Snake bite: Pit vipers, part 1 (Proceedings)

Article

Pit vipers are the largest group of venomous snakes in the United States and are involved in an estimated 150,000 bites annually of dogs and cats.

Pit vipers are the largest group of venomous snakes in the United States and are involved in an estimated 150,000 bites annually of dogs and cats.1 Approximately 99% of all venomous snake bites in the United States are inflicted by pit vipers. In North America members of the family Crotalidae belong to three genera: the rattlesnakes (Crotalus and Sistrurus sp) and the copperheads and cottonmouth water moccasins (Agkistrodon sp).

Pit vipers can be identified by their characteristic retractable front fangs, bilateral heat sensing "pits" between the nostrils and eyes, elliptical pupils, a single row of subcaudal scales distal to the anal plate, and triangular shaped heads. The rattlesnakes have special keratin rattles on the ends of their tails. The copperheads and water moccasins, are found throughout the eastern and central United States. Copperheads are responsible for the majority of venomous snake bites in North America. Water moccasins can be pugnacious and have a greater tendency to deliver venom when they bite. Rattlesnakes are found throughout the continental United States and account for the majority of deaths in animal victims.

Pit vipers control the amount of venom they inject during a bite. The amount of venom injected depends on the snake's perception of the situation. Initial defensive strikes are often nonenvenomating. Offensive bites meter a given amount of venom into the victim, and agonal bites deliver the entire venom load and are therefore the most dangerous. A severed snake head can bite reflexively for up to an hour after decapitation.

The severity of any pit viper bite is related to the volume and toxicity of the venom injected as well as to the location of the bite, which may influence the rate of venom uptake. As a generalization, the toxicity of pit viper venoms ranges in descending order from the rattlesnakes to the water moccasins and then to the copperheads. The toxicity of rattlesnake venom varies widely. Nine species and twelve subspecies of rattlesnakes have populations with venoms containing proteins that are immunologically similar to the potent neurotoxin mojave toxin (Table 1). It is possible for pit viper venom to be strictly neurotoxic with virtually no local signs of envenomation.

Table 1. Species of Rattlesnakes That Have Populations Containing Neurotoxin

Crotalus durissus durissus

Crotalus durissus terrificus var. cumanensis

Crotalus durissus terrificus (Brazil)

Crotalus horridus atricaudatus

Crotalus lepidus klauberi

Crotalus mitchellii mitchellii

Crotalus tigris

Crotalus vegrandis

Crotalus viridis abyssus

Crotalus viridis concolor

Crotalus scutulatus scutulatus (venom A)

Crotalus scutulatus salvini

Sistrurus catenatus catenatus

Pit viper venoms are a complex combination of enzymatic and nonenzymatic proteins. The primary purpose of the venom is not to kill but rather to immobilize the prey and predigest its tissues. The venom is 90% water and has a minimum of 10 enzymes and 3 to 12 nonenzymatic proteins and peptides in any individual snake. The nonenzymatic components, called the "killing fraction," have a median lethal dose (LD50) over 50 times smaller than that of the crude venom.

Differences in venom within a species induced by the age of the snake are highlighted by a study of northern Pacific rattlesnakes in which the adult venoms were shown to have approximately fivefold higher fibrinogenolytic protease activity2 . The complexity of the issue of variation of venom components is highlighted by the differences found in fibrinolysis and complement inactivation of venoms from different Blacktail rattlesnakes. In a study of 72 individual Blacktail rattlesnake venoms, the following conclusion was made: there were no venom differences as a function of geographic distribution; however, individual venom variability was significant enough to be identified as an important clinical reality.3

The enzyme phospholipase A is distributed throughout pit viper venoms. This enzyme catalyzes the hydrolysis of fatty ester linkages in diacyl phosphatides, which form lysophosphatides and release unsaturated and saturated fatty acids. There are many antigenically different isoenzymes. Some controversy exists about the extent of any neurotoxic effects that these isoenzymes may possess. Many cellular substances may be released by this enzyme, including histamine, kinins, slow-reacting substance, serotonin, and acetylcholine. The extent of the release of these physiologically active compounds most likely depends on the ability of phospholipase A to degrade membranes. The enzyme phospholipase B may also be present and is responsible for hydrolyzing lysophosphatides. Direct cardiotoxic effects of venom proteins have been exhibited in some pit viper venoms, particularly the diamondback rattlesnakes.

A key point is that the envenomation syndrome reflects the complexity of the venom. The body has to respond to the effects of multiple venom fractions, metabolize each, and deal with the resultant myriad of metabolites. In addition to the individual pharmacologic properties of these proteins and their metabolites, it has been demonstrated that some components act synergistically in producing specific effects or reactions. The net effect of this interaction of venom with the victim's response is a metabolic stew of toxic peptides and digestive enzymes. Additionally, the traditional categorization of pit vipers as having only hematoxic venoms should be reevaluated because some subpopulations of rattlesnakes possess only neurotoxic venom.

