Updated: Dec 17, 2008
Approximately 40-50 species of venomous coral snakes exist in North America and South America, with the greatest variety from Mexico to northern South America. A number of African and Asian coral snake species also exist. All coral snakes belong to the family Elapidae; Micrurus fulvius (eastern coral snake) and Micrurus tener (Texas coral snake) are the most important species in the United States.
Another US coral snake is Micruroides euryxanthus (Sonoran or Arizona coral snake); this is a relatively innocuous snake, and no deaths have been attributed to its bite.
Coral snakes tend to be relatively shy creatures, and bites are uncommon. Coral snakes account for fewer than 1% of venomous snakebites in the United States. Most people bitten by coral snakes are handling them intentionally. Most bites occur in the spring or fall.
The coral snake venom apparatus is composed of a pair of small, fixed, hollow fangs in the anterior aspect of the upper jaw through which the snake conducts venom via a chewing motion (see Media file 2). Unlike pit vipers, such as rattlesnakes, copperheads, and cottonmouths, which strike quickly, coral snakes must hang on for a brief period to achieve significant envenomation in humans.
Probably fewer than 20 bites per year (though 99 alleged bites were reported to the American Association of Poison Control Centers in 2004).1
No accurate information on international incidence is available.
No deaths related to coral snake bites have been reported in the United States since coral snake antivenom became available. Before that time, the estimated case-fatality rate was 10%, and the cause of death was respiratory or cardiovascular failure. Patients who survive the bite may require respiratory support for up to a week and may suffer persistent weakness for weeks to months.
The vast majority of patients bitten by coral snakes report that a brightly colored snake bit them.
North of Mexico City, including the United States, the color pattern of the snake can be helpful in differentiating a coral snake from a harmless mimic (eg, nonvenomous milk snake). In this region, all coral snakes have a red, yellow, black, yellow, red banding pattern (red and yellow touching, see Media file 1); most harmless mimics have a red, black, yellow, black, red pattern (red and yellow separated by black). The mnemonic "Red on yellow, kill a fellow; red on black, venom lack," may be helpful in this region. South of Mexico City, the banding patterns are much less helpful, and bicolor (red and black) species are also present.
Physical findings of snake bite may include the following:
Snake Envenomations, Brown
Snake Envenomations, Cobra
Snake Envenomations, Moccasins
Snake Envenomations, Mohave Rattle
Snake Envenomations, Rattle
Snake Envenomations, Sea
Of utmost importance is prompt movement of the victim to a medical facility capable of rendering advanced care, including possible antivenom administration and airway support.
In the United States, the product used to treat Micrurus bites for the last several decades, Wyeth's Micrurus fulvius Antivenin, is no longer in production. Other antivenoms are produced in other countries (eg, Brazil, Costa Rica) for non-North American coral snakes. Mexico produces an antivenom that is likely effective for coral snake bites in the United States. It may prove that one of these exotic antivenoms will be required to be imported into the United States for use in serious bites here. In the absence of such an antivenom, care must be entirely supportive.
Care for persons bitten by Sonoran coral snakes is entirely supportive because no specific antivenom is available for this species.
Any appropriate, available antivenom should be administered according to the manufacturer's instructions.
As with any form of bite, tetanus status should be updated as necessary.
Antibiotic prophylaxis is not indicated. Because of the relative paucity of enzymatic necrotic components in their venoms, coral snake bites tend to cause little local tissue damage, and secondary infections are rare.
Imparts passive immunity to the patient against the venom components of the snake(s) for which it is manufactured. Heterologous antibodies administered bind with venom antigens and block their deleterious effects.
Historically the DOC for significant bites by M fulvius (eastern coral snake) and M tener (Texas coral snake); however, it is no longer being produced. Unless another known effective antivenom is available, care for victims bitten by coral snakes in the United States will have to rely entirely on supportive care (as per the text above), though the outcome should still be good.
