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"pregnancy-induced hypertension" OR "preeclampsia" management
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I now have comprehensive content from both textbooks. Here is a full overview:
Pregnancy-Induced Hypertension (PIH)
Definition and Classification
Hypertension complicates up to 8-10% of all pregnancies. PIH falls under a broader classification:
| Category | Definition |
|---|---|
| Gestational hypertension | New BP ≥ 140/90 mmHg during pregnancy, resolves postpartum |
| Preeclampsia | Gestational hypertension after 20 weeks + proteinuria (>300 mg/24 hr) or end-organ damage |
| Eclampsia | Seizures in a patient with signs of preeclampsia |
| HELLP syndrome | Severe preeclampsia: Hemolysis + Elevated Liver enzymes (ALT/AST >70 U/L) + Low Platelets (<100,000/mL) |
| Pregnancy-aggravated hypertension | Chronic hypertension with superimposed preeclampsia/eclampsia |
| Chronic/coincidental hypertension | Present before pregnancy or persisting >6 weeks postpartum |
Actual PIH (gestational + preeclamptic types) complicates 2-7% of pregnancies. Eclampsia, while declining in incidence, remains one of the major causes of maternal mortality.
Risk Factors
- Age <20 years
- Primigravidas
- Twin or molar pregnancies
- Hypercholesterolemia
- Pregestational diabetes
- Obesity
- Family history of PIH
- Chronic hypertension (established risk factor for preeclampsia)
Pathophysiology
PIH/preeclampsia is a vasospastic disease of unknown cause, unique to pregnant women. Key mechanisms:
- Normal pregnancy is a high-output, low-resistance state with depressed vascular responsiveness to vasopressors
- In gestational hypertension: cardiac output rises further, followed by abnormally high peripheral resistance as disease develops
- In preeclampsia: cardiac output eventually drops as peripheral resistance rises
- Endothelial dysfunction releases vasoactive mediators causing vasoconstriction
- Placenta-derived factors disrupt vascular integrity and endothelial function
- Consequences: vasospasm, ischemia, and thrombosis - injuring maternal organs, causing placental infarction and abruption, and fetal death from hypoxia and prematurity
The exact cause of eclamptic seizures is unknown, though vascular responsiveness to endogenous vasopressors is a focus of research.
Clinical Presentation
- New-onset hypertension after 20 weeks
- Proteinuria
- Peripheral edema
- Renal and hepatic dysfunction
- CNS warning signs (severe preeclampsia): headache, visual disturbances, altered mental status
- Fulminant/severe preeclampsia: BP ≥ 160/110 mmHg with epigastric/liver tenderness, visual disturbance, or severe headache
- Eclampsia: seizures and coma
Approximately 20% of eclamptic episodes occur >48 hours after delivery - postpartum women with CNS symptoms must be monitored.
Management
Indications to Start Drug Therapy
- Diastolic BP > 105 mmHg, OR
- Systolic BP > 160 mmHg
Antihypertensive Drugs in Pregnancy
| Drug | Notes |
|---|---|
| Methyldopa (250 mg twice daily) | Centrally acting α-agonist; first-line, well-established fetal safety (former FDA category B) |
| Labetalol (100 mg twice daily oral; 20 mg IV acute) | α1-selective, β-non-selective; reasonable safety profile |
| Nifedipine (30 mg once daily) | Calcium channel blocker; reasonable evidence of safety |
| Hydralazine (5-10 mg IV/IM, repeat every 20 min) | Acute inpatient BP control |
Avoid: ACE inhibitors and angiotensin receptor blockers - unequivocal adverse fetal effects.
BP Targets During Treatment
- Goal: lower by 15-20%, targeting systolic 140-150 mmHg and diastolic 90-100 mmHg
- Rapid lowering risks uterine hypoperfusion - avoid aggressive drops
Seizure Prevention and Treatment - Magnesium Sulfate
Magnesium sulfate is the cornerstone of seizure management. It has little antihypertensive effect but is the most effective anticonvulsant, preventing recurrent seizures while maintaining uterine and fetal blood flow.
- IV loading dose: 4-6 g over 15-20 minutes
- Maintenance: 2 g/hr IV
- Monitor for hypermagnesemia: loss of deep tendon reflexes (~10 mg/dL) and respiratory depression (~12 mg/dL)
- Antidote: IV calcium gluconate 1 g given slowly reverses toxicity
If Seizures Persist Despite Magnesium
(with obstetric consultation)
- Lorazepam 2-4 mg IV (may repeat ×1 after 10-15 min)
- Phenytoin/fosphenytoin 15-20 mg/kg IV
- Levetiracetam 20-60 mg/kg IV
Definitive Treatment
Delivery of the baby is the treatment of choice in severe preeclampsia with end-organ damage, provided the fetus is mature enough. If the baby is very preterm, hospitalization and pharmacotherapy may be used to allow further fetal maturation in utero.
Key Points to Remember
- Preeclampsia → Eclampsia progression is unpredictable and rapid - aggressive BP management is essential
- Magnesium sulfate is for seizure prevention/treatment, NOT primarily for BP control
- ACE inhibitors and ARBs are contraindicated in pregnancy
- HELLP syndrome is a life-threatening variant requiring urgent delivery
- Postpartum eclampsia can occur - monitor for CNS symptoms for at least 48 hours after delivery
Sources: Goodman & Gilman's Pharmacological Basis of Therapeutics; Rosen's Emergency Medicine
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