Bites
A wide variety of bites are seen in children. It is estimated that more than 1 million children are treated annually for bites (Table 12-1).1 In this chapter we concentrate on bites of interest to the surgeon. The reader is referred elsewhere for discussions of management of venomous stings and injuries from marine life and general details of wound management.
TABLE 12-1
Bites and Envenomations to Humans: Calls to Poison Centers in 2010
Data from Bronstein AC, Spyker DA, Cantilena LR, et al, editors. 2010 Annual Report of the American Association of Poison Control Centers National Poison Data System (NPDS): 28th Report. Clin Toxicol 2011;49:910–41, Appendix.
Tetanus
The Gram-positive anaerobic organism Clostridium tetani is the causative agent for tetanus, a severe and often fatal disease. In 2009, there were a total of 18 cases (zero under 14 years of age) reported in the USA.2
There has been a low incidence rate of tetanus since a peak of 102 cases in 1975. Mortality from tetanus is associated with co-morbid conditions such as diabetes, intravenous drug use, and old age, especially when vaccination status is unknown. Infection can occur weeks after a break in the skin, even after a wound has seemed to heal. The ideal anaerobic surroundings allow spores to germinate into mature organisms producing two neurotoxins: tetanolysin and tetanospasmin.3 The latter is able to enter peripheral nerves and travel to the brain, causing the clinical manifestations of uncontrolled muscle spasms and autonomic instability. The incubation period varies from as short as two days to several months, with most cases occurring within 14 days.4 In general, the shorter the incubation period, the more severe the disease and the higher the fatality risk.
All wounds should be cleaned and debrided. Symptomatic and supportive care includes medications such as benzodiazepines to control tetanic spasms and antimicrobials for infection. Metronidazole (oral or intravenous, 30 mg/kg/day, divided into four daily doses, maximum 4 g/day) is the preferred antibiotic because it decreases the number of vegetative forms of C. tetani.5 An alternate choice is parenteral treatment with penicillin G (100,000 U/kg/day every four to six hours, not to exceed 12 million units/day) for ten to 14 days. Human tetanus immune globulin (TIG) is administered to adults and adolescents as a one-time dose of 3000–6000 units intramuscularly. Some experts recommend that children receive 500 units to decrease the discomfort from injection.5 Infiltrating part of the dose locally is controversial. Tetanus prevention in a potentially exposed patient depends on the nature of the wound and history of immunization with tetanus toxoid (Table 12-2).
TABLE 12-2
Wound Tetanus Prophylaxis Guideline
| Vaccination History (Td) | Clean/minor Wounds | All Other Wounds |
| ? or <3 doses | Td or Tdap—No TIG | Td or Tdap—TIG |
| ≥3 doses | Td or Tdap—No TIG if ≥10 years since last dose | Td or Tdap—No TIG if ≥5 years since last dose |
Data from American Academy of Pediatrics: Tetanus (lockjaw), Bite Wounds. In Pickering LK, Baker CJ, Kimberlin DW, Long SS (eds): Redbook: 2009 Report of the Committee on Infectious Diseases, 28th ed. Elk Grove Village, IL, American Academy of Pediatrics, 2009, pp 187-191, 655–60.
Cat, Dog, Human, and Other Mammalian Bites
Children are frequent victims of mammalian bites. The most common complication from bites is infection: cats, 16–50%; dogs, 1–30%, and humans, 9–18%.6 When the bite is from a cat, dog, or other mammal, the most common infectious organisms are Streptococcus, Staphylococcus, Actinomycetes, Pasteurella species, Capnocytophaga species, Moraxella species, Corynebacterium species, Neisseria species, Eikenella corrodens, Haemophilus species, anaerobes, Fusobacterium nucleatum, and Prevotella melaninogenica.5,7,8 Human bites are a potential source not only for bacterial contamination but also for hepatitis B and, possibly, human immunodeficiency virus (HIV) infection.9
Recommendations for bite wound management are presented in Box 12-1. Evidence-based medicine studies concerning whether to close wounds are not conclusive. Distal extremity wounds, especially hand/fist to teeth, are at higher risk for infection. Whether minimal risk wounds require prophylactic antimicrobial therapy is also controversial. Antibiotics started within eight to 12 hours of the bite and continued for two to three days may decrease infection rate.5 The oral drug of choice is amoxicillin-clavulanate. For penicillin-allergic patients, an extended-spectrum cephalosporin or trimethoprim-sulfamethoxazole plus clindamycin should be used.5
Rabies and Postexposure Prophylaxis
Rabies is a viral disease usually transmitted through the saliva of a sick mammal (e.g., dogs, cats, ferrets, raccoons, skunks, foxes, bats, and most other carnivores). The majority of reported cases in the USA are caused by raccoons, skunks, foxes, mongooses, and bats. Small rodents such as rats, mice, squirrels, chipmunks, hamsters, guinea pigs, rabbits and gerbils are almost never infected with rabies. Over the past decade, cats have been the most common domestic animal with rabies. Rabies-related human deaths in the USA occur one to seven times per year since 1975. Modern prophylaxis has proven nearly 100% successful. Worldwide, fatalities are about 40,000–70,000. The rabies virus enters the central nervous system and causes an acute, progressive encephalomyelitis from which survival is extremely unlikely. The human host has a wide range for the incubation period from days to years (most commonly weeks to months).
