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Emergency And Acute Medicine – Preeclampsia/Eclampsia
Hypertensive disorders of pregnancy complicate approximately 1% of all pregnancies and account for 16% of maternal deaths. Gestational hypertension (GH) is defined as new-onset hypertension after 20 weeks of gestation that resolves with delivery and occurs in 6–7% of pregnancies. Preeclampsia is gestational hypertension accompanied by proteinuria and affects 2.2–6.3% of pregnancies. Eclampsia is defined as preeclampsia with the occurrence of seizures. Postpartum preeclampsia develops within 6 weeks of delivery, often without prior history of hypertension, and occurs in approximately 5% of patients, most commonly in African American women. HELLP syndrome—characterized by hemolysis, elevated liver enzymes, and low platelets—may occur in women with preeclampsia or eclampsia. Superimposed preeclampsia refers to preeclampsia developing in a woman with chronic hypertension and complicates up to 25% of such pregnancies.
Preeclampsia is thought to result from incomplete placental implantation leading to placental underperfusion, decreased angiogenic growth factors, and increased placental debris in the maternal circulation. Eclampsia may develop even in patients without prior documented hypertension; approximately one-third of patients who seize have no preceding hypertensive diagnosis. Risk factors include extremes of reproductive age, nulliparity, multiple gestations, molar pregnancy, obesity, diabetes, collagen vascular disease, chronic hypertension, renal disease, smoking, and prior history of preeclampsia.
Gestational hypertension is diagnosed when systolic blood pressure (SBP) exceeds 140 mm Hg or diastolic blood pressure (DBP) exceeds 90 mm Hg on two separate measurements after 20 weeks of gestation in a previously normotensive patient. Severe hypertension is defined as SBP greater than 160 mm Hg or DBP greater than 110 mm Hg. Preeclampsia requires the presence of hypertension and proteinuria, defined as ≥300 mg protein on 24-hour urine collection or ≥1+ protein on urinalysis. Mild preeclampsia presents with SBP <160 mm hg and dbp <110 hg, normal platelets liver function tests, absence of neurologic symptoms. severe preeclampsia includes sbp>160 mm Hg or DBP >110 mm Hg, heavy proteinuria, oliguria, thrombocytopenia, right upper quadrant pain, impaired liver function, cerebral symptoms, visual disturbances, pulmonary edema, or evidence of intrauterine growth restriction. HELLP syndrome may present with pulmonary edema, renal or liver failure, sepsis, stroke, or other systemic complications.
Patients commonly report headache, visual disturbances, abdominal pain (especially right upper quadrant), nausea, vomiting, weight gain, edema, shortness of breath, or neurologic symptoms. A history of prior preeclampsia, chronic hypertension, or renal disease increases suspicion. Physical examination should include serial blood pressure measurements, careful abdominal palpation for right upper quadrant tenderness, evaluation for edema, and detailed neurologic assessment including mental status and deep tendon reflexes.
Evaluation requires serial blood pressure monitoring and urinalysis. Laboratory studies include complete blood count, liver function tests, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, coagulation studies, fibrinogen, and d-dimer levels. Proteinuria greater than 1+ on dipstick warrants 24-hour urine collection. Obstetric ultrasound assesses gestational age, fetal growth, viability, and amniotic fluid volume. Fetal monitoring and nonstress testing are indicated. Head CT should be performed when neurologic deficits or severe symptoms raise concern for intracranial hemorrhage or mass. Lumbar puncture may be necessary if infection or subarachnoid hemorrhage is suspected. Urine toxicology should be considered to exclude cocaine or methamphetamine use.
