Residency · Residency · Emergency Medicine
Emergencies in Pregnancy: Preeclampsia, Eclampsia, and HELLP
Introduction
Hypertensive disorders of pregnancy are among the leading causes of maternal morbidity and mortality worldwide, complicating 5 to 10 percent of all pregnancies. Preeclampsia, eclampsia, and HELLP syndrome represent a spectrum of disease that can rapidly progress to life-threatening complications including seizures, stroke, hepatic rupture, placental abruption, and multi-organ failure. The emergency physician must recognize these conditions early, initiate stabilizing treatment, and coordinate with obstetric services for definitive management.
Classification of Hypertensive Disorders of Pregnancy
Chronic hypertension is defined as blood pressure of 140/90 mmHg or higher before 20 weeks gestation or preexisting hypertension. Gestational hypertension refers to new-onset blood pressure of 140/90 mmHg or higher after 20 weeks without proteinuria or end-organ dysfunction. Preeclampsia is new-onset hypertension after 20 weeks with proteinuria or end-organ dysfunction. Preeclampsia with severe features includes blood pressure of 160/110 mmHg or higher, thrombocytopenia, renal insufficiency, hepatic dysfunction, cerebral or visual symptoms, or pulmonary edema. Eclampsia is defined as new-onset generalized tonic-clonic seizures in a patient with preeclampsia. HELLP syndrome, characterized by hemolysis, elevated liver enzymes, and low platelets, represents a severe variant of preeclampsia. Chronic hypertension with superimposed preeclampsia describes worsening hypertension or new proteinuria and end-organ dysfunction in a patient with chronic hypertension.
| Disorder | Definition | Timing | Key Features |
|---|---|---|---|
| Chronic hypertension | BP ≥ 140/90 before pregnancy or < 20 weeks | Pre-existing | No proteinuria or end-organ dysfunction |
| Gestational hypertension | New BP ≥ 140/90 after 20 weeks | > 20 weeks | No proteinuria or end-organ dysfunction |
| Preeclampsia | New HTN + proteinuria or end-organ dysfunction | > 20 weeks | Proteinuria ≥ 300 mg/24h or organ damage |
| Preeclampsia with severe features | BP ≥ 160/110 or end-organ damage | > 20 weeks | Thrombocytopenia, renal/hepatic dysfunction, cerebral symptoms |
| Eclampsia | New tonic-clonic seizures in preeclampsia | Ante/intra/postpartum | 20% occur without prior severe HTN |
| HELLP syndrome | Hemolysis + elevated liver enzymes + low platelets | Usually > 20 weeks | Can occur without HTN or proteinuria in 15–20% |
Preeclampsia
Pathophysiology
The underlying mechanism involves abnormal placentation, where failed remodeling of uterine spiral arteries leads to placental ischemia. The ischemic placenta releases anti-angiogenic factors, including sFlt-1 and soluble endoglin, that cause widespread endothelial dysfunction. This endothelial dysfunction produces vasospasm, increased vascular permeability, and activation of the coagulation cascade. Target organ effects include cerebral edema and seizures, hepatic periportal necrosis and subcapsular hematoma, renal glomerular endotheliosis, and placental abruption and intrauterine growth restriction.
Diagnostic Criteria (ACOG 2020)
The diagnosis requires blood pressure of 140/90 mmHg or higher on two occasions at least 4 hours apart after 20 weeks gestation (or a single blood pressure reading of 160/110 or higher), combined with at least one of the following: proteinuria (300 mg or more per 24 hours, protein-to-creatinine ratio of 0.3 or higher, or urine dipstick of 2+), thrombocytopenia with platelets below 100,000 per microliter, renal insufficiency with creatinine above 1.1 mg/dL or doubling of baseline, hepatic dysfunction with transaminases above twice the upper limit of normal, new-onset cerebral or visual symptoms such as headache unresponsive to medication or visual disturbances including scotomata and blurred vision, or pulmonary edema.
Severe Features
Severe features include systolic blood pressure of 160 mmHg or higher or diastolic blood pressure of 110 mmHg or higher (measured twice, 15 minutes apart in the ED context), platelet count below 100,000 per microliter, AST or ALT above twice the upper limit of normal or severe persistent right upper quadrant or epigastric pain, creatinine above 1.1 mg/dL, pulmonary edema, and new-onset headache or visual disturbances (which indicate cerebral edema and impending eclampsia).
<image>Pathophysiology diagram of preeclampsia showing the cascade from abnormal placentation and failed spiral artery remodeling to placental ischemia, release of anti-angiogenic factors (sFlt-1 and soluble endoglin), systemic endothelial dysfunction, and the resulting target organ effects on the brain, liver, kidneys, and coagulation system</image>
Emergency Department Management of Preeclampsia
Blood Pressure Control
Blood pressure of 160/110 mmHg or higher must be treated urgently to prevent stroke, the leading cause of death in preeclampsia and eclampsia. First-line agents include IV labetalol (20 mg IV over 2 minutes, escalating to 40 mg then 80 mg if blood pressure remains elevated after 10 minutes, with a maximum total dose of 300 mg), IV hydralazine (5 to 10 mg IV over 2 minutes, repeated every 20 minutes to a maximum total dose of 20 mg), and oral immediate-release nifedipine (10 to 20 mg orally, repeated in 20 to 30 minutes if needed, which is rapidly effective and well-tolerated). The target blood pressure is 140 to 150/90 to 100 mmHg, and precipitous drops that may compromise uteroplacental perfusion must be avoided. ACE inhibitors and ARBs are contraindicated because of teratogenicity, and nitroprusside should be avoided due to fetal cyanide toxicity.
