Updated: Mar 10, 2008
The phylum Echinodermata includes a diverse group of marine animals that are slow moving and nonaggressive, including brittle stars (class Ophiuroidea), starfish (class Asteroidea), sea urchins (class Echinoidea), and sea cucumbers (class Holothuroidea). These animals have pentamerous (5-part) radial symmetry and calcareous skeletons that form thick outer plates and protective spines in some; hence, they are named Echinodermata, which means spiny skin. Injury and envenomation occur almost exclusively from accidental contact or careless handling; bathers, divers, and fishermen are at greatest risk. Poisonous echinoderm ingestions or intoxications are not covered in this article.
While most echinoderms are poisonous, and many have sharp spines or spicules capable of causing injury, only a few members of the Asteroidea, Echinoidea, and Holothuroidea classes are capable of causing venomous injuries in humans. In this article, envenomation refers to the parenteral or topical application of toxins produced in specialized glands and tissues with modified application structures (spines, pedicellaria, tentacles). This definition is in contrast to poisoning or intoxication, which refers to the oral ingestion of toxins produced or accumulated in nonspecialized glands or tissues.
Brittle stars (class Ophiuroidea; see Media file 6) are not generally considered capable of causing venomous injuries in humans. However, some brittle stars (Ophiomastix annulosa) do possess toxins and are capable of causing paralysis and death in small animals. These animals should be handled with care.
Sea urchins (Echinoidea) capable of causing venomous injuries in humans use specialized spines (long or short) and pedicellaria (delicate seizing organs equipped with pincerlike jaws) to deliver their venom. Although both structures are present, generally only one is venomous in a given species. Thus, grouping the venomous urchins into 1 of the following 3 categories is convenient:
Sea cucumbers (Holothuroidea) are generally regarded as nonvenomous, although many are poisonous to eat without proper preparation. The Cuvierian tubules of some sea cucumbers are toxic and may be extruded from the anus as a defensive mechanism when the animal is disturbed or irritated (Bohadschia argus; see Media file 4).
Echinoderm envenomations do not represent a significant public health problem, although little epidemiologic data are available. Venomous echinoderms are encountered principally in tropical seas. Nonvenomous traumatic injuries from echinoderms are not uncommon in the United States, especially in coastal communities where sea urchins live.
Echinoderm envenomations are quite common, although little epidemiologic data are available.
The most common starfish envenomization results from contact with the crown-of-thorns starfish (Acanthaster planci), which populates reefs of the Indo-Pacific from east Africa to Central America. Similarly, sea urchins capable of envenomation tend to be concentrated in tropical and subtropical marine regions. The Indo-Pacific is the home of all categories of venomous urchins, including Diadema, Echinothrix, and Toxopneustes species and the venomous genera of sea cucumbers (Holothuria). For some Chinese, Malay, and Pacific Island gourmets, properly prepared sea cucumbers are prized as a delicacy (eg, beche-de-mer, trepang).
Significant local and systemic effects are possible following echinoderm envenomation from any of the 3 venomous classes, starfish (Asteroidea), sea urchins (Echinoidea), and sea cucumbers (Holothuroidea). However, a clear link between echinoderm envenomation and death (other than subsequent drowning) cannot be found in the literature, despite several anecdotal reports of fatalities.4,2,5,6 Detailed documentation is sparse, and death must be very rare. This is in contrast to poisoning or intoxication following ingestion of certain echinoderms, which has been well documented to result in severe illness and fatality.
Immediate and often incapacitating pain is described following puncture wounds from the crown-of-thorns starfish (Acanthaster planci), long-spined urchins (Diadema species, Echinothrix species), and some short-spined urchins (Phormosoma species). Similarly, pedicellaria-containing urchins (Toxopneustes species, Tripneustes species) and other short-spined urchins (Asthenosoma species, Araeosoma species) may deliver a severe sting at the slightest touch without inflicting any puncture at all. Significant ocular inflammation, dermatitis, and pain may follow topical exposure to the holothurin toxins of venomous sea cucumbers.
The severity of envenomation depends on multiple factors, including the offending species; site and number of stings; the size, maturity, and age of the animal; and the underlying health and individual sensitivity of the individual exposed.
