DIABETES MELLITUS IN

PREGNANCY (INT)
HM Sulchan Sofoewan
Division of Fetomaternal Department of
Obstetrics and Gynecology Faculty of
Medicine Gadjah Mada University
 INTRODUCTION
 DM in pregnancy is a medical complication
of pregnancy
 The incidence is 3,5% of all pregnancy
 DM in pregnancy consist of Gestational
Diabetes (GD) the diagnose is made during
pregnancy (90%), and Pregestational
Diabetes (PGD) the diagnose is made
before pregnancy consist of DM type 1 and
type 2 (10%).
 PATHOPHYSIOLOGY
 Increasing of perinatal morbid and mortality is
correllated with hyperglycemia state.
 Pregnancy is a diabetonic state.
 The placental transfer of glucose is fascilated
difusion, maternal hyperglycemia – fetal
hyperglycemia – hyperplasia of fetal beta cell
Langerhans – fetal hyperinsulinemia – glycogen
and fat deposite – macrosomia (Pedersen
hypothesis)
HIPOTESIS PEDERSEN
 Maternal hyperglycemia
 Fetal hyperglycemia
 Fetal pancreatic hyperplasia
 Fetal hyperinsulinemia
 ___!______!______!_______!________!_____
 Macro Organo Neona Erythro Surfaktan
 Somia megaly tal risk poesis Neonatal
 Traum Neona RDS
 Vag del policyt
GESTATIONAL DIABETES
 CH intolerance with onset / recognition
during pregnancy, induced by pregnacy
 Fasting hyperglycemia ( < 105 class A1, >
105 class A2)
 Fasting hyperglycemia, macrosomia, fetal
anomalies not increase
 Class A2 unexplained stillbirth,
hypertension and increasing of CS
MACROSOMIA
 Maternal hyperglycemia, caused fetal
hyperinsulinemia, excessive fat deposition,
anthropometrically different from LGA
infant
 \shoulder dystocia, cephalopelvic
disproportion
 Neonatal hyperinsulinemia, hypoglycemia
SCREENING
 Performed between 24 – 28 weeks of gest in
women not known to have glucose intoleran
 Using 50 g oral glucose, if value > 140
mg/dl, then are test with 100 g oral glucose
 Dx: with 75 g 2 hours or 100 g 3 hours oral
glucose tolerance test after an overnight fast
DIAGNOSIS
 Dx of GD using 100 g oral glucose
 Plasma glucose
 Timing (1979) (1982)
 Fasting 105 95
 1 hour 190 180
 2 hours 165 155
 3 hours 145 140
MANAGEMENT
 Insulin therapy recommended when
standard diet therapy does not maintain:
 the fasting plasma glucose < 105 mg/dl, 2
hours PP < 120 mg/dl
 Or capillary glucose level < 95 mg/dl
fasting (1997)
 Or nutritional management fails maintain
fasting blood glucose < 95 mg/dl, or 2 hours
PP blood glucose level < 120 mg/dl
 DIET
 The goal of diet therapy: 1) provide nutrient for
the mother and fetus, 2) control glucose level, and
3) prevent starvation ketosis
 Significant caloric restriction (1200-1800
kcal/day) has been shown to reduce
hyperglycemia and and plasma triglyceride with
no increse in ketonuria.
 Although maternal weight gain and macrosomia
may be decrease, the safety has not been
established
OBSTETRICAL
MANAGEMENT
 GD who do not require insulin seldom
require early delivery or intervention
 There is no consessus antepartum fetal
testing necessary
 Elective induction to curtail fetal growth
and prevent shoulder dystocia controversial
 If require insulin, receive antepartum fetal
testing and managed as overt diabetes
POSTPARTUM CARE
 50% women with GD developing overt
diabetes within 20 years
 Should undergo glucose evaluation 6 – 12
weeks after delivery
 A 75 g oral glucose tolerance test is
recommended
 Fasting < 115 mg/dl (no diabetes), < 140
mg/dl (impaired glucose tolerance), > 140
mg/dl (diabetes)
PREGESTATIONAL OVERT
DIABETES
 Known to have diabetes before pregnancy
 Using White classification, the end organ
derangement, involving eyes, kidney and
heart, have significant effects on pregnancy
 Dx ketoacidosis or random plasma glucose
> 200 mg/dl, or fasting plasma glucose >
126 mg/dl
 Embrio, fetus and mother can experiences
complication
 WHITE CLASSIFICATION OF
DIABETIC PREGNANCIES
 A. GTT abnormal, no symptoms, euglycemia with
appropriate diet without insulin
 B. Adult onset (age >=20), short duration (<10
yrs)
 C. Relatively young onset (age 10-19) or relatively
long duration (10-19 yrs)
 D. Very young onset (age < 10 yrs) or very long
duration (>= 20 yrs) or evidence of background
retinopathy.

