Local

Approximately 20% of bites by pit vipers lack any venom injection (dry bites).⁵ The only findings in such cases are puncture wounds or lacerations and minimal pain. Actual envenomation produces burning pain within minutes, followed by edema and erythema. Swelling progresses over the next few hours, and ecchymoses and hemorrhagic bullae may appear (Fig. 22-3). Involvement of the lymphatic system is common and heralded by lymphangitis and lymphadenopathy. With delayed or inadequate treatment, severe tissue necrosis can occur.

FIGURE 22-3 A case of severe envenomation by a western diamondback rattlesnake (Crotalus atrox) 4 days after the bite. Note the soft tissue swelling and hemorrhagic and serum-filled vesicles.

(Courtesy Dr. David Hardy.)

Systemic

Patients may complain of weakness, nausea, vomiting, perioral paresthesias, a metallic taste, and muscle twitching, although these systemic complaints are uncommon.⁶ Diffuse capillary leakage leads to pulmonary edema, hypotension, and eventually shock. In victims of severe bites, a consumptive coagulopathy can develop within 1 hour.⁴ Such patients can bleed spontaneously from almost any anatomic site, although clinically significant bleeding is uncommon, even in the face of significantly abnormal coagulation test results. Multifactorial acute renal failure resulting from direct nephrotoxins, circulatory collapse, myoglobinuria, and consumptive coagulopathy is possible. Laboratory abnormalities may include hypofibrinogenemia, thrombocytopenia, prolonged prothrombin and partial thromboplastin times, increased fibrin split products, elevated creatinine and creatine phosphokinase levels, proteinuria, hematuria, and anemia or hemoconcentration.^4,6

Unlike pit viper venoms, which tend to affect multiple organ systems, coral snake venom is primarily neurotoxic. Local injury is generally minimal or absent. Systemic signs of coral snake bites, including cranial nerve dysfunction and loss of deep tendon reflexes, may progress to respiratory depression and paralysis over a period of several hours. Differences in therapy make it important to distinguish between coral snake and pit viper bites.

Field Treatment

“Do no harm” first aid, consisting of rapid evacuation and proceeding to definitive care and immobilization, is the mainstay of first aid therapy. Removing the victim from the snake and placing him or her at rest is the first step. The wound is cleansed and immobilized at approximately heart level, if possible. Cryotherapy, suction, tourniquets, and electric shock therapy are harmful and ineffective. Therefore, these measures are not recommended. Most pit viper bites in the United States pose more of a threat to local tissues than to the life of the victim, and the use of any method to restrict venom to the bite site may be ill advised. The Australian pressure immobilization technique, in which the entire bitten extremity is snugly wrapped with a bandage, beginning at the bite site, and splinted, has been demonstrated in small studies to significantly limit the systemic spread of various snake venoms. This technique is the field treatment of choice for a non-necrotizing bite, such as from a coral snake,⁷ but may make the local necrosis worse after a pit viper bite. Field measures must not delay transport to the nearest hospital appropriately equipped to handle a venomous snakebite. At least experimentally, antivenom (antivenin) reduces soft tissue loss and improves function,⁸ and is probably time-dependent. In serious envenomations, delay in antivenin administration leads to greater tissue injury.

Hospital Management

Caution must be exercised when handling any snake brought in with the patient for identification. Even dead snakes and severed heads can still have a bite reflex for as long as 1 hour. Handling of these animals by untrained healthcare personnel, even when the animal is dead, is not recommended.

A rapid, detailed history of the incident, type of snake, field management, and previous antivenom exposure is important. Physical assessment emphasizes vital signs, cardiopulmonary status, neurologic examination, and wound appearance and size. The bitten extremity is marked at two or three locations so that circumferences can be measured every 15 minutes to judge the progression of local findings. Such measurements continue until the swelling has clearly stabilized.

Necessary laboratory analyses include a complete blood count, coagulation studies (prothrombin time, partial thromboplastin time, international normalized ratio [INR], fibrin degradation products, fibrinogen level), electrolyte, blood urea nitrogen, creatinine, and creatine phosphokinase levels, and urinalysis. No laboratory studies are necessary for a coral snake bite. A chest radiograph and electrocardiogram are obtained in older patients and anyone with systemic symptoms.

