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

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)
Blood gases (arterial or venous)	May demonstrate hypoxia and/or hypercapnia in the presence of respiratory insufficiency as a result of neurotoxicity	Consider in cases of severe envenomation (hypotension, shock, respiratory distress) or if significant underlying comorbidity is present
Urinalysis	Normal
Electrocardiogram	Variable; possible ischemia	Obtain in cases of severe envenomation or in patients with significant underlying comorbidity
Chest radiograph	Usually normal; possible aspiration	Obtain in cases of severe envenomation or in patients requiring endotracheal intubation
Bedside pulmonary function testing	Variable; may reveal lowered peak flow in early respiratory embarrassment	May use to monitor respiratory status (at first sign of diminished flow, consider early airway control and assisted ventilation)

APTT, Activated partial thromboplastin time; INR, international normalized ratio; PT, prothrombin time

Treatment

Prehospital Management

Field management focuses on providing reassurance and rapid transport to a facility equipped with antivenom. If possible to do so safely, the snake is identified. No attempt should be made to capture or kill the snake, although it may be possible to photograph the animal if a digital camera is available.

No first aid measures have ever been proved to be beneficial in victims of pit viper bites. For victims bitten by a coral snake, the Australian pressure-immobilization technique is applied quickly in the field to limit the spread of venom. This involves wrapping the entire bitten extremity snugly in an occlusive wrap followed by the application of a splint (Fig. 139.8). Victims must then be carried from the field for the technique to be effective.²⁴ Rescuers may have difficulty applying the technique in correct fashion in that they tend to underestimate the degree of pressure that needs to be exerted under the wrap.²⁵ The pressure-immobilization technique has been shown to significantly limit the spread of venom after elapid snakebites²⁶ and was effective in one small animal study using eastern coral snake (M. fulvius) venom.²⁷ Although the pressure-immobilization technique may limit the spread of pit viper venom as well, it may actually exacerbate local tissue damage by restricting tissue-destroying venom to the bite site, and it should not be used for such bites.

Fig. 139.8 Australian pressure-immobilization technique for field management of nonnecrotizing elapid snakebites (e.g., coral snakes).

(Adapted from original drawing by Commonwealth Serum Laboratories. With permission.)

Hospital Management

Hospital management of snakebite victims begins with assessment of respiratory and circulatory status. The patient is initially administered oxygen, and cardiac and pulse oximetry monitoring is begun while the emergency physician takes a directed history and performs a focused physical examination. It is uncommon for snakebite victims in North America to initially be seen with significant respiratory compromise. In patients bitten by coral snakes or rattlesnakes with neurotoxic venom, however, difficulty with airway patency and breathing can develop.

If signs of neurotoxicity are presence and any shortness of breath or difficulty speaking or swallowing develops, the airway should be promptly and definitively secured by endotracheal intubation to prevent aspiration. If the victim shows any signs of dehydration or shock, fluid resuscitation is begun with the administration of 1 to 2 L of normal saline (20 to 40 mL/kg for children). If the blood pressure does not respond promptly to crystalloid infusion, albumin is added because it may remain in the leaky vasculature for a longer period. Vasopressors are used only as a last resort after adequate intravascular volume repletion has been achieved.²⁸ Inadequately treated hypotension is a key aspect in many cases of fatal snake envenomation.^29,³⁰

Once the ABCs (airway, breathing, and circulation) have been addressed, an attempt is made to identify the offending snake. If the victim has brought the snake to the hospital, extreme caution should be used in examining it, even if it appears to be dead. A severed snake head can have a bite reflex for up to an hour following death and is capable of inflicting a serious bite.³¹^–³³

Circumferences of the bitten extremity are marked and measured at the bite site and at one or two sites more proximally every 15 minutes during the early stages of envenomation. This offers an objective measure of the progression of local swelling. If the circumferences are increasing, the envenomation is progressing and administration of antivenom is indicated.

The key to management of significant envenomation is antivenom administration. Initial decisions on antivenom administration are guided by the clinical findings (Box 139.1).

Pit Viper Antivenom

The current antivenom available in the United States for pit viper bites, Crotalidae polyvalent immune Fab, ovine (CroFab; BTG International, Inc., West Conshohocken, PA), is produced by immunizing sheep with the venom of four different pit vipers. The ovine IgG antibodies obtained are further refined by digestion with papain to yield Fc and Fab fragments. The Fc fragments—responsible for inducing many acute anaphylactoid reactions to antivenom—are discarded, and the protective Fab fragments are isolated with affinity column chromatography. CroFab is packaged in a lyophilized state and requires reconstitution before administration.