Echinoderms are slow moving and nonaggressive; injury and envenomation occur as the result of accidental exposure or careless handling.
| Anaphylaxis | Dysbarism |
| Coelenterate and Jellyfish Envenomations | Lionfish and Stonefish |
| Corneal Abrasion | Snake Envenomations, Sea |
| Decompression Sickness | Stingray Envenomations |
Marine wound infections
Retained foreign body
Emergency department (ED) management of echinoderm envenomation involves addressing the venom exposure and the accompanying trauma inflicted by the specific application structures used to deliver the venom (spines, pedicellaria, tentacles). General rules of therapy include prompt analgesia, wound management, and observation for and supportive treatment of significant systemic symptoms.
Medical therapy is directed primarily at local and systemic analgesia, with nonspecific supportive therapy required only in the most severe cases. Prophylactic antibiotics are generally not indicated, except in persons with deep puncture wounds or who are immunocompromised. However, once infection is established, prompt therapy must be instituted with emphasis on coverage for potential marine pathogens. No antivenoms are available. Tetanus prophylaxis is indicated in all marine animal injuries.
Used to provide local or regional anesthesia as adjunctive or alternative pain control.
Any of the commonly used local anesthetics suffice; however, bupivacaine provides superior duration of anesthesia and pain relief for irrigation, wound exploration, and debridement.
10-20 mL of 0.25-0.5% intralesionally; not to exceed 3-4 mg/kg
<12 years: Not established
>12 years: 1.25 mg/kg/dose intralesionally
May enhance effects of CNS depressants; coadministration may increase toxicity of MAOIs, TCAs, beta-blockers, vasopressors, and phenothiazines
Documented hypersensitivity; septicemia; spinal deformities; severe hypertension; existing neurologic disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Test a dose and monitor for CNS toxicity, cardiovascular toxicity, and signs of unintended intrathecal administration; caution with inflammation or sepsis in region of proposed injection; monitor patient's state of consciousness after each injection; caution in hypertension, cerebral vascular insufficiency, peripheral vascular disease or heart block, and arteriosclerotic heart disease
For adjunctive pain control when immersion therapy and local and/or regional anesthesia are not sufficient. Analgesic route (oral or parenteral) is a matter of choice and may not be needed with appropriate local or regional anesthetic.
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 is commonly titrated until desired effect obtained.
0.1 mg/kg IV/IM/SC; may repeat q1-3h prn pain control
Administer as in adults
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Indicated for outpatient treatment of early or minor wound infections and prophylaxis for high-risk wounds (deep puncture wounds, grossly contaminated wounds, persons who are chronically ill or immunocompromised).
Trimethoprim/sulfamethoxazole, ciprofloxacin, tetracycline, and doxycycline are referenced as the initial oral antibiotics of choice in different sources for uncomplicated wound infection or prophylaxis following marine-acquired injuries. Other antibiotics mentioned include cephalexin, amoxicillin, and amoxicillin clavulanate.
Broad-spectrum parenteral antibiotics are indicated for serious wound infections (eg, cellulitis, myositis, gas gangrene) or sepsis following injuries sustained in the marine environment. The mortality rate for a Vibrio species wound infection approaches 50% (usually patients with chronic liver disease), and serious Aeromonas species infection may mimic clostridial gas gangrene.
No controlled studies exist regarding efficacy of therapy. Several references suggest both a tetracycline and either an extended-spectrum cephalosporin or aminoglycoside.
Inhibits bacterial synthesis of dihydrofolic acid by competing with PABA. This results in inhibition of bacterial growth.
160 mg TMP/800 mg SMZ PO bid
15-20 mg/kg/d PO, based on TMP, tid/qid for 14 d
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases prevalence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia caused by folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, individuals with chronic alcoholism, elderly patients, those receiving anticonvulsant therapy, persons with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
Bactericidal antibiotic that inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA-gyrase in susceptible organisms.
500 mg PO bid
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Treats susceptible bacterial infections of gram-positive and gram-negative organisms as well as infections caused by Mycoplasma, Chlamydia, and Rickettsia species. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s) of susceptible bacteria.
500 mg PO qid
<8 years: Not recommended
>8 years: 10-20 mg/lb (25-50 mg/kg) PO qid
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Inhibits protein synthesis and, thus, bacterial growth by binding with 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.
100 mg PO/IV bid
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms.
Arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.
