
Snake Envenomations: More Than Just a Bite
Snake envenomation is a major public health challenge in many parts of the world, and it is included in the World Health Organization's list of neglected tropical diseases.[1] The geographic areas most affected are rural, with the vast majority of dangerous bites occurring in Africa, Southeast Asia, South Asia, and Central and South America.[1] Access to quality emergency and critical care resources and to treatments such as antivenom is generally reduced in these regions.
Snake bites have the potential for significant morbidity and mortality, particularly in pediatric populations. Although likely to be greatly underreported, about 5.4 million snake bites occur each year, resulting in an estimated 2.7 million envenomations and an average of 110,000 deaths; an additional 300,000 people suffer severe disability or amputation.[1] Knowledge of dangerous snake species and their geographic distribution, toxidromes, potential complications, and management are essential to making informed decisions regarding clinical care.
The main image above shows a fer-de-lance snake bite on a researcher's calf. The inset image is that of a fer-de-lance.
Snake Envenomations: More Than Just a Bite
The left image shows a chronic nonhealing ulcer of the right foot and fixed deformities of the toes following a cobra bite. The snake image is that of a giant king cobra.
Three main families encompass most venomous snakes: elapids, viperids, and colubrids.
Elapids
Elapids comprise many highly venomous snake species across Africa, South Asia, Southeast Asia, and the Americas, including cobras, kraits, mambas, coral snakes, sea snakes, and taipan/tiger/brown snakes. Their venoms are often associated with neuromuscular paralysis and the development of bulbar and respiratory compromise. However, significant diversity in venom effects exists, and elapid venom may produce complex and mixed toxidromes (eg, muscle/tissue destruction) as well as dysregulation and consumption of coagulation factors, resulting in hemorrhage.[2,3]
Snake Envenomations: More Than Just a Bite
The main image depicts the bleeding gums of a patient following a bite by a Russell viper (inset image).
Viperids
Viperids inhabit many of the same areas as elapids, but they are also found in North America and Europe. Vipers that pose a danger to humans include Russel vipers, carpet vipers, saw-scaled vipers, adders, asps, and pit vipers. Their venom is thought to produce local and systemic cytotoxic and myotoxic effects, with or without significant dysregulation of coagulation. However, some viper species produce hemotoxic and neurotoxic venoms, with resultant paralysis and hemorrhage.[3]
Snake Envenomations: More Than Just a Bite
The main image depicts (A) hemorrhages in the brainstem, (B) evidence of brainstem herniation, and (C) basal subarachnoid hemorrhages from the brain of a patient who succumbed to an unidentified snake bite. The inset image shows a boomslang snake.
Colubrids
The Colubridae family of snakes are generally nonvenomous or have venoms that are not harmful to humans. It includes species such as the corn snake and the king snake, which are popular pets. However, the boomslang and other similar species of colubrids, including the twig snake, produce a highly hemotoxic venom that causes systemic consumption of clotting factors, leading to widespread hemorrhage.
Boomslang venom has a slow onset of action, with derangement of coagulation often taking place over days. Although this gradual process may allow time to secure antivenom, it may also lead the victim to erroneously conclude the bite was not venomous ("dry bite") or permit healthcare providers to prematurely discharge such victims from clinical observation. Death may occur from hemorrhagic shock and hypovolemia or central nervous system (CNS) hemorrhage.[3,4]
Snake Envenomations: More Than Just a Bite
A southern copperhead snake is shown in the top image. The bottom image depicts a right fourth digit following a bite from a southern copperhead.
Snake Bites in North America
North America also has a variety of venomous snakes capable of producing significant morbidity and even death. Viperids such as rattlesnakes have bites that generally produce a cytotoxic effect, with local tissue damage and possibly rhabdomyolysis. Although deaths are uncommon, extremity bites may result in severe disability or amputation.[2,3]
Copperheads are important viperids native to the southeastern United States. Although dry bites from these snakes are common and their venom is thought to be of low potency relative to other viper venoms, copperhead venom typically produces a cytotoxic toxidrome.[3,4]
Also native to the southeastern United States are cottonmouths (water moccasins), semi-aquatic pit vipers. Their bites may produce significant muscle and tissue destruction. Although deaths are rare, severe scarring, disability, and amputation are not uncommon.[3,4]
Snake Envenomations: More Than Just a Bite
Coral snakes are the sole species of elapids native to North America. Their range includes much of Mexico, Central and South America, and the southern United States, including Arizona, southern California, New Mexico, and Texas. Cytotoxic and hemotoxic effects of their bites have been described, including rhabdomyolysis and hemorrhage; however, coral snake bites typically produce a neurologic toxidrome, with both pre- and postsynaptic neuromuscular junction effects. Neurotoxic effects may be delayed for as long as 12 hours.[3-6]
The banding pattern of coral snakes may be similar to that of harmless milk snakes, leading to their possible misidentification as nonvenomous snakes. Mnemonics such as "red next to black, my friend Jack" or "red next to yellow, watch that fellow" are misleading and potentially dangerous, as banding colors and patterns vary with species and geographic location. If any doubt exists regarding identification of a banded snake in a person who has sustained a bite in the geographic range of coral snakes, a period of observation is indicated to surveil for the development of neurologic symptoms.[3-6]
Snake Envenomations: More Than Just a Bite
The image depicts the arm of a patient on day 3 after a copperhead bite to a finger.
Venomology
Snake venom is a complex mix of proteins, with significant variation in venom composition even amongst snakes of the same species. Thus, venomous bites frequently produce a range of symptoms, and it is not uncommon for victims of venomous snake bites to demonstrate evidence of multiple toxic effects.
