnancy –gestational DM • Abnormally high tissue insulin resistance. 2. Known diabetic controlled on diet may need insulin 3. Medicine dependent need enhanced medication.
CHO. DERANGEMENTS IN PREGNANCY • Established DM: - Type- 1----IDDM (more common in peg.) - Type- 2----NIDDM 2. Gestational DM: - Appear in preg. mostly disappear after preg. 3. Impaired Glucose tolerance: - CHO metabolism altered - Some develop frank DM in later half - So, should be managed as DM
White’s classification Class D Insulin-treated diabetic Onset under age 10 Duration more than 20 years Background retinopathy Class F Diabetic nephropathy Class H Cardiac disease Class R Proliferative retinopathy Class A1 Abnormal glucose tolerance test with normal fasting capillary (95 mg/dl) and postprandial (120 mg/dl) glucose levels Controlled with diet alone Class A2 Abnormal glucose tolerance test with abnormal fasting or postprandial glucose levels Treated with diet and insulin Class B Insulin-treated diabetic Onset over age 20 years Duration less than 10 years No vascular disease or retinopathy Class C Insulin-treated diabetic Onset between ages 10 and 20 years Duration between 10 and 20 years Background retinopathy
EFFECTS OF DM ON PREGNANCY • Fetal glucose level follows maternal one closely until facilitated diffusion saturated or maternal glucose reaches 11-13mmol/l then fetus dose not follow—Fetal protective mechanism • Insulin appear in fetal circulation at 10-12 wk. • In maternal DM, fetus has hyperinsulinemia- acting as growth promoting hormone-- fetal macrosomia • F. hyperinsulinemia rather than F. hyperglycemia is responsible for adverse effects.
ADVERSE FETAL EFFECT OF DM. • Congenital Malformation: 4—10 times higher than normal. Exact mechanism of teratogenicity not known. Said to be directly related to conc. Of glucose at time of organogenesis. So, in known diabetics ---more chance of Cong. abnormality.
ADVERSE FETAL EFFECT OF DM. Cont-- • Structural abnormalities: CVS, Skeletal, CNS, GIT. • Fetal caudal regression syndrome: Abnormality of vertebrae below T10. • Sacral agenesis: missing sacrum. • Dislocation of hips. • Talipes. • Spina bifida. • Renal anomalies. • Urinary or fecal incontinence.
Cong. An. of infants of diabetic mother • Skeletal and central nervous system Caudal regression syndrome Neural tube defects Microcephaly • Cardiac Transposition of the great vessels Ventricular septal defects Coarctation of the aorta defects or patent ductus arteriosus Atrial septal defects Cardiomegaly • Renal • Hydronephrosis • Renal agenesis • Urethral duplication • Gastrointestinal • Duodenal atresia • Anorectal atresia • Small left colon syndrome • Other • Single umbilical artery
ADVERSE FETAL EFFECT OF DM. Cont-- 2.Spontaneous miscarriage: Due to cong. Anomalies. 3.Fetal macrosomia: - Due to f. hyperinsulinaemia. body wt 4kg. - f. macrosomia----large for dates. - Prolonged obstructed labour. - Shoulder dystosia. 4.IUGR: - placental function compromised. - poor prognosis.
ADVERSE FETAL EFFECT OF DM. Cont-- 5. Polyhydramnios: - fetal. polyuria—osmotic diuresis. - premature labour. - malpresentation. 6.Pre-eclempsia: - perinatal mortality double. 7.RDS: - diabetes delays production of surfactant. 8. Unexplained intrauterine death. 9. Perinatal mortality: - 5times higher.
MANAGEMENT. • INITIAL MANAGEMENT: A:known diabetic: - Pre-pregnancy care - Early booking --- optimal control --- USG B:Gestational diabetes: - Many women go unrecognized &diagnosed after poor obs. Outcome.
EFFECTS OF PREGNANCY ON DM CONTROL More difficult RETINOPATHY Proliferative retinopathy may progress so careful ophthalmic assessment. NEPHROPATHY • No permanent deterioration in renal function. • Fetal outcome good if preclampsia does not supervene & glucose control good. • End stage renal disease – termination of pregnancy.
INITIAL MANAGEMENT Cont-- SCREENING: a. Clinical Features: cheap way of screening. women at high risk of gest. D.M. *diabetes in 1st degree relatives. *maternal obesity. Wt.90kg. *persistent glycosuria. * previous hx. of large baby. *previous hx. of unexplained still birth. *previous birth of cong. malformed baby. *polyhydramnios /macrosomia in current preg.
INITIAL MANAGEMENT Cont-- b. Random glucose test. cut of value 6.4 mmol/l with in 2 hr& 5.8mmol/l after 2 hrs of meal-----OGTT. c. Fasting glucose test. cut of value 4.8mmol/l-----OGTT. d. Glucose challenge test: At 28wks. 50g glucose given. 1hr later blood taken--if >7.8mmol/l-OGTT.
DIAGNOSTIC TEST. • Oral glucose tolerance test. Gold standard investigation. If screening test is +v O’SULLIVAN METHOD. - after an overnight fast >8hrs. - a fasting blood sample taken. - Give 100g glucose in 250ml water. - Take blood sample ½ hrly for next 3 hrs.
Abnormal results: if values exceeds this: fasting= 5.0mmol/l 1hr = 9.2mmol/l 2hr = 8.1mmol/l 3hr = 6.9mmol/l
WHO OGTT75 grams glucose in 250ml water after fasting sample
II. Further Management. • Medical management. • Obstetrical management. MEDICAL MANAGEMENT: combined care –obstetrician + endocrinologist. a) TREATMENT MODLITIES: - diet. - diet + insulin.
