Human bites may be the most common bites seen in many urban emergency rooms. The main clinical problem in human bites relates to soft tissue infection since human saliva contains up to 1011 bacteria/mL, and plaque on teeth has even greater numbers of bacteria. Common infecting organisms include Streptococcus viridans, Staphylococcus spp., Eikenella corrodens, Bacteroides spp., and microaerophilic streptococci. The most common serious infections develop when there has been penetration of the joint capsule, which typically occurs when a clenched fist strikes the tooth of the person being assaulted (“fight bite”). These wounds usually involve the metacarpophalangeal (MCP) or the proximal interphalangeal (PIP) joints. These are usually benign-appearing wounds and are frequently missed unless the examiner is aware of the potential problems of joint penetration. Such wounds may not be directly over the MCP joint unless the hand is examined with the fist clenched. These wounds should be seen in consultation with a hand surgeon and are usually best treated with intraoperative irrigation, intravenous antibiotics, and elevation of the hand and arm but should not be treated on an outpatient basis. In general, human bites should not be closed, with the exception of wounds on the face.
Antibiotic prophylaxis for human bites consists of ampicillin plus a beta-lactamase inhibitor (intravenous ampicillin/sulbactam or amoxicillin/clavulanate). Alternative agents include cefoxitin or ampicillin alone or in combination with clindamycin. Although the incidence is unknown, hepatitis and infection with human immunodeficiency virus (HIV) are potentially transmissible by human bites. As with other exposures, the risk of infection depends on the size of the inoculums and the virulence of the viral agent. HIV exists in relatively low concentrations in human saliva and is relatively fastidious, presumably making its transmission difficult. Hepatitis B and C require a much smaller inoculum, and their transmission in a human bite is theoretically a greater risk. If the individual responsible for the bite is known or available for evaluation, serologic testing for HIV and hepatitis B and C is recommended. If the individual responsible for the bite is unavailable for testing, the administration of gamma globulin and hepatitis B vaccination should be considered in nonimmunized patients. Tetanus immunization should be given if indicated40 (see Table 47-4).
Cat bites, like human bites, tend to be heavily contaminated. Cats tend to leave deep, small punctures that may penetrate all the way to bone. Commonly isolated organisms include Pasteurella multocida and Staphylococcus spp. Ampicillin plus a beta-lactamase inhibitor provides reasonable empiric coverage and tetanus and rabies prophylaxis should be given if indicated (Tables 47-3, 47-4, 47-10, and 47-12).
Table 47-10 Treatment Recommendations and Estimates of the Risk of Rabies, According to Type of Exposure and Geographic Area |Favorite Table|Download (.pdf)
Table 47-10 Treatment Recommendations and Estimates of the Risk of Rabies, According to Type of Exposure and Geographic Area
|Treatment Recommendationsch47_fn06,ch47_fn07||Cases of Rabies/10,000 Untreated Exposuresch47_fn07|
|Geographic Area||Animalsch47_fn05||Bite||No Bite||Bite||No Bite|
|Group 1: rabies endemic or suspected in species involved in the exposure||Bats anywhere in the United States; raccoons, skunks, foxes; mongooses in Puerto Rico; dogs in most developing countries and in the United States along Mexican border (3–80% rabid)||Treat||Treat||150–5,000||0.3–160|
|Group 2: rabies not endemic in species involved in the exposure, but endemic in other terrestrial animals in area||Most wild carnivores (wolves, bobcats, bears) and groundhogs (2–20% rabid)||Treat||Treat or consult||10–1,200||0.2–40|
|Dogs and cats (0.1–2% rabid)||Observe or consult||Observe or consult||0.5–120||0.01–4|
|Rodents and lagomorphs except groundhogs (about 0.01% rabid)||Consult or do not treat||Do not treat||0.05–0.6||0.001–0.02|
|Group 3: rabies not endemic in species involved in the exposure or in other terrestrial animals in the area||Dogs, cats, many wild terrestrial animals in Washington, Idaho, Utah, Nevada, Colorado (0.1–0.01% rabid)||Consult or do not treat||Consult or do not treat||0.05–6||0.001–0.2|
