eMedicine Specialties > Emergency Medicine > Obstetrics & Gynecology

Pregnancy, Preeclampsia

Mert Erogul, MD, Assistant Professor of Emergency Medicine, University Hospital of Brooklyn: Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Updated: May 12, 2008

Introduction

Background

Preeclampsia is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 weeks' gestation. It is clinically defined by hypertension and proteinuria.

Preeclampsia is part of a spectrum of disorders that includes gestational hypertension, severe preeclampsia, and eclampsia. Although each of these disorders can appear in isolation, they are thought of as progressive manifestations of a single process and are believed to share a common etiology.

The diagnostic criteria for preeclampsia focus on measurement of elevated blood pressure and proteinuria that develop after 20 weeks' gestation. Consensus is lacking among the various national and international organizations about the values that define the disorder, but a reasonable limit in a woman who was normotensive prior to 20 weeks' gestation is a systolic blood pressure (BP) greater than 140 mm Hg and a diastolic BP greater than 90 mm Hg on 2 successive measurements 4-6 hours apart. Preeclampsia in a patient with preexisting essential hypertension is diagnosed if systolic BP has increased by 30 mm Hg or if diastolic BP has increased by 15 mm Hg.

Proteinuria is defined as 300 mg or more of protein in a 24-hour urine sample. In the emergency department, a urine protein-to-creatinine ratio of 0.19 or greater is somewhat predictive of significant proteinuria (negative predictive value [NPV], 87%).¹  Serial confirmations 6 hours apart increase the predictive value. Although more convenient, a urine dipstick value of 1+ or more (30 mg/dL) is not reliable. 

For the purposes of guiding management, a distinction can be made between mild preeclampsia and severe preeclampsia. 

Diagnostic criteria for severe preeclampsia include at least one of the following:

• Systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg on 2 occasions 6 hours apart with the patient at bed rest
• Proteinuria greater than 5000 mg in a 24-hour collection or more than 3+ on 2 random urine samples collected at least 4 hours apart
• Oliguria with less than 500 mL per 24 hours
• Persistent maternal headache or visual disturbance
• Pulmonary edema or cyanosis
• Concerning abdominal pain
• Impaired liver function test findings
• Thrombocytopenia
• Oligohydramnios, decreased fetal growth, or placental abruption

Eclampsia is defined as seizures in a patient with preeclampsia.

For more information, see Medscape’s Pregnancy Resource Center.

For a related CME activities, see CME - Hypertension in Pregnancy: Emerging Risk Factor for Cardiovascular Disease, CME/CE – Folic Acid in Early Second Trimester May Reduce Risk of Preeclampsia, and CME – Antioxidants May Not Reduce Risk for Preeclampsia.

Pathophysiology

The mechanism by which preeclampsia occurs is not certain, and the diagnosis may represent a diversity of pathophysiologies that proceed to a common final pathway. The inciting event is believed to be placental hypoperfusion, which may result because the uteroplacental spiral arterioles are abnormally formed, leaving them highly sensitive to vasoconstriction. Both maternal and paternal factors have been implicated in the development of preeclampsia.

Placental hypoperfusion leads by an unclear pathway to the release of systemic vasoactive compounds that cause an exaggerated inflammatory response, vasoconstriction, endothelial damage, capillary leak, hypercoagulability, and platelet dysfunction, all of which contribute to organ dysfunction and the various clinical features of the disease.

Preeclampsia is a state of high systemic vascular resistance with normal or relatively low intravascular volume.

Frequency

United States

Preeclampsia occurs in approximately 5% of all pregnancies. The incidence of preeclampsia is 23.6 cases per 1,000 deliveries in the United States.

International

The global incidence of preeclampsia has been estimated at 5-14% of all pregnancies.

Mortality/Morbidity

Preeclampsia is the third leading pregnancy-related cause of death, after hemorrhage and embolism. Preeclampsia is the cause in an estimated 790 maternal deaths per 100,000 live births.