Antivenom administration is described in detail in Box 139.2 and in the Tips and Tricks box. Antivenom is effective in reversing most systemic and laboratory derangements seen following snake envenomation. However, its ability to reverse thrombocytopenia, rhabdomyolysis, or myokymia is variable.^9,^35,³⁶ Antivenom’s efficacy in preventing local tissue damage has never been definitively demonstrated. If given very early in the course, it may reduce or limit permanent local damage to some slight degree.

Box 139.2 Administration of Antivenom

Pit Viper Antivenom Administration

Obtain informed consent if possible.

Expand the patient’s intravascular volume with normal saline if safe to do so (e.g., no history of congestive heart failure).

Begin reconstitution of antivenom as soon as its need is evident because this process takes time (see the Tips and Tricks box).

Have epinephrine at the bedside, ready to administer immediately in the event of an acute reaction to the antivenom.

CroFab

Dilute the starting dose in 250 mL of normal saline.

Starting dose (children receive the same dose of antivenom as adults):

• Nonenvenomation (dry bite)—0 vials

• Progressive local findings only—4 vials

• Evidence of systemic toxicity—4 to 6 vials

Initially administer antivenom intravenously at a slow rate with the emergency physician at the bedside to intervene in the event of an acute (anaphylactoid) adverse reaction.

If tolerated, after 5 to 10 minutes increase the rate of infusion to allow the entire dose to be administered in 1 hour.

Observe the patient for 1 hour after administration—if findings of envenomation continue to worsen, repeat the starting dose (and continue this sequence until stable; generally no more than two initial doses are required).

Once the patient’s condition is stabilized, admit the patient (to an intensive care unit if any evidence of instability, otherwise to a regular bed) for observation and further management (e.g., wound care; see text).

After stabilization, repeat the dosing of CroFab, 2 vials every 6 hours for 3 additional doses, to prevent recurrence of the effects of the venom.

Coral Snake Antivenom Administration

The basic principles (e.g., informed consent and presence of epinephrine at the bedside) are the same as for pit viper antivenom administration.

Use the manufacturer’s product information to determine proper dosing.

Victims bitten by a coral snake should be admitted to a closely observed setting to allow early detection of any deterioration.

Tips and Tricks

As soon as it is clear that antivenom is indicated, have the pharmacy or nursing staff begin reconstitution of the appropriate number of vials to be given. Reconstitution can be labor-intensive and, if the manufacturer’s recommended procedure is used, can take almost 30 minutes to prepare each vial.

By using 25 mL of sterile water per vial (as opposed to the 10 mL recommended by the manufacturer) and hand mixing via continuous rolling and inverting of the vials, the reconstitution time can be reduced to less than 2 minutes per vial.³⁴

Coral Snake Antivenom

At the time of this writing, production of coral snake antivenom has ceased in the United States, with the current remaining stock set to expire October 31, 2012. Coral snake antivenom is still produced in Mexico (Coralmyn, Instituto Bioclon), but it is not commercially available in the United States. There is reportedly a plan in place for Pfizer to resume production of Micrurus antivenom in the United States.³⁷

Even though the onset of neurotoxic findings following a bite by a coral snake may be delayed, once they start, they may be rapidly progressive and relatively unresponsive to antivenom administration. Management of a victim of a serious bite by a coral snake (definitively identified Micrurus specimen, particularly M. fulvius, and effective penetration of the fangs into the victim’s skin) ideally includes prompt administration of antivenom before evidence of neurotoxicity begins. In the absence of appropriate coral snake antivenom, these victims must be managed conservatively, including securing the airway at the first sign of difficulty swallowing or breathing and providing mechanical ventilation (possibly for many days). If appropriate antivenom is available, it should be administered according to the manufacturer’s guidelines, and all the precautions outlined for administration of pit viper antivenom should be taken (see Box 139.2). Pit viper antivenom is of no benefit to victims of bites by a coral snake.

No antivenom is available for Sonoran coral snake (M. euryxanthus) bites, but this species is quite small and inoffensive and has never caused a known fatality.³⁸ Management is purely supportive.

Other Treatment Considerations

Blood products are rarely needed for victims of venomous snakebites, even with significant coagulopathy noted on laboratory tests.³⁹ Aggressive antivenom administration always precedes the administration of any blood products to avoid feeding further substrate to an ongoing venom-induced consumptive coagulopathy.