Continue
 F. Renal disease
 R. Proliferative retinopathy
 RF. Both renal disease and proliferative
retinopathy
 G. Multiple reproductive failure (habitual
abortion and/stillbirths)
 H. Arteriosclerotic heart disease
 T. Pregnancy after renal transplantation
 EFFECTS ON THE FETUS-
NEONATE
 Abortion: Initial glycohemoglobin A1 >12%.
 Malformation: incidence 5-10%, is not associated
with chromosomal abnormalities, poorly controle
preconception and early in pregnancy, lower
glycosylated hemoglobin values.
 Unexplained fetal demise: no factor, no plac insuf,
growth restiction, oligohydramnion
 Hypothesis: hyperglycemia mediated chronic
aberration in transport of oxygen and fetal metab
 Macrosomia, hydramnios (fetal polyuria), preterm
NEONATAL EFFECTS
 Respiratory distress: lung maturation delaye
 Hypoglycemia: hyperplasia beta islet cell
 Hypocalcemia: cause has not been explain
 Hyperbilirubinemia: pathogenesis uncertain
 Cardiac hypertrophy: macrosomia,
hyperinsulinemia
 Inheritance of diabetes: if both parents has
diabetes, the risk 20%.
MATERNAL COMPLICATION
 Preeclampsia:
 Ketoacidosis
 Infections
 Diabetic nephropathy
 Diabetic retinopathy
 Diabetic neuropathy
MANAGEMENT
 Preconception: prevent early pregnancy loss
and congenital marformation,
preconceptional glucose control by insulin
preprandial glucose level 70-100 mg/dl,
postprandial <140 and < 120 at 1 and 2
hours respectively, folate 400 ug given
preconceptional and during early pregnancy
Continue
 First trimester: Monitoring of glucose control,
hospitalized during firs trim to glucose control
program, education and to assess the extent of
vacular complication, total caloric intake 30-35
kcal/kg, given as three meals and three snacks
daily intake of: 55 % CH, 20% protein, and 25 %
fat, less than 10% saturated fat.
 Obese may be manage with lower caloric as long
as weight loss and ketonuria are avoided
 Continue
 Second trim:
 US at 18-20 weeks to detect NTD
 Third trim:
 Weekly visit to monitor glucose control and
evaluate for PE, serial US at 3-4 weeks interval to
evaluate exessive and insufficiency growth and
AF volume
 Hospitalized for poorly control and hypetension
Continue
 Fetal suveillance program begin between
26-32 weeks depend on clinical risk factor
for fetal death, ante partum testing at least
weekly
DELIVERY
 Delivery is planned after 38 weeks
 Class B and C recommended CS to avoid
traumatic birth
 More advanced diabetes, with vascular
disease CS
 Labor induction when fetus not large and
cervix favorable
DELIVERY
 1. Low risk:
 - Good glucose control
 - No vasculopathy
 - Normal fetal growth
 - Good fetal monitoring
 - No prior stillbirth
 Delivery on 40 weeks of gestation,
expectative spontan vaginal delivery.
DELIVERY
 2. High risk:
 - Bad glucose control
 - There is vasculopathy
 - Abnormal fetal growth
 - Polyhydramnion
 - Hystory of stillbirth
 Delivery around 38 weeks of gestation if lung is
mature, CS depend on obstetric indication.
DELIVERY
 3. Macrosomia:
 Estimation of fetal weight > 4500 g the
 methode of delivery is CS.
 THANK YOU