If the patient is completely asymptomatic 6 hours after a pit viper bite or 24 hours after a coral snake bite and all laboratory results are normal, it is unlikely that envenomation has occurred, and discharge is acceptable. All envenomated patients are best observed for at least 24 hours in the hospital.

Fasciotomy

The great majority of snakebites result in the subcutaneous deposition of venom. Venom that is deposited by larger snakes into muscle compartments, however, can result in an increase in intracompartmental pressure. Subfascial deposition of venom is more likely in areas with less subcutaneous tissue (e.g., fingers, toes, anterior lower leg). Clinically differentiating a true compartment syndrome from the typical swollen, painful extremity seen after subcutaneous envenomation is difficult and may require measurement of compartment pressure. Fasciotomies are considered only if pressures are documented to exceed 30 to 40 mm Hg despite antivenom treatment and elevation (Fig. 22-4). There is no role for routine or prophylactic fasciotomy in venomous snakebites.¹⁵ Preliminary animal evidence has suggested that fasciotomy may actually increase the severity of local myonecrosis in snake venom–induced compartment syndrome.¹⁶ When a fasciotomy is required for treatment of compartment syndrome, antivenom should be aggressively administered and no débridement of injured tissue should be performed, because this tissue may be viable with antivenin therapy.⁸ Negative-pressure wound therapy would seem a logical choice in the postoperative care of the patient following fasciotomy for intramuscular envenomation.

FIGURE 22-4 Fasciotomy of the forearm compartments in a victim of a severe rattlesnake bite on the hand. Intracompartmental pressures were documented to be exceedingly elevated in this patient, despite limb elevation and large doses of antivenom.

(Courtesy Dr. Robert Norris.)

Evaluation

Humans attacked by animals are at risk for blunt and penetrating trauma. Animals produce blunt injuries by striking with their extremities, biting with their powerful jaws, and crushing with their body weight. Teeth and claws can puncture body cavities, including the cranium, and amputate extremities. Patients with serious injuries are managed in a similar fashion as other potential polytrauma victims, with special attention given to wound management. Useful laboratory tests include a hematocrit when blood loss is of concern and cultures when an infection is present. Radiographs are obtained to diagnose potential fractures, joint penetration, severe infections, and retained foreign bodies, such as teeth. The patient’s tetanus status needs to be updated, as necessary.

Wound Care

Local wound management reduces the risk for infection and maximizes functional and aesthetic outcomes. Early wound cleansing is the most important therapy for preventing infection and zoonotic diseases such as rabies. Intact skin surrounding dirty wounds is scrubbed with a sponge and 1% povidone-iodine or 4% chlorhexidine gluconate solution. Alternatively, a 1% povidone-iodine solution can be used for irrigation, as long as the wound is flushed afterward with normal saline or water. Scrubbing the wound surface itself can increase tissue damage and infection and thus needs to be avoided. Wounds that are dirty or contain devitalized tissue are cleansed lightly with gauze or a porous sponge and sharply débrided.¹⁷

Options for wound repair include primary, delayed primary, and secondary closure. The anatomic location of the bite, source of the bite, and type of injury determine the most appropriate method. Primary closure is appropriate for head and neck wounds that are initially seen within 24 hours of the bite and for which aesthetic results are important and infection rates are low.^17,19,20 Primary closure can also be used for low-risk wounds to the arms, legs, and trunk if seen within 6 to 12 hours of the bite. Severe human bites and avulsion injuries of the face that require flaps have been successfully repaired by primary closure; however, this technique remains controversial. Wounds prone to the development of infection (Box 22-1), such as those initially seen longer than 24 hours after the bite (or longer than 6 hours if ear or nose cartilage is involved), are covered with moist dressings and undergo delayed primary closure after 3 to 5 days. Puncture wounds have an increased incidence of infection and are not sutured. Deep irrigation of small puncture wounds and wide excision have not proved beneficial. Larger puncture wounds, however, usually benefit from irrigation and débridement.²¹ Healing by secondary intention generally produces unacceptable scars in cosmetic areas. The clinician should be alert to the fact that significant dog bites may have extensive undermined areas created by the large canine teeth. These wounds require operative intervention under general or regional anesthesia.

