eMedicine Specialties > Emergency Medicine > Obstetrics & Gynecology

Pregnancy, Eclampsia

Allysia M Guy, MD, Staff Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn, New York
Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn

Updated: Aug 11, 2009

Introduction

Background

Ten percent of all pregnancies are complicated by hypertension (HTN). Eclampsia and preeclampsia account for about half of these cases worldwide and have been recognized and described for years despite the general lack of understanding of the disease.¹ In the fifth century, Hippocrates noted that headaches, convulsions, and drowsiness were ominous signs associated with pregnancy. In 1619, Varandaeus coined the term eclampsia in a treatise on gynecology.²

Eclampsia is defined as the clinical presentation of an unexplained seizure, convulsion, or altered mental status in the setting of the signs and symptoms of preeclampsia. It is considered a complication of severe preeclampsia.² It typically occurs during or after the 20th week of gestation or in the postpartum period.

The clinical manifestations of maternal preeclampsia are hypertension and proteinuria with or without coexisting systemic abnormalities involving kidney, liver, or blood. There is also a fetal manifestation of preeclampsia involving fetal growth restriction, reduced amniotic fluid, and abnormal fetal oxygenation.¹ HELLP syndrome is a severe form of preeclampsia and involves hemolytic anemia, elevated LFTs, and low platelet count.

Pathophysiology

Eclampsia is the progression from severe preeclampsia to seizures and coma and is thought to be due to hypertensive encephalopathy, vasogenic edema associated cortical ischemia, edema, or hemorrhage. The cause of preeclampsia and later eclampsia remains unclear. The main etiologic theories include abnormal trophoblastic invasion, coagulation abnormalities, vascular endothelial damage, cardiovascular maladaptation, immunologic phenomena, genetic predisposition, and dietary deficiencies or excess.²

It is believed that there is abnormal cerebral blood flow in the setting of extreme hypertension. Compensatory cerebral perfusion mechanisms are interrupted. Vessels become dilated with increased permeability and cerebral edema occurs and results in ischemia and encephalopathy. In extreme hypertension, the normal compensatory vasoconstriction may become defective. Several autopsy findings support this model and consistently reveal swelling and fibrinoid necrosis of vessel walls.²

Many uterovascular changes occur when a woman is pregnant. It is believed that these changes are due to the interaction between fetal and maternal allografts and result in systemic and local vascular changes. These system changes contribute to the brain pathology in eclampsia by inhibiting the regulation of cerebral perfusion. It has been shown that, in patients with eclampsia, the development of uteroplacental arteries is hindered.²

Many factors may contribute to this phenomenon. Endothelial cell dysfunction occurs in the vessels of these hypertensive women. Factors associated with endothelial dysfunction such as cellular fibronectin, von Willebrand factor, cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion molecule-1 [VCAM-1], and intercellular adhesion molecule-1 [ICAM-1]), and cytokines (ie, interleukin-6 [IL-6] and tumor necrosis factor-α [TNF-α]) have been shown to be increased in the systemic circulation of women suffering from this disease.¹ It is believed that antiangiogenic factors such as placental protein fms-like tyrosine kinase 1 (sFlt-1) and activin A antagonizes VEGF.³ Elevated levels of these proteins cause a reduction of VEGF and induce systemic and local endothelial cell dysfunction.¹

Reactive oxygen species have been shown to be pertinent for many cellular processes including angiogenesis, growth, and differentiation. Oxidative stress has been shown to stimulate activin A production and secretion from the placental and endothelial cells. Elevated levels of activin A are significantly associated with excessive oxidative stress.³ Additionally, oxidative stress has also been linked to endothelial dysfunction in preeclamptic patients. Studies in pregnant mouse models have proposed that there is a dysregulation in the ROS signaling pathway.^4,5 Leakage of proteins from circulation and generalized edema are sequelae of the endothelial dysfunction and thus a defining factor associated with preeclampsia and eclampsia.

