Diabetes in Pregnancy Ryan Agema MS III.

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Presentation transcript:

Diabetes in Pregnancy Ryan Agema MS III

Diabetes in Pregnancy Epidemiology Classification Pathophysiology Morbidity Fetal Maternal Diagnosis Treatment and Management References

Epidemiology 4-6% 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 DM Prevalence also varies by race 1.5-2% in Caucasians, 5-8% in Hispanic, Asian and African Americans, and up to 15% in some SW Native American groups.

Classification

Pathophysiology Normal pregnancy is characterized by: Mild fasting hypoglycemia Postprandial hyperglycemia Hyperinsulinemia Due to peripheral insulin resistance which ensures an adequate supply of glucose for the baby.

Pathophysiology Human Placental Lactogen (HPL) Produced by syncytiotrophoblasts of placenta. Acts to promote lipolysis  increased FFA and to decrease maternal glucose uptake and gluconeogenesis. “Anti-insulin” Estrogen and Progesterone Interfere with insulin-glucose relationship. Insulinase Placental product that may play a minor role.

A Vicious Cycle???

Fetal Morbidity Miscarriages Preterm Delivery Frequency directly related to degree of maternal glycemic control. Up to 44% with poorly controlled DM (HbA1C >12). Preterm Delivery Increase in both spontaneous and indicated preterm labor (<35 wks).

Fetal Morbidity Birth Defects 1-2% 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 Morbidity Macrosomia Defined 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 Morbidity Growth Restriction Although 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 Morbidity Polycythemia Hypoglycemia Hyperglycemia stimulates fetal erythropoeitin production. Can lead to tissue ischemia and infarction. Hypoglycemia Think 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 Morbidity Postnatal hyperbilirubinemia Occurs in appox. 25%, double that of normal. Thought to be due in large part to polycythemia. Respiratory distress syndrome 5-6 fold increased frequency. May be due to a delay in lung maturation or simply due to the increased frequency of preterm deliveries.

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

Maternal Morbidity Increased 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 retinopathy Diabetic nephropathy

Maternal Morbidity Diabetic neuropathy Preeclampsia 2-fold increase

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

Diagnosis Glucose Tolerance Test Draw a fasting glucose level (normal<95). Give 100 gram glucose load with glucose levels drawn after 1, 2 and 3 hours. Normal levels vary widely depending on who you ask but should be in the following ranges: 1 hr:<180 2 hr:<155 3 hr:<140 2 or more abnormal values = GDM.

Treatment and Management Obviously 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 Management Obstetrical management Serial US to trend fetal growth, AFI and fetal anatomy Fetal well-being monitored with kick counts, NSTs, BPPs Postpartum, 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.

References www.acog.org Current Obstetric & Gynecologic Diagnosis & Treatment (2003) Williams Obstetrics (2005)