Cobra Envenomation
Updated: Aug 03, 2022
Author: Bobak Zonnoor , MD, MMM; Chief Editor: Joe Alcock, MD, MS more...
OVERVIEW
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.
Prognosis
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)
Diagnostics
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.
Treatment
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.
Background
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 ulcerations, uveitis, and permanent visual impairment or blindness have been
reported in untreated cases. About half of the cases ascribed to the African spitting cobras (N
nigricollis, N mossambica, N pallida, N 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.
Pathophysiology
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]
Lethality
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.
Epidemiology
Frequency
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]
International
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).
Sex
Because of increased exposure to snakes, men are bitten more often than women.
Mortality/Morbidity
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.
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.