Although vipers are typically thought of as producing cytotoxic and/or hemotoxic venoms, and elapid venoms are associated with neurotoxins, there is substantial overlap. Bites from some vipers produce a principally neurotoxic effect, whereas some elapid bites may cause significant local and systemic tissue and muscle breakdown, with or without derangements in coagulation, as well as induce paralysis. Moreover, some snake venoms have direct toxic effects on specific organs, resulting in primary cardiac or renal damage, that occurs in addition to secondary damage that may be due to other venom effects (eg, hypovolemia, rhabdomyolysis, hyperkalemia).[3,4,7,8]
Snake Envenomations: More Than Just a Bite
The image shows the lower leg of a young boy 2 weeks after he was bitten by a species of pit viper. The extensive tissue necrosis required above-knee amputation.
Cytotoxins
Various snake venoms from different snake families and geographic regions generate cytotoxic effects. These venoms typically consist of a mixture of proteolytic and myotoxic enzymes, which may cause extensive local tissue damage, and even systemic muscle and tissue destruction. Severe muscle breakdown can result in compartment syndrome and rhabdomyolysis, with subsequent acute renal injury and hyperkalemia. Bites may result in significant local damage and produce severe disability or even amputation.[4,9]
Snake Envenomations: More Than Just a Bite
Paralysis of the neck flexor muscles ("broken neck" sign) is shown in a teenage girl bitten by a Russell viper.
Neurotoxins
Neurotoxic snake venoms generally cause a descending paralysis with cranial nerve findings of diplopia, ptosis, dysphagia, and dysarthria. Generalized muscle weakness and paralysis may follow and the diaphragm and thoracic cage muscles may be affected, resulting in respiratory compromise.[3,9]
Neurotoxic snake venoms typically exert their effects at the neuromuscular junction, either at the pre- or postsynaptic nerve ending. Venom-mediated presynaptic nerve toxicity may not be reversible; once the venom has been taken up by the presynaptic nerve, medications or antivenom may have little impact. Thus, the rapid administration of antivenom is particularly crucial in regions known to have presynaptically-acting snake venoms (Australia, South Asia, and Southeast Asia elapid species such as the taipan and tiger snakes). Late administration of antivenom should still be considered in affected patients however, as some snake species produce venoms with mixed pre- and postsynaptic effects, and some benefit may be obtained from neutralizing any remaining circulating venom or reducing the postsynaptic effect.
Snake Envenomations: More Than Just a Bite
The image reveals (1) intracerebral hemorrhages that appear to be older than (2) the hemorrhages in the lateral ventricles of the brain from a patient who succumbed to the bite of an unknown snake.
Hemotoxins
Some snake species, including the boomslang and many viper species, produce derangements in the coagulation pathway, resulting in systemic hemorrhage. The mechanism of action of these venoms is variable, with multiple points of the coagulation cascade targeted; in general, consumption of platelets and coagulation factors results, which leads to systemic hemorrhage. Victims demonstrate spontaneous hemorrhage at the bite site and injection or intravenous sites, as well as petechiae, epistaxis, and gingival hemorrhage. Death may occur from hypovolemia due to internal and external hemorrhage as well as CNS hemorrhage.
Antivenom is particularly effective in addressing hemotoxic effects, and it can rapidly reverse coagulopathy.[3,8,9]
Snake Envenomations: More Than Just a Bite
Management Overview
Management of snake bites involves limiting the systemic spread of venom and appropriate supportive care, including wound care, cardiorespiratory support and, when available, early administration of antivenom and/or tetanus prophylaxis, if appropriate. Focus wound care on immobilization of the affected extremity or body part; in the setting of bacterial infection, administer antibiotics. Compressive dressings may be considered in regions or situations where generalized neurotoxicity is a significant threat and local wound effects are minimal. Bitten extremities should be kept either at the level of the heart in the case of cytotoxic bites, or below the level of the heart when envenomation with a neurotoxic venom is suspected.[3,9]
Some neurotoxic venoms respond well to anticholinesterase agents (eg, edrophonium, neostigmine). Antivenom can dramatically improve outcomes in many envenomation cases; however, presynaptic neurotoxins can be irreversible and result in long-term flaccid paralysis that is unresponsive to acetylcholinesterase medications and antivenoms.[3,9]
In all cases of snake envenomation, consult with a toxicologist or physician with experience administering antivenom.[3,9] In the United States, Poison Control consultation is available 24 hours per day, 7 days a week, by calling 1-800-222-1222 or using the online tool webPOISONCONTROL. A list of available antivenoms by region is available at www.toxinology.com.
Snake Envenomations: More Than Just a Bite
Diagnostics
In many instances of snake bites, there is little information to suggest if the snake was indeed dangerous or if the bite was dry. Some regions (eg, Australia) use wound venom tests to determine if a snake bite was venomous. However, negative tests may occur even in the setting of envenomation; therefore, administer wound care/cleaning and clinical care on the basis of the victim's condition. If toxicity is suspected or feared, patient observation for at least 24 hours is usually indicated.[10]
Diagnostic studies may be useful in addition to observation for the evaluation of the presence of venom effects. In general, laboratory studies are targeted at detecting evidence of significant muscle or tissue damage, and/or coagulopathy.[3,9] Consider obtaining the following laboratory studies:
- Complete blood cell count
- Levels of electrolytes (including potassium), creatine kinase, and lactate
- Renal function tests
- Prothrombin time (PT) / partial thromboplastin time (PTT) / international normalized ratio (INR)
- Levels of D-dimer / fibrinogen
- Urinalysis
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