Studies also suggest that the oxidative stress, inflammation, and endothelial cell dysfunction is further mediated by increased systemic leukocyte activity. Histochemistry studies indicate that there is predominantly an increase in neutrophil infiltration of vasculature in patients with eclampsia.⁵

Evidence does exist demonstrating an increase in leptin molecules in the circulation, which induces oxidative stress on cells as well as induces platelet aggregation. This most likely contributes to the coagulopathy associated with the disease.^4,2 Additionally, imbalanced prostanoid productions as well as increased plasma antiphospholipids have also been implicated in the pathogenesis of eclampsia, though poorly understood.^6,2

Inflammation, neutrophil invasion, oxidative stress with endothelial injury, and angiogenesis impedance have all been implicated in the pathogenesis of preeclampsia; however, the pathophysiology as a whole remains to be elucidated.

Frequency

United States

The reported incidence of eclampsia ranges from 1 in 2,000 to 1 in 3,448 pregnancies in the Western world. This rate is increased in lower socioeconomic populations, in woman younger than 20 years, in multifetal gestations, and in those without access to prenatal care.²

International

An estimated 10% of pregnancies are affected by hypertension worldwide.¹ Approximately one half of all hypertensive pregnancy disorders are due to preeclampsia.¹

Mortality/Morbidity

The preeclampsia-eclampsia case-fatality rate is approximately 6.4 cases per 10,000 cases at delivery.¹
The most significant maternal complications of eclampsia are related to permanent CNS damage secondary to recurrent seizures or intracranial bleeding. The maternal mortality rate is 8-36% in these cases.⁷
The fetal mortality rate varies from 13-30% due to premature delivery and its complications. Placental infarcts, abruptio placentae, and intrauterine growth retardation also contribute to fetal demise.²
Maternal death risk is approximately 1.8% in western countries. Higher mortality rates are associated with patients who have multiple seizures outside the hospital and those without prenatal care.
In developing countries, mortality is as high as 14% and is associated with lack of resources and intensive care facilities required for supportive management.¹
Mortality risks are increased for women aged 30 years and older, those without prenatal care, and black women.²
Women who have eclampsia before 28 weeks' gestation have also been found to have a higher risk of death.²

Race

Black woman have an increased risk of mortality associated with preeclampsia, most likely due to inadequate access to prenatal care and increased incidences of genetic diseases associated with circulating antiphospholipids.² It has been proven that patients with elevated antiphospholipid plasma levels have a higher incidence of preeclampsia/eclampsia; however, whether this is due to the antiphospholipids themselves or some other underlying process is not clear.⁶

Age

Eclampsia usually occurs in patients at both extremes of reproductive age; however, the risk of eclampsia is greatest in women younger than 20 years. Mortality risk is higher for women older than 35 years who have suffered from eclampsia previously.²

Clinical

History

Most eclamptic patients present with hypertension and seizures, with some combination of proteinuria and edema. However, hypertension, edema, and proteinuria may be absent in the setting of preeclampsia.⁷
Hypertension has been absent 16% of the time, proteinuria absent 14%, and edema absent 26%.²
Eclampsia can occur during the antepartum, intrapartum, and postpartum periods. Ninety percent of eclampsia cases occur after 28 weeks' gestation.²
The natural progression of the disease is from symptomatic severe preeclampsia (differentiated from preeclampsia by specific vital signs, symptoms, and laboratory abnormalities) to seizures.
Features of eclampsia include the following:
- Seizure or postictal state (100%)
- Headache (80%), usually frontal
- Generalized edema (50%)
- Vision disturbance (40%), such as blurred vision and photophobia
- Right upper quadrant (RUQ) abdominal pain with nausea (20%)
- Amnesia and other mental status changes

Physical

Findings at physical examination may include the following:

Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg
Tachycardia
Tachypnea
Rales
Mental status changes
Hyperreflexia
Clonus
Papilledema
Oliguria or anuria
Localizing neurologic deficits
Right upper quadrant (RUQ) or epigastric abdominal tenderness
Generalized edema
Small fundal height for the estimated gestational age
Apprehension

Causes

The etiology of eclampsia is not fully understood:

Studies in animal modes have suggested dysfunction of the uteroplacental bed related to altered endothelial, angiogenic factors, and vascular implantation.¹ This results in decreased uteroplacental perfusion pressure and ischemia with a subsequent release of cytokines and reactive oxygen species. The effect is a sympathetic and neurohormonal dysregulation of blood pressure, generalized vasoconstriction, and cellular and organ system dysfunction.³
Other causes may include the following:
- Altered cardiovascular reactivity
- Increased capillary permeability
- Widespread vasospasm
- Microthrombi
- Hypertension
- Improper implantation of the placenta

Risk factors include the following:

Nulliparity
Family history of preeclampsia, prior preeclampsia and eclampsia²
Poor outcome of previous pregnancy, including intrauterine growth retardation, abruptio placentae, or fetal death
Preexisting medical condition - Obesity, chronic hypertension, renal disease, thrombophilias-antiphospholipid antibody syndrome, protein C deficiency and protein S deficiency, antithrombin deficiency, vascular and connective tissue disorders, gestational diabetes, and systemic lupus erythematosus²
Multifetal gestations, hydatid mole, fetal hydrops, primigravida
Teen pregnancy
Primigravida
Patient older than 35 years
Lower socioeconomic status

Differential Diagnoses

Adrenal Insufficiency and Adrenal Crisis	Shock, Septic
Encephalitis	Stroke, Hemorrhagic
Hypertensive Emergencies	Stroke, Ischemic
Hypoglycemia	Subarachnoid Hemorrhage
Meningitis	Systemic Lupus Erythematosus
Neoplasms, Brain	Withdrawal Syndromes
Pregnancy, Preeclampsia

Workup

Laboratory Studies

Urinalysis to detect for proteinuria (>300 mg/24 h or > 1 g/L): A timed collection has been the criterion standard. Protein per unit time measured over 24 hours has been used traditionally; however, 12-hour collections have been proven to be as accurate.⁸
The CBC may reveal the following:
- Anemia due to microangiopathic hemolysis, hemoconcentration due to third spacing, or physiologic hemodilution of pregnancy
- Peripheral smear (schistocytes, burr cells, echinocytes)
- Increased bilirubin >1.2 mg/dL
- Thrombocytopenia (<100,000) due to hemolysis and low platelet count associated with HELLP syndrome (seen in 20-25% of patients with eclampsia)²
- Low serum haptoglobin levels
- Elevated lactate dehydrogenase (LDH) levels (threshold of 180–600 U/L)
The serum creatinine level is elevated because of decreased intravascular volume and a decreased glomerular filtration rate (GFR). Creatinine clearance (CrCl) may be less than 90 mL/min/1.73 m².
Liver function test results may reveal the following (20-25% of patients with eclampsia):
- Aspartate aminotransferase (SGOT) level higher than 72 IU/L, total bilirubin levels higher than 1.2 mg/dL, and LDH level higher than 600 IU/L²
- Elevated levels due to hepatocellular injury and HELLP syndrome
The coagulation profile may reveal normal prothrombin (PT) and activated partial thromboplastin (aPTT) times, fibrin split products, and fibrinogen levels. Rule out associated disseminated intravascular coagulation (DIC).
Rule out hypoglycemia as cause of seizure or result of seizure, and rule out hyperglycemia as cause of mental status changes.
Uric acid levels may be increased mildly.

Imaging Studies

Head CT scanning
- Obtain a CT scan of the head in patients with severe preeclampsia or eclampsia and associated neurologic deficits or severe headache.
- CT scan is used to assess intracranial hemorrhage, subarachnoid hemorrhages, or cerebrovascular accidents.
Transabdominal ultrasonography
- Transabdominal ultrasonography is used to estimate gestational age.
- This may also be used to rule out abruptio placentae that can complicate eclampsia.

Treatment

Prehospital Care

Emergency medical services personnel should (1) secure an intravenous line with a large-bore catheter, (2) initiate cardiac monitoring and administer oxygen, and (3) transport the patient in the left lateral decubitus position.
Supportive care includes airway support and attempted termination of any ongoing seizure with diazepam.