2 g IV q8h
50 mg/kg IV q8h; not to exceed 6 g/d
Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase ceftazidime levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment
May be indicated for treatment of delayed tissue reactions. These occur in the form of either nodular or diffuse granulomatous lesions, occurring up to 3 months after penetrating echinoderm injuries, particularly those from sea urchins. Generally, though not exclusively, these result from unrecognized retained spine fragments. Intralesional and/or systemic corticosteroid therapy may be beneficial, although clearly less efficacious than surgical removal of spine fragments. Topical corticosteroids may be useful for treatment of dermatitis.
Useful in treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.
5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve
4-5 mg/m2/d
Alternatively, administer 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Treats inflammatory dermatosis that is responsive to steroids. Decreases inflammation by suppressing migration of PMNs and reversing capillary permeability.
Administer 60 mg IM followed by additional doses of 20-100 mg given when signs and symptoms recur; taper over 2 wk as symptoms resolve
<6 years: Not established
6-12 years: 0.03-0.2 mg/kg IM at 1- to 7-d intervals
>12 years: Administer as in adults; taper over 2 wk as symptoms resolve
Coadministration with barbiturates, phenytoin, and rifampin decreases effects of triamcinolone
Documented hypersensitivity; fungal, viral, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation of glucocorticoids may cause adrenal crisis
Has mineralocorticoid activity and glucocorticoid effects. Decreases inflammation by suppression of migration of PMNs and reversal of increased capillary permeability. Useful in management of inflammation caused by immune response.
100 mg IV bolus initially; followed by continuous infusion of 100 mg q8h for 24-48 h
Once patient is stable, oral hydrocortisone may be started at dose of 50 mg PO q8h for another 48 h; taper over 2 wk as symptoms resolve
<12 years: 1-2 mg/kg IV bolus; followed by 25-150 mg/d divided q6-8h
>12 years: 1-2 mg/kg IV bolus; followed by 150-250 mg/d divided q6-8h; taper over 2 wk as symptoms resolve
Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia
Documented hypersensitivity; viral, fungal, or tubercular skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis
These agents are used to generate passive immunity.
Used for passive immunization of any person with a wound that may be contaminated with tetanus spores.
For prophylaxis: 250-500 U IM in opposite extremity to tetanus toxoid lesion
Clinical tetanus: 3000-10,000 U IM for clinical tetanus
For prophylaxis: 250 U IM in opposite extremity as tetanus toxoid
Clinical tetanus: 3000-10,000 U IM
None reported
Since antibodies in globulin preparation may interfere with immune response to vaccination, do not administer within 3 mo of live virus immune globulin administration; may be necessary to revaccinate persons who received immune globulin shortly after live virus vaccination
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Persons with isolated IgA deficiency have potential for developing antibodies to IgA and can have anaphylactic reactions to subsequent administration of blood products that contain IgA; do not perform skin testing because intradermal injection of concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing medication to be withheld from a patient not allergic to this material; true allergic responses to human gamma globulin given in prescribed IM manner are extremely rare; do not admix with other medications because usually incompatible
Generally, immunization against tetanus is considered for this type of envenomation. A booster injection in previously immunized individuals is recommended to prevent this potentially lethal syndrome. Patients who may not have been immunized against Clostridium tetani products should receive tetanus immune globulin (Hyper-Tet).
Used to induce active immunity against tetanus in selected patients. Immunizing agents of choice for most adults and children >7 y. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is midlateral thigh.
Primary immunization: 0.5 mL IM; give 2 injections 4-8 wk apart and a third dose 6-12 mo after second injection
Give 0.5 mL booster dose q10y
Administer as in adults
Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization because of poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol because it may impair amnestic response to tetanus toxoid; concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction is nevertheless clinically insignificant and does not preclude concurrent use)
Documented hypersensitivity; history of any type of neurologic symptoms or signs following administration of this product; FDA recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are an important cause of provocative poliomyelitis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use to treat actual tetanus infections or for immediate prophylaxis of unimmunized individuals (use tetanus antitoxin instead, preferably human tetanus immune globulin); diminished antibody response to active immunization may be observed in patients receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued; routine immunization of symptomatic and asymptomatic HIV-infected persons is recommended
Williamson JA, Fenner PJ, Burnett JW. Venomous and Poisonous Marine Animals: Medical and Biological Handbook. 1996:88-97, 106-117, 312-325.
Marsh L, Slack-Smith S, Gurry D. Sea Stingers. Perth: Western Australian Museum; 1986:133.
Underhill D. Australia's Dangerous Creatures. Sydney: Reader's Digest; 1987:368.
