Volume 61 | Issue 1 Article 8 1999 Pit Viper Envenomation In Dogs: Pathophysiology and Treatment David Senter Iowa State University Tom Carson Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Veterinary Pathology and Pathobiology Commons, Veterinary Physiology Commons, Veterinary Toxicology and Pharmacology Commons, and the Zoology Commons Recommended Citation Senter, David and Carson, Tom (1999) "Pit Viper Envenomation In Dogs: Pathophysiology and Treatment," Iowa State University Veterinarian: Vol. 61 : Iss. 1 , Article 8. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol61/iss1/8 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Pit Viper Envenomation In Dogs: Pathophysiology and Treatment DAVID SENTER, DVMt, AND TOM CARSON, DVM, PH.D.tt inflicted by rattlesnakes. 1 Members of the Crotalidae (pit viper) family account for the large majority (95%) of poisonous snakebites. The three main genera in this family are Cro­ talus (rattlesnake),Agkistrodon (copperhead, cottonmouth water moccasin), and Sistrurus (pygmy rattler, massasauga).2 Among these groups, there are at least 26 subspecies of rattlesnakes, five subspecies of copperheads, three subspecies of cottonmouths, three sub­ species of pygmy rattlesnakes, and three sub­ species of massasauga.1 Members of the pit viper family get their name from the facial pits that exist between the nostril and the eye which function to detect heat and vibration. 1,2 Other distinguishing characteristics of the Copperhead (Agkistrodon contortix). This species crotalids include triangular shaped heads, re­ enjoys widespread distribution across the U.S., tractable fangs, a single row of subcaudal ranging from Texas and Oklahoma in the south· west, Iowa to the northwest, New York and Massa· scales, and vertical, elliptical shaped pupils. chusetts to the northeast, and Florida to the south· All pit vipers have movable fangs that inject east. This species is among the most commonly a voluntarily controlled amount ofvenom.2 encountered pit vipers in the U.S., however it is also among the least dangerous in terms of venom toxicity and volume of injection. Pathophysiology In general, pit viper venom is considered Venomous snakes occur throughout a very hemotoxic and proteolytic as opposed to many wide geographic area within the United snakes that are predominately neurotoxic. 3 States. In certain areas of the country, snake­ The Mojave green rattlesnake (Crotalus bites in dogs are diagnosed on a regular basis scutulatus scutulatus) is an exception as its during the warm months of the year when venom contains a very substantial quantity snakes are most active and people and their of neurotoxin. Venom constituents vary con­ pets are most likely to be spending time in siderably between snakes of different species areas that snakes inhabit. The best treatment as well as between individuals within a spe­ for snakebite is a controversial subject among cies depending on geographic location, age, veterinarians and there is no single treatment and season of the year. protocol. Therefore, it is necessary for a clini­ Of the three genera in the pit viper fam­ cian to understand the pathophysiology be­ ily, the rattlesnakes have the most potent hind envenomation in order to make educated venom with the eastern and western diamond­ decisions as to the treatment of each indi­ back rattlesnakes accounting for 95% of fa­ vidual patient. talities in man.2The relative toxicity of venom An estimated 15,000 domestic animals are from several North American snakes are listed bitten by snakes annually in the United in Table 1. States. Approximately 80% of fatal bites are Snake venom consists of a diverse mix­ ture of peptides, enzymes, and proteins. At 'Dr. David Senter is a 1998 graduate of the Iowa State least 26 different enzymes have been defined, University College of Veterinary Medicine. ten of these are common to all pit viper ven­ "Dr. Tom Carson is a professor in the Department of Pathology specializing in toxicology at the Iowa State oms. One major enzyme is hyaluronidase University College of Veterinary Medicine. which allows the venom to spread and pen- VOL 61, No 1; SPRING 1999 21 Table 1. Venom Toxicity of Some North American Snakes! Snake Median Lethal Dose LD50(mg / kg-l}* Rattlesnakes (Crotalus) Mojave (C. scutulatus scutulatus) 0.23 Eastern diamondback (C. adarnanteus) 1.68 Western diamondback (C. atrox) 2.18 Timber (C. horridus horridus) 2.69 Pygmy rattlesnakes (Sistrurus) Pygmy (8. miliaris) 2.85 Massassauga (8 catentatus) 2.91 Moccasins (Agkistrodon) Cottonmouth (A. piscivorus) 4.19 Copperhead (A. contortrzx) 10.92 LD50 values are from a study which adminisU!red venom intravenously in 18 to 26 gm mice. etrate tissues by decreasing the viscosity of ocytopenia. Several attempts to measure the connective tissue. 