eMedicine Specialties > Emergency Medicine > Environmental

Spider Envenomation, Redback

Rebecca L Rubin, MD, Clinical Assistant Instructor and Resident Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital Center
Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Updated: Sep 23, 2009

Introduction

Background

The redback spider (Latrodectus hasseltii) belongs to the family Theridiidae, the comb-footed spiders. Its genus Latrodectus also includes black widows, whose name may be more familiar to North American readers. The redback spider can be found throughout Australia, although it is more commonly seen in the temperate regions than in the colder, southern areas. The spider exists in higher numbers in Australia's urban and suburban areas and is virtually absent in the continent's forests. Outside of Australia, similar species of Latrodectus include Karakurt in Central Asia, Malmignatte in Europe, the Koppie spider in South Africa, and the Night Stinger in New Zealand.

The redback spider bite is the most common envenomation requiring antivenom in Australia. The female redback spider is responsible for most occurrences of envenomations. She is usually 10 mm in length and has a small cephalothorax and a large, globular abdomen that bears a red, orange, or brown stripe. The male redback spider is considerably smaller than the female and is only occasionally able to cause mild envenomation.^{[1,2 ]}

Female redback spider showing a distinctive red stripe over the abdomen. Image courtesy of John Paterson.

Female redback spider with egg sacs. Image courtesy of John Paterson.

Pathophysiology

The redback spider can cause a clinical condition referred to as latrodectism following a bite. The active ingredient in the redback's venom responsible for its toxic properties in vertebrates is a 130-kd protein, alpha-latrotoxin (aLTX). aLTX is a potent neurotoxin that works in 2 ways to produce efflux of neurotoxins from presynaptic nerve cells. 

In one mechanism of action, aLTX aggregates into tetramers that form pores in neuronal presynaptic cell membranes allowing calcium influx into the cytosol and resulting in exocytosis of neurotransmitters such as norepinephrine, dopamine, acetylcholine, glutamate, and GABA. The membrane pores formed by aLTX may also be large enough for a direct efflux of small intracellular compounds that are vital for cytoplasm function.

The monomeric aLTX can also act by activating latrophilin (LPH), an aLTX receptor found on the cell surface of neuronal cells, without incorporating into the cell membrane. Latrophilin is a G protein-coupled receptor that activates phospholipase C, which, in turn, increases the cytosolic concentration of IP3 leading to release of calcium from intracellular stores. This rise in cytosolic calcium increases the rate of spontaneous exocytosis of neurotransmitters and the amplitude of evoked release. Alpha-latrotoxin is a potent venom, with an LD-50 in mice, which is 20-40 µg/kg of body weight.^{[3,4,5 ]}

Frequency

United States

Only the black widow spider, a close relative of the redback spider, lives in the United States. These arachnids cause approximately 2500 envenomations each year.

International

The redback spider is found in Australia, New Zealand, and southern Asia. In Australia, the spider has been blamed for 250 envenomations requiring antivenom annually. Perhaps many more cases are mild or unrecognized and do not receive antivenom.

Mortality/Morbidity

Accurate data regarding morbidity/mortality is difficult to gather, as there is no mandatory reporting of spider bites in Australia. There appears to be greater morbidity in pediatric and elderly patients. There have been no recorded deaths caused by redback spider bites in the past several decades.^{[6 ]}

Race

All races are susceptible to redback spider envenomation if the patient lives in an endemic area inhabited by the redback spider. One article shows more severe envenomation in Aboriginal patients, but states that this is due to a significantly longer time from envenomation to presentation in ED as compared to non-Aboriginal patients.^{[7 ]}

Sex

In one study of redback envenomations in Australia, 60% of victims were female. However, most other sources do not quote a male/female sex discrepancy.^{[8 ]}

Age

Redback envenomation may occur at any age; the median age is 35 years. Envenomation may be more dangerous in babies and small children because of the difficulty in making a specific diagnosis in that group of patients in addition to the small body size bearing the same dose of injected poison as an adult would tolerate.^{[8 ]}

