Step 2 CK · Obstetrics & Gynecology

Hypertensive & Medical Disorders of Pregnancy

Name: Hypertensive & Medical Disorders of Pregnancy
Creator: Veli Bakalov, MD

Preeclampsia, magnesium, and the medical problems that ride along with pregnancy

Obstetrics & Gynecology·Medical Disorders of Pregnancy·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

Study materialsNo account needed

Card deckActive-recall cards · quick checks · quiz

High-yield

BP ≥140/90 before 20 weeks (or persisting >12 weeks postpartum) is chronic HTN; after 20 weeks, HTN alone is gestational, plus proteinuria or organ dysfunction is preeclampsia, plus seizures is eclampsia.
Severe features: BP ≥160/110, platelets <100,000, transaminases ≥2× normal or RUQ/epigastric pain, creatinine >1.1 or doubled, pulmonary edema, cerebral/visual symptoms; proteinuria amount does not count.
Magnesium sulfate (4–6 g load, 1–2 g/hr, continued 24 hours postpartum) prevents and treats eclamptic seizures but is not an antihypertensive.
Lost patellar reflexes are the first sign of magnesium toxicity, followed by respiratory depression; stop the infusion and give calcium gluconate.
Treat BP ≥160/110 within 30–60 minutes with IV labetalol, IV hydralazine, or oral nifedipine; never use ACE inhibitors, ARBs, or nitroprusside in pregnancy.
Deliver gestational HTN and preeclampsia without severe features at 37 weeks, severe features at 34 weeks, and eclampsia or HELLP after stabilization regardless of gestational age.
Low-dose aspirin 81 mg from 12–28 weeks (ideally before 16) prevents preeclampsia in high-risk women (prior preeclampsia, chronic HTN, diabetes, renal or autoimmune disease, multiples).
HELLP (hemolysis, elevated liver enzymes, low platelets) can present with RUQ pain and normal BP; it risks hepatic rupture and is treated by delivery.
GDM failing diet (fasting ≥95) gets insulin; raise levothyroxine ~30% in pregnancy; PTU in the first trimester, methimazole after; treat VTE with LMWH, never warfarin or DOACs.

Classifying hypertension in pregnancy

The 20-week line. Hypertension (BP ≥140/90) before 20 weeks is chronic; new hypertension after 20 weeks is gestational hypertension or preeclampsia, depending on proteinuria and end-organ involvement.

Hypertensive disorders of pregnancy

Disorder	Timing	Defining features
Chronic hypertension	Before 20 weeks or persisting >12 weeks postpartum	BP ≥140/90
Gestational hypertension	After 20 weeks	BP ≥140/90; no proteinuria, no severe features
Preeclampsia	After 20 weeks	Hypertension plus proteinuria or end-organ dysfunction
Superimposed preeclampsia	Chronic HTN, then after 20 weeks	New proteinuria or end-organ dysfunction on top of chronic hypertension
Eclampsia	Usually after 20 weeks, including postpartum	Preeclampsia plus new tonic-clonic seizures

Diagnosing preeclampsia. BP ≥140/90 on two readings 4 hours apart after 20 weeks, plus either proteinuria (≥300 mg/24 h, protein:creatinine ≥0.3, or dipstick 2+ only if quantitative testing is unavailable) or end-organ signs—thrombocytopenia, elevated transaminases, renal insufficiency, pulmonary edema, or cerebral/visual symptoms. Proteinuria is no longer required if organ dysfunction is present.

Severe features change management:

BP ≥160/110
Platelets <100,000/μL
Transaminases ≥2× normal or severe RUQ/epigastric pain
Creatinine >1.1 mg/dL or doubled
Pulmonary edema
New cerebral or visual symptoms (headache, scotomata)

The amount of proteinuria is not a severe feature: massive proteinuria alone does not upgrade the diagnosis.

Magnesium and blood pressure control

Magnesium sulfate is first-line both for treating eclamptic seizures and for seizure prophylaxis in preeclampsia with severe features; it outperforms phenytoin and diazepam. Load 4–6 g IV, then infuse 1–2 g/hr, continuing 24 hours postpartum. It is not an antihypertensive. For refractory seizures, add a benzodiazepine.

Protect the airwayABCs, left lateral position to prevent aspiration
IV magnesium sulfate4–6 g load, then infusion
Control severe-range BPlabetalol, hydralazine, or nifedipine
Deliverthe only definitive cure, once the mother is stabilized

Magnesium toxicity. Magnesium is renally cleared, so toxicity accumulates with oliguria or renal insufficiency; monitor deep tendon reflexes, respiratory rate, and urine output. Toxicity progresses predictably: loss of deep tendon reflexes first (~9–12 mg/dL), then respiratory depression (~12–15 mg/dL), then cardiac conduction defects and cardiac arrest at higher levels (conduction changes above about 18 mg/dL, or 15 mEq/L; cardiac arrest near 30 mg/dL, or 25 mEq/L).

