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Gestational diabetes and the hypertensive disorders of pregnancy read like a pile of numbers to memorize: screening windows, glucose cutoffs, blood pressure thresholds, severe features. This episode turns them into two clean sequences and one definitions ladder, so you can separate chronic hypertension from gestational hypertension from preeclampsia from eclampsia from HELLP, and never lose sight of the one thing that actually treats any of them.
Gestational Diabetes Mellitus (GDM)
Glucose intolerance first recognized during pregnancy, distinct from pre-existing diabetes that predates or is present before 20 weeks.
Risk Factors
- Obesity (BMI >30) → strongest modifiable risk factor.
- Prior GDM → recurrence rate ~50% in subsequent pregnancies.
- Prior macrosomic infant (birthweight >4 kg).
- Family history of type 2 diabetes (T2DM).
- Polycystic ovary syndrome (PCOS).
- Glycosuria on prenatal urinalysis.
- Ethnicity: Hispanic, Black, Asian, Native American, Pacific Islander.
- Advanced maternal age, multiparity.
Clinical Presentation
- GDM is asymptomatic, detected entirely through screening.
- Complications drive the clinical picture:
- Maternal: preeclampsia, polyhydramnios, increased C-section rate, T2DM later in life (up to 50% within 10 years).
- Fetal/neonatal: macrosomia → shoulder dystocia, birth trauma, brachial plexus injury; neonatal hypoglycemia (fetal hyperinsulinemia continues after cord clamping); neonatal hyperbilirubinemia; respiratory distress syndrome; stillbirth (with poorly controlled disease).
- Important distinction: congenital anomalies (cardiac, neural tube) are a complication of pregestational DM, not GDM. Organogenesis occurs in the first trimester, before GDM is ever diagnosed.
- The question stem would likely describe a screening result or ask about a complication, or give a macrosomic infant and ask what the mother had.
Diagnostics / Screening
- Universal screening at 24-28 weeks for all pregnant patients.
- Step 1: 1-hour glucose challenge test (GCT): 50g oral glucose load, no fasting required. Cutoff ≥130-140 mg/dL (varies by institution) → abnormal, proceed to 3-hour GTT.
- Step 2: 3-hour glucose tolerance test (GTT): 100g oral glucose load, requires fasting. Diagnose GDM if 2 or more values meet or exceed thresholds:
- Fasting ≥95 mg/dL
- 1-hour ≥180 mg/dL
- 2-hour ≥155 mg/dL
- 3-hour ≥140 mg/dL
- High-risk patients (prior GDM, obesity, strong family history): screen at first prenatal visit with fasting glucose or HbA1c. If abnormal at first visit → overt (pregestational) diabetes, not GDM.
Treatment
- Class A1 vs A2 GDM: A1 is controlled with diet and exercise alone; A2 requires medication (insulin preferred) and drives more fetal surveillance and earlier delivery.
- First line: medical nutrition therapy (MNT) + exercise. Carbohydrate restriction and aerobic exercise. Adequate to control glucose in ~70-80% of patients.
- Self-monitoring of blood glucose: fasting and 1-2 hours postprandial.
- Targets: fasting <95 mg/dL; 1-hour postprandial <140 mg/dL; 2-hour postprandial <120 mg/dL.
- If diet and exercise fail after 1-2 weeks:
- Insulin: preferred pharmacologic agent. Does not cross the placenta. NPH + regular insulin or long-acting analogs (glargine, detemir).
- Metformin: used but crosses the placenta; long-term fetal effects not fully established. Acceptable when insulin is refused or unavailable.
- Glyburide: used but associated with higher rates of neonatal hypoglycemia and macrosomia compared to insulin. Less preferred.
- Fetal surveillance: growth ultrasound, non-stress test (NST), biophysical profile (BPP) as indicated for poorly controlled disease.
- Delivery timing: 39-40 weeks for well-controlled GDM. Earlier delivery considered with macrosomia, poor glucose control, or other complications.
- Postpartum: 75g oral glucose tolerance test (OGTT) at 6-12 weeks postpartum. GDM resolves after delivery but ~50% develop T2DM within 10 years.
Exam Keys
- GDM screening: 1-hour GCT (no fasting) at 24-28 weeks. Abnormal → 3-hour GTT (fasting, 2+ values).
- GDM is asymptomatic. Complications define the presentation.
- Macrosomia, shoulder dystocia, neonatal hypoglycemia = GDM complications.
- Congenital anomalies = pregestational DM. Not GDM. First trimester organogenesis is the key.
- Insulin is the preferred pharmacologic treatment. Doesn’t cross the placenta.
- Postpartum OGTT at 6-12 weeks. Screen for persistent T2DM.
Hypertensive Disorders of Pregnancy
A spectrum of blood pressure disorders occurring during pregnancy, classified by timing, presence of proteinuria, and end-organ dysfunction.
Risk Factors for Preeclampsia
- Prior preeclampsia → highest recurrence risk.
- Nulliparity (first pregnancy).