The onset of clinical signs after a snake bite may be delayed for several hours. This phenomenon is highlighted by the fact that 40% of all severe envenomations in humans are graded as mild to nonenvenomating sometime during the syndrome. In humans it is estimated that 20% of all pit viper bites are nonenvenomating (i.e., dry), with an additional 25% classified as mild envenomations. It is for this reason that so many antidotal treatments are championed, and it also emphasizes the need to rely on scientific evaluation for the various treatment modalities proposed.

The victim affects the severity of an envenomation by such factors as species of victim, body mass, location of bite, post-bite excitability, underlying pre-existing medical conditions and resultant medications. The snake affects the severity of the envenomation by species and size of snake, age of snake, motivation of snake, and degree of venom regeneration since last use (Table 2).

Table 2. Variables Affecting the Severity of Envenomation

Victim

Body mass

Bite location

Time to medical facility

Type of first aid applied

Concurrent medications (nonsteroidal anti-inflammatory drugs, etc.)

Snake

Species

Size

Age of snake

Motivation for bite

Time since last venom use

Time of year

Cats are more resistant, on the basis of milligram of venom per kilogram body mass, to pit viper venom than dogs. However, cats generally present for veterinary care in a more advanced clinical condition. This is likely due to the cat's smaller body size and the proclivity of cats to play with the snake, thereby antagonizing it and inducing an offensive strike, often to the torso. Because dogs generally receive more defensive strikes, have a larger body mass, and more frequently seek immediate human companionship after injury, they are more likely to receive medical attention promptly.

It is possible that a life-threatening envenomation may occur with no local clinical signs other than the puncture wounds themselves. Local tissue reactions to pit viper envenomation include puncture wounds, one to six from a single bite, which may be bleeding. Occasionally these fang wounds appear as small lacerations. Rapid onset of pain may ensue with development of progressive edema. Ecchymosis and petechiation may become manifest. Tissue necrosis may occur, particularly in envenomations to areas without a significant subcutaneous tissue mass. The presence of fang marks does not indicate that envenomation has occurred, only that a bite has taken place.

Systemic clinical manifestations include pain, weakness, dizziness, nausea, severe hypotension, thrombocytopenia, fasciculations, regional lymphadenopathy, alterations in respiratory rate, increased clotting times, decreased hemoglobin, abnormal electrocardiogram, increased salivation, echinocytosis of red cells, cyanosis, proteinuria, bleeding (e.g., melena, hematuria, hematemesis), obtundation, and convulsions. Not all of these clinical manifestations are seen in each patient, and they are listed in descending order of frequency as seen in human victims.

Severe hypotension results from pooling of blood within the shock organ of the species bitten (i.e., the hepatosplanchnic [dogs] or pulmonary [cats] vascular bed) and fluid loss from the vascular compartment secondary to severe peripheral swelling. This swelling can be significant.

The victim's clotting anomalies largely depend on the species of snake involved. Coagulopathies range from direct blockage or inactivation of various factors in the patient's clotting cascade to the possible destruction of megakaryocytes in the circulating blood and bone marrow. Approximately 60% of envenomated patients develop a coagulopathy, by far the most common is hypofibrinogenemia with prolonged clotting times. Venom induced thrombocytopenia occurs in approximately 30% of envenomations with an untreated nadir usually occurring between 72 and 96 hours.

Monitoring of the severity and progression of the clinical envenomation syndrome may be difficult. A tool that has proven useful is the envenomation severity score system (figure 1). Use of this system more accurately quantifies the severity of the patient's condition over time, and allows a more objective assessment of the patient.4 It is recommended that a severity score be acquired upon entry, 6 hours, 12 hours and 24 hours post initial hospitalization.

Figure 1.

Snakebite Severity Score

Pulmonary System

0: Signs within normal limit

1: Minimal - slight dyspnea

2: Moderate - respiratory compromise, tachypnea, use of accessory muscles

3: Severe - cyanosis, air hunger, extreme tachypnea, respiratory insufficiency or respiratory arrest from any cause

Cardiovascular System

0: Signs within normal limits

1: Minimal - tachycardia, general weakness, benign dysrhythmia, hypertension

2: Moderate - tachycardia, hypotension (but tarsal pulse still palpable)

3: Severe - extreme tachycardia, hypotension (non-palpable tarsal pulse or systolic blood pressure < 80 mmHg), malignant dysrhythmia or cardiac arrest

Local Wound

0: Signs within normal limits

1: Minimal - pain, swelling, ecchymosis, erythema limited to bite site

2: Moderate - pain, swelling, ecchymosis, erythema involves less than half of extremity and may be spreading slowly

3: Severe - pain, swelling, ecchymosis, erythema involves most or all of one extremity and is spreading rapidly

4: Very severe - pain, swelling, ecchymosis, erythema extends beyond affected extremity, or significant tissue slough