Emergency Department Care

Hospitalization, labor followed by delivery. In 1772, De la Motte recognized that prompt delivery of pregnant women with convulsions favored their recovery.⁹ Delivery is the only definitive treatment.
The initial step for supportive care is to maintain adequate oxygenation. Supportive care for eclampsia consists of close monitoring, invasive if clinically indicated; airway support; adequate oxygenation; anticonvulsant therapy; and BP control.
Intravenous magnesium sulfate is the initial drug administered to terminate seizures and lower BP. Seizures usually terminate after the loading dose of magnesium. A loading dose of 6 g (15-20 min) and a maintenance dose of 2 g per hour as a continuous intravenous solution. Once the seizures terminate, 85% of patients note improved blood pressure control.^7,2 Note: Magnesium toxicity can cause coma, and, if mental status changes with these infusion rates, this should be considered.²
Severe hypertension must be addressed after magnesium infusions. Hydralazine or labetalol can then be administered IV for BP control. The goal is to maintain systolic BP between 140 and 160 mm Hg and diastolic BP between 90 and 110 mm Hg. Recommended intravenous bolus of hydralazine (5-10 mg) or labetalol (20-40 mg q15min prn). Other potent antihypertensive medications such as sodium nitroprusside or nitroglycerin can be used but are rarely required.²
Diuretics are used only in the setting of pulmonary edema.
Care must be taken not to decrease the BP too drastically; an excessive decrease can cause inadequate uteroplacental perfusion and fetal distress.⁹
Benzodiazepine or phenytoin can be used for seizures that are not responsive to magnesium sulfate.
Maintaining a diastolic BP of 90 mm Hg is the goal of antihypertensive therapy. Oral nifedipine (40-120 mg/d) with or without labetalol (600-2400 mg/d) is given to keep systolic BP between 140 and 155 mm Hg and diastolic pressure between 90 and 105 mm Hg.²
A dose of antenatal steroids may be administered in anticipation of emergent delivery when gestational age is less than 32 weeks. Betamethasone (12 mg IM q24h X 2 doses) or dexamethasone (6 mg IM q12h X 4 doses) is recommended.^9,2
Several organizations have developed screening, treatment, and prevention guidelines for preeclampsia and eclampsia.^10,11,12

Consultations

Recommend immediate consultation with in-house obstetrician and maternal fetal medicine for emergent delivery. ICU services may also be involved to facilitate close monitoring.

Medication

The goal of therapy is to decrease BP, prevent or control convulsions, and deliver a viable neonate. The antihypertensive agent of choice is hydralazine. Alternative antihypertensives include labetalol, diazoxide, and occasionally, nitroprusside.

Anticonvulsants

Convulsive generalized status epilepticus in pregnancy jeopardizes both the mother and fetus. The anticonvulsant agent of choice is magnesium sulfate. However, when seizures continue after administration of magnesium, benzodiazepines are the drugs of choice.

Magnesium sulfate (MgSO4)

Used to treat and prevent seizures. May cause hyporeflexia, respiratory depression, and bradycardia. Monitor patient's reflexes and discontinue infusion if reflexes are absent or if magnesium level exceeds 6-8 mEq/L. Use IV/IM route for seizure prophylaxis in preeclampsia. When treating true eclampsia, use IV route for quicker action. Calcium gluconate 10% solution 10-20 mL IV can be given as an antidote for clinically significant hypermagnesemia. Discontinue as soon as desired effect is obtained. Repeat doses depend on continuing presence of patellar reflex and adequate respiratory function.

Dosing

Adult

4 g IV initially, followed by 1-4 g IM q4h prn
Alternatively, 1-4 g/h continuous infusion

Pediatric

20-100 mg/kg/dose IV q4-6h prn; doses as high as 200 mg/kg/dose have been used in severe cases

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycoside use and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone; may increase cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May alter cardiac conduction, leading to heart block inpatients taking digitalis; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; may produce significant hypertension or asystole; in overdose, calcium gluconate 10-20 mL IV of 10% solution can be given as antidote for clinically significant hypermagnesemia; use in eclampsia is reserved for immediate control of life-threatening convulsions

Diazepam (Valium)

For treatment of seizures resistant to magnesium sulfate. Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Dosing

Adult

5-10 mg IV q10-20min; repeat in 2-4 h prn; not to exceed 30 mg in 8 h

Pediatric

0.05-0.3 mg/kg/dose IV over 2-3 min q15-30min; not to exceed 10 mg; repeat in 2-4 h prn

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Antihypertensives

A systolic BP of 160-180 mm Hg or greater or a diastolic BP of 110 mm Hg or greater should be treated with IV antihypertensives to prevent cerebral hemorrhage. Hydralazine is the DOC for BP control in eclampsia. However, parenteral hydralazine is provided to pharmacists only through special emergency request. Therefore, be prepared to use other antihypertensive agents when hydralazine is not available immediately. Labetalol has alpha-adrenergic and beta-adrenergic blocking effects and can be used for rapid control of severe hypertension.