Clinical

History

• In Australia, most bites occur during the warmer months between December and April. Bites to the limbs comprise approximately three quarters of cases, and bites to the distal limbs are twice as common as to the proximal limbs; 46% in distal extremity and 26% in proximal limb.^{[8 ]}
• The cardinal symptoms of redback spider envenomation include immediate pain at the site of the bite with or without erythema, which usually progresses over hours to involve the entire limb and draining lymph nodes in the axilla or groin. The pain may persist longer than 24 hours, with a median duration of 36 hours. Other common complaints include nausea, vomiting, abdominal pain, headache, and migratory arthralgias.^{[3 ]}
• In infants, nonspecific symptoms may be present, including inconsolable crying and refusal to eat.
• Most cases are mild or unrecognized and do not receive antivenom. The only way to accurately diagnose a redback spider bite is for the patient to recognize the typical markings on the spider's abdomen or bring the spider in with the patient for proper identification.^{[8 ]}

Physical

• Common physical findings in a patient with redback spider envenomation include tenderness and erythema at the bite site. Occasionally, one can see localized or generalized sweating, which may be unrelated to the bite site. Local piloerection may also be present.^{[8 ]}
• Systemic findings in redback spider envenomation, seen in approximately 35% of all bites, include fever, hypertension, and tachycardia.^{[8 ]}
• Neurological symptoms may include restlessness and insomnia, muscle weakness and twitching, and paralysis. The median duration of all effects is 48 hours.
• Rare complications include myocarditis, rhabdomyolysis, and death.

Differential Diagnoses

Other Problems to Be Considered

Redback spider envenomation has been mistaken for sepsis, acute abdomen, acute hepatitis, testicular torsion, anaphylaxis, and premature labor.

Workup

Laboratory Studies

• The serum creatine kinase level may be elevated if the kidneys are involved, and peripheral white blood cell count may also be elevated.
• In a female patient, a pregnancy test may be useful to differentiate the presentation from premature labor and to guide the medication choice for treatment of latrodectism.

Imaging Studies

• Plain radiographs of the affected limb may be indicated to evaluate for subcutaneous air if a concern for necrotizing fasciitis exists.
• Venous Doppler ultrasonography of the affected extremity may be indicated to evaluate for deep vein thrombosis.

Other Tests

• ECG may be prove helpful in a patient with autonomic instability, chest pain, or if comorbidities are present.

Treatment

Prehospital Care

• Pressure immobilization of the bitten limb is not recommended due to the slow and non–life-threatening progression of symptoms. Pressure dressings may also exacerbate pain in the affected area.
• Ice packs to the bite site and simple oral analgesia may be helpful.
• Do not administer antivenom in the field due to the risk of a severe allergic reaction.
• Collection of the spider may aid its proper identification at the emergency department.

Emergency Department Care

• In patients with severe symptoms and signs of envenomation, treatment with redback spider antivenom should be considered. The benefit of treatment with antivenom should be weighed against the risk of its possible complications, including but not limited to, anaphylaxis and serum sickness.

Consultations

• The local poison control center may be consulted for spider identification and management of severe envenomations.
• A surgeon may be consulted if compartment syndrome is suspected.

Medication

Most cases of redback spider envenomation are mild and can be managed symptomatically using common oral analgesics and sedatives.

Redback spider antivenom provides specific treatment in severe cases of envenomation.

Ensure that the patient's tetanus status is up to date.

Antivenom

Redback spider antivenom is the primary treatment of severe latrodectism. Before the introduction of the antivenom in 1995, 14 deaths due to redback spider envenomation were documented in Australia. The antivenom consists of equine IgE fragments raised against aLTX. Each ampule contains 500 units of neutralizing capacity against the Australian redback spider venom, with an average volume of 1-1.5 mL per ampule. The antivenom is usually administered by intramuscular injection. Indications for use of antivenom include severe headache, vomiting, abdominal pain, hypertension, arthralgia, or myalgia. Severe pain at the envenomation site is not considered an indication for antivenom administration.^{[1 ]}

Increasing concerns exist about the possible ineffectiveness of the IM route of administration of the redback antivenom. A recent study showed no significant difference in relief of symptoms or patient outcome between IV and IM administration of antivenom.^{[9 ]}

The risk of allergic reaction to the antivenom is 0.5% and is higher in patients with a history of horse allergy or prior exposure to equine immunoglobulin. Before using the antivenom, ensure the ability to manage hypersensitivity reaction and check for availability of the appropriate resuscitation/intubation equipment. The risk of serum sickness after exposure to the antivenom is 1.4%.