Morbidity and mortality is related to systemic endothelial dysfunction; vasospasm and small-vessel thrombosis leading to tissue and organ ischemia; CNS events such as seizures, strokes, and hemorrhage; acute tubular necrosis; coagulopathies; and placental abruption in the mother. 

Hemolysis, elevated liver enzyme levels, and low platelets (HELLP) syndrome may be an outcome of severe preeclampsia, although some authors believe it to have an unrelated etiology.

Race

The frequency of mortality differs among race and ethnicity, with African Americans having a worse mortality rate than white women.

Age

Preeclampsia occurs more frequently in women at the extremes of reproductive age.

• Younger women (<20 y) have a slightly increased risk. Primigravid patients in particular seem to be predisposed.
• Older women (>35 y) have a markedly increased risk.

Clinical

History

Mild-to-moderate preeclampsia may be asymptomatic. Many cases are detected through routine prenatal screening. Patients with severe preeclampsia display end-organ effects and may complain of the following:

• CNS  
  • Headache
  • Visual disturbances - Blurred, scintillating scotomata
  • Altered mental status
  • Blindness - May be cortical or retinal
• Dyspnea
• Edema: This exists in many pregnant women but sudden increase in edema or facial edema is more concerning for preeclampsia. The edema of preeclampsia occurs by a distinct mechanism that is similar to that of angioneurotic edema.
• Epigastric or right upper quadrant (RUQ) abdominal pain: Hepatic involvement occurs in 10% of women with severe preeclampsia.
• Weakness or malaise: This may be evidence of hemolytic anemia.

Physical

Findings on physical examination may include the following:

• Increased BP compared with the patient's baseline or greater than 140/90 mm Hg
• Altered mental status
• Decreased vision
• Papilledema
• Epigastric or RUQ abdominal tenderness
• Peripheral edema: Edema can be normal in pregnancy, but a sudden increase in edema or swelling of the face is more suggestive of preeclampsia.
• Hyperreflexia or clonus
• Seizures
• Focal neurologic deficit

Causes

• Pregnancy-associated risk factors
  • Chromosomal abnormalities
  • Hydatidiform mole
  • Multifetal pregnancy
  • Oocyte donation or donor insemination
  • Urinary tract infection
• Maternal-specific risk factors
  • Extremes of age
  • Black race
  • Family history of preeclampsia
  • Nulliparity
  • Preeclampsia in a previous pregnancy
  • Diabetes
  • Obesity
  • Chronic hypertension
  • Renal disease
  • Periodontal disease²

Differential Diagnoses

Workup

Laboratory Studies

• CBC count
  • Microangiopathic hemolytic anemia (HELLP)
  • Thrombocytopenia
  • Hemoconcentration may occur in severe preeclampsia.
• Liver function tests: Transaminase levels are elevated from hepatocellular injury and in HELLP syndrome.
• Serum creatinine level: levels are elevated due to decreased intravascular volume and decreased glomerular filtration rate (GFR).
• Urinalysis  
  • Proteinuria is one of the diagnostic criteria for preeclampsia.
  • Proteinuria is defined as greater than or equal to 1+ protein on urine dipstick. Alternatively, protein concentration of 300 mg/L or more on urine dipstick.
  • Proteinuria is also defined as 300 mg or more of protein in a 24-hour urine sample.
• Elevated PT, aPTT, fibrin split products, and decreased fibrinogen
• Disseminated intravascular coagulopathy testing
• Uric acid  
  • Uric acid levels are increased in preeclampsia.
  • Serial levels may be useful to indicate disease progression.

Imaging Studies

• Head CT: This study is used to detect intracranial hemorrhage in selected patients with sudden severe headaches, focal neurologic deficits, or seizures with a prolonged post-ictal state.
• Ultrasonography: This is used for fetal assessment.

Treatment

Prehospital Care

• Oxygen via facemask
• Intravenous access
• Cardiac monitoring
• Transportation of patient in left lateral decubitus position
• Seizure precautions

Emergency Department Care

In the emergency setting, control of BP and seizures should be priorities. Definitive therapy is delivery of the fetus, although preeclampsia may paradoxically emerge in postpartum patients. In general, the further the pregnancy is from term, the greater the impetus to manage the patient medically.

