Residency · Residency · Obstetrics Gynecology
Hypertensive Disorders of Pregnancy
Classification
Chronic Hypertension
Chronic hypertension in pregnancy is defined as blood pressure of 140/90 mmHg or greater diagnosed before pregnancy or before 20 weeks' gestation. It persists beyond 12 weeks postpartum. The cause may be essential hypertension or secondary to conditions such as renal artery stenosis, pheochromocytoma, or Cushing syndrome. Prevalence is increasing with rising maternal age and obesity rates.
Gestational Hypertension
Gestational hypertension is new-onset blood pressure of 140/90 mmHg or greater after 20 weeks' gestation without proteinuria or other signs of preeclampsia. It resolves by 12 weeks postpartum. Up to 50% of patients progress to preeclampsia, making close surveillance essential.
Preeclampsia
Preeclampsia is new-onset hypertension (140/90 mmHg or greater) after 20 weeks' gestation with either proteinuria (300 mg or more per 24 hours, protein-to-creatinine ratio of 0.3 or greater, or dipstick 2+) or end-organ dysfunction without proteinuria, including thrombocytopenia (platelets below 100,000), renal insufficiency (creatinine above 1.1 mg/dL or doubling of baseline), impaired liver function (transaminases at or above twice normal), pulmonary edema, or new-onset headache or visual disturbances not explained by an alternative diagnosis.
Preeclampsia with Severe Features
Severe features include blood pressure of 160/110 mmHg or greater on two occasions at least 4 hours apart (or once if antihypertensives started), platelets below 100,000, liver transaminases at or above twice the upper limit of normal with or without severe persistent right upper quadrant or epigastric pain, creatinine above 1.1 mg/dL or doubling of baseline, pulmonary edema, or new-onset cerebral or visual disturbances.
| Classification | Definition | Key Features |
|---|---|---|
| Chronic hypertension | BP ≥140/90 before pregnancy or <20 weeks | Persists >12 weeks postpartum |
| Gestational hypertension | New-onset BP ≥140/90 after 20 weeks | No proteinuria or end-organ dysfunction; up to 50% progress to preeclampsia |
| Preeclampsia without severe features | BP ≥140/90 after 20 weeks + proteinuria or end-organ dysfunction | Deliver at 37+0 weeks |
| Preeclampsia with severe features | BP ≥160/110 or end-organ dysfunction criteria | Deliver at ≥34 weeks; immediate delivery for certain indications |
| Eclampsia | Generalized tonic-clonic seizures in preeclampsia | Can occur antepartum, intrapartum, or postpartum |
| Superimposed preeclampsia | Chronic HTN + new proteinuria or end-organ dysfunction after 20 weeks | Highest risk for adverse outcomes |
Chronic Hypertension with Superimposed Preeclampsia
This applies when a patient with preexisting hypertension develops worsening hypertension or new-onset proteinuria or end-organ dysfunction after 20 weeks. It carries the highest risk for adverse maternal and fetal outcomes.
Eclampsia
Eclampsia is new-onset generalized tonic-clonic seizures in a patient with preeclampsia. It can occur antepartum, intrapartum, or postpartum (up to 6 weeks, most within 48 hours) and may develop without preceding severe hypertension.
<image>Diagram showing the classification of hypertensive disorders of pregnancy as a hierarchical flowchart, distinguishing chronic hypertension, gestational hypertension, preeclampsia without severe features, preeclampsia with severe features, eclampsia, and superimposed preeclampsia</image>
Pathophysiology
Placental Origin
Preeclampsia originates in the placenta. In normal pregnancy, trophoblast cells invade and remodel the spiral arteries into low-resistance, high-capacity vessels. In preeclampsia, this invasion is incomplete, leaving high-resistance spiral arteries that provide inadequate placental perfusion. The resulting ischemia triggers release of anti-angiogenic factors -- primarily sFlt-1 and soluble endoglin -- that antagonize VEGF and PlGF, causing systemic endothelial dysfunction.
