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.

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 insulin3. Medicine dependent need enhanced medication.

CHO. DERANGEMENTS IN PREGNANCY1. Established DM: - Type- 1----IDDM (more common in peg.) - Type- 2----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

White’s classificationClass A1Abnormal glucose tolerance test with normal

fasting capillary (95 mg/dl) and postprandial (120 mg/dl) glucose levels Controlled with diet alone

Class A2Abnormal glucose tolerance test with abnormal

fasting or postprandial glucose levels Treated with diet and insulin

Class BInsulin-treated diabeticOnset over age 20 yearsDuration less than 10 yearsNo vascular disease or retinopathy

Class CInsulin-treated diabeticOnset between ages 10 and 20 yearsDuration between 10 and 20 yearsBackground retinopathy

Class DInsulin-treated diabeticOnset under age 10Duration more than 20 yearsBackground retinopathy

Class FDiabetic nephropathy

Class HCardiac disease

Class RProliferative 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.

1. 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 systemCaudal regression syndromeNeural tube defectsMicrocephaly

• CardiacTransposition of the great

vessels Ventricular septal defectsCoarctation of the aortadefects or patent ductus

arteriosusAtrial septal defectsCardiomegaly

•RenalHydronephrosisRenal agenesisUrethral duplication

•GastrointestinalDuodenal atresiaAnorectal atresiaSmall left colon syndrome

•OtherSingle 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.

Infant of diabetic mother.

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

CONTROL More difficultRETINOPATHY 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

Blood Sample Glucose Level Remarks

Fasting < 6 mmol/l D M excluded

6- <7.8 mmol/l Impaired glucose tolerance

> 7.8 mmol/l Frank D M

2 Hours PP <7.8 mmol/l D M excluded

> 7.8-< 11 mmol/l Impaired glucose tolerance

>11 mmol/l Frank 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 snacks30-35 Kcal/Kg ideal body weightNo more than 10-12 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

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

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/dayC. 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 MANAGEMENT1. ANTENETAL CARE:A. -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 weekly3. 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 CARECARE OF THE MOTHER

Fall in insulin requirement in the puerperium. CARE OF THE BABY1. RESPIRATORY SYSTEM

1. Resp distress syndrome2. Transient tachypnoea of the newborn

2. HYPOGLYCAEMIA1. 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 RUBINAEMIA1. Vit K 1mg Inj.2. Phenobarbitone 2.5-5mg /kg daily3. 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)

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

THANK YOU