Cobra Envenomation

Updated: Aug 03, 2022
  • Author: Bobak Zonnoor , MD, MMM; Chief Editor: Joe Alcock, MD, MS  more...
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Practice Essentials

Cobra envenomation is an extremely variable process. The lethality of the venom itself varies significantly - depending on the species, age of the individual snake, suspected seasonal variation in venom composition, route of enoculation (intravenous, intradermal, subcutaneous, etc), and many more factors.


Many patients recover with no specific treatment.

The neurotoxic effects of cobra venom are reversible, though motor recovery may take up to 7 days - and as many as 10 weeks. [1]

Reports of death within 1 hour of cobra bite exist, but a timeframe of 2-6 hours is more typical of fatal cases.

Digit or limb amputation may result with secondary infections following an initial bite. Marjolin ulcers may also form from chronic lesions.

Corneal erosions can develop secondary infections which may lead to permanent blindness with venom introduced into the eyes.

Patient education

Advise amateur herpetoculturists bitten by a venomous snake in their collection to not keep such animals. If they previously have received antivenom, their risk for an allergic reaction may be increased should antivenom use be required again in the future.

Signs and symptoms

Signs and symptoms following a cobra bite can be extremely variable:

  • Immediate, local pain (almost always present)

  • Soft tissue swelling (may be progressive)

  • Tissue necrosis with surrounding blistering and regional lymphadenopathy

  • Nausea and vomiting (earliest sign of systemic envenomination, typically within 6 hours) [1]

  • Early neurologic findings: contraction of frontalis muscle causing elevation of brows, ptosis, ophthalmoplegia, blurred vision (ocular muscles highly sensitive to neuromuscular blockade), loss of visual accommodation due to mydriasis, perioral paresthesia

  • Later neurologic findings: dysphagia, dysphasia, paralysis of palate and jaw muscles, tongue paralysis, neck paralysis, respiratory arrest. Despite occuring later, findings may be rapidly progressive within minutes to hours. [1]

  • Autonomic dysfunction: profuse salivation, nausea, vomiting, abdominal pain, blood pressure and heart rate abnormalities

  • Alteration of mental status (eg, drowsiness, occasionally with euphoria)

  • Chest pain or tightness, shortness of breath

  • Eye pain, tearing, blurred vision (with eye exposure to venom from spitting cobras)


Laboratory studies offer no diagnostic benefit for snake envenomation. Baseline labs (eg, complete blood count [CBC], electrolyte tests, renal function studies, coagulopathy panels) may be reasonable in severe bites or if the patient has significant underlying medical problems. Coagulopathy is not an expected feature of bites by most cobras, though prolonged bleeding and failure of clot retraction have been reported following bites by African spitting cobras and anticoagulant proteins have been identified in the venom of the African ringhals (Hemachatus haemachatus).

An arterial or venous blood gas may be helpful in gauging respiratory status.

In some regions of the world, researchers are developing immunologic tools, such as enzyme-linked immunosorbent assays (ELISAs), to aid in species identification and possibly in severity grading.

Consider a chest radiograph for patients requiring intubation or showing evidence of cardiorespiratory failure.

An electrocardiogram (ECG) should be obtained if the victim complains of chest pain or if there is evidence of dysrhythmia.


For a full discussion, see Treatment and Medication.

The definitive therapy for cobra envenomation is antivenom administration. This should be started as soon as possible if evidence of systemic envenomation is present. Supportive care should be provided throughout the patient's course - from pre-hospital until discharge with follow-up.



Venomous snakes are divided into families, of which the major ones are elapidae and viperidae. Physically, elapidae have shorter fangs, smaller heads, and smooth scales. Viperidae have stockier triangular heads wider than their necks, hingeable fangs that fold against the roof of their mouths, and ridged scales. However the distinction of interest for this article is venom. As a general rule-of-thumb, elapidae venom causes neuromuscular deficits - mainly flaccid paralysis - while viperidae venom focuses on local effects, including tissue necrosis, rhabdomyolysis, coagulopathy, and bleeding. As a disclaimer, these descriptors are generalized and individual species may differ from them. For example, venom of African spitting cobras primarily cytotoxic and coagulopathic effects with significantly less neurologic impact.

Cobras belong to the elapidae family and is the common name for snakes belonging to the Naja genus. Although primarily found in Africa and southern Asia, they are well recognized around the world - in large part due to its unique neck hood but also because of its debilitating venom. They have long held importance in their respective local cultures as creatures of danger but have permeated beyond into literature, media, folklore, etc. To many people, the cobra is the quintessential venomous snake.

As for physical attributes, cobras are generally large snakes, measuring 1.2 to 2.5 meters in length. The king cobra, which may reach 5.2m, is the longest of the cobras - and in fact, they are the longest venomous snake in the world. When encountered, cobras usually try to escape but occasionally defend themselves boldly and may appear aggressive. Cobras will elevate their head and spread their characterstic neck hood, typically only seen in a defensive mode. They are also said to produce a growl-like sound.

