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Cobra Envenomation Medication

  • Author: Robert L Norris, MD; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Oct 27, 2015
 

Medication Summary

The definitive therapy for cobra envenomation is antivenom administration, which should be started as soon as possible if evidence of systemic envenoming is present. If specific antivenom is not rapidly available, the patient must be supported using conservative measures alone. Measures include securing the airway and supporting respirations as necessary. Hypotension should be treated initially with intravenous fluids (initially crystalloids but if blood pressure/tissue perfusion fails to improve, then albumin). If hypotension persists after the intravascular volume is replete, vasopressor agents may be necessary.

Evidence supports the trial of cholinesterase-inhibiting drugs, such as edrophonium or neostigmine, as a temporizing measure in a situation of severe cobra venom poisoning with significant neurologic abnormalities until antivenom can be obtained.[13, 14]   These temporizing drugs should not, however, delay securing the airway of a victim who is developing respiratory distress or inability to handle secretions.

Antivenom can be started according to the manufacturer's instructions regarding route and dose.  Although some manufacturers advise use of an intradermal skin test to predict an acute reaction to antivenom, this procedure is terribly unreliable and only serves to waste precious time.  Such recommendations for skin testing should be ignored.

As with any form of bite, update the tetanus status as necessary. Antibiotic prophylaxis is not necessary.

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Antivenom

Class Summary

These agents impart passive immunity to the victim against the venom components of the snake(s) for which it is manufactured. The heterologous antibodies bind with venom antigens and block their deleterious effects.

Antivenom (variable, see below)

 

Several different cobra antivenoms are produced by various countries. They are of variable purity and efficacy. The most appropriate agent for the species involved should be determined and obtained. Given venom variability, antivenom produced in the country of origin of the offending species is preferred. An intradermal skin test for potential acute sensitivity is often recommended by manufacturers before administration. Such skin tests are, however, completely unreliable predictors of anaphylactic/anaphylactoid reactions, and should be omitted. Before administration, intravascular volume should be expanded using crystalloids such as normal saline or Ringer's lactate unless some contraindication (eg, congestive heart failure) is present. Pretreatment with antihistamines (H1 and H2 blockers) can be considered, though their efficacy at preventing adverse reactions to antivenom is unproven. Epinephrine should be immediately available for treatment of an anaphylactoid response to the heterologous serum.

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Antihistamines

Class Summary

Antihistamines (H1 and H2 blockers) may blunt or prevent an acute allergic reaction when given before the administration of antivenom. If an anaphylactic/anaphylactoid reaction occurs despite pretreatment, further antihistamine dosing may be required. These agents are useful in managing pruritus in cases of delayed serum sickness, which may appear days to weeks following antivenom treatment.

Diphenhydramine (Benadryl)

 

Diphenhydramine can be administered parenterally. It is often the H1 blocker of choice in treating or preventing anaphylactoid reactions. It is also effective orally in treating itching associated with serum sickness. If an acute allergic reaction subsequently occurs, further administration may be required.

Cimetidine (Tagamet)

 

Cimetidine is an H2 antagonist coadministered with an H1 antagonist if there is no response to the H1 antagonist alone; it treats itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.

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Cardiovascular agents

Class Summary

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.

Epinephrine (Epi-Pen)

 

With its combined alpha- and beta-adrenergic effects, Epinephrine is the drug of choice for the treatment of an acute anaphylactoid reaction because it halts and reverses the major abnormalities associated with such reactions (eg, hypotension, laryngospasm, bronchospasm, edema, urticaria); it must be available immediately for administration if such a reaction to antivenom occurs.

Dopamine (Intropin)

 

Dopamine may be required to support blood pressure in the face of hypotension caused by an anaphylactic/anaphylactoid reaction (unresponsive to fluids, epinephrine) or by direct snake venom effects (unresponsive to fluids, antivenom).

Norepinephrine (Levophed)

 

Norepinephrine may be used as an alternative to dopamine to support blood pressure in the face of hypotension caused by an anaphylactic/anaphylactoid reaction that is unresponsive to fluids and epinephrine.

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Corticosteroids

Class Summary

Used in management of both acute and delayed allergic phenomena following antivenom administration. Corticosteroids, however, have no primary role in the management of snake venom poisoning.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

 

Steroids ameliorate the delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce the inflammatory effects of this immune-complex mediated disease.