Seizure Prophylaxis
Magnesium sulfate is the drug of choice for seizure prevention in preeclampsia with severe features. The loading dose is 4 to 6 grams IV over 15 to 20 minutes, followed by a maintenance infusion of 1 to 2 grams per hour. The therapeutic range is 4 to 7 mEq/L. Toxicity monitoring includes checking patellar reflexes (lost at 7 to 10 mEq/L), respiratory rate (respiratory depression at 10 to 13 mEq/L), and cardiac conduction (cardiac arrest at levels above 25 mEq/L). Magnesium toxicity is treated with calcium gluconate 1 gram IV over 2 to 3 minutes. Magnesium should be continued for 24 to 48 hours postpartum.
Laboratory Evaluation
The laboratory workup includes CBC with platelet count, comprehensive metabolic panel (creatinine, liver function tests, glucose), coagulation studies (PT, PTT, fibrinogen), LDH, uric acid, type and screen, and urinalysis.
Eclampsia
Eclampsia is defined as new-onset generalized tonic-clonic seizures in a patient with preeclampsia and can occur antepartum (53 percent), intrapartum (19 percent), or postpartum (28 percent). It can occur up to 4 to 6 weeks postpartum as late postpartum eclampsia. Notably, 20 percent of eclamptic seizures occur without preceding severe hypertension or proteinuria. Management begins with protecting the airway, positioning the patient on the left lateral side, and preventing aspiration. Magnesium sulfate 4 to 6 grams IV bolus should be administered if the patient is not already receiving it; seizures typically self-terminate within 1 to 2 minutes. If seizures recur, an additional 2 grams of magnesium IV is given. For seizures refractory to magnesium, lorazepam 4 mg IV or propofol/thiopental for intubation may be required. Immediate fetal monitoring should follow seizure control. Eclampsia is an indication for delivery regardless of gestational age, after maternal stabilization.
HELLP Syndrome
Diagnostic Criteria
The diagnosis of HELLP requires hemolysis (schistocytes on peripheral smear, LDH above 600 IU/L, elevated indirect bilirubin, low haptoglobin), elevated liver enzymes (AST or ALT above twice the upper limit of normal), and low platelets (below 100,000 per microliter). HELLP can occur without hypertension or proteinuria in up to 15 to 20 percent of cases. Symptoms include right upper quadrant or epigastric pain (65 percent), nausea and vomiting (36 percent), headache, and malaise, and the presentation may mimic gastritis, hepatitis, or cholecystitis.
Complications
Hepatic subcapsular hematoma or rupture is a catastrophic complication presenting with sudden severe abdominal pain, shoulder pain, and hemodynamic collapse. CT or ultrasound shows subcapsular hematoma, and management includes immediate transfusion, surgery, and delivery. DIC is present in 20 percent of severe HELLP and is managed with blood products including cryoprecipitate, FFP, and platelets. Placental abruption occurs in 16 percent of HELLP cases. Other complications include acute renal failure, ARDS, and stroke.
Management
Delivery is the definitive treatment for HELLP regardless of gestational age if the patient is at 34 weeks or beyond or if the patient is deteriorating. Between 24 and 34 weeks, a 48-hour course of betamethasone for fetal lung maturity may be considered if the patient can be safely stabilized. Blood pressure control and seizure prophylaxis follow the same protocols as for preeclampsia with severe features. Platelet transfusion is indicated if the count is below 20,000 per microliter or below 50,000 if the patient requires cesarean delivery or has active bleeding. Corticosteroids (dexamethasone 10 mg IV every 12 hours) may temporarily improve platelet count and liver function tests, though evidence is mixed, and they are not a substitute for delivery.
<image>Clinical comparison table illustration showing the distinguishing features of preeclampsia, eclampsia, and HELLP syndrome side-by-side, including typical presentation, blood pressure patterns, laboratory abnormalities, key complications, and management priorities, organized in a color-coded grid format</image>
Postpartum Considerations
Preeclampsia and eclampsia can present for the first time in the postpartum period, up to 6 weeks after delivery. The emergency physician should consider this diagnosis in any postpartum patient with headache, visual changes, hypertension, or seizures. Posterior reversible encephalopathy syndrome (PRES) is associated with severe preeclampsia and eclampsia, presenting with headache, visual disturbances, seizures, and altered mental status. MRI shows vasogenic edema in the posterior white matter, and the condition is generally reversible with blood pressure control. Peripartum cardiomyopathy can coexist with preeclampsia, presenting with dyspnea, orthopnea, and signs of heart failure, and bedside echocardiography is diagnostic.
Clinical Pearls
Blood pressure of 160/110 mmHg or higher in pregnancy is a hypertensive emergency requiring treatment within 30 to 60 minutes to prevent stroke. Magnesium sulfate is superior to all other anticonvulsants for seizure prevention and treatment in eclampsia. HELLP syndrome can occur without hypertension or proteinuria, and it should be considered in any pregnant or postpartum patient with right upper quadrant pain and thrombocytopenia. Eclampsia can present up to 6 weeks postpartum, and it should always be considered in the differential for new postpartum seizures. Delivery is the only definitive treatment for preeclampsia, eclampsia, and HELLP, and the decision to deliver involves balancing maternal safety against fetal maturity.
References
- ACOG Practice Bulletin No. 222: Gestational hypertension and preeclampsia. Obstet Gynecol. 2020;135(6):e237-e260.
- Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol. 2004;103(5 Pt 1):981-991.
- Altman D, Carroli G, Duley L, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359(9321):1877-1890.
- Tuffnell DJ, Jankowicz D, Lindow SW, et al. Outcomes of severe pre-eclampsia/eclampsia in Yorkshire 1999/2003. BJOG. 2005;112(7):875-880.