• BP control  
  • The goal is to lower BP to prevent cerebrovascular and cardiac complications while maintaining uteroplacental blood flow.
  • Control of mildly increased BP does not appear to improve perinatal morbidity or mortality, and, in fact, it may reduce birth weight.
  • Antihypertensive treatment is indicated for diastolic blood pressure above 105 mm Hg and systolic pressure above 160 mm Hg, though patients with chronic hypertension may tolerate higher values.
  • Patients with severe preeclampsia who have BP below 160/105 mm Hg may benefit from antihypertensives because of the possibility of unpredictable acceleration of the disease and sudden increases in hypertension.
  • The goal is to maintain diastolic blood pressure between 90 and 100 mm Hg and systolic pressure between 140 and 155 mm Hg.
• Control of seizures  
  • Active seizures should be treated with intravenous magnesium sulfate as a first-line agent.
  • Prophylactic treatment with magnesium sulfate is indicated for all patients with severe preeclampsia. No consensus exists about whether patients with mild preeclampsia (elevated blood pressure without evidence of end-organ damage) need to be on magnesium seizure prophylaxis.
  • Magnesium levels, respiratory rate, reflexes, and urine output must be monitored to detect magnesium toxicity.
  • For seizure refractory to magnesium sulfate therapy, benzodiazepines and/or phenytoin may be considered.
• Fluid management  
  • Despite the peripheral edema, patients with preeclampsia are intravascularly volume depleted with high peripheral vascular resistance. Diuretics should be avoided. 
  • Aggressive volume resuscitation may lead to pulmonary edema, which is a common cause of maternal morbidity and mortality. Because volume expansion has no demonstrated benefit, patients should be fluid restricted when possible, at least until the period of postpartum diuresis.
  • Central venous or pulmonary artery pressure monitoring may be indicated in critical cases.
  • Careful measurement of fluid input and output is advisable, particularly in the immediate postpartum period.
• Delivery  
  • This is not an immediate consideration for emergency physicians.
  • Patients with mild preeclampsia are often induced after 37 weeks' gestation.
  • In patients with severe preeclampsia, induction of delivery should be considered after 34 weeks' gestation. In these cases, the severity of disease must be weighed against the risks of prematurity.   
  • Eclampsia is common after delivery and has occurred up to 6 weeks after delivery. Patients at risk for eclampsia should be carefully monitored postpartum.

Consultations

Immediate obstetric consultation is warranted for all patients who present with preeclampsia.

Medication

Magnesium sulfate is the first-line treatment of prevention of primary and recurrent eclamptic seizures. For eclamptic seizures refractory to magnesium sulfate, lorazepam and phenytoin may be used as second-line agents.

In the setting of severe hypertension (systolic BP, >160 mm Hg; diastolic BP, >110 mm Hg), antihypertensive treatment is recommended. Antihypertensive treatment decreases the incidence of cerebrovascular problems but does not alter the progression of preeclampsia.

Traditionally, hydralazine has been used for control of severe hypertension in women with preeclampsia. However, the evidence regarding the side effects and maternal/fetal outcomes when compared with labetalol and nifedipine is conflicting.

Anticonvulsants

Agents that inhibit smooth muscle contractions are used.

Magnesium sulfate

First-line therapy for seizure prophylaxis. Antagonizes calcium channels of smooth muscle. Indicated in severe preeclampsia, eclampsia, and preeclampsia in the near term. Administer IV/IM for seizure prophylaxis in preeclampsia. Use IV for quicker onset of action in true eclampsia.

Dosing

Adult

4-6 g IV over 20 min with maintenance of 1-2 g/h

Pediatric

Not established

Interactions

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

Magnesium sulfate may alter cardiac conduction leading to heart block in digitalized patients; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering magnesium sulfate dose since may produce significant hypotension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
Important to monitor patient's blood pressure after administering dose. Adjust as necessary.