1. Diet: Three meals and three snacks 30-35 Kcal/Kg ideal body weight No more than 10-12 Kg weight gain 50% of energy carbohydrates (unrefined), 30% fat and 20% proteins Review diet history to identify major areas of reduction of caloric intake Insulin: see later Alert the patients and relatives about the possibility of hypoglycemia and measures to counteract
2.INSULIN THERAPY. • Tm of choice - does not cross placenta. - Short acting. - Long acting. • Insulin regimen: • four times daily regimen; - short acting insulin---3 times after meal. - long acting---------------at night.
2.INSULIN THERAPY Cont-- BIPHASIC REGIMEN: • Fixed combination of medium & short acting insulin 70:30 is given in 2DD dosage. • One before breakfast and other before dinner • 2/3rd of daily dose before breakfast.2/3-p.insulin+1/3-NPH. • 1/3rd in evening.1/2+ 1/2. p.insulin+NPH.
DOSAGE SCHEDULE • In insulin dependent, adjust dose especially in later half of pregnancy • If started during preg. Initially start 6 hourly short acting 6 units/dose but at night long acting 10 units For biphasic regimen start 20units/day • In NIDDM control on diet, start insulin if Pre-prandial glucose persistantly > 6mmol/l
OTHER FORMULAS TO CONTROL DIABETES. 1.wt× 0.7------6_15 wks. Wt× 0.8 ---15_25wks wt×0.9 ---25_35wks. Wt×1 u----36-40 wks. 2.wt/2. total dose. 3. Sliding scale. 4. BSL -5/20= single dose. 5. Mean of all readings of bld sugar profile/5.
MONITORING • Objective is to maintain - Fasting glucose------< 5.5 mmol/l - P P ---------------------<7.5 mmol/l a. Blood glucose level: - In U K ---- test 4 times (3 pre-meal & 1 at bed time) - In U S A – after meal measurements also taken b/c it correlate better with fetal wt. - Pre-breakfast high measurement may be due to rebound phenomenon after nocturnal hypoglycemia
b. HbA1C (glycosilated Hb.): Glucose irreversibly bound to Hb. - Indicates previous 2 months glucose control - Repeat monthly basis - For good control should be <8%.
OBSTETRICAL MANAGEMENT • ANTENETAL CARE: • -1ST trimester : - good glucose control & - USG - 2nd trimester: - USG at 18-20 wk.(cong. An.) - USG at 20-22wk.(cardiac An.) - 3rd trimester: - Care for . Polyhydramnios . PIH . F. macrosomia . IUD . Pre-term labour
2. DELIVERY: a) Time of Delivery: - Well controlled DM --- 39-40 weeks - Uncontrolled DM ----- 38 weeks b) Mode of Delivery: - Vaginal delivery is mode of choice - Low threshold for C- section
c) Management During Labour: *Insulin therapy: Give I/V insulin 1 unit/h if, . Labour established . Induction of labour . Elective C-section Dilute insulin 20 U (0.2ml) in 19.8 ml N/S . Infuse 1 ml (1 U)/ hour. Measure glucose 1 hourly Aim: Maintain glucose between 4.5-5.5 mmol/l Give also 10% D/W in other I/ V line @ 1L/8 hourly
* OBSTETRIC Mx:- Induction of labour – as usual - good pain relief - avoid milking of U cord - Early clamping of U cord - call neonatologist
2. VISIT FREQUENCY: -Fortnightly from 24-32 wk. followed by weekly 3. FETAL SURVEILLANCE: a) USG: - AC– good indicator of fetal wt. so, - AC+ AFI from 24 weeks , fortnightly b) CTG: - 2-3 times/week from 36 weeks onward c) Doppler: d) Biophysical Profile:
POST PARTUM CARE • CARE OF THE MOTHER • Fall in insulin requirement in the puerperium. • CARE OF THE BABY • RESPIRATORY SYSTEM • Resp distress syndrome • Transient tachypnoea of the newborn • HYPOGLYCAEMIA • Blood glucose checked at 2,4,6& 12 hours of age. • If <1.4mmol/l at 4 hours, I/v 10% dextrose. • Start feeding by 2 hours & continue at 3-4 hours interval. • HYPERBILI RUBINAEMIA • Vit K 1mg Inj. • Phenobarbitone 2.5-5mg /kg daily • Phototherapy • Exchange transfusion
NEWBORN MAANAGEMENT • SERIALLY ASSESS CAPILLARY GLUCOSE OF THE NEONATE ESPECIALLY IN THE FIRST 12 HOURS. REPLACE GLUCOSE IF THE GLUCOSE LEVEL IS LESS THAN 45 MG/DL • IF THE HEMATOCRIT VALUE EXCEEDS 70, EXCHANGE TRANSFUSION • SERIALLY MONITOR BILIRUBIN LEVEL.
CONTRACEPTION • Estrogen containing allowed with need for tight control unless vascular disease • Progestin only allowed • IUCD allowed increased method failure • Barrier methods allowed • Sterilization should be considered especially women with contraindications to pregnancy (proliferative retinopathy, cardiopathy, nephropathy, gastropathy and other vascular lesions)
DON’T FORGET • OGTT at 6 weeks to confirm disappearance of impaired glucose tolerance
SUMMARY • DM is a common and serious problem for the mother and fetus • Prompt management of preexisting DM should start BEFORE pregnancy • Insulin dosage schemes differ but the therapeutic aim is the same • GDM should be sought in all pregnant women with few exceptions