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Cobra Envenomation

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

Background

To many people, the cobra is the quintessential venomous snake. Cobras discussed in this article include species in the genus Naja and other similar venomous snakes, such as Ophiophagus hannah (king cobra), Hemachatus haemachatus (ringhals), Walterinnesia aegyptia (desert black snake), Boulengerina species (water cobras), and Pseudohaje species (tree cobras).

Most cobras are large snakes, 1.2-2.5 m in length. The king cobra, which may reach 5.2 m, is the largest venomous snake in the world. Cobras live throughout most of Africa and southern Asia. Their habitats vary, and some species adapt readily to life in cultivated areas and around villages.

When encountered, cobras usually try to escape but occasionally defend themselves boldly and may appear aggressive. Most of these snakes elevate the head and spread the neck as a threat gesture. However, a number of other snakes, venomous and nonvenomous, use this defense as well.

Most snakebites are inflicted on body extremities. Because cobras are popular as show snakes, bites on the hands and fingers are common.

By far, rural agricultural workers and other people in Asia and Africa receive most bites while working outdoors without protective footwear or when cutting tall grass with a hand blade. In North America and Europe, captive cobras may cause bites to zookeepers or amateur collectors.[1, 2]

Not all snakebites result in envenomation. In the case of cobras, the percentage of dry bites may be quite high, 45% in one series of 47 cases from Malaysia. In another series, 1 of 3 snake charmers bitten by large king cobras showed no signs of envenomation.

In addition to biting, some cobra species have a unique defense; they eject or spit jets of venom toward an aggressor, usually and accurately directly at the eyes. The fangs of these species are specially modified with the discharge orifice on the anterior face rather than at the tip. The effective discharge range of a large snake is at least 3 m. The ringhals and certain African species of Naja are the most effective spitters, but the spitting behavior also is observed among some Asian Naja species.

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Pathophysiology

Cobra envenomation is an extremely variable process. The envenomations of some species cause profound neurological abnormalities (eg, cranial nerve dysfunction, abnormal mental status, muscle weakness, paralysis, and respiratory arrest). With other cobras, local tissue damage is of primary concern.

Necrosis is typical of bites by the African spitting cobras (Naja nigricollis, Naja mossambica, Naja pallida, and Naja katiensis), the Chinese cobra (Naja atra), the Monocellate cobra (Naja kaouthia), and the Sumatran spitting cobra (Naja sumatrana). Although the venoms of these cobras contain neurotoxins, necrosis often is the chief or only manifestation of envenoming in humans. Occasionally, a combination of neurologic dysfunction and tissue necrosis may occur as with the Indian cobra (Naja naja). The images below depict several species.


Naja atra (Chinese cobra). Photo by Sherman Minto Naja atra (Chinese cobra). Photo by Sherman Minton, MD.

Naja kaouthia (Monocellate cobra). Photo by Sherm Naja kaouthia (Monocellate cobra). Photo by Sherman Minton, MD.

Naja naja (Indian Cobra). Photo by Robert Norris, Naja naja (Indian Cobra). Photo by Robert Norris, MD.

Cobra venoms have been studied extensively. As with all snake venoms, they are multicomponent products whose toxins are mostly proteins and polypeptides.

Venoms can be divided into the following categories:

  • With most species, excluding some of the African spitting cobras, the most clinically significant toxins are postsynaptic neurotoxins that competitively bind to nicotinic acetylcholine receptors to produce depolarizing neuromuscular blockade. One group in this category has 60-62 amino acids and 4 disulfide bridges. Another has 71-74 amino acids and 5 disulfide bridges.
  • The second venom category comprises so-called cardiotoxins, which are actually generalized cell-membrane poisons that produce irreversible cell depolarization. Such depolarization may cause dysrhythmia, hypotension, and death.
  • Toxins in the third category activate complement via the alternative pathway (C3-C9 sequence).
  • The fourth category is composed of enzyme toxins, such as phospholipase A 2 (variable toxicity), hyaluronidase (facilitates tissue dispersion of other toxins), L -amino acid oxidase (gives many venoms a characteristic yellow coloration), and acetylcholine acetylhydrolase (unknown toxicity). Other proteolytic enzymes are found in the venom of the king cobra.