As per the manufacturer's package insert for the appropriate, available product
Pediatric doses of snake antivenoms are the same as for adults
None reported
Documented hypersensitivity; may still be indicated for significant envenomation despite allergy if the reaction is easily reversed with appropriate medications (eg, epinephrine, antihistamines, steroids)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Anaphylactic/anaphylactoid reactions and delayed serum sickness are a concern; appropriate therapeutic agents for anaphylaxis treatment should be ready for immediate use; while use in pregnancy has not been well studied, it is generally felt that the benefits of antivenom administration outweigh the risks
H1 and H2 blockers may blunt or prevent acute allergic reaction when given before the administration of antivenom. If an anaphylactoid reaction occurs despite pretreatment, further antihistamine dosing may be required. They are also useful in managing pruritus in cases of delayed serum sickness, which may appear days to weeks following antivenom treatment.
Administered parenterally and often is the H1 blocker of choice in treating or preventing anaphylactic/anaphylactoid reactions. Also effective in oral form for treating itching associated with serum sickness.
Pretreatment for antivenom: 1 mg/kg/dose IV; not to exceed 100 mg/dose; if acute allergic reaction subsequently occurs, additional doses may be required; not to exceed 300 mg/d
Serum sickness: 1 mg/kg PO q6h prn itching; not to exceed 400 mg/d
Pretreatment for antivenom: Administer as in adults
Serum sickness: 1 mg/kg PO q6h prn itching; not to exceed 300 mg/d
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions
Documented hypersensitivity; MAOIs
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction
Administered parenterally and often is the H2 blocker of choice in treating or preventing anaphylactoid reactions. Use this medication in addition to H1 antihistamines.
300 mg IV q6h prn
5-10 mg/kg IV q6h prn; not to exceed 300 mg/dose
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
These agents are useful in treating acute allergic reactions that may occur with antivenom administration and in supporting the blood pressure and tissue perfusion of hypotensive patients with shock unresponsive to IV fluids and antivenom.
DOC for treating anaphylactoid reactions. Has alpha-agonist effects that increase peripheral vascular resistance and reverse peripheral vasodilatation, systemic hypotension, and vascular permeability. Conversely, beta-agonist activity of epinephrine produces bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
0.01 mL/kg of 1:1000 (1 mg/mL) IM/SC; not to exceed 0.5 mL
0.01 mL/kg of 1:1000 (1 mg/mL) IM/SC; not to exceed 0.3 mL; may be repeated q10-20min prn
For severe hypotension: 0.05 mcg/kg/min IV initially (ie, 1 mg in 500 mL isotonic saline, starting at 0.025 mL/kg/min); titrate to effect
Concurrent use with alpha- or beta-blockers is not recommended; nonselective beta-blockade allows alpha-receptor effects to predominate; increasing vascular resistance leads to increased BP and reflex bradycardia; closely monitor vital signs if the patient is taking a beta-blocker; pressor action is increased when coadministered with alpha-agonists; increases toxicity of halogenated inhalational anesthetics
Documented hypersensitivity; cardiac dysrhythmias or angle-closure glaucoma; do not use during labor (may delay second stage of labor)
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in elderly persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac dysrhythmias
May be required to support BP with hypotension caused by anaphylactoid reaction that is unresponsive to fluids and epinephrine or by direct coral snake venom effects that are unresponsive to fluids and antivenom.
5-20 mcg/kg/min IV; titrate to effect
Administer as in adults
Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong the effects
Documented hypersensitivity; pheochromocytoma; ventricular fibrillation
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Closely monitor urine flow, cardiac output, pulmonary wedge pressure, and BP during infusion; prior to infusion, correct hypovolemia as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia
May be used as alternative to dopamine to support BP in the face of hypotension caused by anaphylactoid reaction unresponsive to fluids and epinephrine.
0.5-1 mcg/min IV; titrate to effect
0.1 mcg/kg/min IV; titrate to effect
Atropine may enhance pressor response by blocking reflex bradycardia
Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia may be increased and area of infarct extended
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
If possible, correct intravascular volume depletion before therapy; extravasation may cause severe tissue necrosis and, thus, should be administered into a large vein; caution in occlusive vascular disease
Essential for management of acute and delayed allergic phenomena following antivenom administration. Steroids have no primary role in the management of snake envenomation.
Ameliorates the delayed effects of anaphylactoid reactions and may prevent biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may reduce the inflammatory effects of this immune-complex mediated disease.
125 mg IV q6-8h
1-2 mg/kg IV q6-8h
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
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
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
This or other PO forms of corticosteroids (eg, prednisolone) are useful in managing mild-to-moderate serum sickness on an outpatient basis.
