Venomous Snakebites in North America

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139 Venomous Snakebites in North America

Epidemiology

Pit vipers inflict approximately 99% of the 7000 to 8000 venomous snakebites that occur in the United States each year.2,3 The incidence of venomous snakebite is lower in Canada and higher in Mexico, although precise numbers are hard to determine.

Pathophysiology

Snake venom, particularly pit viper venom, is a complex mixture of enzymes, low-molecular-weight (nonenzymatic) proteins, metallic ions, and other constituents.4,5 The venom is highly variable, depending on the species of snake; its geographic origin; its age, health, and diet; and the time of year.6 Among the most important components found in pit viper venom are phospholipase A2 enzymes, which cause cellular disruption and tissue damage; hyaluronidase, which facilitates the distribution of venom within tissues; and thrombin-like enzymes, which affect various aspects of the coagulation cascade and lead to coagulation abnormalities.

Also of major importance in pit viper venom–induced coagulopathy are metalloproteinases known as hemorrhagins, which increase vascular permeability and damage endothelial cells.7,8 Some rattlesnakes, such as certain specimens of Mohave rattlesnakes (Crotalus scutulatus), possess neurotoxic components in their venom. These presynaptically acting toxins prevent the release of acetylcholine at neuromuscular junctions. Depending on their geographic location, Mohave rattlesnakes may possess this component and are termed venom A–producing rattlesnakes.9,10

Other rattlesnakes that may, based on their geographic origin, possess neurotoxic components closely related to Mohave toxin include the eastern diamondback rattlesnake (Crotalus adamanteus), the timber rattlesnake (Crotalus horridus), the southern Pacific rattlesnake (Crotalus oreganus helleri), and the tiger rattlesnake (Crotalus tigris).1115

Coral snake venom is less complex than pit viper venom but is among the most toxic venom in North America. The primary effects of coral snake venom are neurotoxic and are due to a component in the venom that blocks the postsynaptic end plates at neuromuscular junctions.16,17

Anatomy

Pit vipers get their name from the sensitive heat receptors (foveal organs) located on the anterior of their heads, slightly below and between the nostril and eye (Fig. 139.1). These organs aid the snake in finding prey, aiming its strike, and determining the volume of venom to be injected. Other characteristics typical of a pit viper include a triangular-shaped head (also found in many nonvenomous snakes), elliptical (catlike) pupils, and in the United States, the presence of a single row of scales that spans the underside of its tail (Fig. 139.2). Nonvenomous snakes in the United States generally have a double row of scales crossing the ventral aspect of the tail. Rattlesnakes can also usually be identified by the keratin plates that make up their unique caudal rattle.

image

Fig. 139.1 The heat-sensing pits or foveal organs of pit vipers.

(Adapted from original drawing by Marlin Sawyer. With permission.)

Pit vipers range in size from the diminutive pygmy rattlesnake (Sistrurus miliarius), typically 40 to 50 cm in length, to the massive eastern diamondback rattlesnake (C. adamanteus), which can attain lengths of greater than 1.5 m (Fig. 139.3).18

Coral snakes are identified in the United States by their characteristic color pattern—red, yellow, and black bands that completely encircle the body, with the red and yellow bands being contiguous. In harmless coral snake mimics, such as milk snakes (Lampropeltis spp.), the red and yellow bands are separated by a band of black (Fig. 139.4). Color patterns cannot, however, be used outside the United States to reliably identify coral snakes.

Venomous snakes possess venom-producing glands in the upper jaw, behind the eyes (Fig. 139.5). These glands produce the venom that at the time of a bite is passed via ducts to the hollow, needle-like fangs on the anterior maxillae. In pit vipers, these fangs range in length (proportional to the snake’s overall length) from just a few millimeters to more than 2.5 cm.18 The fangs are folded up against the roof of the snake’s mouth when not in use. During a bite, the pit viper opens its mouth widely and swings its fangs into an upright position to drive them into the tissues of its target. Venom is then injected via a set of investing musculature. The speed of a pit viper’s strike has been clocked at 8 feet per second19—faster than a human being can react.

image

Fig. 139.5 The venom apparatus of pit vipers.

(Adapted from original drawing by Marlin Sawyer. With permission.)