Bites involving the hands or feet have a much greater chance of becoming infected and are left open.¹⁷ The primary goal in repairing bite wounds on the hand is to maximize functional outcome. Approximately one third of dog bites on the hand become infected, even with adequate therapy.²¹ Healing by secondary intention is recommended for most hand lacerations. After thorough exploration, irrigation, and débridement, the hand is immobilized, wrapped in a bulky dressing, and elevated.

A common human bite wound associated with high morbidity is a clenched fist injury (fight bite) resulting from striking another person’s mouth. Regardless of the history obtained, injuries over the dorsum of the metacarpophalangeal joints are treated as clenched fist injuries. These minor appearing wounds often result in serious injury to the extensor tendon or joint capsule and have significant oral bacterial contamination. The extensor tendon retracts when the hand is opened, so evaluation needs to be carried out with the hand in the open and clenched positions. Minor injuries are irrigated, débrided, and left open. Potentially deeper injuries and infected bites require exploration and débridement in the operating room and administration of IV antibiotics.²²

All bite injuries are reevaluated in 1 or 2 days to rule out secondary infection.

Microbiology

Given the large variety and concentration of bacteria in mouths, it is not surprising that wound infection is the main complication of bites, with 3% to 18% of dog bite wounds approximately 50% of cat bite wounds becoming infected. Infected wounds contain aerobic and anaerobic bacteria and yield an average of five isolates/culture (Box 22-2). Although many wounds are infected by Staphylococcus and Streptococcus spp. and anaerobes, Pasteurella spp. are the most common bacterial pathogen, found in 50% of dog bites and 75% of cat bites. Human bite wounds are frequently contaminated with Eikenella corrodens in addition to the microorganisms found after dog and cat bites.^22,23

Systemic diseases such as rabies, cat scratch disease, cowpox, tularemia, leptospirosis, and brucellosis can be acquired through animal bites. Human bites can transmit hepatitis B and C, tuberculosis, syphilis, and human immunodeficiency virus (HIV).²⁰ Although HIV transmission from human bites is rare, seroconversion is possible when a person with an open wound, either from a bite or a preexisting injury, is exposed to saliva containing HIV-positive blood.²⁴ In this scenario, baseline and 6-month postexposure HIV testing is performed and prophylactic treatment with anti-HIV drugs is considered.

Antibiotics

Although data are limited, preventive antibiotics are recommended for patients with high-risk bites.^17,21 The initial antibiotic choice and route are based on the type of animal and severity and location of the bite. Cat bites often cause puncture wounds that require antibiotics. Patients with low-risk dog and human bites do not benefit from prophylactic antibiotics unless the hand or foot is involved.²³ Patients seen 24 hours after a bite without signs of infection do not usually need prophylactic antibiotics. Routine cultures of uninfected wounds have not proved useful and are reserved for infected wounds.

Initial antibiotic selection needs to cover Staphylococcus and Streptococcus spp., anaerobes, Pasteurella spp. for dog and cat bites, and E. corrodens for human bites. Amoxicillin-clavulanate is an acceptable first-line antibiotic for most bites. Alternatives include second-generation cephalosporins, such as cefoxitin, or a combination of penicillin and a first-generation cephalosporin. Penicillin-allergic patients can receive clindamycin combined with ciprofloxacin (or combined with trimethoprim-sulfamethoxazole if the patient is pregnant or a child).^17,20 Moxifloxacin has also been suggested as monotherapy. Infections developing within 24 hours of the bite are generally caused by Pasteurella spp. and are treated by antibiotics with appropriate coverage. Patients with serious infections require hospital admission and parenteral antibiotics such as ampicillin-sulbactam, piperacillin-tazobactam, cefoxitin, ticarcillin-clavulanate or clindamycin combined with a fluoroquinolone, or trimethoprim-sulfamethoxazole.