Systemic Effects
Endothelial dysfunction drives multiorgan involvement. Vascular effects include increased peripheral resistance, vasospasm, and endothelial injury. Renal manifestations include glomerular endotheliosis, decreased GFR, and proteinuria. Hepatic involvement ranges from periportal fibrin deposition and hepatocellular necrosis to subcapsular hematoma. Hematologic consequences include microangiopathic hemolysis and platelet consumption (HELLP syndrome). The CNS may develop cerebral edema, posterior reversible encephalopathy syndrome (PRES), and seizures.
Risk Factors and Prevention
Risk Factors
Major risk factors include nulliparity, advanced maternal age (35 or older), obesity (BMI 30 or greater), prior preeclampsia, family history, chronic hypertension, renal disease, diabetes, SLE, antiphospholipid syndrome, multiple gestation, assisted reproductive technology, and interpregnancy interval greater than 10 years.
Low-Dose Aspirin Prophylaxis
ACOG and USPSTF recommend aspirin 81 mg daily starting at 12 to 16 weeks (ideally by 16 weeks) and continued until delivery for patients with one or more high-risk factors or two or more moderate-risk factors. This reduces preeclampsia risk by approximately 15 to 25%. Calcium supplementation (1 g or more daily) may also reduce risk in calcium-deficient populations.
Diagnosis and Evaluation
Baseline Labs at Diagnosis
The workup includes CBC with platelet count, comprehensive metabolic panel (creatinine, AST, ALT, albumin), LDH, uric acid, urinalysis with protein-to-creatinine ratio or 24-hour urine protein, and coagulation studies if platelets are declining or DIC is suspected.
Monitoring
Serial blood pressure monitoring (at least twice daily inpatient), labs every 6 to 12 hours if severe features are present (daily to every other day otherwise), fetal surveillance with NST and/or BPP plus umbilical artery Doppler, and growth ultrasound every 3 to 4 weeks for suspected IUGR.
<image>Comparison table showing laboratory findings in preeclampsia without severe features versus HELLP syndrome, including typical ranges for platelets, LDH, AST/ALT, haptoglobin, and peripheral smear findings</image>
Management
Preeclampsia Without Severe Features
Expectant management with close surveillance until 37 weeks 0 days. Serial labs twice weekly minimum, daily kick counts, twice-weekly NST. Antihypertensives not routinely needed unless BP reaches severe range. Delivery by induction at 37 weeks 0 days; do not continue beyond 37 weeks.
Preeclampsia with Severe Features
At 34 weeks 0 days or beyond, deliver after maternal stabilization. At 24 to 34 weeks, expectant management may be considered at a tertiary center if BP is controlled, labs are stable, and fetal status is reassuring. Betamethasone should be given for fetal lung maturity. Magnesium sulfate is administered during the steroid window. Immediate delivery is required regardless of gestational age for uncontrollable severe BP, eclampsia, pulmonary edema, placental abruption, DIC, non-reassuring fetal status, or refractory severe headache or visual changes.
Antihypertensive Therapy
Severe-range BP (160/110 or greater) must be treated within 30 to 60 minutes to prevent stroke. Options include IV labetalol (20 mg, then 40 mg, then 80 mg at 10-minute intervals, max 300 mg), IV hydralazine (5 to 10 mg every 20 minutes, max 20 mg), or oral immediate-release nifedipine (10 to 20 mg every 20 to 30 minutes, max 50 mg in the first hour). For chronic control, labetalol 200 to 800 mg orally two to three times daily or nifedipine XL 30 to 120 mg daily. The CHAP trial supports targets below 140/90.