Dog bite wounds are another common clinical problem. Wound concerns center around injury to soft tissue since large dogs can generate tremendous force with their muscles of mastication. Soft tissue infections following dog bites are not as common as after cat and human bites, but they do occur. The bite wound should be copiously irrigated, and empiric preventive antibiotics are generally recommended. Facial dog bite wounds are usually closed, while wounds in other locations are managed with delayed primary closure or healing by secondary intention. Common infecting organisms include P. multocida, S. viridans, Bacteroides spp., Fusobacterium, and Capnocytophaga. As in the case of human and cat bite wounds, ampicillin plus a beta-lactamase inhibitor provides reasonable empiric coverage for dog bite wounds. Tetanus and rabies prophylaxis should be administered if indicated (see Tables 47-3, 47-4, 47-10, and 47-12).40
A number of different strains of highly neurotropic viruses cause clinical rabies infection. Most of these viruses belong to a single serotype in the genus Lyssavirus, family Rhabdoviridae. The virion contains a single-stranded, nonsegmented, negative-sense RNA genome, which encodes for five structural proteins.102 Guidelines for the administration of rabies vaccine as well as for tetanus among others vaccines following traumatic injuries have been published by the Surgical Infection Society of North America.40
Susceptibility to rabies infection varies according to species, although most wild mammals can become infected with the virus. Foxes, coyotes, wolves, and jackals are most susceptible; skunks, raccoons, bats, bobcats, mongooses, and monkeys are intermediate; and opossums are surprisingly resistant.102
In the United States, rabies is found in terrestrial animals in 10 distinct geographic areas. In each of these areas, one species is the predominant reservoir, with one of the distinct antigenic variants predominating. Bats account for an additional eight variants, accounting for sporadic outbreaks throughout the United States. The majority of the cases of rabies encephalitis acquired in the United States probably originate from exposure to bats. The epidemiology of human rabies reflects the geographic distribution of animals, emphasizing the fact that rabies is primarily a disease of nonhuman mammals. Vaccination programs for domestic animals in the United States have been responsible for a dramatic decline in rabies acquired from domestic dog and cat bites (Tables 47-10 and 47-11). Internationally, the majority of human rabies is still acquired from dog bites, where canine rabies is still endemic.102
Table 47-11 Human Rabies Cases in the United States by Exposure Category, 1946–1995a |Favorite Table|Download (.pdf)
Table 47-11 Human Rabies Cases in the United States by Exposure Category, 1946–1995a
|Years||Domestic||Wildlife||Other||Unknown (%)||Case Total|
In humans, the established disease is almost always fatal. The diagnosis is relatively straightforward when a history of an animal bite is obtained; however, the history of a probable bite is inconsistently reported. Clinical symptoms of human rabies include pain at the bite site, dysphagia, pharyngeal spasms, paralysis, hydrophobia, and seizures. Distinguishing rabies from other causes of viral encephalitis or tetanus can be difficult. An effective vaccine is available for preventing the onset of clinical rabies. The dismal prognosis of rabies encephalitis emphasizes the importance of appropriate use of the vaccine and Ig preparations to prevent infection.
The risk of acquiring rabies depends on the probability of rabies infection in the animal and the amount of inoculum delivered into the wound, with the greatest risk from a bite. All animal wounds should be irrigated and cleansed with soap or a detergent. This has been shown to protect 90% of experimental animals from infection following inoculation of rabies virus into a wound.
Because public health officials monitor the incidence of rabies in populations of domestic and wild animals, a treating physician should be familiar with the local incidence of rabies in his or her region. Several historical clues may be of benefit in determining the likelihood that the animal was rabid. If the bite was unprovoked or the animal was behaving erratically prior to the bite, the chance of rabies inoculation is increased. Bites from most wild carnivores, skunks, raccoons, and bats should be considered as rabid, while bites from immunized animals should be considered low risk. Healthy dogs and cats in nonendemic areas are low risk. Tables 47-10 and 47-12 summarize recommendations regarding the risk of transmission of rabies and treatment. If there is any question concerning prophylaxis, public health officials should be promptly consulted.