Naja philippinensis (Philippine cobra) venom is the most toxic, with a subcutaneous median lethal dose (LD50) of 0.14 mg/kg in mice. In comparison, the corresponding LD50 for Naja naja (Indian cobra) venom is 0.29 mg/kg, for Naja haje (Egyptian cobra) venom is 1.75 mg/kg, for king cobra venom is 1.73 mg/kg, and for Naja nigricollis (black-necked spitting cobra) venom is 3.05 mg/kg.

An additional, unique form of toxicity with some Asian and African species is acute ophthalmia, which occurs when venom is spit into the eyes. Spitting cobras can spit venom into a person's eyes from up to 3 m away. Immediate and intense pain results, with blepharospasm, tearing, and blurring of vision. Systemic toxicity does not occur with eye exposure, but corneal ulcerations, uveitis, and permanent blindness have been reported in untreated cases. Occasionally, ocular exposure occurs when a person has venom on their hands (as following laboratory venom extraction from a snake) and rubs his or her eyes.[3]

About half of the cases ascribed to the African spitting cobras (N nigricollis, N mossambica, N pallida, N katiensis) showed corneal ulceration, and some patients experienced permanent visual impairment or blindness. Cases ascribed to the Asian spitting cobras and the African ringhals are usually less severe.

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Epidemiology

Frequency

United States

Envenomations result from human interaction with cobras in zoos, research laboratories, and private collections in the United States and other countries where cobras lack natural habitat. In a series of 54 consultations regarding bites by non-native snakes in the United States, 23 involved cobras. One fatality occurred, and 7 other cases involved serious envenoming. In Russell's 1980 series, cobras inflicted 18 of the 85 bites by non-native snakes.[4] No comparable data are available for other nations, though it was reported that only 3 cobra bites among 32 bites inflicted by non-native venomous snakes occurred in Britain (rattlesnakes were implicated most often in this series).

International

Snakebites are a significant medical problem in parts of Africa and Asia. In West Africa, the annual bite incidence is 40-120 bites per 100,000 population. Two rural Congolese regions report an annual incidence of 430 bites per 100,000 population. In a 7-year survey, the Natalese incidence was 24 bites per 100,000 population.

Sex

Because of increased exposure to snakes, men are bitten more often than women.

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Mortality/Morbidity

In India, the annual mortality incidence is 5.6-12.6 per 100,000 population. At one time, Burma listed snakebite as its fifth leading cause of death. More recently, the annual mortality incidence was 3.3 per 100,000 population.[5] Data from Thailand and Malaysia in the 1980s demonstrate an annual mortality incidence of 0.1 per 100,000 population.[6, 7]

Determining the exact contribution of cobras to overall snakebite morbidity and mortality is difficult. In most cases, bitten individuals are unable to identify the snake. In India, the tendency is to ascribe all fatal or serious bites to cobras. Physicians are also likely to attribute all bites with neurotoxic symptoms to cobras.

In a Thai survey, cobras made up 17% of the 1145 snakes identified in bites and were responsible for 25% of the fatalities associated with those bites.[8] In northern Malaysia, cobras accounted for 23 of 854 bites in which the snake was identified. In a survey in Taiwan, cobras were blamed for 100 of 851 bites in which the snake was identified; none was fatal.[9] Cobras accounted for 2 of 95 bites on a Liberian rubber plantation.[10] The ringhals was responsible for 18 of 314 envenomations in Natal. Based on patients' symptoms alone, 18 other bites in this series were ascribed to cobras.

King cobra bites are considered more serious than bites from other cobra species because of the greater volumes of injected venom and the more rapid onset of neurotoxic symptoms. Mortality is also higher. In a series of 35 cases, 10 deaths occurred. Ringhals bites are similar to other cobra bites but are less serious both locally and systemically. Deaths are rare. A medical report of 4 bites by the desert black snake described relatively mild symptoms and reported recovery without specific treatment. Anecdotal reports of fatal bites exist. No medical accounts of bites by water cobras or tree cobras exist. Anecdotal evidence suggests both are dangerous.

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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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