Prednisone (Deltasone, Orasone, Sterapred)

 

Prednisone is useful orally in managing mild-to-moderate serum sickness treated on an outpatient basis.

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Cholinesterase inhibitors

Class Summary

Cholinesterase inhibitors may be effective in temporarily reversing muscle weakness until antivenom can be obtained. Their use might obviate intubation, but airway protection should not be delayed if there is any doubt of the patient's respiratory status or ability to protect the airway.

Edrophonium (Enlon, Reversol)

 

Edrophonium is a short-acting anticholinesterase agent; it may provide significant improvement in muscle strength (eg, ability to open eyes) within 2 minutes and its effect peaks in 5 minutes. Weakness rapidly returns, however, and can be subsequently treated with a longer-acting agent, such as neostigmine.

Neostigmine (Prostigmin)

 

Neostigmine is a longer-acting cholinesterase inhibitor that can be used if a trial of edrophonium is effective; it inhibits the destruction of acetylcholine by acetylcholinesterase, which facilitates the transmission of impulses across the myoneural junction.

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Immune globulins

Class Summary

Consists of administration of immunoglobulin pooled from serum of immunized subjects.

Tetanus immune globulin (TIG)

 

Tetanus immune globulin is used for passive immunization of any person with a wound that might be contaminated with tetanus spores when the person has not previously completed a primary tetanus immunization series.

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Toxoids

Class Summary

Toxoids are used to induce active immunity against the respective antigens.

Tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Adacel, Boostrix)

 

This is a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine. It promotes active immunity to diphtheria, tetanus, and pertussis by inducing the production of specific neutralizing antibodies and antitoxins. It is indicated for active booster immunization for tetanus, diphtheria, and pertussis prevention for persons aged 10-64 years (Adacel approved for 11-64 y, Boostrix approved for 10-18 y). It is the preferred vaccine for adolescents scheduled for booster.

Tetanus toxoid adsorbed or fluid

 

The immunizing agent of choice for most adults and children older than 7 years is tetanus and diphtheria toxoids. It is 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, it may be administered into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally.

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Contributor Information and Disclosures
Author

Robert L Norris, MD Professor, Department of Emergency Medicine, Stanford University Medical Center

Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, International Society of Toxinology, American Medical Association, California Medical Association, Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and 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; Physician Advisor for Case Management, Wellspan Health System, York

David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, American Society of Pediatric Nephrology, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Special thanks to the family of Dr. Sherman A. Minton who died on June 15, 1999. Dr. Minton, a renowned herpetologist and toxinologist, was instrumental in co-authoring the first edition of this chapter.

References
  1. Minton SA. Bites by non-native venomous snakes in the United States. Wilderness Environ Med. 1996. 4:297-303.

  2. Reid HA. Bites by foreign venomous snakes in Britain. Br Med J. 1978 Jun 17. 1(6127):1598-1600. [Medline].

  3. Goldman DR, Seefeld AW. Ocular toxicity associated with indirect exposure to African spitting cobra venom. Wilderness Environ Med. 2010 Jun. 21(2):134-6. [Medline].

  4. Russell FE. Snake venom poisoning in the United States. Annu Rev Med. 1980. 31:247-59. [Medline].

  5. Tin-Myint, Rai-Mra, Maung-Chit, et al. Bites by the king cobra (Ophiophagus hannah) in Myanmar: successful treatment of severe neurotoxic envenoming. Q J Med. 1991 Sep. 80(293):751-62. [Medline].

  6. Looareesuwan S, Viravan C, Warrell DA. Factors contributing to fatal snake bite in the rural tropics: analysis of 46 cases in Thailand. Trans R Soc Trop Med Hyg. 1988. 82(6):930-4. [Medline].

  7. Reid HA, Thean PC, Martin WJ. Epidemiology of snake bite in north Malaya. Br Med J. 1963. 1:992-997.

  8. Viravan C, Looareesuwan S, Kosakarn W, et al. A national hospital-based survey of snakes responsible for bites in Thailand. Trans R Soc Trop Med Hyg. 1992 Jan-Feb. 86(1):100-6. [Medline].

  9. Sawai Y, Tseng CS. Snakebites on Taiwan. Snake. 1969. 1:9-18.

  10. Stahel E. Epidemiological aspects of snake bites on a Liberian rubber plantation. Acta Trop. 1980 Dec. 37(4):367-74. [Medline].