Other antihypertensive drugs have significant adverse effects and should not be used as primary agents. Diazoxide may cause hyperglycemia and inhibit labor. Nitroprusside may cause fetal cyanide toxicity. Diuretics should be avoided because of the relative intravascular volume depletion in the patient with eclampsia.

Hydralazine (Hydrea)

Decreases systemic resistance through direct vasodilation of arterioles.

Dosing

Adult

5 mg IV initially, then 5-10 mg IV q20-30min prn; not to exceed 30 mg

Pediatric

0.1-0.2 mg/kg/dose IV q4-6h prn; not to exceed 20 mg or 1.7-3.5 mg/kg/d divided into 4-6 doses

Interactions

MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Implicated in myocardial infarction; caution in suspected coronary artery disease

Labetalol (Normodyne)

Used as alternative to hydralazine in eclampsia. It blocks alpha-adrenergic, beta1-adrenergic, and beta2-aderenergic receptor sites.

Dosing

Adult

20-30 mg IV over 2 min followed by 40-80 mg IV at 10-min intervals; not to exceed 300 mg/dose

Pediatric

Not established
Suggested dose: 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia from nitroglycerin use, without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock; uncompensated congestive heart failure; bradycardia; pulmonary edema; reactive airway disease; atrioventricular block; severe bradycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy with signs of liver dysfunction; in elderly patients, a lower response rate and higher incidence of toxicity may be observed

Diazoxide (Hyperstat)

Produces direct smooth-muscle relaxation of the peripheral arterioles, decreasing BP.

Dosing

Adult

1-3 mg/kg IV as a single injection, not to exceed 150 mg/dose
Repeat dose in 5-15 min prn until BP is adequately reduced

Pediatric

Administer as in adults

Interactions

May decrease serum hydantoins, possibly resulting in decreased anticonvulsant effects; thiazide diuretics may potentiate hyperuricemic and antihypertensive effects

Contraindications

Documented hypersensitivity; aortic coarctation; pheochromocytoma; arteriovenous shunts; aortic aneurysm

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with diabetes mellitus may require treatment for hyperglycemia; when given prior to delivery, may produce fetal or neonatal hyperbilirubinemia, thrombocytopenia, altered carbohydrate metabolism, and other adverse reactions

Nitroprusside (Nitropress)

Used occasionally for treatment of eclampsia. It causes peripheral vasodilation by directly acting on venous and arteriolar smooth muscle, reducing peripheral resistance.

Dosing

Adult

0.3-0.5 mcg/kg/min IV, increase in increments of 0.5 mcg/kg/min, titrate to desired hemodynamic effect; average dose is 3 mcg/kg/min

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic; atrial fibrillation or flutter

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, hypothyroidism; in renal or hepatic insufficiency, levels may increase and cause cyanide toxicity; can lower BP and should be used only in patients with mean arterial pressures >70 mm Hg

Follow-up

Further Inpatient Care

Patients with eclampsia require immediate obstetric consultation and admission to an intensive care setting for supportive care and treatment until delivery of the neonate.
Patients require hospitalization, with bed rest in left lateral decubitus position.
Airway management and adequate oxygenation should be continued.
Anticonvulsant therapy with magnesium sulfate may be required.
Treat continued hypertension with hydralazine or labetalol.
Delivery of the neonate is the definitive treatment.

Transfer

Perinatal morbidity and mortality rates vary in relation to the level of care rendered by the medical center. Patients with eclampsia require transfer to a high-risk obstetric facility that provides neonatal and maternal intensive care.
When initially evaluating a patient with eclampsia, become familiar with the level of care that the medical center can offer the patient.