1,4 Another major component amount of histamine released after contact is phospholipase ~ which disrupts cell mem­ with snake venom have been perfQrmed by branes, uncouples phosphorylation, inhibits various in vitro tests with mixed results. How­ cellullar respiration, and may release hista­ ever, no in vivo direct test of the histamine­ mines, kinins, and serotonin. Phospholipase releasing activity of Crotalus species venom A;, acts by liberating arachidonic acid from has been reported.3 The nonenzymatic polypeptide component of Crotalidae venom has more of a direct effect on the cardiovascu­ lar and respiratory system. Cardiovascular System A lethal factor in Crotalus species venom dis­ rupts the basal lamina and collagen of the capillaries allowing for leakage of red blood cells and plasma through the endothelial membrane.l ,3 Petechia, ecchymosis, and exten­ sive edema are commonly seen due to the vas­ Prairie rattlesnake, Western rattlesnake, Green cular destruction and increased vascular per­ rattlesnake (Crotalus viridis). This species is meability. Approximately one-third of the total found in all U.S. states west of a line from the circulating fluid volume can be lost into an Dakotas to Texas. It is a locally common species affected extremity within hours of envenoma­ with a variable temperanlent. Despite its rela­ I tively small size, envenomation by this species tion. ,3 Furthermore, severe hypotension com­ has resulted in human fatalities. monly occurs due to pooling of blood in the hepatosplanchnic bed in dogs. 4 This combina­ membrane phospholipids which is then con­ tion can ultimately lead to hemoconcentration, verted to various prostaglandins (PGI2, PGE2, lactic acidosis, and hypovolemic shock. PGF2<) and thromboxane A;,.3 Prostaglandin Some envenomated patients will have E2 and PGI2 cause vasodilation and decrease concurrent thrombocytopenia which may be systemic arterial pressure that contributing due to the aggregation of platelets to areas of to hypotension. Another component, throm­ damaged endothelium and the production of boxane A;" is a potent inducer of platelet ag­ thromboxane A;,and PGE2 from phospholipase gregation which may contribute to thromb- A;,. Venoms from several species of rattle- 22 IOWA STATE UNIVERSITY VETERINARIAN flaccid paralysis. However, its greatest effect is on motor axon terminals of the diaphragm and respiratory paralysis may not occur for several hours after envenomation. Urinary System Most pit viper venoms, especially those of the western diamondback rattlesnake and the prairie rattlesnake, cause myonecrosis which could cause the release ofmyoglobin.5 There­ fore, if severe envenomation has occurred, the Mojave rattlesnake, l ..U .....'., nephrotoxic effects of myoglobinuria may re­ (Crotalus scutulatus). Mojave rattlers are sult in acute renal failure. Other potential unique among rattlesnake species in that their venom contains a significant neurotoxic compo­ nephrotoxic factors include hemoglobinuria nent. Per volume, this venom is the most highly (some venoms cause intravascular hemolysis), toxic of all the North American pit vipers. This defibrination syndrome, and hypovolemic species ranges from southwest Utah to south· shock. ern Nevada and the Mojave De ert region and southward to central Mexico. Clinical Signs and Diagnosis snakes have been shown to have direct plate­ Snake envenomation can be difficult to diag­ let-aggregating properties.3 nose ifthe incident was not witnessed. Clini­ In general, snake venom has very com­ cal signs may vary greatly depending on the plex effects on blood coagulation. Many ofthe species of snake involved and the quantity and rattlesnake venoms studied cause the forma­ . toxicity of the venom injected. The potency of tion of an imperfect fibrin clot which results the venom depends on several factors such as in pure defibrination and high levels of fibrin age ofthe snake (young snakes have high pep­ degradation products.3 This cause is differen­ tide fractions), the volume of venom regener­ tiated from disseminated intravascular coagu­ ated since the last bite, aggressiveness of the lation (DIC) by the fact that platelets and fac­ snake, and motivation of the snake (offensive tor VIII are not consumed. Unlike with DIC, strikes are usually more severe).! In addition, this condition is not inhibited by heparin. the enzymatic fraction ofthe venom is