  11. Norris RL, Ngo J, Nolan K. 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].

  12. Ang LJ, Sanjay S, Sangtam T. Ophthalmia due to spitting cobra venom in an urban setting--a report of three cases. Middle East Afr J Ophthalmol. 2014 Jul-Sep. 21 (3):259-61. [Medline].

  13. Gold BS. Neostigmine for the treatment of neurotoxicity following envenomation by the Asiatic cobra. Ann Emerg Med. 1996 Jul. 28(1):87-9. [Medline].

  14. Watt G, Theakston RD, Hayes CG, et al. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. N Engl J Med. 1986 Dec 4. 315(23):1444-8. [Medline].

  15. Lim BL. Venomous land snakes of Malaysia. In: Chou LM, Gopalkrishnakone P, eds. Snakes of Medical Importance - Asia-Pacific Region. National of University of Singapore. 1990:387-417.

  16. Warrell DA. Clinical toxicology of snakebite in Africa and the Middle East and Asia. In: Clinical Toxicology of Animal Venoms and Poisons. CRC Press. 1995:433-594.

 
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Naja naja (Indian Cobra). Photo by Robert Norris, MD.
Naja atra (Chinese cobra). Photo by Sherman Minton, MD.
Naja kaouthia (Monocellate cobra). Photo by Sherman Minton, MD.
Naja nivea (Cape cobra). Photo by Sherman Minton, MD.
Necrosis from a cobra bite. Photo by Sherman Minton, MD.
Necrosis from a Naja atra (Chinese cobra) bite. This resulted in a severe deformity. The patient had few systemic signs or symptoms. Photo by Sherman Minton, MD.
Table of antivenom choices for cobra bites. As antivenom manufacturers come and go in the market, choices in this list may or may not be available. Consultation with regional poison control centers, which have access to the Antivenin Index, may help identify and locate an appropriate product for use.
Cobra antivenoms and their manufacturers (part 1). As antivenom manufacturers come and go in the market, choices in this list may or may not be available. Consultation with regional poison control centers, which have access to the Antivenin Index, may help identify and locate an appropriate product for use.
Cobra antivenoms and their manufacturers (part 2). As antivenom manufacturers come and go in the market, choices in this list may or may not be available. Consultation with regional poison control centers, which have access to the Antivenin Index, may help identify and locate an appropriate product for use.
The Australian pressure immobilization technique. This technique has been shown to be helpful in delaying systemic absorption of elapid venoms, but its use in cobra bites remains controversial. A broad pressure bandage is immediately wrapped, beginning distally (illustration 1 of 5), around as much of the extremity as possible (illustrations 2 and 3). No effort should be spent removing clothing prior to bandage application. The bandage is wrapped snugly, as for a severely sprained ligament. A splint (or sling when applied to the upper extremity) is then placed (illustrations 4 and 5), and the victim is carried from the scene. The victim should expend no effort in getting to definitive care. Pressure immobilization should remain in place until the victim has reached medical care. The doctor will decide when to remove the bandages. If venom has been injected, it will move into the bloodstream quickly once the bandages are removed. The doctor should leave the bandages and splint in position until appropriate antivenom is available. Used with permission from Commonwealth Serum Laboratories.
The Australian pressure immobilization technique, illustration 2 of 5. A broad pressure bandage is immediately wrapped, beginning distally (as shown above), around as much of the extremity as possible. No effort should be spent removing clothing prior to bandage application. The bandage is wrapped snugly, as for a severely sprained ligament. Used with permission from Commonwealth Serum Laboratories.
The Australian pressure immobilization technique, illustration 3 of 5. A broad pressure bandage is immediately wrapped, beginning distally (as shown above), around as much of the extremity as possible. No effort should be spent removing clothing prior to bandage application. The bandage is wrapped snugly, as for a severely sprained ligament. Used with permission from Commonwealth Serum Laboratories.
The Australian pressure immobilization technique, illustration 4 of 5. A splint (or sling when applied to the upper extremity) is then placed and the victim is carried from the scene. The victim should expend no effort in getting to definitive care. Pressure immobilization should remain in place until the victim has reached medical care. Used with permission from Commonwealth Serum Laboratories.
The Australian pressure immobilization technique, illustration 5 of 5. A splint (or sling when applied to the upper extremity) is then placed and the victim is carried from the scene. The victim should expend no effort in getting to definitive care. Pressure immobilization should remain in place until the victim has reached medical care. Used with permission from Commonwealth Serum Laboratories.
 
 
 
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