Deterrence/Prevention

High protein, low salt diet²
Protein supplementation
Magnesium
Calcium
Zinc
Fish and evening primrose
Antihypertensive drugs
Antithrombotic agents
Low-dose aspirin
Dipyridamole
Heparin
Vitamins E an C

Note: Studies have not been able to prove risk benefits of most of these preventative measures; thus, they are not recommended as prophylaxis at this time.²

Complications

Permanent neurologic damage from recurrent seizures or intracranial bleeding
Studies suggest increased risk for CVA and CAD in eclamptic mothers later in life.¹
Renal insufficiency and acute renal failure
Fetal changes - IUGR, abruptio placentae, oligohydramnios
Hepatic damage and rarely hepatic rupture
Hematologic compromise and DIC
Increased risk of recurrent preeclampsia/eclampsia with subsequent pregnancy⁴
Death

Prognosis

Approximately 25% of women with eclampsia have hypertension in subsequent pregnancies.
Eclamptic multiparous women may have an increased risk for essential hypertension.
Eclamptic multiparous women have an increased mortality rate in subsequent pregnancies compared with primiparous women.

Miscellaneous

Medicolegal Pitfalls

Preeclampsia can progress quickly to eclampsia.
Immediately consult an obstetrician/gynecologist when the diagnosis of eclampsia is being considered.
Seizures in the first trimester or well into the postpartum period probably are due to CNS pathology and warrant full evaluation, including CT scanning of the head, lumbar puncture (if clinical evidence of meningitis or concern for hemorrhage exists), determination of electrolyte levels, and urine or serum toxicologic screening.
Preventing the development of preeclampsia in high-risk patients could theoretically decrease the risk of eclampsia and its complications later in pregnancy. Aspirin blocks platelet aggregation and vasospasm in preeclampsia, and it may be effective in preventing preeclampsia. Recent studies have shown that low-dose aspirin in women at high risk for preeclampsia can contribute to a decreased risk of preeclampsia, a reduction in preterm delivery rates, and a reduction in fetal death rates without increasing the risk of placental abruption. An obstetrician should directly supervise aspirin therapy in high-risk patients.