Most snakebites are inflicted on body extremities. By far, rural agricultural workers and other people in Asia and Africa receive most bites while working outdoors without protective wear. Children and young people tend to suffer more morbidity and mortality. In North America and Europe, captive cobras may cause bites to zookeepers or amateur collectors. [2, 3]

Not all snakebites result in envenomation, that is the introduction of venom into a victim typically via injection by fangs. Reports of dry bites is skewed given difficulties in accurately determining if venom was injected and in general lack of reporting of bites. Given this however, a literature review showed a wide incidence of dry bites based on snake species, ranging from 4% to 50%. [4]

In addition to biting, some cobra species have the ability to eject or spit jets of venom toward an aggressor, usually directed at the eyes in an effort to temporarily blind it in order to stage an escape. 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 is 1 meter but can reach up to 3 meters. This ability is found in African and Asian spitting cobras as well as South African ringhals, belonging to the Elapidae family that appear very similar to but are not true cobras.

When venom contacts the eye, acute ophthalmia occurs with symptoms of immediate and intense pain, blepharospasm, tearing, and blurring of vision. Systemic toxicity does not occur with eye exposure, but corneal ulcerationsuveitis, and permanent visual impairment or blindness have been reported in untreated cases. About half of the cases ascribed to the African spitting cobras (N nigricollisN mossambicaN pallidaN katiensis) showed corneal ulceration, and some resulted in permanent blindness. 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. [5]  Cases ascribed to the Asian spitting cobras and the African ringhals are usually less severe.



The envenomation of some cobra species causes profound neurological abnormalities (eg, cranial nerve dysfunction, abnormal mental status, muscle weakness, paralysis, and respiratory arrest). However with other cobras, cytotoxicity and local tissue damage is the primary concern and presentation - especially regarding bites from 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) - despite their venoms also containing some amount of neurotoxins. Occasionally, a combination of neurologic dysfunction and tissue necrosis may occur as with the Indian cobra (Naja naja).

Venom Composition

As with all snake venoms, cobra venoms are multicomponent products. Variations in composition occur between species as a result of evolutionary adaptions. Some of cobra venom components include:

  • α-neurotoxins (or α-cobratoxins). Also called three-fingered toxins due to their molecular shape, this family of neurotoxins competitively binds to post-synaptic nicotinic acetylcholine receptors to produce block depolarization, resulting in paralysis. The most concerning outcomes are bulbar and respiratory muscle paralysis resulting in death. [1]
  • Cardiotoxins. These cause a host of issues - including irreversible cell depolarization and contraction of muscular cells, cellular lysis,  dysfunction of platelet aggregation, inhibition of protein kinase C and Na+/K+ ATPase, and more - leading to dysarrhythmias and hemodynamic instability. [6]

  • Complement-activating proteins. Complement-depleting cobra venom factor (CVF) activates the alternative complement pathway without the standard antigen-antibody complex. It also dysregulates the pathway’s ability to halt the activation, overall leading to a depletion of complement factors and proteins and ultimately hindering the complement system from opsonizing and neutralizing venom. [7]

  • Enzymes. The major enzymatic toxins include phospholipase A2 (damages mitochondria, hematocytes, skeletal muscles, and vascular endothelium), hyaluronidase (facilitates tissue dispersion of other toxins by degrading extracellular matrix at bite site), L -amino acid oxidase (gives many venoms a characteristic yellow coloration), and acetylcholinesterase (terminates cholingeric neurotransmission impairing muscle contraction). [1, 7]


Naja philippinensis (Philippine cobra) venom is the most toxic of the cobra venoms, 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.

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.





About 5.4 millions snake bites occur every year, according to the World Health Organization. Of these, envenomations account for 1.8 to 2.7 million - resulting in 81,000 to 138,000 fatalities and nearly three times this in terms of permanent sequelae and amputations. Under-reporting of snake bites, resulting complications, and death is likely ubiquitous. Countries in which bites occur often have less developed healthcare infrastructure and reporting and data collecting systems in place. [8]


Snakebites are a significant medical problem in parts of Africa and Asia. The majority of envenomations, up to 2 million, occur in Asia. Roughly half a million occur in Africa yearly resulting in 20,000 deaths. 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. [8]

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. [9] 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).


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



Determining the exact contribution of cobras to overall snakebite morbidity and mortality is difficult. This stems from a larger issue of having reliable  counts of snake bites in general, as community and government based reporting grossly undercounts numbers while population-based surveys likely more accurately reflect morbidity and mortality. [1, 8] In most cases, bitten individuals are unable to identify the snake. Physicians are may by default attribute bites with neurotoxic symptoms to cobras without substantiation.

In India, the annual mortality incidence is 5.6-12.6 per 100,000 population from overall snake bites. 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. [10] Data from Thailand and Malaysia in the 1980s demonstrate an annual mortality incidence of 0.1 per 100,000 population. [11, 12]

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. [13] 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 were fatal. [14] Cobras accounted for 2 of 95 bites on a Liberian rubber plantation. [15] 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. [1] King cobras are also reputed for their short bite-to-death times, ranging from minutes to hours, while other envenominations can take days. Ringhals bites are similar to other cobra bites but are less serious both locally and systemically with deaths being 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. [16]

Prevalance of chronic and permanent morbidity (such as amputations and physical disfigurement resulting in handicap) due to snake bites is unknown.