Overview

This overview discusses the clinical features and treatment of snakebites in Kentucky and nearby regions. Victims may suffer a wide range of symptoms ranging from local irritation with the dry bite (no envenomation), to life threatening systemic toxicity necessitating antivenin administration. The fatality rate is surprisingly low. The greatest challenge in treating these patients centers on the decision to give antivenin.

Epidemiology

The American Association of Poison Control Centers National Data Collection System reported 2814 crotalid snakebites in 2003, one of which was fatal. (15) Most bites in the United States result from snakes of the family Crotalidae. These are commonly referred to as Crotalids, or pit vipers. The term pit viper comes from the infrared heat sensing pits located just behind and below each nostril.(9) There are three genera of Crotalidae. The genera Crotalus and Sistrurus comprise all species of rattlesnakes, and the genus Agkistrodon comprises copperheads and cottonmouths (water moccasins). The family Elapidae are responsible for less than 0.5% of all bites. They are not endemic to the Midwestern region, existing only in the southeastern and Southwestern United States. An example of the typical elapid would be the brightly colored coral snake.

In Kentucky, four species of Crotalids are responsible for most envenomations. The exceptions are bites from non-indigenous snakes occurring in zoo personnel or with private collectors. The four species are Agkistrodon contortrix or copperhead, Agkistrodon piscivorus or cottonmouth, Crotalus horridus or timber rattlesnake, and Sistrurus miliarius or pigmy rattlesnake. The Kentucky Regional Poison Center annually receives reports on 60 - 100 copperhead bites, 2 - 10 timber rattlesnake bites, and 1 -2 cottonmouth bites. Pigmy rattlesnake bites are uncommon.

The bite of the copperhead is usually the least severe of the group, requiring antivenin administration less frequently. However, significant local effects were reported in one third of patients in one study. (11) Most bites occur in the summer months. Both the snakes, and the victims are more active and more likely to come in contact with one another then. One study cited 95% of all bites occurring between the months of April and October.(7) All of the bites in this particular study were on the extremities; 60% were on the lower extremity. Although there was a wide age range, the means age was 26 with males bitten more commonly than females.

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Snake identification

The pit vipers have triangular shaped heads, elliptical pupils, and a single row of subcaudal scales distal to the anal plate. As the name implies, copperheads are distinguished by their copper colored heads. The head of the cottonmouth is dark, with a distinctive white buccal mucosa. The rattles on rattlesnakes are located distal to the subcaudal plates.

Pharmacology/Pathophysiology

Crotalid venom is a complex mixture of many different toxins.(5) Ninety percent of the dry weight consists of protein and polypeptides. Venom components will vary not only between species, but also within the same species depending on geography, season, age and nutritional status of the snake. Crotalid venom contains proteolytic enzymes, which cause tissue damage. Various neurotoxins, hematologic toxins, and cardiac toxins are also found.

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Clinical Features

The clinical features of snakebite are distinct, with a wide range of severity.(5) The amount of venom injected will vary depending on the age and health of the snake. Snakes attempt to regulate the amount of venom injected relative to the size of their prey, an ability that is believed to be underdeveloped in juvenile snakes. It is thought that the size of a human being confuses the sensory input of the snake, often resulting in a dry bite. (14) Dry bites occur in up to 20% of cases. Venom is typically deposited in the dermal or subcutaneous tissue, and rarely intramuscularly. It is subsequently absorbed by lymphatic tissue.

The dry bite will present with local pain and irritation, whereas the most severe envenomations may result in coagulopathy, hypotension, shock, or even death. Pain is a generally an early and persistent feature of snakebites. Fang marks may or may not be present. Envenomation may occur without obvious fang marks. (7) If envenomation does occur, tissue edema and ecchymoses will ensue as the toxins begin to affect the microvasculature. Tissue edema commonly progresses to involve the entire extremity. Ecchymoses may progress as well and hemorrhagic blebs commonly appear. Frank tissue necrosis may occur in later stages. Lymphadenopathy and lymphangitis may occur, and usually represent inflammation rather than secondary bacterial infection.

Rarely compartment syndrome will occur. It is more commonly described with intramuscular injection of venom. Compartment syndrome presents with typical symptoms of pain (especially with passive motion), parasthesias, pallor, and sometimes paralysis. The clinical diagnosis of compartment syndrome can be difficult in light of ongoing pain, edema, hemorrhage, and swelling. Elevated CK levels are expected secondary to muscle necrosis and rhabdomyolysis and may occur in the absence of compartment syndrome.

