Incidence 2-3% of pregnancies are complicated by diabetes mellitus Normal Physiology in Pregnancy in early pregnancy (T1) i...
Incidence
- 2-3% of pregnancies are complicated by diabetes mellitus
Normal Physiology in Pregnancy
- in early pregnancy (T1) insulin secretion is increased and its anabolic
actions are potentiated, decreasing fasting maternal glucose levels and
promoting maternal energy storage - in later pregnancy (T2,T3) insulin resistance develops due to anti-insulin factors: human placental lactogen (increased secretion with
growth of the placenta) and cortisol - result: higher fasting glucose and enhanced lipolysis (increased FFA,TG, lipids, ketones) to supply energy for fetal growth
Classification of Diabetes Mellitus (DM)
- Insulin Dependent DM (Type I)
- Non-Insulin Dependent DM (Type II)
- Gestational Diabetes: DM diagnosed during pregnancy
- Maternal
- hypertension/PET, polyhydramnios, pyelonephritis/UTI
- ketoacidosis, diabetic coma, worsening retinopathy in Type I or Type II, NOT in GDM
- Fetal
- maternal hyperglycemia leads to fetal hyperinsulinism : accelerated anabolism and macrosomia result
- increased congenital anomalies and miscarriage from preconception or T1 hyperglycemia
- cardiac (VSD), neural tube, genitourinary, gastrointestinal and MSK (sacral agenesis) defects
- IUGR if mother has end-organ damage
- delayed fetal lung maturity
- preterm labour/prematurity
- increased incidence of stillbirth
pregnancies complicated by GESTATIONAL diabetes do not manifest an increased risk of congenital anomalies because it develops later (i.e. after T1)
- Neonatal macrosomia and associated birth trauma, hypoglycemia, hyperbilirubinemia and jaundice, hypocalcemia, polycythemia, and RDS
Treatment of DM in Pregnancy
T1
- see prior to pregnancy to optimize glycemic control (will reduce risk of congenital anomalies)
- since oral hypoglycemics are contraindicated, Type IIÃs must be switched to insulin
- counsel : potential complications and risks
- advise preconception folic acid
- see early and date pregnancy
- consult internist and dietitian to manage insulin and diet
- measure hemoglobin A 1C early in T1 or preconception if possible; this gives an indication of glycemic control during embryogenesis and can be used to estimate risk of birth defects
- initial evaluations: 24 hour urine (protein and creatinine clearance), retinal exam, ECG, urine C&S, hemoglobin A 1C
- throughout pregnancy monitor BP, urine dip (protein/glucose/ketones), weight gain, blood glucose (self-monitor) every visit and occasional urine C&S and hemoglobin A1 C
- in early pregnancy transfer of glucose and amino acids to the fetus results in a tendency toward maternal hypoglycemia
- nausea and vomiting may reduce food intake, therefore may need to decrease insulin dose
- clinic visits 2 weekly
- MSAFP (at 16 weeks) and 3 detailed U/S examinations
- consider fetal echocardiography to exclude congenital heart defect
- admit for blood sugar control if needed
- in the second half of pregnancy, the diabetogenic action of placental hormones outweigh the continuous siphoning of glucose by the fetus
- demand for insulin is increased, hence insulin dosages need to be increased
- clinic visits weekly
- fetal surveillance (BPP, NST); frequency depends on risk
- < 36 weeks = weekly
- > 36 weeks = weekly or biweekly
- timing of delivery dependent upon fetal and maternal risk factors
- can wait for spontaneous labour if glucose well-controlled and BPP normal
- induce by 40 weeks
Labor
- increased risk of CPD (Cephalopelvic Disproportion), shoulder dystocia with babies weighing over 4000 g
- elective C-section for predicted birth weights of greater than 4500 g (controversial)
- during labour monitor sugars 1h with patient on insulin and dextrose drip and aim for blood sugar of 3.5 to 6.5 to reduce the risk of neonatal hypoglycemia
Postpartum
- increased risk of hypoglycemia
- once eating a regular diet, resume insulin at two-thirds of prepregnancy dose and monitor 6 hourly