Possible contraindications to antivenom use include current beta-blocker therapy, as this may reduce the patient's responsiveness to resuscitative therapy in the event of anaphylaxis.^{[1 ]}

Redback spider antivenom

Produced by Commonwealth Serum Laboratories Ltd, Australia.

Dosing

Adult

500 Units IM
Same dose, diluted in 100-150 mL of crystalloid, may be administered as IV infusion over 15-30 min in presence of severe stings and symptoms; additional dose of antivenom should be considered if patient does not respond to first dose within 60 min; diagnosis of redback spider envenomation should be reconsidered if no improvement is observed after second dose of antivenom

IV dose of antivenom may be warranted in confirmed cases of redback envenomation, where no response is observed after administering 2 IM doses of antivenom

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity to horse serum

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 patients with documented allergy to horse serum (be prepared to treat anaphylaxis with IV fluids, diphenhydramine, and epinephrine)

Analgesics

Patients may experience severe pain at the bite site, and pain control is essential to quality patient care.

Acetaminophen with codeine (Tylenol With Codeine, Capital and Codeine)

Combines analgesic effects of a centrally acting opium-derived alkaloid (codeine) and a peripherally acting nonopioid analgesic (acetaminophen). Indicated for treatment of mild to moderate pain.

Dosing

Adult

1-2 tab Tylenol #2 (15 mg codeine phosphate plus 300 mg acetaminophen), Tylenol #3 (30 mg codeine phosphate plus 300 mg acetaminophen), or 1 tab Tylenol #4 (60 mg codeine phosphate plus 300 mg acetaminophen) PO q4-6h prn, not to exceed 360 mg codeine and 4 g acetaminophen/24h

Pediatric

Based on codeine: 0.5-1 mg/kg/dose PO q4-6h
Based on acetaminophen: 10-15 mg/kg/dose PO q4h; not to exceed 75 mg/kg/d or 2.6 g/d
<3 years: Not established
3-6 years: 5 mL (1 tsp) PO qid prn
7-12 years: 10 mL (2 tsp) PO qid prn
>12 years: Administer as in adults

Interactions

Multiple drug interactions exist; please refer to Micromedex for a complete list of drug interactions; toxicity of codeine increases with CNS depressants, tricyclic antidepressants, MAO inhibitors, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity of acetaminophen

Contraindications

Documented hypersensitivity to drug or related products

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

Hypersensitivity to drug or tablet components, respiratory depression, paralytic ileus, G6PD deficiency, CNS depression, acute abdomen, head injury, increased ICP, impaired liver function, hypothyroidism, adrenal insufficiency, biliary disease, GU/GI obstruction, alcohol and drug abuse history; caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction; hepatotoxicity with acetaminophen possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products and combined use with these products may result in cumulative acetaminophen doses and exceed recommended maximum dose

Morphine sulfate, injectable (Duramorph, Infumorph, Astramorph).

DOC for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated to the desired effect.

Dosing

Adult

2-10 mg IV administered over 4-5 min or 5-20 mg IM/SC q4-6h prn

Pediatric

0.1-0.2 mg/kg IV/IM/SC q2-4h (not to exceed 15 mg/dose)

Interactions

May cause severe respiratory depression when used with other CNS depressants; phenothiazines may antagonize the analgesic effects of opiates

Contraindications

Documented hypersensitivity to morphine; asthma, hypotension, respiratory depression, upper airway obstruction, paralytic ileus

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

Concurrent administration of other opioid analgesics or CNS depressants, alcohol consumption, circulatory shock, head injury or increased intracranial pressure, respiratory compromise, atrial flutter and other supraventricular tachycardias, elderly and debilitated patients

Benzodiazepines

Patients may experience significant restlessness and anxiety, which may require the use of sedatives for symptomatic control.

Lorazepam (Ativan)

A sedative hypnotic in the benzodiazepine class that has a short onset of effect and relatively long half-life.

Dosing

Adult

1-2 mg IV/IM (not to exceed 10 mg/d)

Pediatric

0.05-0.1 mg/kg IV/IM (not to exceed 4 mg)

Interactions

CNS toxicity increases when concurrently used with other CNS depressants

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; untreated open-angle glaucoma; severe respiratory depression

Precautions

Pregnancy

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

Precautions

Concurrent use of other CNS depressants, respiratory depression, elderly/debilitated patients, depressed patients

Diazepam (Valium)

Modulates postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. Also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.
Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of CIndividualize dosage and increase cautiously to avoid adverse effects.