Dosing

Adult

4 mg/dose IV slowly over 2-5 min and repeat in 10-15 min prn; cumulative dose of 8 mg/d typically considered maximum
1-10 mg/d PO/IV/IM divided bid/tid

Pediatric

Infants and children: 0.1 mg/kg IV slowly over 2-5 min; repeat prn in 10-15 min at 0.05 mg/kg; not to exceed 4 mg/dose
Adolescents: 0.07 mg/kg IV slowly over 2-5 min and repeat in 10-15 min prn; not to exceed 4 mg/dose

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAO inhibitors

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma; reversal agents (eg, flumazenil) contraindicated when lorazepam used for life-threatening conditions (eg, control of intracranial pressure or status epilepticus)

Precautions

Pregnancy

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

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Phenytoin (Dilantin)

Phenytoin has been used successfully in eclamptic seizures, but cardiac monitoring is required secondary to associated bradycardia and hypotension.
Central anticonvulsant effect of phenytoin is by stabilizing neuronal activity by decreasing the ion flux across depolarizing membranes.
Some benefits to using phenytoin are that it can be continued orally for several days until the risk of eclamptic seizures has subsided, it has established therapeutic levels that are easily tested, and no known neonatal adverse effects are associated with short-term usage.

Dosing

Adult

10 mg/kg loading dose infused IV no faster than 50 mg/min, followed by maintenance dose started 2 h later at 5 mg/kg

Pediatric

Administer as in adults

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity
Phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate
Phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, valproic acid

Contraindications

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Precautions

Pregnancy

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

Precautions

Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugar levels); discontinue use if hepatic dysfunction occurs

Antihypertensives

These agents are used to decrease systemic resistance and to help reverse uteroplacental insufficiency.

Hydralazine (Apresoline)

First-line therapy against preeclamptic hypertension. Decreases systemic resistance through direct vasodilation of arterioles, resulting in reflex tachycardia. Reflex tachycardia and resultant increased cardiac output helps reverse uteroplacental insufficiency, a key concern when treating hypertension in a patient with preeclampsia. Adverse effects to the fetus are uncommon.

Dosing

Adult

5-10 mg IV; repeat q20min to maximum of 60 mg

Pediatric

Not established

Interactions

MAO inhibitors 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

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

Hydralazine has been implicated in myocardial infarction; caution in suspected coronary artery disease

Labetalol (Normodyne)

Second-line therapy that produces vasodilatation and decreases in systemic vascular resistance. Has alpha-1 and beta-antagonist effects and beta2-agonist effects. Has more rapid onset than hydralazine and less overshoot hypotension. Dosage and duration of labetalol is more variable. Adverse effects to fetus are uncommon.

Dosing

Adult

50-100 mg IV; repeat q30min to a maximum of 300 mg

Pediatric

Not established

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia, resulting 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; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; 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 if signs of liver dysfunction; in elderly patients, a lower response rate and higher incidence of toxicity may be observed

Nifedipine (Procardia)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Sublingual administration is generally safe, despite theoretical concerns.

Dosing

Adult

10-30 mg IR cap PO tid; not to exceed 120-180 mg/d
30-60 mg SR tab PO qd; not to exceed 90-120 mg/d

Pediatric

0.25-0.5 mg/kg/dose PO tid/qid prn

Interactions

Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)

Contraindications

Documented hypersensitivity

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

May cause lower extremity edema; allergic hepatitis has occurred but is rare

Follow-up

Further Inpatient Care

• Hospitalization is indicated for all women with severe preeclampsia. The goals of hospitalization include the following:
  • Daily weigh-ins
  • Blood pressure readings every 4 hours
  • Prophylactic anticonvulsive therapy
  • Corticosteroids to enhance fetal lung maturity

Further Outpatient Care

• Outpatient management of preeclampsia has a limited role. The decision to treat on an outpatient basis must be made in consultation with an obstetrician. Detailed instructions on signs and symptoms of progression of disease, including headache, visual changes, abdominal pain, vaginal bleeding, or decreased fetal movement, as well as strict bed rest is recommended.

Transfer

• Patients with severe preeclampsia must be stabilized in the ED as much as possible prior to transfer to a tertiary care facility.

