Diabetes in PregnancyHasanuddin, MD

Diabetes in PregnancyEpidemiologyClassificationPathophysiologyMorbidityFetalMaternalDiagnosisTreatment and ManagementReferences

Epidemiology4-6% of pregnancies in the U.S are complicated by DM, accounting for 50-150 thousand babies per year.88% GDM, 8% Type II DM, 4% Type 1 DMPrevalence also varies by race1.5-2% in Caucasians, 5-8% in Hispanic, Asian and African Americans, and up to 15% in some SW Native American groups.

Classification

PathophysiologyHuman Placental Lactogen (HPL)Produced by syncytiotrophoblasts of placenta.Acts to promote lipolysis increased FFA and to decrease maternal glucose uptake and gluconeogenesis. Anti-insulinEstrogen and ProgesteroneInterfere with insulin-glucose relationship.InsulinasePlacental product that may play a minor role.

A Vicious Cycle???

Fetal MorbidityMiscarriagesFrequency directly related to degree of maternal glycemic control.Up to 44% with poorly controlled DM (HbA1C >12).Preterm DeliveryIncrease in both spontaneous and indicated preterm labor (

Fetal MorbidityBirth Defects1-2% risk among the general population.4-8 fold increased risk among preexisting diabetics.Most common defects are CNS and CV, but also an increase in renal and GI abnormalities.Up to a 600 fold increase in caudal regression syndrome.

Fetal MorbidityMacrosomiaDefined as birthweight above 90th % or >4000 grams.Occurs in 15-45% of diabetic pregnancies, a 4-fold increase over normal.Carries many morbidities including birth trauma, RDS, neonatal jaundice and severe hypoglycemia.

Fetal MorbidityGrowth RestrictionAlthough we typically associate maternal DM with macrosomia, growth restriction is fairly common among Type 1 diabetic mothers.Best predictor is presence of maternal vascular disease.

Fetal Morbidity

Fetal MorbidityPolycythemiaHyperglycemia stimulates fetal erythropoeitin production.Can lead to tissue ischemia and infarction.HypoglycemiaThink of as an overshoot mechanism.Baby is used to having lots of maternal glucose so it makes lots of insulin. When born, maternal glucose is no longer available but insulin remains high hypoglycemia.Can lead to seizures, coma and brain damage.

Fetal MorbidityPostnatal hyperbilirubinemiaOccurs in appox. 25%, double that of normal.Thought to be due in large part to polycythemia.Respiratory distress syndrome5-6 fold increased frequency.May be due to a delay in lung maturation or simply due to the increased frequency of preterm deliveries.

Fetal MorbidityPolyhydramniosAmniotic fluid volume >2000 mL.Occurs in 10% of diabetics.Increased risk of placental abruption and preterm labor.

Maternal MorbidityIncreased risk of DKA due to increasingly resistant DM.Increased incidence of UTI due to glucose-rich urine and urinary stasis.Glucosuria is a normal finding of pregnancy but may be much higher in diabetics.Diabetic retinopathyDiabetic nephropathy

Maternal MorbidityDiabetic neuropathyPreeclampsia2-fold increase

DiagnosisGlucose Challenge Test (24-28 wks)50 gram glucose load with blood level 1 hour later.Does NOT require fasting state.Normal finding is 140, need to do a 3 hour glucose tolerance test.

DiagnosisGlucose Tolerance TestDraw a fasting glucose level (normal

Treatment and ManagementObviously the main goal is to maintain good glycemic control.Typically controlled with insulin but oral hypoglycemic agents like glyburide are also showing promise.

Treatment and ManagementObstetrical managementSerial US to trend fetal growth, AFI and fetal anatomyPostpartum, 95% of GDM mothers return to normal glucose tolerance, and require no further insulin.Glucose tolerance screen 2-4 mo. postpartum to detect those that remain diabetic.

Referenceswww.acog.orgCurrent Obstetric & Gynecologic Diagnosis & Treatment (2003)Williams Obstetrics (2005)