- Chronic hypertension, chronic kidney disease, diabetes mellitus.
- Obesity, multiple gestation, autoimmune disease (SLE, antiphospholipid syndrome).
- Advanced maternal age (>35), Black race.
- Donor egg or assisted reproductive technology (ART).
Definitions and Classification
- Chronic hypertension: BP ≥140/90 present before pregnancy or before 20 weeks. Pre-existing. Persists postpartum.
- Gestational hypertension: new-onset BP ≥140/90 after 20 weeks WITHOUT proteinuria or severe features. Resolves within 12 weeks postpartum.
- Preeclampsia: new-onset BP ≥140/90 after 20 weeks WITH:
- Proteinuria (spot protein:creatinine ratio ≥0.3, or 24-hour urine protein ≥300 mg, or dipstick ≥2+), OR
- Any severe feature (even without proteinuria):
- BP ≥160/110 on two readings ≥4 hours apart
- Thrombocytopenia (platelets <100,000)
- Renal insufficiency (creatinine >1.1 mg/dL or doubling of baseline)
- Impaired liver function (transaminases 2x normal) or severe RUQ or epigastric pain
- Pulmonary edema
- New-onset headache unresponsive to medication, or visual disturbances (scotomata, blurry vision)
- Eclampsia: preeclampsia + new-onset generalized seizures. No prior seizure history.
- HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets. Considered a variant of severe preeclampsia. May present with RUQ or epigastric pain, nausea, malaise, and bruising, sometimes without classic hypertension or proteinuria. Do not miss it.
- Hyperreflexia and clonus are warning signs of impending eclampsia, not diagnostic severe features of preeclampsia. Brisk, exaggerated reflexes signal CNS irritability and rising seizure risk. Watch the direction: worsening preeclampsia drives reflexes up (hyperreflexia, clonus), while magnesium therapy is monitored for reflexes going down → areflexia is the earliest sign of magnesium toxicity, before respiratory depression and cardiac arrest.
- The question stem would likely describe a patient with HTN + proteinuria, or a question about what constitutes a severe feature. Know the definitions cold.
Diagnostics
- BP measurement: ≥2 readings at least 4 hours apart to confirm sustained elevation.
- Urinalysis: spot protein:creatinine ratio or 24-hour urine protein.
- CBC (platelets), comprehensive metabolic panel (creatinine, LFTs), LDH, uric acid.
- HELLP labs: hemolysis (LDH ≥600 IU/L, schistocytes on peripheral smear, low haptoglobin), AST/ALT ≥2x upper limit of normal, platelets <100,000.
- Continuous fetal monitoring (NST, BPP, growth ultrasound).
Prevention
- Low-dose aspirin 81 mg/day: start at 12-16 weeks (no later than 28 weeks) for high-risk patients. Indications: prior preeclampsia, chronic HTN, CKD, DM, autoimmune disease, multiple gestation, or ≥2 moderate risk factors.
Treatment
- Only definitive treatment is delivery.
- Gestational HTN or mild preeclampsia, remote from term: expectant management with close monitoring. Antihypertensives only if BP ≥160/110.
- Preeclampsia ≥37 weeks: deliver.
- Preeclampsia with severe features: deliver at ≥34 weeks. If <34 weeks and maternal-fetal status allows, brief stabilization and corticosteroids, then deliver.
- Eclampsia (seizure): magnesium sulfate IV to abort seizure and prevent recurrence. Stabilize, then deliver.
- Magnesium sulfate: given IV for seizure prophylaxis in severe preeclampsia (during labor and 24 hours postpartum) and for treatment of eclampsia.
- Toxicity sequence: loss of deep tendon reflexes (DTRs) → respiratory depression → cardiac arrest.
- Monitor: DTRs, respiratory rate, urine output.
- Antidote: calcium gluconate IV.
- Acute severe hypertension (BP ≥160/110): treat within 30-60 minutes to prevent maternal stroke.
- IV labetalol, IV hydralazine, or oral nifedipine (immediate-release).
- Avoid ACE inhibitors and ARBs in pregnancy (fetal renal toxicity).
- HELLP syndrome: delivery is the treatment. Corticosteroids may be given for platelet count <50,000 or to accelerate fetal lung maturity.
- Postpartum: BP can worsen in the first 3-5 days after delivery. Monitor closely. HTN may require antihypertensive therapy for weeks postpartum.
Exam Keys
- Preeclampsia = HTN after 20 weeks + proteinuria OR severe feature. Know the severe features.
- Eclampsia = preeclampsia + seizures. Magnesium is the treatment, not an anticonvulsant for other causes.
- HELLP = hemolysis + elevated LFTs + low platelets. RUQ pain + thrombocytopenia = think HELLP.
- Preeclampsia before 20 weeks = think gestational trophoblastic disease.
- Magnesium toxicity: DTRs lost first. Calcium gluconate reverses it.
- Acute severe HTN (≥160/110): treat immediately. Options: IV labetalol, IV hydralazine, oral nifedipine.
- Only cure = delivery. Everything else is temporizing.
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