A lost patellar reflex is the earliest clinical warning. With areflexia or respiratory depression, stop the infusion and give IV calcium gluconate, the antidote.

Severe-range blood pressure. BP ≥160/110 needs treatment within about 30–60 minutes to prevent maternal stroke. First-line options are IV labetalol, IV hydralazine, or oral immediate-release nifedipine, aiming for roughly 140–150/90–100—not normotension, which can compromise placental perfusion. Avoid labetalol in asthma or heart block.

Safe and unsafe drugs. Safe chronic antihypertensives are labetalol, nifedipine, methyldopa, and hydralazine. Avoid ACE inhibitors and ARBs (fetal renal dysgenesis, oligohydramnios, skull ossification defects)—stop them as soon as pregnancy is recognized and switch to labetalol—and nitroprusside (fetal cyanide toxicity).

Delivery timing, prevention, and HELLP

Delivery timing by diagnosis

Diagnosis	Deliver
Gestational hypertension	At 37 weeks
Preeclampsia without severe features	At 37 weeks
Preeclampsia with severe features	At 34 weeks (corticosteroids if earlier delivery is likely)
Eclampsia, HELLP, or unstable mother or fetus	Stabilize, then deliver regardless of gestational age

Delivery is the only cure; mode is obstetric, and vaginal delivery is preferred when feasible.

Aspirin prophylaxis. Low-dose aspirin 81 mg daily, started at 12–28 weeks (ideally before 16 weeks) and continued until delivery, lowers preeclampsia risk in high-risk women: prior preeclampsia, chronic hypertension, pregestational diabetes, renal disease, autoimmune disease (lupus, antiphospholipid syndrome), or multiple gestation. It is also offered with several moderate risk factors such as nulliparity, obesity, and age ≥35.

HELLP syndrome is a severe variant of preeclampsia: Hemolysis (schistocytes, high LDH, low haptoglobin), Elevated Liver enzymes, and Low Platelets. It presents with RUQ pain and malaise, sometimes with normal-range BP and little proteinuria, and risks hepatic subcapsular hematoma or rupture and DIC. Treatment is delivery after stabilization, with magnesium.

HELLP can masquerade as a GI illness—check the platelets in any late-pregnancy RUQ pain. Acute fatty liver of pregnancy differs by prominent hypoglycemia, coagulopathy, and hepatic failure.

Diabetes in pregnancy

Screening. At 24–28 weeks, a 50 g 1-hour glucose challenge ≥140 mg/dL leads to a 100 g 3-hour tolerance test; two or more abnormal values confirm gestational diabetes (GDM).

Treatment. Start with diet and exercise. If targets are missed (fasting <95, 1-hour <140, or 2-hour <120 mg/dL), insulin is the preferred pharmacotherapy; metformin and glyburide cross the placenta and are second-line. Complications include macrosomia, shoulder dystocia, and neonatal hypoglycemia (from fetal hyperinsulinemia). Retest with a 75 g OGTT at 4–12 weeks postpartum, because type 2 diabetes risk remains high for life.

Pregestational diabetes, unlike GDM, raises the risk of congenital anomalies—cardiac defects, neural tube defects, and caudal regression—in proportion to periconception HbA1c, so optimize control before conception.

Thyroid disease and thromboembolism

Hypothyroidism. Increase levothyroxine by about 30% as soon as pregnancy is confirmed, because demand rises and the fetus depends on maternal thyroxine early; untreated hypothyroidism risks impaired fetal neurodevelopment.

Graves disease. Use PTU in the first trimester, because methimazole causes aplasia cutis and embryopathy, then switch to methimazole in the second and third trimesters, because PTU is hepatotoxic. Maternal thyroid-stimulating antibodies can cross the placenta and cause fetal or neonatal hyperthyroidism, even in women previously treated with radioiodine or thyroidectomy who now take levothyroxine; check TSH receptor antibodies and monitor the fetus if they are elevated.

Venous thromboembolism. Pregnancy is hypercoagulable (more clotting factors, less protein S, venous stasis). Treat or prevent VTE with LMWH (enoxaparin), which does not cross the placenta. Avoid warfarin (embryopathy: nasal hypoplasia, stippled epiphyses) and DOACs. Diagnose DVT with compression ultrasound and PE with CT angiography or V/Q scan.