Endocrinology · Reproductive Endocrinology
The facts most likely to be tested
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Universal screening for gestational diabetes mellitus (GDM) occurs at 24–28 weeks gestation using a one-hour 50g glucose challenge test.
A positive screen requires a diagnostic three-hour 100g oral glucose tolerance test (OGTT), where two or more elevated values confirm the diagnosis.
The primary pathophysiology involves placental human placental lactogen (hPL) inducing peripheral insulin resistance to ensure adequate glucose supply to the fetus.
First-line management for GDM is medical nutrition therapy (MNT) and lifestyle modification including moderate exercise.
Pharmacologic therapy is indicated if glycemic targets are not met, with insulin being the preferred agent; metformin may be used as an alternative (glyburide is discouraged because of worse neonatal outcomes including macrosomia, neonatal hypoglycemia, and birth injury; note that metformin also readily crosses the placenta).
Infants born to mothers with poorly controlled GDM are at highest risk for macrosomia, neonatal hypoglycemia, and shoulder dystocia.
Postpartum management requires a two-hour 75g OGTT at 4–12 weeks postpartum to screen for persistent type 2 diabetes mellitus.
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A 28-year-old G2P1 woman at 26 weeks gestation presents for a routine prenatal visit. Her BMI is 32 kg/m². She undergoes a 50g glucose challenge test, which returns a value of 155 mg/dL. She has no history of pre-gestational diabetes. Her fundal height is measured at 30 cm, which is slightly large for gestational age.
What is the most appropriate next step in the management of this patient?
Perform a three-hour 100g oral glucose tolerance test (OGTT).
The patient's 50g glucose challenge test is elevated (>130-140 mg/dL depending on institutional threshold), necessitating a diagnostic 100g OGTT to confirm gestational diabetes.
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Etiology / Epidemiology
Caused by placental insulin resistance in the 2nd/3rd trimester. Obesity, prior GDM, and family history are primary risk factors.
Clinical Manifestations
Usually asymptomatic; screen all patients at 24-28 weeks. Look for macrosomia on ultrasound.
Diagnosis
Screen with 50g glucose challenge test (≥130-140 mg/dL). Confirm with 100g 3-hour OGTT.
Treatment
First-line is lifestyle modification (diet/exercise). If failed, insulin is the gold standard.
Prognosis
Risk of shoulder dystocia and neonatal hypoglycemia. 50% risk of developing Type 2 DM later.
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Epidemiology & Etiology
GDM occurs when the pancreas cannot overcome the insulin resistance induced by placental hormones. High-risk groups include patients with BMI >30, history of macrosomic infants, and polycystic ovary syndrome.
Pertinent Anatomy
The placenta acts as an endocrine organ, secreting hormones like human placental lactogen that antagonize maternal insulin. This creates a state of relative insulin deficiency during the late second and third trimesters.
Pathophysiology
Placental hormones increase maternal insulin resistance to ensure glucose availability for the fetus. When maternal pancreatic beta-cell compensation is insufficient, hyperglycemia ensues. Excess glucose crosses the placenta, causing fetal hyperinsulinemia, which acts as a growth hormone leading to macrosomia.
Clinical Manifestations
Most patients are asymptomatic and identified via universal screening. Polyhydramnios and macrosomia on ultrasound are clinical red flags. Post-delivery, neonates are at high risk for hypoglycemia, respiratory distress syndrome, and hypocalcemia.
Diagnosis
Universal screening occurs at 24-28 weeks. The 100g 3-hour OGTT is diagnostic if two of the following are met: fasting ≥95, 1hr ≥180, 2hr ≥155, or 3hr ≥140 mg/dL. The Carpenter-Coustan criteria are the standard thresholds used in clinical practice.
Treatment
Initial management is medical nutrition therapy and moderate exercise. If glucose targets are not met, insulin is the preferred pharmacologic agent as it does not cross the placenta. Metformin may be used when a patient cannot take or declines insulin, but it readily crosses the placenta and long-term offspring data are lacking; glyburide should not be used in place of insulin because of worse outcomes including macrosomia and birth injury.
Prognosis
Maternal complications include preeclampsia and increased risk of future Type 2 DM. Fetal complications include shoulder dystocia and birth trauma. Patients require a 4-12 week postpartum glucose tolerance test to screen for persistent diabetes.
Differential Diagnosis
Pre-gestational Diabetes: elevated A1c in the first trimester
Impaired glucose tolerance: a single abnormal value on the 3-hour OGTT, below the two-value diagnostic threshold
Monogenic diabetes (MODY): mild stable fasting hyperglycemia with a strong autosomal dominant family history and young age at onset
Physiologic glycosuria of pregnancy: glucose detectable in urine from the increased glomerular filtration rate despite normal plasma glucose
Stress or glucocorticoid-induced hyperglycemia: transient glucose elevation after betamethasone or acute illness, resolving within 3-5 days