Gastrointestinal System

0: Signs within normal limits

1: Minimal - abdominal pain, tenesmus

2: Moderate - vomiting, diarrhea

3: Severe - repetitive vomiting, diarrhea, or hematemesis

Hematological System

0: Signs within normal limits

1: Minimal - coagulation parameters slightly abnormal, PT<20 sec, PTT <50 sec, platelets 100,000-150,000/mm3

2: Moderate - coagulation parameters abnormal, PT 20-50 sec, PTT 50-75 sec, platelets 50,000-100,000/mm3

3: Severe - coagulation parameters abnormal, PT 50-100 sec, PTT 75-100 sec, platelets 20,000-50,000/mm3

4: Very Severe - coagulation parameters markedly abnormal with bleeding present or the threat of spontaneous bleeding, including PT unmeasurable, PTT unmeasurable, platelets < 20,000/mm3

Central Nervous System

0: Signs within normal limits

1: Minimal – apprehension

2: Moderate - chills, weakness, faintness, ataxia

3: Severe - lethargy, seizures, coma

Total Score Possible.......................................0 to 20

A complete blood count with differential, including platelet counts, should be obtained; red blood cell morphology along with baseline serum chemistry with electrolytes should be collected. A coagulation profile should be obtained including activated clotting times, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and fibrin degradation products. Urinalysis with macro- and microscopic evaluations including free protein and hemoglobin-myoglobin should be performed. These laboratory tests should be repeated periodically to monitor the progression of the syndrome and/or the effectiveness of therapy.

Circumferential measurements of the affected body part at, above, and below the bite site at set time intervals aid in objective monitoring of the progression of the swelling secondary to many pit viper bites. Transient (within 48 hours) echinocytosis has been reported in dogs after envenomation, and its presence is an indicator of envenomation. However, absence of this morphologic change is not an indicator of lack of envenomation.5

References

1. Peterson M, Meerdink G: Venomous bites and stings. In Kirk R (ed): Current Veterinary Therapy X. Philadelphia, WB Saunders, 1989, pp. 177–186.

2. MacKessy S: Fibrinogenolytic proteases from venoms of juvenile and adult northern Pacific rattlesnakes (Crotalus viridis oreganus). Comp Biochem Physiol B Comp Biochem 1993; 106: 181–186.

3. Rael E, Rivas J, Chen T, et al: Differences in fibrinolysis and complement inactivation by venom from different northern blacktail rattlesnakes (Crotalus molossus molossus). Toxicon 1997; 35: 505–513.

4. Dart R, Hulburt K, Garcia R, Brown J: Validation of a severity score for the assessment of crotalid snakebite. Ann Emerg Med 1996; 27:3: 321-326.

5. Brown D, Meyer D, Wingfield W, et al: Echinocytosis associated with rattlesnake envenomation in dogs. Vet Pathol 1994; 31: 654–657.

6. Stewart M, Greenland S, Hoffman J: First-aid treatment of poisonous snakebite: Are currently recommended procedures justified? Ann Emerg Med 1981; 10: 331–335.

7. McNalley J, Dart R, O'Brien P: Southwestern rattlesnake envenomation database (abstract). Vet Hum Toxicol 1987; 29: 486.

8. Johnson E, Kardong K, MacKessy S: Electric shocks are ineffective in treatment of lethal effects of rattlesnake envenomation in mice. Toxicon 1987; 25: 1347–1349.

9. Howe N, Meisenheimer Jr J: Electric shock does not save snakebitten rats. Ann Emerg Med 1988; 17: 254–256.

10. Russell F, Ruzic N, Gonzales H: Effectiveness of antivenin (crotalidae) polyvalent following injection of crotalus venom. Toxicon 1973; 11: 461–464.

11. Brown J: Effects of pH, temperature, antivenin and functional group inhibitors on the toxicity and enzymatic activities of Crotalus atrox venom. Toxicon 1966; 4: 99–105.

12. Snyder C, Knowles J, Pickens J, et al: Snakebite poisoning. In Catcott E (ed): Canine Medicine. Santa Barbara, American Veterinary Publications, 1968, p. 256.

13. Smith M, Ownby C: Ability of polyvalent (crotalidae) antivenin to neutralize myonecrosis, hemorrhage and lethality induced by timber rattlesnake (Crotalus horridus horridus) venom. Toxicon 1985; 23: 409–424.

14. Malasit P, Warrell D, Chanthavanich P: Prediction, prevention, and mechanism of early (anaphylactic) antivenom reactions in victims of snakebites. Br Med J 1986; 292: 17–20.

15. Christopher D, Rodning C: Crotalidae envenomation. South Med J 1986; 79(2): 159–162.

16. Bond R, Burkhart K: Thrombocytopenia following timber rattlesnake envenomation. Ann Emerg Med 1997; 30: 40–44.

17. Kerrigan K, Mertz B, Nelson S, et al: Antibiotic prophylaxis for pit viper envenomation: prospective controlled trial. World J Surg 1997; 21: 369–372.

18. Clark R, Selden B, Furbee B: The incidence of wound infection following crotalid envenomation. J Emerg Med 1993; 11: 583–586.

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