Management begins with stabilization of airway, breathing, and circulation. Patients should receive 100% oxygen and be placed in the left lateral decubitus position to reduce inferior vena cava compression and improve cardiac output. Continuous maternal cardiopulmonary and fetal monitoring is essential. Magnesium sulfate (MgSO₄) is the first-line agent for seizure prophylaxis and treatment. A typical regimen includes a 4 g IV loading dose (or 10 g IM) followed by a continuous infusion of 1–2 g/hour, with a target serum magnesium level of 4–7 mEq/L. The infusion rate should not exceed 1 g/min during bolus administration. Signs of magnesium toxicity include hypotension, loss of patellar reflexes, respiratory depression, decreased urine output, and elevated creatinine; calcium gluconate 1 g IV is the antidote.
Blood pressure control is achieved with intravenous hydralazine (5–20 mg IV) or labetalol (initial 10 mg IV, followed by incremental dosing). The goal is to reduce blood pressure by approximately 25% initially, then gradually to <160 />00 mm Hg over several hours. If seizures persist despite magnesium, second-line therapy includes diazepam, fosphenytoin, or phenytoin. Intubation is required for airway protection, refractory seizures, or hypoxia.
Delivery is the definitive treatment for preeclampsia and eclampsia. Obstetric consultation is mandatory in all cases. Expectant management may be considered in select patients less than 30 weeks’ gestation with stable disease, but delivery is recommended beyond 30 weeks or in the presence of severe features. Emergent induction or cesarean section is indicated for maternal or fetal instability.
All patients with preeclampsia, eclampsia, or HELLP syndrome require admission, often to intensive care or labor and delivery units. Patients with isolated hypertension who have negative evaluation for preeclampsia and are asymptomatic may be discharged with close obstetric follow-up. Patients should return immediately for headache, visual changes, abdominal pain, dyspnea, leg swelling, or decreased urine output.
Clinicians must remember that preeclampsia and eclampsia can occur up to 30 days postpartum and should be considered in any postpartum patient presenting with edema, headache, shortness of breath, or seizure. Airway management may be challenging due to airway edema and engorgement; smaller-diameter endotracheal tubes and fiberoptic techniques may be required. Early recognition, aggressive stabilization, and timely delivery are critical to reducing maternal and fetal morbidity and mortality.
Hypertensive disorders of pregnancy complicate approximately 1% of all pregnancies and account for 16% of maternal deaths. Gestational hypertension (GH) is defined as new-onset hypertension after 20 weeks of gestation that resolves with delivery and occurs in 6–7% of pregnancies. Preeclampsia is gestational hypertension accompanied by proteinuria and affects 2.2–6.3% of pregnancies. Eclampsia is defined as preeclampsia with the occurrence of seizures. Postpartum preeclampsia develops within 6 weeks of delivery, often without prior history of hypertension, and occurs in approximately 5% of patients, most commonly in African American women. HELLP syndrome—characterized by hemolysis, elevated liver enzymes, and low platelets—may occur in women with preeclampsia or eclampsia. Superimposed preeclampsia refers to preeclampsia developing in a woman with chronic hypertension and complicates up to 25% of such pregnancies.
Preeclampsia is thought to result from incomplete placental implantation leading to placental underperfusion, decreased angiogenic growth factors, and increased placental debris in the maternal circulation. Eclampsia may develop even in patients without prior documented hypertension; approximately one-third of patients who seize have no preceding hypertensive diagnosis. Risk factors include extremes of reproductive age, nulliparity, multiple gestations, molar pregnancy, obesity, diabetes, collagen vascular disease, chronic hypertension, renal disease, smoking, and prior history of preeclampsia.
Gestational hypertension is diagnosed when systolic blood pressure (SBP) exceeds 140 mm Hg or diastolic blood pressure (DBP) exceeds 90 mm Hg on two separate measurements after 20 weeks of gestation in a previously normotensive patient. Severe hypertension is defined as SBP greater than 160 mm Hg or DBP greater than 110 mm Hg. Preeclampsia requires the presence of hypertension and proteinuria, defined as ≥300 mg protein on 24-hour urine collection or ≥1+ protein on urinalysis. Mild preeclampsia presents with SBP <160 mm hg and dbp <110 hg, normal platelets liver function tests, absence of neurologic symptoms. severe preeclampsia includes sbp>160 mm Hg or DBP >110 mm Hg, heavy proteinuria, oliguria, thrombocytopenia, right upper quadrant pain, impaired liver function, cerebral symptoms, visual disturbances, pulmonary edema, or evidence of intrauterine growth restriction. HELLP syndrome may present with pulmonary edema, renal or liver failure, sepsis, stroke, or other systemic complications.