Wound management of pit viper bites includes placing the extremity in a well-padded splint and elevating it above heart level to reduce swelling. Tetanus prophylaxis is given if needed. Prophylactic antibiotics are not necessary unless misdirected first aid measures included incisions into the bite wound or mouth suction. In such cases, a broad-spectrum antibiotic (to cover both gram-positive and gram-negative bacteria) is administered in standard doses. Pit viper bites in the United States rarely become infected. When they do, however, antibiotic therapy is guided by wound culture testing. Tissue that is clearly necrotic is débrided after the patient is stabilized and once any attendant coagulopathy has been reversed. Intact blebs and blisters are left undisturbed, and those that rupture are conservatively unroofed. Physical therapy is started as early as possible to return the patient to an optimal level of functioning.

Indications for obtaining any consultations that may be needed are listed in Box 139.3.

Next Steps: Admission and Discharge

All patients with any evidence of envenomation are admitted to the hospital for further observation and management. If the envenomation is severe, the victim is admitted to an intensive care unit. If it appears that the snake did not inject any venom (i.e., a dry bite—no signs or symptoms of envenomation, simple puncture wounds only), the victim is observed in the emergency department for a minimum of 8 hours. After 8 hours, victims who remain asymptomatic, with normal vital signs and laboratory results, are discharged in the care of a responsible adult and told to return if any evidence of envenomation occurs. Dry bites occur in as many as 20% of pit viper bites, although the precise reason for this remains unclear.^6,⁴⁰ Any child with a possible venomous snakebite is admitted to the hospital regardless of the presence or absence of signs or symptoms of poisoning. Likewise, victims of a possible bite by a coral snake are admitted for observation because of the significant delay that can occur before any evidence of envenomation is apparent.

Documentation

Record a careful history in the patient’s own words, including a description of the snake.

Record the results of a thorough screening physical examination.

Have nursing staff measure and record the circumferences of the bitten extremity every 15 minutes until the swelling has stabilized and then every hour for 24 hours.

Note the specifics of any discussion with consultants (e.g., poison control specialists).

Measure and record intracompartmental pressures if concern arises about the development of compartment syndrome.

Document informed consent (for antivenom administration or fasciotomy) if possible.

Complications

Adverse Reactions to Antivenom

Adverse reactions to antivenom include early, acute reactions (which are probably anaphylactoid in nature [also known as nonallergic anaphylaxis]) and delayed serum sickness, an immunoglobulin (IgG and IgM) immune complex–mediated disease. Anaphylactoid reactions may be manifested as hives, wheezing, laryngeal edema, abdominal pain, vomiting, diarrhea, and hypotension. The incidence of anaphylactoid reactions to CroFab is approximately 15%,⁴¹ with most reactions being minor and easily treated (Box 139.4).⁴² Serum sickness occurs in approximately 3% of patients treated with CroFab⁴¹ and may be manifested approximately 1 to 2 weeks after administration as fever, urticaria, myalgia, arthralgia, renal dysfunction, or neuropathy (or any combination of these signs). Serum sickness is easily treated with oral steroids (e.g., prednisone, 1 to 2 mg/kg orally per day) administered until the symptoms resolve, followed by a 2-week tapering of the dose. Oral antihistamines may provide additional symptomatic relief. Before discharge from the hospital, patients are warned to watch for signs and symptoms of serum sickness and told to return if they occur.

Box 139.4 Management of Acute Reactions to Antivenom (Allergic or Nonallergic Anaphylaxis)

Immediately stop the infusion.

Treat the signs and symptoms in standard fashion (airway management as needed, epinephrine, crystalloid infusion, antihistamines [H₁ and H₂ blockers], steroids, and vasopressors as needed).

In most cases the antivenom can be restarted (with the emergency physician at the bedside) once the reaction abates. If the reaction was severe and appears more life-threatening than the envenomation, a decision may be made to withhold further antivenom therapy. It is very helpful to consult an expert on snake envenomation in such cases.

Compartment Syndrome

Some larger rattlesnakes have fangs long enough to penetrate deeply into muscle compartments. Because many significant pit viper bites result in swollen extremities that are discolored and painful on any attempted range of motion, it can be difficult to determine when a compartment syndrome is imminent. This complication is actually rare following pit viper bites, but if there is concern about rising intracompartmental pressure, it is objectively measured with any standard technique. If the pressure is elevated above 30 to 40 mm Hg, the limb is further elevated, more antivenom is administered, and mannitol is given (1.0 g/kg intravenously over a 30-minute period) if the patient is hemodynamically stable.⁴³ If the compartment pressure remains high 1 hour after these measures have been carried out, fasciotomy is considered. Although animal research has suggested an actual increase in myonecrosis following fasciotomy,⁴⁴ there is still a risk for ischemic neuropathy following unabated rises in compartment pressure. It is important to obtain informed consent, if possible, before proceeding with fasciotomy.

