2DIABETES IN PREGNANCYINCIDENCE -- 3—4/1000 pregnancy.
3CARBOHYDRATE 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 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.
4INFLUENCE 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 DMAbnormally high tissue insulin resistance.2. Known diabetic controlled on diet may need insulin3. Medicine dependent need enhanced medication.
5CHO. DERANGEMENTS IN PREGNANCY Established DM:- Type IDDM (more common in peg.)- Type NIDDM2. 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
6White’s classification Class A1Abnormal glucose tolerance test with normal fasting capillary (95 mg/dl) and postprandial (120 mg/dl) glucose levels Controlled with diet aloneClass A2Abnormal glucose tolerance test with abnormal fasting or postprandial glucose levels Treated with diet and insulinClass BInsulin-treated diabeticOnset over age 20 yearsDuration less than 10 yearsNo vascular disease or retinopathyClass COnset between ages 10 and 20 yearsDuration between 10 and 20 yearsBackground retinopathyClass DInsulin-treated diabeticOnset under age 10Duration more than 20 yearsBackground retinopathyClass FDiabetic nephropathyClass HCardiac diseaseClass RProliferative retinopathy
7EFFECTS 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 mechanismInsulin appear in fetal circulation at wk.In maternal DM, fetus has hyperinsulinemia- acting as growth promoting hormone-- fetal macrosomiaF. hyperinsulinemia rather than F. hyperglycemia is responsible for adverse effects.
8ADVERSE 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 ofCong. abnormality.
9ADVERSE 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.
10Cong. An. of infants of diabetic mother Skeletal and central nervous systemCaudal regression syndromeNeural tube defectsMicrocephalyCardiacTransposition of the great vesselsVentricular septal defectsCoarctation of the aortadefects or patent ductus arteriosusAtrial septal defectsCardiomegalyRenalHydronephrosisRenal agenesisUrethral duplicationGastrointestinalDuodenal atresiaAnorectal atresiaSmall left colon syndromeOtherSingle umbilical artery
11ADVERSE 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.
14MANAGEMENT. INITIAL MANAGEMENT: A:known diabetic: - Pre-pregnancy care - Early booking optimal control--- USGB:Gestational diabetes:- Many women go unrecognized&diagnosed after poor obs. Outcome.
15EFFECTS OF PREGNANCY ON DM CONTROL More difficultRETINOPATHY Proliferative retinopathy may progress so careful ophthalmic assessment.NEPHROPATHYNo permanent deterioration in renal function.Fetal outcome good if preclampsia does not supervene & glucose control good.End stage renal disease – termination of pregnancy.
16INITIAL 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.
17INITIAL 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.
18DIAGNOSTIC TEST. Oral glucose tolerance test. Gold standard investigation.If screening test is +vO’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.
20WHO OGTT 75 grams glucose in 250ml water after fasting sample Blood SampleGlucose LevelRemarksFasting< 6 mmol/lD M excluded6- <7.8 mmol/lImpaired glucose tolerance> 7.8 mmol/lFrank D M2 Hours PP<7.8 mmol/l> 7.8-< 11 mmol/l>11 mmol/lFrank D M
21II. Further Management. Medical management. Obstetrical management. combined care –obstetrician + endocrinologist.a) TREATMENT MODLITIES:- diet.- diet + insulin.
221. Diet:Three meals and three snacks30-35 Kcal/Kg ideal body weightNo more than Kg weight gain50% of energy carbohydrates (unrefined), 30% fat and 20% proteinsReview diet history to identify major areas of reduction of caloric intakeInsulin: see laterAlert the patients and relatives about the possibility of hypoglycemia and measures to counteract
232.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.
242.INSULIN THERAPY Cont-- BIPHASIC REGIMEN:Fixed combination of medium & short actinginsulin 70:30 is given in 2DD dosage.One before breakfast and other before dinner2/3rd of daily dose before breakfast.2/3-p.insulin+1/3-NPH.1/3rd in evening.1/2+ 1/2. p.insulin+NPH.
25DOSAGE SCHEDULEIn insulin dependent, adjust dose especially in later half of pregnancyIf started during preg. Initially start 6 hourly short acting 6 units/dose but at night long acting 10 unitsFor biphasic regimen start 20units/dayIn NIDDM control on diet, start insulin ifPre-prandial glucose persistantly > 6mmol/l
26OTHER 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.
27MONITORING Objective is to maintain - Fasting glucose------< 5.5 mmol/l- P P <7.5 mmol/la. Blood glucose level:- In U K ---- test 4 times (3 pre-meal & 1 at bed time)- In U S A – after meal measurements also takenb/c it correlate better with fetal wt.- Pre-breakfast high measurement may be due torebound phenomenon after nocturnal hypoglycemia
28b. HbA1C (glycosilated Hb. ): Glucose irreversibly bound to Hb b. HbA1C (glycosilated Hb.): Glucose irreversibly bound to Hb. - Indicates previous 2 months glucose control - Repeat monthly basis - For good control should be <8%.
29OBSTETRICAL MANAGEMENT ANTENETAL CARE:-1ST trimester : good glucose control &- USG- 2nd trimester: - USG at wk.(cong. An.)- USG at 20-22wk.(cardiac An.)- 3rd trimester: Care for. Polyhydramnios PIH. F. macrosomia IUD. Pre-term labour
302. 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
31c) Management During Labour: 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
32* OBSTETRIC Mx:- Induction of labour – as usual - good pain relief- avoid milking of U cord- Early clamping of U cord- call neonatologist
332. VISIT FREQUENCY: -Fortnightly from 24-32 wk. followed by weekly 3 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:
34POST PARTUM CARE CARE OF THE MOTHER CARE OF THE BABY Fall in insulin requirement in the puerperium.CARE OF THE BABYRESPIRATORY SYSTEMResp distress syndromeTransient tachypnoea of the newbornHYPOGLYCAEMIABlood 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 RUBINAEMIAVit K 1mg Inj.Phenobarbitone 2.5-5mg /kg dailyPhototherapyExchange transfusion
35NEWBORN MAANAGEMENTSERIALLY ASSESS CAPILLARY GLUCOSE OF THE NEONATE ESPECIALLY IN THE FIRST 12 HOURS. REPLACE GLUCOSE IF THE GLUCOSE LEVEL IS LESS THAN 45 MG/DLIF THE HEMATOCRIT VALUE EXCEEDS 70, EXCHANGE TRANSFUSIONSERIALLY MONITOR BILIRUBIN LEVEL.
36CONTRACEPTIONEstrogen containing allowed with need for tight control unless vascular diseaseProgestin only allowedIUCD allowed increased method failureBarrier methods allowedSterilization should be considered especially women with contraindications to pregnancy (proliferative retinopathy, cardiopathy, nephropathy, gastropathy and other vascular lesions)
37DON’T FORGETOGTT at 6 weeks to confirm disappearance of impaired glucose tolerance
38SUMMARY DM is a common and serious problem for the mother and fetus Prompt management of preexisting DM should start BEFORE pregnancyInsulin dosage schemes differ but the therapeutic aim is the sameGDM should be sought in all pregnant women with few exceptions