The venom delivery apparatus of a coral snake is less sophisticated than that of a pit viper. Coral snakes have slightly enlarged, anterior, maxillary fangs fixed in an erect position, with which they inject venom (Fig. 139.6). For a coral snake to produce envenomation, it must chew on its victim for a few seconds. Bites by coral snakes frequently involve someone intentionally picking the snake up, often after misidentifying it as a harmless snake.20

Presenting Signs and Symptoms

The signs and symptoms of pit viper envenomation are broken down into local and systemic findings. Locally, the victim will have puncture wounds, although the pattern may be misleading and cannot be used to reliably differentiate between a venomous bite and a bite by a harmless snake. Generally, severe, burning pain develops at the bite site within minutes, followed shortly by local swelling that can progress over time to involve the entire bitten extremity and even the trunk. There may be persistent bloody oozing from the fang marks, indicative of coagulopathy. Ecchymosis may be present at the site and, more remotely, as hemorrhagins induce vascular leaks and loss of red blood cells, in tissues (Fig. 139.7). Over several hours to days, blisters and blebs may form on the extremity, particularly at the bite site. These lesions are filled with clear serous fluid or bloody exudate.

Systemically, victims have a myriad of complaints, which can include nausea, vomiting, and dizziness; numbness of the mouth, tongue, or extremities; muscle fasciculations (myokymia); and shortness of breath. The victim’s vital signs may be abnormal. Patients with severe bites may be tachycardic and hypotensive.

In the early stages, hypotension is due to systemic vasodilation. Later, the hypotension is compounded by third spacing of fluids into the bitten extremity and potentially hemolysis.19 Some pit vipers, such as venom A–producing Mohave rattlesnakes, may produce few local signs and symptoms but may cause more systemic toxicity, particularly neurotoxic findings such as ptosis and difficulty swallowing and breathing.

Bites by a coral snake generally cause little in the way of local findings, and their fang marks may be difficult to see.21 Swelling is usually slight and pain is variable (mild to more pronounced). Victims of significant bites by a coral snake may have a delay in the onset of systemic findings, sometimes for many hours.22 Signs of neurotoxicity may then develop, with the earliest findings being altered mental status and cranial nerve dysfunction (e.g., ptosis). Neurotoxicity can progress to frank skeletal muscle paralysis and respiratory failure.

Diagnostic Testing

In the initial phase of evaluating a victim of a potential pit viper bite, a complete blood count and coagulation studies are repeated every 1 to 2 hours as long as the findings are normal (Table 139.1). If an abnormality appears (e.g., diminished platelets or fibrinogen), antivenom should be administered (see later) and laboratory tests rechecked every 6 hours thereafter until stable. This 6-hour period after antivenom administration is necessary for a healthy liver to replete coagulation factors.

Table 139.1 Diagnostic Testing in Victims of a Potential Venomous Snakebite in North America

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DIAGNOSTIC STUDY VENOM EFFECTS COMMENTS
Potential Pit Viper Bite
Complete blood count
 White blood cell count May be elevated without evidence of infection Caused by stress demargination
 Hemoglobin/hematocrit Variable; may be normal, elevated, or decreased May be elevated if dehydrated, may be low if bleeding or hemolysis is present
 Platelets May be low or very low May see early profound thrombocytopenia
Metabolic panel
 Renal function tests Usually normal May be abnormal if delayed renal dysfunction occurs
 Hepatic function tests Usually normal May be abnormal with delayed hepatic dysfunction or underlying liver disease (e.g., alcohol abuse)
Coagulation studies
 PT, APTT, INR May be elevated Abnormalities related to consumptive coagulopathy
 Fibrinogen May be reduced
 Fibrin degradation products May be elevated
 D-dimer May be elevated
Type and screen Venom effects and antivenom can interfere with this process23 Obtain on first available blood drawn; blood product replacement is rarely necessary, however
Blood gases (arterial or venous) May demonstrate metabolic acidosis or hypoxia, depending on the clinical scenario Consider in cases of severe envenomation (hypotension, shock, respiratory distress) or if significant underlying comorbidity; use caution in those with coagulopathy
Urinalysis Hematuria, proteinuria Test each voided sample until the patient is stable; positive blood on bedside testing in the absence of red blood cells on microscopic analysis may indicate myoglobinuria
Electrocardiogram Variable; possible ischemia Obtain in cases of severe envenomation or in patients with significant underlying comorbidity
Chest radiograph Pulmonary edema, aspiration Obtain in cases of severe envenomation or in patients with significant underlying comorbidity
Computed tomography Variable May be indicated if evidence of intracranial, intraabdominal, or retroperitoneal bleeding in patients with consumptive coagulopathy (based on clinical findings)
Potential Coral Snake Bite
Complete blood count
 White blood cell count May be elevated without evidence of infection Caused by stress demargination
 Hemoglobin/hematocrit Normal  
 Platelets Normal  
Metabolic panel
 Renal function tests Normal  
 Hepatic function tests Normal May be abnormal if underlying liver disease (e.g., alcohol abuse)
Coagulation studies All normal  
Type and screen   Unnecessary (no need for blood products)