Table 47-12 Schedule of Prophylaxis Recommended in the United States after Possible Exposure to Rabies |Favorite Table|Download (.pdf)
Table 47-12 Schedule of Prophylaxis Recommended in the United States after Possible Exposure to Rabies
|Not previously vaccinated|
|Local wound cleansing||Immediate cleansing with soap and water|
|Rabies immune globulin||20 IU/kg of body weight (if anatomically feasible, up to half the dose be infiltrated around the wound or wounds and the rest should be administered intramuscularly in the gluteal area. Never give more than the recommended dose. Do not use the syringe used for vaccine or inject into the same anatomic site)|
|Vaccine||1.0 mL of HDCV or RVA intramuscularly in the deltoid areach47_10 on days 0, 3, 7, 14, and 28|
|Local wound cleansing||Immediate cleansing with soap and water|
|Rabies immune globulin||Should not be given|
|Vaccine||1.0 mL of HDCV or RVA intramuscularly in the deltoid areach47_10 on days 0 and 3|
Snakebite is a challenging but rare problem that is more common in the Southern United States and Mexico than elsewhere in North America. Like most other traumatic illnesses, it is more common in men than it is in women. Approximately 50% of patients are bitten during recreational activity or while working outdoors, while the remaining half are bitten by pet snakes or snakes being handled for some other reason. Snakebites are responsible for an average of only 12 deaths per year in the United States with rattlesnakes causing the majority of severe envenomations. Venomous snakes indigenous to the continental United States are either crotalids, which include rattlesnakes, copperheads, and cottonmouths, or elapids, of which coral snakes are the only indigenous species in the United States (Table 47-13 reviews the common Crotalidae of North America).
Table 47-13 Crotalidae of North America |Favorite Table|Download (.pdf)
Table 47-13 Crotalidae of North America
|Agkistrodon||Moccasins, copperheads||No rattles, large plates on crown||North America, Southeastern Europe, Asia|
|Crotalus||Rattlesnakes||Rattles, small scales on crown||North, Central, and South America|
|Sistrurus||Massasaugas and pygmy rattlesnakes||Rattles, large plates on crown||North America|
Since no evidence-based recommendations can be made for the treatment of snakebite, treatment recommendations are based on clinical series, animal studies, and common sense. While the clinical data are conflicting, the experimental animal data are clear. In this chapter, a treatment regimen for snakebite is proposed, pertinent controversies are discussed, and a rationale for the treatment scheme is presented (Fig. 47-6).
Algorithm for the treatment of snakebite, only in a setting in which anaphylaxis can be treated.
Identification of the Snake
Because the majority of snakebites in the United States are nonvenomous, an attempt should be made to identify the snake. This is possible by history as well as direct observation, particularly if the victim brings the snake to the emergency department for this to occur. If at all possible, the snake should be identified by someone knowledgeable in herpetology and no identification should be attempted by hospital personnel unless the snake is dead or completely contained. For patients who are snake handlers or those bitten by pet snakes, the patients themselves will be the best resource to identify the type of snake. Fig. 47-7 summarizes the physical characteristics of crotalid snakes. The three important genera of Crotalidae in the United States are Crotalus and Sistrurus (rattlesnakes) and Agkistrodon (copperheads and water moccasins; Table 47-13). These snakes are characterized by a broad triangular head, relatively thick body, elliptical pupils, and facial pits. All but one species of rattlesnakes have rattles, which distinguishes them from copperheads and water moccasins. The only other snakes of clinical importance in the continental United States are the coral snakes. The two species of these that are common to the United States are Micrurus fulvius fulvius (Eastern coral snake) and the Micrurus fulvius tenere (the Texas coral snake). The Sonoran coral snake (Micrurus euryxanthus) is present in a small area of Southern Arizona, but is mostly indigenous to Mexico. These snakes are brightly colored, with red, yellow, white, and black rings. They are relatively small bodied and have small nontriangular heads without facial pits. Their rings encircle the body and the mouth area is black. Their characteristic coloring pattern of a red band adjacent to a yellow one distinguishes coral snakes from other snakes that are brightly colored but nonvenomous, which is the justification for the idiom, “Red on yellow, kill a fellow, red on black, venom lack.” Coral snakes belong to the family Elapidae, or elapid, which includes cobras, kraits, mambas, and the poisonous snakes of Australia. Coral snakes tend to be secretive, burrowing, and nonaggressive, accounting for the low incidence of bites by these animals. They do not have large fangs, and when they do bite, they tend to chew on the offending animal or part.
Characteristics of poisonous and nonpoisonous snakes.