Coagulopathy may range from mild to severe. Bleeding is usually a problem only in the most severe cases. Although true DIC is rare, it has been reported. Bleeding times may become prolonged and thrombocytopenia may develop. Fibrin split products may be elevated, but d-dimer, anti-thrombin III, and factor XIII levels are normal (except in true DIC).

Fluid losses from third spacing, and sometimes vomiting, may cause hypovolemia and hypotension. Rarely, anaphylaxis may occur, particularly if the patient has been sensitized from a previous bite. Rapid cardiovascular collapse and refractory hypotension have been described for the rare case when venom is injected intravascularly.

Renal damage may occur, usually in the form of acute tubular necrosis (ATN). ATN is usually due either to hypoperfusion secondary to hypovolemia, or rhabdomyolysis. However, cortical necrosis has been described in severe envenomations.

Rarely pulmonary edema will occur, but usually represents ARDS rather than left ventricular failure. Bites to the face, mouth, or tongue may result in life threatening edema and prompt, pre-emptive intubation is mandatory.

Many patients experience various nonspecific symptoms. Nausea and vomiting are common, and diarrhea may be a feature as well. Weakness, diaphoresis, malaise, perioral or digital parasthesias may occur. Myokymia is seen with timber rattler bites and mild fasciculations are possible with most crotalid bites. Weakness or paralysis are extremely rare, and are more commonly described with the Mojave rattlesnake of the southwestern United States.

These signs and symptoms generally manifest early on, and progress steadily depending upon degree of envenomation. If no clinical or laboratory evidence of venom toxicity exist six hours after a bite from a snake indigenous to Kentucky, then envenomation is highly unlikely. It is important to realize that significant coagulopathy and thrombocytopenia may occur without significant edema or pain at the bite site. Possible late sequelae include persistent extremity pain and edema, and wound infection.

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Treatment of crotalid envenomation

Pre-hospital
The most important measure is rapid transport to a health care facility that has the ability to administer antivenin. Many different pre-hospital treatments have been proposed.8 Their efficacy is generally controversial. Immobilization of the patient is recommended. Movement may promote propagation of the venom and increase risk of systemic effects prior to reaching the controlled hospital environment. Local ice should not be used as necrosis related to vasoconstriction in poorly perfused tissues may occur. Some authors recommend constricting bands, but only if they can be precisely pressure regulated so as to obstruct lymphatic and superficial drainage without obstructing venous or arterial flow. Constricting bands carry the risk of increasing tissue necrosis distal to the band.

Although some older studies have advocated incision and suction, this practice is fraught with danger. In addition to local skin, nerve or tendon damage, necrosis is promoted and increased wound infection rates may result. Commercial venom extractors have been shown to remove some venom in animal models. However, these devices have not been shown to decrease morbidity and mortality. Incisions should never be made and the use of commercial suction devices should not delay or substitute for trained medical attention.

Hospital
The wound should be cleansed and immobilization continued. Elevation may decrease edema. It is helpful to demarcate the limits of edema so as to monitor propagation. Serial circumferential limb measurements may be useful. It is best not to bandage the wound, and tape should not be used, as further tissue damage may occur when later removed

Intravenous access in the uninvolved limb is essential. Inadequate fluid resuscitation is common. If symptoms are present or if the bite is suspected to have been caused by a venomous snake, obtain a CBC, PT and PTT. If the patient presents with significant symptoms or if the bite is suspected to be from a venomous snake other than a copperhead, then other laboratory studies may be required, such as fibrinogen and fibrin split products.

Tetanus immunization should be administered as needed. Although the incidence of wound infection is low, it may be difficult to distinguish between infection and tissue effects related to the envonomation. Antibiotic use may be warranted based on clinical judgment.

For a suspected crotaline bite from an indigenous snake in Kentucky, the patient should be observed for a minimum of 4 to 6 hours. If other than mild local symptoms develop, or if laboratory abnormalities such as coagulopathy are present, hospitalization is warranted. Opioid analgesia may be necessary. Aspirin and non-steroidal anti-inflammatory agents should be avoided because of their platelet inhibiting effects. Antivenin is generally the initial treatment for coagulopathy. Consider blood products if antivenin is ineffective, for active bleeding, or if the patient is unstable. Fasciotomy is rarely necessary. (4) If compartment syndrome is suspected, measurement of compartment pressures should be done (not possible in the digits). The initial treatment of compartment syndrome is antivenin. Fasciotomy should be done only if antivenin is not effective.