References

Craici I, Wagner S, Garovic VD. Preeclampsia and future cardiovascular risk: formal risk factor or failed stress test?. Ther Adv Cardiovasc Dis. Aug 2008;2(4):249-59. [Medline].
Gabbe. Hypertension. In: Obstetrics: Normal and Problem Pregnancies. 5^th ed. Churchill Livingstone, An Imprint of Elsevier; 2007:[Full Text].
Reddy A, Suri S, Sargent IL, Redman CW, Muttukrishna S. Maternal circulating levels of activin A, inhibin A, sFlt-1 and endoglin at parturition in normal pregnancy and pre-eclampsia. PLoS One. 2009;4(2):e4453. [Medline].
Banerjee S, Randeva H, Chambers AE. Mouse models for preeclampsia: disruption of redox-regulated signaling. Reprod Biol Endocrinol. Jan 15 2009;7:4. [Medline].
Cadden KA, Walsh SW. Neutrophils, but not lymphocytes or monocytes, infiltrate maternal systemic vasculature in women with preeclampsia. Hypertens Pregnancy. 2008;27(4):396-405. [Medline].
Nodler J, Moolamalla SR, Ledger EM, Nuwayhid BS, Mulla ZD. Elevated antiphospholipid antibody titers and adverse pregnancy outcomes: analysis of a population-based hospital dataset. BMC Pregnancy Childbirth. Mar 16 2009;9:11. [Medline].
Rivers EP. Preeclampsia, eclampsia, and other hypertensive disorders of pregnancy. In: The Clinical Practice of Emergency Medicine. 2^nd ed. 1996:315-21.
Hofmeyr GJ, Belfort M. Proteinuria as a predictor of complications of pre-eclampsia. BMC Med. Mar 24 2009;7:11. [Medline].
ACOG. ACOG Practice Bulletin: Diagnosis and Management of Preeclampsia and Eclampsia: The American College of Obstetricians and Gynecologists Number 33. Jan 2002.
[Guideline] Milne F, Redman C, Walker J, Baker P, Bradley J, Cooper C, et al. The pre-eclampsia community guideline (PRECOG): how to screen for and detect onset of pre-eclampsia in the community. BMJ. Mar 12 2005;330(7491):576-80. [Medline]. [Full Text].
[Guideline] Tuffnell DJ, Shennan AH, Waugh JJ, Walker JJ. The management of severe pre-eclampsia/eclampsia. London (UK): Royal College of Obstetricians and Gynaecologists. Mar 2006;[Full Text].
[Guideline] Magee LA, Helewa M, Moutquin JM, von Dadelszen P, Hypertension Guideline Committee, Society of Obstetricians and Gynaecologists of Canada. Prediction, prevention, and prognosis of preeclampsia. In: Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. J Obstet Gynaecol Can. Mar 2008;30(3 Suppl 1):S16-23. [Full Text].
Abbott J. Complications related to pregnancy. In: Emergency Medicine: Concepts and Clinical Practice. 3^rd ed. 1992:1984-7.
Brady WJ, DeBehnke DJ, Carter CT. Postpartum toxemia: hypertension, edema, proteinuria and unresponsiveness in an unknown female. J Emerg Med. Sep-Oct 1995;13(5):643-8. [Medline].
Coomarasamy A, Honest H, Papaioannou S. Aspirin for prevention of preeclampsia in women with historical risk factors: a systematic review. Obstet Gynecol. Jun 2003;101(6):1319-32. [Medline].
Duley L, Henderson-Smart D, Knight M, King J. Antiplatelet drugs for prevention of pre-eclampsia and its consequences: systematic review. BMJ. Feb 10 2001;322(7282):329-33. [Medline].
[Guideline] Hals G, Crump T. The pregnant patient: guidelines for management of common life-threatening medical disorders in the emergency department. Emerg Med Rep. Mar 13 2000;21(6):57-9.
Hansen WF. Problems in pregnancy. In: Emergency Medicine: A Comprehensive Study Guide. 4^th ed. 1996:573.
Moussouttas M, Abubakr A, Grewal RP. Eclamptic subarachnoid haemorrhage without hypertension. J Clin Neurosci. May 2006;13(4):474-6. [Medline].
Rigourd V, Chauvet C, Chelbi ST, Rebourcet R, Mondon F, Letourneur F, et al. STOX1 overexpression in choriocarcinoma cells mimics transcriptional alterations observed in preeclamptic placentas. PLoS One. 2008;3(12):e3905. [Medline].
Robinson CJ, Johnson DD, Chang EY. Evaluation of placenta growth factor and soluble Fms-like tyrosine kinase 1 receptor levels in mild and severe preeclampsia. Am J Obstet Gynecol. Jul 2006;195(1):255-9. [Medline].
Stennett AK, Khalil RA. Neurovascular mechanisms of hypertension in pregnancy. Curr Neurovasc Res. May 2006;3(2):131-48. [Medline].
Thangaratinam S, Coomarasamy A, O'Mahony F, Sharp S, Zamora J, Khan KS, et al. Estimation of proteinuria as a predictor of complications of pre-eclampsia: a systematic review. BMC Med. Mar 24 2009;7:10. [Medline].
Which anticonvulsant for women with eclampsia?. Evidence from the Collaborative Eclampsia Trial. Lancet. Jun 10 1995;345(8963):1455-63. [Medline].

Keywords

eclampsia, hypertension of pregnancy, seizures in pregnancy, toxemia of pregnancy, coma in pregnancy, preeclampsia, hypertensive disorder, proteinuria

Contributor Information and Disclosures

Author

Allysia M Guy, MD, Staff Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn, New York
Disclosure: Nothing to disclose.

Coauthor(s)

Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn
Mark A Silverberg, MD, FACEP, MMB is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine; Program Director, Emergency Medicine Residency, Summa Health System
Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Mark Zwanger, MD, MBA, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University
Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Medicines Company Consulting fee Consulting; Pfizer Salary Employment

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Stephen Morris, MD, to the development and writing of this article.

Further Reading