An assessment for envenomation must be made in cases of bites by poisonous snakes. If there are no fang marks, envenomation is not possible and even with the presence of fang marks, approximately 20–25% of patients will not have been envenomated. It is estimated that another 50% have minimal to mild envenomation, which would not be a threat to life or limb. Agkistrodon (moccasin and copperhead) bites tend to be less severe than rattlesnake bites and rarely require antivenin or invasive treatment. With rattlesnake bites, it is usually easy to assess whether envenomation has occurred. Crotalid venoms are a mixture of enzymes, polypeptides, and glycosylated peptides that have broad biologic actions; however, one of the common features of these venoms is local tissue destruction. This locally destructive action is an accurate marker of the degree of envenomation. A great deal of pain, edema, and frequently discoloration or formation of bullae is associated with envenomation. Recent data appear to point to the presence of metalloproteinases in crotalid venom as a major source of local and systemic adverse effects.103
Given the relatively rare nature of severe envenomation, there is little in the literature pertaining to scoring the severity of the injury. One group has proposed and validated a Snakebite Severity Score (SSS).104 This takes into account not only the potential for the dose of the envenomation but also the variability in response between patients. The scoring system reviews both the local wound of the bite and any possible systemic (pulmonary, GI, cardiovascular) symptoms, and was useful in determining the level and type of care needed.
Since the signs and symptoms of envenomation have a rapid onset, it is probable that if by the time the patient arrives there is no edema or pain, a significant envenomation has not occurred, or the patient was bitten by a moccasin or copperhead. These points are emphasized because no treatment advocated for a rattlesnake bite is free of risk (most actually have a relatively high risk) and because, in the absence of envenomation or with mild exposure only, supportive care alone will suffice. This point is one that makes evaluation of the snakebite literature difficult. If the clinical series in question includes a large number of Agkistrodon bites or patients with mild envenomations, the outcome will almost always be favorable, regardless of the treatment applied. The real concern in the treatment of snakebite relates to the patient with a severe envenomation associated with extensive destruction of local tissue or systemic signs of toxicity. The outcome for this type of patient is harder to assess from clinical series involving humans.
First aid is defined as the care delivered to the patient prior to arrival in the hospital. “First do no harm” should be loudly emphasized for first aid in the treatment of snakebites. A large number of first aid measures have been proposed for the treatment of venomous snakebites, and many, if not most, have carried a high risk of harm to the patient. The atmosphere at the scene of a snakebite is usually characterized as chaotic at best, punctuated by poorly trained first aid providers. This combination sets the stage for a therapeutic disaster if overly aggressive therapy is initiated at the scene of the bite. The most common potentially harmful treatments include incision and suction, electrical shock therapy, use of tourniquets, and limb immersion in ice.
Incision and suction have been shown experimentally to remove subcutaneously injected venom from animals; however, unless this is done very soon after envenomation, the yield of extracted venom is low.105 The risk of incision and suction is significant when one considers that the person making the incision is probably doing it for the first time, the patient is in pain and unanesthetized, and there is probably no knowledge of anatomy by either person involved in the procedure. It should also be remembered that 25% of the victims of snakebite will have no envenomation or a trivial one. For these reasons, incision and suction has fallen into disfavor as a first aid measure.
In a series of letters to the editor of the Lancet, a group of physicians practicing medicine in Ecuador advocated the use of electrical shock therapy for snakebite. They presented a series of 34 patients who were treated with electrical current using a modification of a stun gun.106 A stun gun is a personal protective device that delivers an extremely high voltage with very little current, which when used on attackers, temporarily disables them. The Ecuadorean investigators used this device on a group of patients with snakebite, probably from Bothrops atrox. All of the patients were said to have fared well, with immediate improvement. Follow-up in this series was not described, and there were no controls. This report led to the widespread use and indeed to the marketing of the stun gun for use in human snakebite. This treatment is typical of snakebite therapy throughout history. A theoretical treatment plan, usually with the potential for great pain or harm, is proposed, implemented, and adopted without any degree of scrutiny. Several controlled animal studies have now shown electrical shock therapy to be ineffective in the treatment of snakebite.
Ice therapy for snakebite has been advocated on the basis of decreasing the optimal temperature range for the enzyme component of the venom, and thus decreasing local tissue damage.107 This topic has been hotly debated without any clear resolution; however, the weight of the evidence would suggest that ice therapy is not efficacious. It has the potential for harm in cases of snakebite, and its use is discouraged. While putting a topical ice pack on the wound carries no risk, it is immersion of the extremity containing a bite or adding salt to the ice that has been associated with problems.
The use of a tourniquet has also been a debated issue in first aid for snakebite. A loosely applied venous tourniquet may decrease systemic absorption of the venom and delay the onset of symptoms; however, it certainly does not help the affected extremity and, if applied too tightly or if excessively tightened by the formation of edema, it carries the potential for causing great harm. Data from Australia suggest a treatment that would seem to be logical and safer that involves the application of a compression bandage and immobilization of the bitten extremity, instead of a tourniquet. With a compression bandage alone there is a great delay in the systemic absorption of venom.108 A splint and elastic bandage wrap or an inflatable air splint could also be used for this purpose. These measures have much less associated risk than placing a tourniquet on the involved extremity.