1 mg/kg PO qd until symptoms resolve; taper over 1-2 wk
Administer as in adults
Coadministration with estrogens may decrease 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, connective tissue, fungal, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Abrupt discontinuation of glucocorticoids after long-term therapy 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
Immune globulins bind toxoids, stimulate an immune response, and offer transient protection while the host immune system develops antibodies.
Used for passive immunization if wound might be contaminated with tetanus spores when the patient has no history of completing a primary tetanus immunization series.
Prophylaxis: 250-500 U IM in different anatomical site than tetanus toxoid administration
Clinical tetanus: 3000-10,000 U IM
Prophylaxis: 250 U IM in different anatomical site than tetanus toxoid administration
Clinical tetanus: Administer as in adults
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 immunoglobulin A (IgA) deficiency have potential for developing antibodies to IgA and could have anaphylactic reactions to subsequent administration of blood products that contain IgA; do not perform skin testing since intradermal injection of concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing the 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 since usually incompatible
Used to induce active immunity against tetanus.
The immunizing agent of choice for most adults and children >7 y is tetanus and diphtheria toxoids. 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 the mid-thigh laterally.
Suggested dosing:
Primary immunization: 0.5 mL IM, give 2 injections 4-8 wk apart and a third dose 6-12 mo after second injection
Booster dose: 0.5 mL q10y
Administer as in adults
Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization due to poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol since 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 its concurrent use)
Documented hypersensitivity; a history of any type of neurological 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 instead tetanus antitoxin, preferably human tetanus immune globulin), diminished antibody response to active immunization may be seen 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
Complications of snake bite may include the following:
Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2005;23(5):589-666. [Medline].
Davidson TM, Eisner J. United States coral snakes. Wilderness Environ Med. 1996;1:38-45.
German BT, Hack JB, Brewer K, et al. Pressure-immobilization bandages delay toxicity in a porcine model of eastern coral snake (Micrurus fulvius fulvius) envenomation. Ann Emerg Med. Jun 2005;45(6):603-8. [Medline].
Gray S. Pressure immobilization of snakebite. Wilderness Environ Med. Spring 2003;14(1):70-1. [Medline].
Kitchens CS, Van Mierop LH. Envenomation by the Eastern coral snake (Micrurus fulvius fulvius). A study of 39 victims. JAMA. Sep 25 1987;258(12):1615-8. [Medline].
Norris RL, Bush SP. North American venomous reptile bites. In: Auerbach PS, ed. Wilderness Medicine. 4th ed. St. Louis: Mosby; 2001:896-926.
Norris RL, Dart RC. Apparent coral snake envenomation in a patient without visible fang marks. Am J Emerg Med. Jul 1989;7(4):402-5. [Medline].
Norris RL, Ngo J, Nolan K, et al. Physicians and lay people are unable to apply pressure immobilization properly in a simulated snakebite scenario. Wilderness Environ Med. 2005;16(1):16-21. [Medline].
Parrish HM, Khan MS. Bites by coral snakes: report of 11 representative cases. Am J Med Sci. May 1967;253(5):561-8. [Medline].
Simpson ID, Tanwar PD, Andrade C, et al. The Ebbinghaus retention curve: training does not increase the ability to apply pressure immobilisation in simulated snake bite--implications for snake bite first aid in the developing world. Trans R Soc Trop Med Hyg. May 2008;102(5):451-9. [Medline].
snake envenomation, snakebite, snake bite, coral snake, Elapidae, Micrurus fulvius, eastern coral snake, Micrurus tener, Texas coral snake, coral snake envenomations, coral snake bite, Micruroides euryxanthus, Sonoran coral snake, Arizona coral snake
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.
Edmond A Hooker II, MD, DrPH, FAAEM, Assistant Professor, Department of Health Services Administration, Xavier University; Associate Clinical Professor, Department of Emergency Medicine, University of Louisville; Assistant Clinical Professor, Department of Emergency Medicine, Wright State University
Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association
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.
David Eitel, MD, MBA, Associate Professor, Department of Emergency Medicine, York Hospital
David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
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: eMedicine.com, Inc. Consulting fee Consulting
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)