Patients commonly report headache, visual disturbances, abdominal pain (especially right upper quadrant), nausea, vomiting, weight gain, edema, shortness of breath, or neurologic symptoms. A history of prior preeclampsia, chronic hypertension, or renal disease increases suspicion. Physical examination should include serial blood pressure measurements, careful abdominal palpation for right upper quadrant tenderness, evaluation for edema, and detailed neurologic assessment including mental status and deep tendon reflexes.
Evaluation requires serial blood pressure monitoring and urinalysis. Laboratory studies include complete blood count, liver function tests, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, coagulation studies, fibrinogen, and d-dimer levels. Proteinuria greater than 1+ on dipstick warrants 24-hour urine collection. Obstetric ultrasound assesses gestational age, fetal growth, viability, and amniotic fluid volume. Fetal monitoring and nonstress testing are indicated. Head CT should be performed when neurologic deficits or severe symptoms raise concern for intracranial hemorrhage or mass. Lumbar puncture may be necessary if infection or subarachnoid hemorrhage is suspected. Urine toxicology should be considered to exclude cocaine or methamphetamine use.
Management begins with stabilization of airway, breathing, and circulation. Patients should receive 100% oxygen and be placed in the left lateral decubitus position to reduce inferior vena cava compression and improve cardiac output. Continuous maternal cardiopulmonary and fetal monitoring is essential. Magnesium sulfate (MgSO₄) is the first-line agent for seizure prophylaxis and treatment. A typical regimen includes a 4 g IV loading dose (or 10 g IM) followed by a continuous infusion of 1–2 g/hour, with a target serum magnesium level of 4–7 mEq/L. The infusion rate should not exceed 1 g/min during bolus administration. Signs of magnesium toxicity include hypotension, loss of patellar reflexes, respiratory depression, decreased urine output, and elevated creatinine; calcium gluconate 1 g IV is the antidote.
Blood pressure control is achieved with intravenous hydralazine (5–20 mg IV) or labetalol (initial 10 mg IV, followed by incremental dosing). The goal is to reduce blood pressure by approximately 25% initially, then gradually to <160 />00 mm Hg over several hours. If seizures persist despite magnesium, second-line therapy includes diazepam, fosphenytoin, or phenytoin. Intubation is required for airway protection, refractory seizures, or hypoxia.
Delivery is the definitive treatment for preeclampsia and eclampsia. Obstetric consultation is mandatory in all cases. Expectant management may be considered in select patients less than 30 weeks’ gestation with stable disease, but delivery is recommended beyond 30 weeks or in the presence of severe features. Emergent induction or cesarean section is indicated for maternal or fetal instability.
All patients with preeclampsia, eclampsia, or HELLP syndrome require admission, often to intensive care or labor and delivery units. Patients with isolated hypertension who have negative evaluation for preeclampsia and are asymptomatic may be discharged with close obstetric follow-up. Patients should return immediately for headache, visual changes, abdominal pain, dyspnea, leg swelling, or decreased urine output.
Clinicians must remember that preeclampsia and eclampsia can occur up to 30 days postpartum and should be considered in any postpartum patient presenting with edema, headache, shortness of breath, or seizure. Airway management may be challenging due to airway edema and engorgement; smaller-diameter endotracheal tubes and fiberoptic techniques may be required. Early recognition, aggressive stabilization, and timely delivery are critical to reducing maternal and fetal morbidity and mortality.
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