In summary, immobilization, neutral positioning, and a compression dressing of some sort are recommended as first aid in cases of snakebite, followed by rapid transport of the patient to a hospital. If a skilled surgeon is present and there is a significant and obvious envenomation, immediate incision and suction or local excision of the bite wound may be considered.109
The care of the patient in the hospital is no less controversial than is first aid for snakebite.110 The principal debates center around: (a) the use of antivenin therapy, (b) aggressive debridement and fasciotomy, and, more recently, (c) observation with supportive care alone. For severe bites, antivenin use is favored along with the aggressive use of supportive care. Fasciotomy is reserved only in the treatment of compartment syndrome. The use of antivenin for mild or even moderate envenomations is not appropriate since the patient will almost certainly do well without any therapy. Immediate surgical debridement for the purpose of removal of venom and nonviable muscle is also not recommended. Experimentally, this approach does not remove the venom, and it is impossible to determine if muscle tissue is viable on the basis of the usual clinical criteria.111 Supportive care alone is not recommended for severe envenomations, although patients with all but the most massive envenomations could probably survive with aggressive modern intensive care and replacement of blood factors.112 In the case of rattlesnake bites there is a relatively effective treatment that limits the amount of tissue damage and systemic action of the venom if administered early. The problem is not efficacy but safety. Antivenin therapy carries a definite risk of anaphylaxis and serum sickness; however, the risk of its use is outweighed by the potential benefits in victims with life- or limb- threatening bites.
A polyvalent equine antivenin (Wyeth-Ayerst Laboratories, Marietta, Pennsylvania) and an ovine Crotalidae polyvalent immune Fab antivenin, consisting of cleaved Fab antibody fragments (CroFab; Protherics, Inc, Nashville, Tennessee), are currently commercially available for the treatment of crotalid envenomations. These products are manufactured by immunizing animals to crotalid venoms and then pooling the globulin fraction containing the antibodies. The ovine Fab product, CroFab, undergoes further modification by cleavage of the Fab antibody fragments and purification with affinity chromatography. Experimentally, antivenin has been shown to be effective in preventing death following the injection of rattlesnake venom. In an animal model, it also preserves muscle function and minimizes the systemic side effects of the venom.
Like all antibody therapies, the equine antivenin is most effective if given immediately before envenomation; however, it is also effective when given after envenomation.111 It has also been shown to be effective if given up to 4 hours after envenomation, although there is little evidence to support its use beyond 4 hours. There have been anecdotal reports of clinical responses when it is given later than this, however, and it is recommended for use in life-threatening envenomations for up to 24 hours following a crotalid bite. Nevertheless, it must be emphasized that if antivenin therapy is going to be used, it should be used as soon as possible after envenomation.
Although widely used clinically, there are significant problems with the unmodified polyvalent equine antivenin. It is a foreign, impure horse serum protein fraction and has been associated with severe and even life-threatening anaphylactic reactions. The exact incidence of such reactions is unclear, ranging from 1% to as high as 39%. The antivenin infusion should be started at a very slow rate and stopped with any signs of an allergic reaction. The antivenin may also cause a dose-dependent, delayed-type serum sickness, which is much less severe than an anaphylactic response, although probably more common with massive infusions of antivenin. These side effects have fueled a debate over use of the antivenin. CroFab is an attempt to make the immunotherapy safer by purification of Ig and cleavage of the Fc fragment to produce Fab fragments.113 An increasing body of evidence supports the safety and efficacy of the Fab product, although additional postmarketing clinical data will ultimately be required.114 The Fab fragment has not been directly compared with other antivenin products. CroFab appears to be different than the older equine antivenin in that it probably requires repeat dosing in the immediate period after administration.113,114
In addition to being given as early as possible and in doses large enough to effect a difference, antivenin should not be administered in any setting in which anaphylaxis cannot be treated (i.e., in the field) and should initially be infused very slowly, with the infusion stopped with signs of hypersensitivity as noted earlier. The dose of antivenin to be given is empiric and based on the physician’s assessment of the amount of venom injected. The dose is the same in children as in adults, again being based on the amount of venom to be neutralized rather than on the weight of the patient. A minimum of 6–10 vials of CroFab is used for severe bites, although this amount is increased as needed. Various schemes have been devised for assessing the dose of antivenin based on the severity of envenomation. As the antivenin should not be used for mild or uncomplicated, moderate envenomations, these classification schemes are not clinically useful. Skin testing prior to antivenin administration should probably be eliminated and replaced by a very small, very slow intravenous injection of the antivenin, with constant monitoring for signs of anaphylaxis. The manufacturer recommends skin testing, but there have been anaphylactic reactions to the skin test, and the presence or absence of a wheal does not always predict anaphylaxis. The treatment of anaphylaxis is reviewed in Table 47-14.