Freyvogel TA. Poisonous and venomous animals in East Africa. Acta Trop. 1972;29(4):401-51. [Medline].
Edmonds C. Dangerous Marine Creatures. Frenchs Forest, NSW: Reed Books; 1989:192.
Smith MM. Sea and Shore Dangers: Their Recognition, Avoidance, and Treatment. 1977. Grahamstown, South Africa: JLB Smith Institute of Ichthyology, Rhodes University; 21-31.
Auerbach PS. Marine envenomations. N Engl J Med. Aug 15 1991;325(7):486-93. [Medline].
Auerbach PS. Medical Guide to Hazardous Life. 2nd ed. Best Pub Co; 1991:21-23, 33-34.
Auerbach PS. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 4th ed. Mosby-Year Book; 2001:1473-1479.
Bove AA, Davis J. Bove and Davis' Diving Medicine. 3rd ed. WB Saunders Co; 1997:310-311.
Cracchiolo A, Goldberg L. Local and systemic reactions to puncture injuries by the sea urchin spine and the date palm thorn. Arthritis Rheum. Jul-Aug 1977;20(6):1206-12. [Medline].
Cunningham P, Goetz P. Venomous and Toxic Marine Life of the World. 2nd ed. Lonely Planet Publications; 1996:77-91.
Edmonds C. Dangerous Marine Creatures: Field Guide for Medical Treatment. 2nd ed. Best Pub Co; 1995:136-140, 149-153.
Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 3rd ed. Mosby-Year Book; 1996:488-489, 493.
Halstead BW, Auerbach PS. With prevention, first aid and treatment. In: Dangerous Aquatic Animals of the World: A Color Atlas. Darwin Press Inc; 1992:45-49.
Kizer KW. Marine envenomations. J Toxicol Clin Toxicol. 1983-84;21(4-5):527-55. [Medline].
Liram N. Sea urchin puncture resulting in PIP joint synovial arthritis: case report and MRI study. J Travel Med. 2000;7 (1):43-5. [Medline].
McGoldrick J, Marx JA. Marine envenomations. Part 2: Invertebrates. J Emerg Med. Jan-Feb 1992;10(1):71-7. [Medline].
Meier J, White J. Clinical Toxicology of Animal Venoms and Poisons. C R C Press LLC; 1995:2-5, 129-133.
Perkins RA. Poisoning, envenomation, and trauma from marine creatures. Am Fam Physician. 2004;69 (4):885-90. [Medline].
Perkins RA, Morgan SS. Poisoning, envenomation, and trauma from marine creatures. Am Fam Physician. Feb 15 2004;69(4):885-90. [Medline].
Schwartz S, Meinking T. Venomous marine animals of Florida: morphology, behavior, health hazards. J Fla Med Assoc. Oct 1997;84(7):433-40. [Medline].
Singletary EM, Rochman AS, Bodmer JC. Envenomations. Med Clin North Am. Nov 2005;89(6):1195-224. [Medline].
Soppe GG. Marine envenomations and aquatic dermatology. Am Fam Physician. Aug 1989;40(2):97-106. [Medline].
Strauss MB, MacDonald RI. Hand injuries from sea urchin spines. Clin Orthop Relat Res. Jan-Feb 1976;(114):216-8. [Medline].
Trott AT. Wounds and Lacerations: Emergency Care and Closure. 2nd ed. Mosby-Year Book; 1997:285-295.
Echinodermata, brittle stars, Ophiuroidea, starfish, starfish envenomation, sea cucumber envenomation, brittle star envenomation, Asteroidea, sea urchins, long-spined sea urchins, short-spined sea urchins, Echinoidea, sea cucumbers, Holothuroidea, echinoderm envenomation, echinoderm sting, crown-of-thorns starfish, Acanthaster planci, Echinaster, Plectaster, Solaster, Diadema, Echinothrix, Phormosoma, Asthenosoma, Araeosoma, Toxopneustes pileolus, Tripneustes, Bohadschia argus, marine envenomations
Scott A Gallagher, MD, FACEP, Chairman, Department of Emergency Medicine, Aspen Valley Hospital; Senior Clinical Instructor, Department of Surgery, School of Medicine, University of Colorado Health Sciences Center
Scott A Gallagher, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
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.
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.
James Steven Walker, DO, MS, Clinical Professor of Surgery, Department of Surgery, University of Oklahoma Health Sciences Center
James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association
Disclosure: Nothing to disclose.
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.
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.
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