Dosing

Adult

2-10 mg IM/IV q3-4h prn (not to exceed 30 mg/8 h)

Pediatric

0.04-0.2 mg/kg IV/IM q2-4h prn (not to exceed 0.6 mg/kg/8 h)

Interactions

CNS toxicity increases when concurrently used with other CNS depressants

Contraindications

Documented hypersensitivity; acute narrow-angle glaucoma; untreated open-angle glaucoma; hypotension; severe respiratory depression

Precautions

Pregnancy

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

Precautions

Concurrent use of other CNS depressants, respiratory depression, elderly/debilitated patients, hepatic insufficiency, depressed patients

Midazolam (Versed)

Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

Dosing

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion

Interactions

Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when using together

Contraindications

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent)

Precautions

Pregnancy

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

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and in elderly patients; monitor for respiratory depression with high or repeated doses; consider lower dosages in patients with organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Immunizations

Tetanus immunization should be administered following a redback spider bite. A booster vaccination is recommended in previously immunized individuals.

Diphtheria-tetanus toxoid vaccine (Adacel, Boostrix, Decavac)

Manufactured by first culturing Clostridium tetani and then detoxifying the toxin with formaldehyde. This toxoid commonly is combined with diphtheria toxoid, and both serve to induce production of serum antibodies to toxins produced by the bacteria.
Used to induce active immunity against tetanus in selected patients. Immunizing agent of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid, not a product containing diphtheria antigen.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is the mid thigh laterally.

Dosing

Adult

0.50 mL IM in extremity other than the one that bears the lesion

Pediatric

Administer as in adults

Interactions

Chloramphenicol may impair the amnestic response to tetanus toxoid; patients receiving concurrent immunosuppressants may remain susceptible despite immunization; concurrent use of tetanus immunoglobulin may delay development of active immunity by several days

Contraindications

Documented hypersensitivity to vaccine's components; presence of febrile illness or acute infection; poliomyelitis outbreak

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

Arthus-type hypersensitivity reaction or fever following a prior dose of vaccine, immunosuppression, latex sensitivity, thrombocytopenia, coagulation disorders

Follow-up

Further Inpatient Care

• Hospitalization is generally not required, after a period of observation, for patients whose symptoms have been alleviated with antivenom. Patients who have contraindications to antivenom and those requiring large doses of opioid analgesics and sedatives for symptomatic control should be hospitalized.^{[8 ]}Hospitalization should be considered in the following situations:
  • Pregnant women
  • Severely symptomatic children
  • Elderly patients with significant comorbidities
  • Patients who develop anaphylaxis to antivenom
  • Patients with complications of envenomation
  • Patients with hemodynamic instability

Further Outpatient Care

• Patients should be given thorough instructions listing the symptoms of serum sickness (fever, pruritus, and arthropathy) and cellulitis and advised to seek medical care if such symptoms occur.^{[1 ]}

Inpatient & Outpatient Medications

• Patients may need to undergo a short course of steroid treatment should serum sickness occur.

Deterrence/Prevention

• Use of pesticides may prevent exposure to spiders in the home. In endemic areas, patients should be advised to inspect their clothes and shoes for spiders before wearing them.

Complications

• Hypertensive emergency
• Acute myocardial infarction
• Myocarditis
• Rhabdomyolysis
• Paralysis
• Death
• Antivenom-associated complications
  • Anaphylaxis (type I hypersensitivity reaction) is characterized by urticaria, wheezing, and circulatory collapse. The risk of allergic reaction in patients receiving redback antivenom is 0.5% and is higher in patients with prior exposure to horse serum proteins or history of reactive airway disease. Anaphylaxis is treated with epinephrine, corticosteroids, antihistamines, intravenous fluids, and ventilatory support in the usual medical fashion.
  • Serum sickness (type III hypersensitivity reaction) is characterized by fever, urticaria, pruritus, nephritis, and arthritis. This condition occurs in 1.4% of patients receiving antivenom and is self-limiting. Treatment is usually conservative. Antihistamines and topical steroids may be used for dermatitis and aspirin for arthralgia. In severe reactions, including glomerulonephritis, corticosteroid therapy may be necessary.