Complications

• Abruptio placentae with disseminated intravascular coagulopathy
• Renal insufficiency or failure
• Hemolysis, elevated liver enzyme levels, and low platelet count (or HELLP syndrome)
• Eclampsia
• Cerebral hemorrhage
• Death, either maternal and/or fetal

Prognosis

• Early detection and frequent obstetric assessment markedly improves prognosis.
• A history of preeclampsia increases a woman's subsequent risk of vascular disease, including hypertension, thrombosis, ischemic heart disease, and stroke.³

Patient Education

• For excellent patient education resources, visit eMedicine's Pregnancy and Reproduction Center and Circulatory Problems Center. Also, see eMedicine's patient education articles Pregnancy and High Blood Pressure.

Miscellaneous

Medicolegal Pitfalls

• Immediate obstetric consultation is required for all patients who present with preeclampsia.
• Maintain a high index of suspicion for preeclampsia when evaluating any complaint in a pregnant patient with abnormally elevated BP.
• Any pregnant patient, regardless of age, is at risk for preeclampsia.

References

1. Rodriguez-Thompson D, Lieberman ES. Use of a random urinary protein-to-creatinine ratio for the diagnosis of significant proteinuria during pregnancy. Am J Obstet Gynecol. Oct 2001;185(4):808-11. [Medline].

2. [Best Evidence] Conde-Agudelo A, Villar J, Lindheimer M. Maternal infection and risk of preeclampsia: systematic review and metaanalysis. Am J Obstet Gynecol. Jan 2008;198(1):7-22. [Medline].

3. [Best Evidence] Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta-analysis. BMJ. Nov 10 2007;335(7627):974. [Medline].

4. Doan-Wiggins L. Hypertensive disorders of pregnancy. Emerg Med Clin North Am. Aug 1987;5(3):495-508. [Medline].

5. Frakes MA, Richardson LE 2nd. Magnesium sulfate therapy in certain emergency conditions. Am J Emerg Med. Mar 1997;15(2):182-7. [Medline].

6. Lew M, Klonis E. Emergency management of eclampsia and severe pre-eclampsia. Emerg Med (Fremantle). Aug 2003;15(4):361-8. [Medline].

7. Lipstein H, Lee CC, Crupi RS. A current concept of eclampsia. Am J Emerg Med. May 2003;21(3):223-6. [Medline].

8. Ogle ME, Sanders AB. Preeclampsia. Ann Emerg Med. May 1984;13(5):368-70. [Medline].

9. Powers DR, Papadakos PJ, Wallin JD. Parenteral hydralazine revisited. J Emerg Med. Mar-Apr 1998;16(2):191-6. [Medline].

10. Probst BD. Hypertensive disorders of pregnancy. Emerg Med Clin North Am. Feb 1994;12(1):73-89. [Medline].

11. Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet. Feb 26-Mar 4 2005;365(9461):785-99. [Medline].

12. Wagner LK. Diagnosis and management of preeclampsia. Am Fam Physician. Dec 15 2004;70(12):2317-24. [Medline].

13. Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol. Nov 1998;92(5):883-9. [Medline].

Keywords

preeclampsia, HTN, hypertensive disease in pregnancy, pregnancy-induced hypertension, toxemia of pregnancy, hypertension, proteinuria, new-onset nondependent edema, seizure activity, eclampsia, seizure in pregnancy, microangiopathic hemolytic anemia, HELLP syndrome, hypertensive encephalopathy, oliguria, pulmonary edema, cyanosis, thrombocytopenia, oligohydramnios, vasospasm, seizures, acute tubular necrosis, placental abruption

Contributor Information and Disclosures

Author

Mert Erogul, MD, Assistant Professor of Emergency Medicine, University Hospital of Brooklyn: Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Mert Erogul, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Assaad J Sayah, MD, Chief, Department of Emergency Medicine, Cambridge Health Alliance
Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

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: Nothing to disclose.

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, Associate Professor, Program Director, Department of Medicine, Division of Emergency Medicine, University of California at Los Angeles School of Medicine
Pamela L Dyne, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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

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