Perspective

The two families of dangerously venomous snakes in North America are the pit vipers (family Crotalidae, subfamily Crotalinae) and the elapids (family Elapidae). Pit vipers found in the United States are the rattlesnakes (genera Crotalus and Sistrurus), cottonmouth water moccasins (Agkistrodon piscivorus), and copperheads (Agkistrodon contortrix). Mexico has a number of species of rattlesnakes and other genera of pit vipers (e.g., Bothrops, Bothriechis, Porthidium). The only indigenous elapids in North America are the coral snakes, which are found in the southern and southwestern part of the United States and Mexico. The coral snakes of the United States belong to two different genera—Micrurus (the eastern coral snake Micrurus fulvius and the Texas coral snake Micrurus tener) and Micruroides (the Sonoran coral snake Micruroides euryxanthus). Sixteen species of coral snakes are found in Mexico.¹

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).^11–15

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.

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

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

Fig. 139.2 Anatomic comparison of pit vipers, coral snakes, and nonvenomous snakes of the United States.

Pit vipers have a triangular-shaped head, elliptical pupils, heat-sensing pits, and a single row of subcaudal scales on the ventral aspect of the tail. Coral snakes are identified by their color pattern (see Fig. 139.4) because they have round pupils and a single row of subcaudal scales, as do most harmless snakes in the United States.

(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

Fig. 139.3 The eastern diamondback rattlesnake (Crotalus adamanteus), found in the southeastern United States, is the largest of the rattlesnakes in North America.

(Courtesy Michael Cardwell, Extreme Wildlife Photography.)

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.

Fig. 139.4 Venomous coral snakes in the United States can be identified by their color pattern, with the red and yellow bands being contiguous (bottom, the Texas coral snake, Micrurus tener). Harmless mimics such as the milk snake (top, the Mexican milk snake, Lampropeltis triangulum annulata) have red and yellow bands separated by black bands.

(Courtesy Charles Alfaro.)

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.

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

Fig. 139.6 Coral snake skull demonstrating the smaller fixed anterior maxillary fangs of these reptiles.

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

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.

Fig. 139.7 Extensive ecchymosis several days after a bite by a northern Pacific rattlesnake (Crotalus oreganus oreganus) on the victim’s pretibial region.

(Photo © Dr. Robert L. Norris.)

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.

Differential Diagnosis and Medical Decision Making

The differential diagnosis in a snakebite victim is generally limited. Most often the victim can recount being bitten by a snake. On rare occasion the victim may not have seen a snake, as when walking through high grass when bitten. In such cases, the presence of at least one puncture wound and progression of local and systemic findings are usually diagnostic. If the victim saw the snake but cannot adequately describe it, careful observation over time will reveal whether envenomation has occurred. Having color photographs on hand of the snakes found locally can aid in proper identification of the offending reptile.

Victims bitten by a coral snake almost always see the snake because of its need to actually chew on them to produce a significant bite. When a coral snake is implicated, the difficulty may be in differentiating the snake as a true coral snake versus a harmless coral snake mimic. Here again, color photos may help if the victim can recall the color pattern of the animal. All victims of a potential bite by a coral snake are observed carefully for at least 24 hours in the hospital because of the possible delay in onset of toxicity.

Young children have no innate fear of snakes and may be unable to describe precisely what bit them, particularly if they are preverbal. All children with possible venomous snakebites are admitted to the hospital for monitoring for at least 24 hours.

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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Jun 14, 2016 | Posted by admin in EMERGENCY MEDICINE | Comments Off on Venomous Snakebites 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)