Recurrent Coagulopathy

Patients in whom coagulopathy develops during the initial stages of pit viper envenomation may have delayed recurrence of abnormal coagulation studies for up to 2 weeks following the bite.^42,⁴⁵ This is probably related to continued absorption of venom components from the depot site after all antivenom administered has been cleared from the body, particularly when a low-molecular-weight Fab antivenom (e.g., CroFab) is used. In most cases, delayed coagulopathy is benign, without evidence of clinically significant bleeding, but severe complications, including intracranial bleeding, have been reported.^46,⁴⁷ Patients are warned of this possibility and instructed to avoid any elective surgery, contact sports, and other high-risk activities for a few weeks following the bite. Although administration of antivenom for delayed coagulopathy may be helpful, it is likely to be less effective than in the acute stages of envenomation. Reasonable indications for administering further antivenom in these cases are outlined in Box 139.5.

Patient Teaching Tips

Never approach, torment, or attempt to catch or kill a venomous or unidentified species of snake.

Do not keep any species of venomous snake as a “pet.”

Never handle a venomous snake that you believe is dead. These snakes may still have a bite reflex and can inflict a serious or fatal bite.

If bitten by a venomous or unknown snake, proceed immediately to the nearest hospital for evaluation. No first aid measures are effective or necessary following bites by pit vipers.

If you have been treated for a venomous snakebite with antivenom, watch for signs of serum sickness (fever, muscle aches, joint aches, hives, or bleeding) in the first 2 weeks after you leave the hospital. If such signs occur, follow up immediately with your physician.

Avoid any elective surgery, contact sports, or high-risk activities for 2 to 3 weeks after a pit viper bite because your blood may not clot normally during this period.

Facts and Formulas

Measurement of Intracompartmental Pressure

If lower than 30 to 40 mm Hg, continue antivenom as indicated along with limb elevation and monitoring.

If higher than 30 to 40 mm Hg, give additional antivenom, keep the limb elevated, administer mannitol (1 g/kg intravenously if the patient’s hemodynamic status allows), observe for 1 hour, and then recheck intracranial pressure.

If the pressure falls below 30 to 40 mm Hg, continue nonoperative treatment. If intracranial pressure remains elevated, consider fasciotomy (with informed patient consent).

Red Flags

Cautions for the Physician

Remain vigilant for worsening severity of venom poisoning; it can progress rapidly and suddenly. Conversely, the onset of clinical findings may be delayed for hours.

Obtain consultation early from a clinician knowledgeable in snake envenomation (e.g., a regional poison control center specialist) whenever needed.

Obtain informed consent whenever possible before giving antivenom.

Give antivenom as soon as possible after its need is identified.

Remain at the patient’s bedside during the initiation of antivenom therapy to intervene if an acute reaction occurs.

Have epinephrine available at the bedside before beginning antivenom infusion.

If a compartment syndrome is suspected, obtain objective measurements of intracompartmental pressure.

If fasciotomy is indicated, obtain and document informed consent.

Cases involving snake envenomation in the United States often end up in medicolegal litigation. Document carefully.

Prognosis

Deaths attributable to bites by endemic snakes are rare in the United States, with only 33 reported to the American Association of Poison Control Centers in the 26-year period from 1983 to 2008.¹ This is an underestimate of the total number of deaths because snakebite is not a reportable condition, but it does reflect the limited toll of snakebite in terms of loss of life in the United States. Deaths are even more infrequent in Canada, whereas in Mexico, as many as 150 people die each year of venomous snakebites.⁴³ The case fatality rate following venomous snakebite in the United States when antivenom is used is less than 1%.⁴⁹ However, long-term complications, such as loss of some degree of function in the bitten extremity, are more likely. Approximately 10% of victims will be left with some functional disability following pit viper bites, and this does not include permanent dysfunction directly related to surgical procedures.⁴³ The incidence of disability may actually be higher if careful, delayed evaluation of extremity function is performed (e.g., using goniometry and precise sensory testing).⁵⁰

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Venomous Snakebites in North America

Perspective

Epidemiology

Pathophysiology

Anatomy

Presenting Signs and Symptoms

Differential Diagnosis and Medical Decision Making

Diagnostic Testing

Treatment

Prehospital Management

Hospital Management

Pit Viper Bite

Coral Snake Bite

Pit Viper Antivenom

Pit Viper Antivenom Administration

CroFab

Coral Snake Antivenom Administration

Coral Snake Antivenom

Other Treatment Considerations

Next Steps: Admission and Discharge

Complications

Adverse Reactions to Antivenom

Compartment Syndrome

Recurrent Coagulopathy

Prognosis

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