Snake Bites: Corals and Crotalids
Lauren Harris, DVM, DACVECC
Envenomation by snakes is a common environmental emergency presented to the small animal veterinarian practicing in Florida. The eastern coral snake (Micurus fuvius fulvius, family Elapidae) has the most toxic venom of all North American snakes on a dry weight basis; however, the pit vipers (cottonmouth, rattlesnakes, copperhead), which belong to the family Crotalidae, are more commonly encountered.
The eastern coral snake is typically a brightly colored snake that has red and black rings interposed by bright yellow rings, and a black snout. The size of these snakes varies, and larger snakes are able to deliver 4-5 times the lethal dose of venom for an adult human. These snakes have short, hollow fangs, which typically induce minimal tissue reaction at the site of the bite.
The most relevant toxic component of the eastern coral snake venom is a neurotoxin, which blocks nicotinic acetylcholine receptors at the neuromuscular junction, leading to vasomotor instability, central nervous system depression, and muscular paralysis. Common clinical signs associated with eastern coral snake envenomation in dogs include weakness, vomiting, hypersalivation, decreased segmental reflexes, tetraparesis, and respiratory depression. The most common cause of death is respiratory paralysis. Hematologic abnormalities such as hemolysis, anemia, and ecchinocytosis may be seen in up to 50% of cases. In cats, acute, ascending, flaccid tetraparesis can be seen, as well as hypothermia and mental depression. Increases in creatinine kinase and aspartate aminotransferase activity are also commonly seen in cats.
While coral snake envenomation is rare, it should be considered as a differential diagnosis for acute lower motor neuron signs in any patient living in an environment where coral snakes are endemic. Other differentials for lower motor neuron disease include botulism, tick paralysis, polyradiculoneuritis, myasthenia gravis, drug reactions, anaphylaxis, and neuropathies associated with metabolic disease.
Treatment for coral snake envenomation includes coral snake antivenom if a bite is confirmed, however, coral snake antivenom is commonly unavailable (as its purchase requires a USDA import permit and approval by the state veterinarian) and efficacy is not always guaranteed. If envenomation is not known, it is reasonable to observe patients closely in the hospital for 36-48 hours as clinical signs may be delayed. If antivenom is not available, patients may be successfully managed with supportive care (including mechanical ventilation as required). Infection associated with coral snake bites have not been reported, therefore, antimicrobial therapy is not deemed necessary. Medications that suppress respiratory drive (such as narcotics) should be avoided. Unfortunately, there is no way to determine which envenomated patients will develop more severe clinical signs necessitating more advanced monitoring and treatment. In a recent retrospective study of coral snake envenomation in dogs and cats, the median time from envenomation to the development of clinical signs was 105 minutes. In this study, 71% of envenomated patients survived to discharge regardless of the treatment instituted.
Pit viper (crotalid) envenomation is relatively common in the United States. Physical characteristics of crotalids include their vertically elliptical pupils, a facial pit (heat sensing organ) between the eye and nostril, a triangular-shaped head, and two elongated canalicular maxillary fangs that rotate forward 90-degrees from the roof of the mouth at the time of the bite. In human envenomation by crotalids, 25% of the bites are considered to be “dry” bites.
Clinical signs associated with pit viper envenomation are commonly seen within 30 minutes of the bite; however, delayed effects may be seen over the first 24 hours of envenomation. The most common immediate signs may include hemorrhage, swelling, and pain at the bite site and around the site of the wound. Many (at least 50) enzymes contained within the snake venom have been identified. These enzymes lead to hematological abnormalities (including ecchinocytosis, spherocytosis, thrombocytopenia, hemolysis, coagulopathy), local wound damage (swelling, pain, bleeding, necrosis), and occasionally neurological impairment (depression, weakness, ataxia). A “snakebite severity score” should be used to assess the patient’s local wound, pulmonary, cardiovascular, gastrointestinal, hematologic, and nervous systems. This score can also be used for monitoring progression of disease associated with envenomation, however, it should not directly guide prognosis on an individual basis.
Hematological abnormalities, such as thrombocytopenia, coagulopathy, and ecchinocytosis, have been reported in 81% of pit viper envenomations. Diagnostic tests used to assess hematologic abnormalities associated with pit viper envenomation should include complete blood count, coagulation profile, and fibrinogen levels. Pigmenturia is also commonly seen, and may be a result of hematuria, myoglobinuria, or hemoglobinuira. Delayed, and often life-threatening complications may include severe anemia, renal failure secondary to pigmentary nephritis, and disseminated intravascular coagulation.
Treatment for the patient envenomated by a pit viper includes IV fluids for hypovolemia, antivenom to neutralize the venom, and analgesia. Fresh whole blood or packed red blood cell transfusions may be considered if there is substantial hemorrhage. The use of fresh frozen plasma is controversial, as its administration may provide more substrate for the venom. It is generally recommended that in the case of coagulopathy, additional antivenom should be given to neutralize the effects of the venom, rather than attempting to replenish clotting factors with fresh frozen plasma.
Antivenom administration is the mainstay of treatment for crotalid envenomation as it limits the progression of swelling and reverses coagulopathy. It is ideally given within 4 hours of envenomation; however, it may still have some beneficial effect if given within 24 hours. There are currently two approved antivenom products in the United States. Antivenin polyvalent (ACP) is a whole immunoglobulin product isolated from hyperimmunized horses. Crofab is a polyvalent immune Fab (Fab molecules cleaved from immunoglobulin of hyperimmunized sheep) that is more potent and less antigenic than the ACP product, however, due to its smaller molecular size, is also cleared more rapidly from the bloodstream. Anaphylaxis is a rare, but potentially life threatening complication of antivenom therapy.
The use of antihistamines and glucocorticoids for the treatment of crotalid snakebite envenomation is not recommended, as no studies have shown these drugs to be beneficial in terms of treating primary venom effects. Non-steroidal anti-inflammatory drugs are also not recommended, as they impair platelet function and can worsen the bleeding associated with envenomation. While antibiotics are commonly administered in the treatment of snakebite envenomation to prevent infection, a recent prospective study of 102 dogs with acute rattlesnake envenomation showed that only one of these patients developed infection. In both human and veterinary medicine, the use of prophylactic antibiotics for infection associated with snake envenomation is not recommended. Antibiotics should only be used when there is evidence of necrosis or abscessation associated with bite, and antibiotic selection should ideally be based on culture results.
Prognosis for crotalid envenomation depends on the severity of envenomation and institution of appropriate treatment in a timely manner. Veterinary studies have reported mortality rates ranging from 1-30%.