Presentation on theme: "DIABETES IN PREGNANCY BY DR. SHUMAILA ZIA. DIABETES IN PREGNANCY INCIDENCE -- 34/1000 pregnancy."— Presentation transcript:
DIABETES IN PREGNANCY BY DR. SHUMAILA ZIA
DIABETES IN PREGNANCY INCIDENCE -- 34/1000 pregnancy.
CARBOHYDRATE METABOLISM DURING PREGNANCY: Increased tissue resistance to insulin. Normally glucose level stays constant b/w mmol/l except after meals. With increasing insulin resistance, homeostasis can only be maintained by doubling insulin secretion from the end of 1 st to 3 rd 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. 1.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 1.Established DM: - Type IDDM (more common in peg.) - Type 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
Whites classification 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 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
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 followFetal protective mechanism Insulin appear in fetal circulation at 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. 1.Congenital Malformation: 410 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.
MANAGEMENT. I.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 CONTROLMore difficult RETINOPATHYProliferative 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 1 st 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 OSULLIVAN 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.
WHO OGTT 75 grams glucose in 250ml water after fasting sample Blood SampleGlucose LevelRemarks Fasting< 6 mmol/lD M excluded 6- <7.8 mmol/lImpaired glucose tolerance > 7.8 mmol/lFrank D M 2 Hours PP<7.8 mmol/lD M excluded > 7.8-< 11 mmol/lImpaired glucose tolerance >11 mmol/lFrank D M
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 Kcal/Kg ideal body weight No more than 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 2/3 rd of daily dose before breakfast.2/3- p.insulin+1/3-NPH. 1/3 rd in evening.1/2+ 1/2. p.insulin+NPH.
DOSAGE SCHEDULE A.In insulin dependent, adjust dose especially in later half of pregnancy B.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 C.In NIDDM control on diet, start insulin if Pre-prandial glucose persistantly > 6mmol/l
OTHER FORMULAS TO CONTROL DIABETES. 1.wt× _15 wks. Wt× _25wks wt× _35wks. Wt×1 u 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 1.ANTENETAL CARE: A.-1 ST trimester : - good glucose control & - USG - 2 nd trimester: - USG at wk.(cong. An.) - USG at 20-22wk.(cardiac An.) - 3 rd trimester: - Care for. Polyhydramnios. PIH. F. macrosomia. IUD. Pre-term labour
2. DELIVERY: a) Time of Delivery: - Well controlled DM weeks - Uncontrolled DM 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 mmol/l Give also 10% D/W in other I/ V 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 wk. followed by weekly 3. FETAL SURVEILLANCE: a) USG: - AC– good indicator of fetal wt. so, - AC+ AFI from 24 weeks, fortnightly b) CTG: 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 1.RESPIRATORY SYSTEM 1.Resp distress syndrome 2.Transient tachypnoea of the newborn 2.HYPOGLYCAEMIA 1.Blood glucose checked at 2,4,6& 12 hours of age. 2.If <1.4mmol/l at 4 hours, I/v 10% dextrose. 3.Start feeding by 2 hours & continue at 3-4 hours interval. 3.HYPERBILI RUBINAEMIA 1.Vit K 1mg Inj. 2.Phenobarbitone 2.5-5mg /kg daily 3.Phototherapy 4.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)
DONT 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