Antivenin is indicated for pit viper bites which result in systemic manifestations (eg coagulopathy, hypotension) or significant local manifestations (eg compartment syndrome). Exact indications for antivenin in some settings are poorly defined and controversial. When in doubt, consult with someone familiar with snakebites such as a poison center (1-800-222-1222) or medical toxicologist. Antivenin is seldom needed for copperhead bites. However, this is under study and future recommendations may change. (6) Although copperheads uncommonly cause systemic symptoms, they do result in significant local manifestations and morbidity. (11,13)

A newer antivenin, CroFab(R) was recently introduced in the US. (2,3,10) It is an ovine-derived product, composed of purified Fab antibody fragments derived from the venoms of the Western Diamondback, Eastern Diamondback, Mojave Rattlesnake, and Water Moccasin. Although CroFab(R) would be expected to be active against Copperheads, initial studies did not address this. A recent retrospective study suggests that CroFabÒ may be effective in the treatment of Copperhead bites. (6) Its Fab structure results in significantly fewer immunologic side effects as compared to the polyvalent crotaline antivenin marketed by Wyeth. The Wyeth product is expected to be phased out and is unlikely to be available in the near future.

Skin testing is not necessary with CroFabÒ. The package insert recommends that initial 4 to 6 vials should be used. If initial control of envenomation effects is not achieved, an additional dose of 4 to 6 vials should be used. Subsequent maintenance doses of 2 vials every 6 hours (X3) are recommended. Patients need to be monitored for immunologic side effects, although this is less likely with CroFabÒ than the older whole antibody product. Recurrent coagulopathy and bleeding complications may occur and patients need to be monitored for this. (1,10,12)

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References/Bibliography

1. Boyer LV, Seifert SA, Cain JS: Recurrence phenomena after immunoglobulin therapy for snake envenomations: part 2. Guidelines for clinical management with crotaline Fab antivenom. Ann Emerg Med 2001;37:196-201.
2. Dart RC, McNally J: Efficacy, safety, and use of snake antivenoms in the United States. Ann Emerg Med 2001;37:181-188.
3. Dart RC. Seifert SA, Carroll L, et al: Affinity-purified, mixed monospecific crotalid antivenom ovine fab for the treatment of crotalid venom poisoning. Ann Emerg Med 1997;30:33-39.
4. Hall EL: Role of surgical intervention in the management of crotaline snake envonomation. Ann Emerg Med 2001;37:175-180.
5. Holstege CP, Miller MB, Wermuth M, et al: Crotalid snake envenomation. Crit Care Clin 1997;13:889-921.
6. Lavonas EJ, Gerardo CJ, O’Malley G, et al: Initial experience with crotalidae polyvalent immune fab (ovine) antivenom in the treatment of copperhead snakebite. Ann Emerg Med 2004;43:200-208.
7. Lawrence WT, Giannopoulos A, Hansen A: Pitviper bites: rational management in locales in which copperheads and cottonmouths predominate. Annals of Plastic Surgery 1996;36:276-285.
8. McKinney PE: Out-of-hospital and interhospital management of crotaline snakebite. Ann Emerg Med 2001;37:168-174.
9. Roberts JR, Otten EJ: Snakes and Other Reptiles. In: Goldfrank LR, Flomenbaum NE, Lewin NE, Howland MA, Hoffman RS, Nelson LS, eds: Goldfrank's Toxicologic Emergencies, 7th ed. New York, NY, McGraw-Hill, pp. 1552-1567.
10. Ruha AM, Curry SC, Beuhler M, et al: Initial postmarketing experience with crotalidae polyvalent immune fab for treatment of rattlesnake envenomation. Ann Emerg Med 2002;39:609-615.
11. Scharman EJ, Noffsinger VD: Copperhead snakebites: clinical severity of local effects. Ann Emerg Med 2001;38:55-61.
12. Seifert SA, Boyer LV: Recurrence phenomena after immunoglobulin therapy for snake envenomations: part 1: pharmacokinetics and pharmacodynamics of immunoglobulin antivenoms and related antibodies. Ann Emerg Med 2001;37:189-195.
13. Spiller HA, Bosse GM: Prospective study of morbidity associated with snakebite envenomation. J Toxicol Clin Toxicol 2003;41:125-130.
14. Strong JL, Hunter KS, Enderson BL: Venomous snakebites, Tenn Med 1997; pp 414 – 415.
15. Watson WA, Litovitz TL, Klein-Schwartz W. 2003 annual report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 2004;22:335-404.

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AUTHOR INFORMATION

Written by: Jason Mattingly, M.D. and George Bosse, M.D. 3/2001
Revised: Geroge Bosse, M.D. 11/2005

Reviewed by: Henry Spiller, M.S., D.ABAT 3/2001

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