| Agent | Route | Dosing | Maximum | Key Considerations |
|---|---|---|---|---|
| Labetalol | IV | 20 mg → 40 mg → 80 mg q10min | 300 mg total | Avoid in asthma, heart block |
| Hydralazine | IV | 5-10 mg q20min | 20 mg | May cause reflex tachycardia |
| Nifedipine (immediate-release) | PO | 10-20 mg q20-30min | 50 mg in first hour | Do not give sublingually |
| Labetalol (chronic) | PO | 200-800 mg BID-TID | 2400 mg/day | First-line for chronic control |
| Nifedipine XL (chronic) | PO | 30-120 mg daily | 120 mg/day | First-line for chronic control |
Magnesium Sulfate
Loading dose 4 to 6 g IV over 20 to 30 minutes, maintenance 1 to 2 g/hour, continued 24 to 48 hours postpartum. Monitor deep tendon reflexes (loss indicates toxicity), respiratory rate (at least 12/min), and urine output (at least 30 mL/hour). Check serum levels if renal impairment (therapeutic range 4 to 7 mEq/L). Antidote for toxicity: calcium gluconate 1 g IV over 3 minutes.
HELLP Syndrome
Diagnosis
Defined by hemolysis (schistocytes, LDH above 600 IU/L, elevated indirect bilirubin, low haptoglobin), elevated liver enzymes (AST/ALT at or above twice ULN), and low platelets (below 100,000). May present as RUQ/epigastric pain, nausea, vomiting, and malaise. Can occur without significant hypertension or proteinuria.
Management
Delivery is definitive. Stabilize with magnesium, antihypertensives, and blood products. Corticosteroids for fetal maturity if below 34 weeks. Platelet transfusion if below 20,000 or below 50,000 with planned cesarean or active bleeding. Monitor for DIC, hepatic rupture, and abruption. Labs typically nadir 24 to 48 hours postpartum, then improve.
<image>Peripheral blood smear showing schistocytes and helmet cells characteristic of microangiopathic hemolytic anemia seen in HELLP syndrome, with arrows pointing to fragmented red blood cells</image>
Eclampsia Management
Secure airway, position in left lateral decubitus, prevent injury. Give magnesium sulfate 4 to 6 g IV bolus (or 2 g if breakthrough seizure on maintenance). Do not use benzodiazepines or phenytoin as first-line -- magnesium is superior. Expect prolonged fetal decelerations that typically recover within 3 to 10 minutes. Do not rush to cesarean during active seizure; stabilize first, then plan delivery.
Postpartum Considerations
Continue magnesium 24 to 48 hours postpartum. BP may worsen postpartum days 3 to 6. Discharge with antihypertensives if BP remains elevated; follow up within 72 hours and at 1 to 2 weeks. NSAIDs are safe and preferred over opioids for postpartum pain. Counsel about 15 to 25% recurrence risk and 2- to 4-fold increased lifetime cardiovascular risk (HTN, stroke, ischemic heart disease). Recommend annual BP checks and cardiovascular risk modification.
Clinical Pearls
Preeclampsia is a clinical diagnosis -- proteinuria is not required if other end-organ dysfunction is present.
Severe-range BP (160/110 or greater) is a medical emergency requiring treatment within 30 to 60 minutes to prevent stroke.
HELLP can present atypically as epigastric pain, nausea/vomiting, or "flu-like" symptoms.
The CHAP trial (2022) showed that treating chronic hypertension to a target below 140/90 in pregnancy reduces preeclampsia and preterm birth.
Magnesium sulfate works for eclampsia; benzodiazepines do not.
Postpartum preeclampsia can present de novo -- educate patients about warning signs at discharge.
Aspirin prophylaxis must be started by 16 weeks to be effective; there is no benefit if initiated later.
References
- ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia (2020)
- ACOG Committee Opinion No. 767: Emergent Therapy for Acute-Onset, Severe Hypertension During Pregnancy and the Postpartum Period (2019)
- Tita AT et al. Treatment for Mild Chronic Hypertension during Pregnancy (CHAP Trial). N Engl J Med. 2022;386:1781-1792
- Magee LA et al. Less-tight versus tight control of hypertension in pregnancy (CHIPS). N Engl J Med. 2015;372:407-417
- ACOG Practice Advisory: Low-Dose Aspirin for Prevention of Preeclampsia (updated 2023)
- Sibai BM. Diagnosis, controversies, and management of HELLP syndrome. Obstet Gynecol. 2004;103:981-991