Prognosis

• Most patients with redback spider envenomation recover fully.

Patient Education

• Following web sites contain additional information and photographs on redback spider:
  • CSIRO Entomology Web site
  • eMedicine's Consumer Health Bites and Stings Center
  • Museum Victoria Web site

Miscellaneous

Medicolegal Pitfalls

• Administration of antivenom may require informed consent.
• Discharging a patient who subsequently returns with persistent symptoms requiring antivenom treatment and/or admission may constitute a legal pitfall.
• Administration of antivenom to a patient with a documented prior hypersensitivity to horse serum or history of asthma and multiple medication allergies, who subsequently develops anaphylaxis may serve as grounds for malpractice.

Multimedia

Media file 1: Female redback spider showing a distinctive red stripe over the abdomen. Image courtesy of John Paterson.

Media file 2: Female redback spider with egg sacs. Image courtesy of John Paterson.

Media file 3: Female redback spider. Image courtesy of John Paterson.

Media file 4: Female redback spider. Image courtesy of John Paterson.

References

1. White J. CSL Antivenom Handbook. 2nd ed. 2001. Available at http://www.toxinology.com/generic_static_files/cslb_index.html.

2. Nimorakiotakis B, Winkel KD. Spider bite--the redback spider and its relatives. Aust Fam Physician. Mar 2004;33(3):153-7. [Medline]. [Full Text].

3. Graudins A. Widow spider envenomation: Lactrodectism. In: Dart RC, ed. Medical Toxicology. 3^rd ed. Lippincott Williams & Wilkins; 2003:1592-1595/248. [Full Text].

4. Nicholson GM, Graudins A. Spiders of medical importance in the Asia-Pacific: atracotoxin, latrotoxin and related spider neurotoxins. Clin Exp Pharmacol Physiol. Sep 2002;29(9):785-94. [Medline].

5. Ushkaryov YA, Volynski KE, Ashton AC. The multiple actions of black widow spider toxins and their selective use in neurosecretion studies. Toxicon. Apr 2004;43(5):527-42. [Medline].

6. Australian Museum. Available at http://australianmuseum.net.au/Redback-Spiders.

7. Mollison L, Liew D, McDermott R, Hatch F. Red-back spider envenomation in the red centre of Australia. Med J Aust. Dec 5-19 1994;161(11-12):701, 704-5. [Medline].

8. Isbister GK, Gray MR. Latrodectism: a prospective cohort study of bites by formally identified redback spiders. Med J Aust. Oct 20 2003;179(8):455; author 455-6. [Medline].

9. Isbister GK, Brown SG, Miller M, Tankel A, Macdonald E, Stokes B, et al. A randomised controlled trial of intramuscular vs. intravenous antivenom for latrodectism--the RAVE study. QJM. Jul 2008;101(7):557-65. [Medline].

10. Hahn IH, Lewin N. Chapter 115: Arthropods. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfrank's Toxicologic Emergencies. 8^th ed. New York, NY: McGraw-Hill; 2006.

11. Isbister GK. Failure of intramuscular antivenom in Red-back spider envenoming. Emerg Med (Fremantle). Dec 2002;14(4):436-9. [Medline].

12. Isbister GK, Sibbritt D. Developing a decision tree algorithm for the diagnosis of suspected spider bites. Emerg Med Australas. Apr 2004;16(2):161-6. [Medline].

Keywords

spider bite, redback spider, spider envenomation, Latrodectus, Latrodectus hasselti, Jockey spider, latrodectism, latrotoxin, aLTX, neurotoxin, redback spider bite, spider bite treatment

Contributor Information and Disclosures

Author

Rebecca L Rubin, MD, Clinical Assistant Instructor and Resident Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital Center
Rebecca L Rubin, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Norris, MD, Associate Professor, Department of Surgery; Chief, Division of Emergency Medicine, Stanford University Medical Center
Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Matthew M Rice, MD, JD, FACEP, Senior Vice President, Chief Medical Officer, Northwest Emergency Physicians; Assistant Clinical Professor of Medicine, University of Washington at Seattle
Matthew M Rice, MD, JD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Washington State Medical Association
Disclosure: Team Health  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

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Alexandr Rafailov, MD, and Mark A Silverberg, MD, to the development and writing of this article.

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