Table 47-14 Treatment for Anaphylaxis |Favorite Table|Download (.pdf)
Table 47-14 Treatment for Anaphylaxis
Epinephrine, 0.5 mg SQ (may be given IV with major anaphylactic reaction). May be repeated every 20 min
H1 antagonists (diphenhydramine, 25–50 mg IV or IM)
H2 antagonists (ranitidine, 50 mg IV)
Glucocorticoids (hydrocortisone, 125 mg IV). No effect for several hours, but may prevent recurrence of symptoms
Inhaled β2 agonist for recurrent bronchospasm (albuterol, 0.5 mg)
Removal of bee stinger
An ongoing debate during the past several decades has concerned the role of surgery in treating a rattlesnake bite. The theoretical rationale for surgical intervention is based on several observations. Crotalid venoms have very powerful, locally destructive effects. Part of the venom can be removed by incision and suction when this follows immediately after injection of the venom but intramuscular injection of the venom produces extensive edema that can lead to a compartment syndrome. These three observations lead to the conclusion that a rattlesnake bite is a local problem that should be amenable to local therapy (i.e., excision of the venom, dead muscle, and relief of a compartment syndrome). Excellent results have been claimed in clinical series in which this approach has been used.115 Unfortunately, no controlled trials have been conducted, and there are large series in which excellent results have been reported without operative intervention.116,117
An animal study performed in rabbits using an intracompartmental injection of western diamondback rattlesnake (Crotalus atrox) venom has yielded interesting results.111 In this study, animals were randomized to undergo fasciotomy with debridement alone, fasciotomy with antivenin alone, fasciotomy with debridement plus antivenin, or to have no treatment. Antivenin therapy prevented loss of muscle and improved survival, while surgery alone did not. It was also clear that muscle that would have survived was removed in the group that had the combination of antivenin plus surgery, since late muscle function was significantly worse in this group than it was in that treated with antivenin alone. The authors concluded, therefore, that although the theory of local treatment of rattlesnake bite was attractive, it was not supported by the data. The issue of fasciotomy alone was not addressed in this study. Based on these unanswered questions, fasciotomy should be done infrequently, and should be reserved for the usual indication of compartment syndrome, which would only occur if there is an intramuscular or intracompartmental envenomation.112 Although rare, this does occur, being more common over the anterior leg, fingers, and the hand. If there is a tight compartment with evidence of compartment syndrome, a fasciotomy should be performed.112 No debridement should be done acutely, as injured muscle may be salvaged with immunotherapy.
Supportive care should consist of fluid resuscitation, tetanus prophylaxis, appropriate monitoring, and the correction of coagulopathy. The bacteriology of rattlesnake mouths has been studied. Commonly present organisms include Pseudomonas spp., Enterobacteriaceae, Staphylococcus spp., and Clostridia.118,119 An extended-spectrum penicillin with a beta-lactamase inhibitor would provide reasonable empiric coverage; however, the weight of evidence supports not using empiric antibiotics.120,121 Coagulopathy due to fibrinolysis is a common complication of envenomation and should be corrected with fresh frozen plasma and cryoprecipitate. The patient’s prothrombin time/international normalized ratio, partial thromboplastin time, fibrinogen concentration, and platelet count should all be monitored, with replacement therapy based on these values and evidence of clinical bleeding.122
The symptoms of coral snake envenomation include local pain at the bite site, but the venom has primarily systemic effects consisting of respiratory depression and changes in CNS function.123 Antivenin and supportive care are the mainstays of treatment for coral snake envenomations. A commercially available antivenin exists for subspecies of Micrurus fulvius (the Eastern and Texas coral snake). This product probably has little cross-reactivity with the venom of M. euryxanthus (the Sonoran coral snake). Patients with fang marks or fang scratches should be admitted for observation. Any signs or symptoms should be treated with between three and five vials of antivenin. It is probably not wise to wait for full-blown systemic symptoms to develop before initiating treatment. If signs of respiratory distress develop, the patient should be treated supportively with intubation and mechanical ventilation as needed.