Prophylactic treatment for humans potentially exposed to rabies includes immediate and thorough wound cleansing followed by passive vaccination with human rabies immune globulin and cell culture rabies vaccines, either human diploid or purified chick embryo.10–12 Many factors help determine the risk assessment in deciding which patient benefits from post exposure prophylaxis and which regimen should be given. The risk of infection depends on the type of exposure, surveillance, epidemiology of animal rabies in the region of contact, species of animal, animal behavior causing it to bite, and availability of the animal for observation or laboratory testing for the rabies virus. The final decision for treatment with vaccines is complex. Therefore local, state, or CDC (Centers for Disease Control) experts are available for assistance. There is no single effective treatment for rabies once symptoms are evident.
Spider Bites
There are about 40,000 species of spiders that have been named and placed in about 3000 genera and 105 families.13 In regard to medically relevant spiders, few are known to cause significant clinical effects. In 2010, about 11,000 calls were made to USA Poison Control Centers (PCC) regarding spider bites.1 It is rare that a spider bite requires surgical care. Few spiders have been shown to have the ability to bite humans because their fangs cannot pierce the skin. The two most medically important spiders in the USA are Sicariidae (brown spiders) and Lactrodectus (widow spiders).
Brown Recluse Spiders
Loxoscelism is a form of cutaneous–visceral (necrotic–systemic) arachnidism found throughout the world with predilection for North and South America.14 There are four species of brown spiders within the USA that are known to cause necrotic skin lesions (Loxosceles deserta, L. arizonica, L. rufescens, and L. reclusa). L. deserta and L. arizonica can be found in the southwestern USA L. reclusa is the most common species associated with human bites. It is usually found in the south central USA, especially Missouri, Kansas, Oklahoma, Arkansas, Tennessee, and Kentucky.15 Spiders can be transported out of their natural habitat but rarely cause arachnidism in nonendemic areas. L. reclusa is tan to brown with a characteristic dark, violin-shaped marking on its dorsal cephalothorax, giving it the nickname ‘fiddleback’ or ‘violin’ spider. The spider can measure up to 1 cm in total body length with a 3 cm or longer leg span (Fig. 12-1). These spiders only have three pairs of eyes whereas most spiders have four pairs.
FIGURE 12-1 Loxosceles reclusa (brown recluse, ‘fiddleback’) spider showing the classic violin-shaped marking on the back (dorsal side) of the cephalothorax. Note the long slender legs and oval body segment with short hairs. The arrow is pointing toward the classic violin marking. (From Ford M, Delaney K, Ling L, et al. Clinical Toxicology. Philadelphia: Elsevier; 2001.)
The incidence of L. reclusa bites predominantly occurs from April through October in the USA. The venom of the brown recluse spider contains at least 11 protein components. Most are enzymes with cytotoxic activity.16 Sphingomyelinase D is believed to be the enzyme responsible for dermonecrosis and activity on red blood cell membranes.17–19 In addition to the local effects, the venom has activity against neutrophils and the complement pathway that induces an immunologic response.19–21 The resulting effect is a necrotic dermal lesion and the possibility that a systemic response will be life threatening.
The prevalence of brown recluse spider envenomations is unknown. The victim may not feel the bite or may only feel a mild pinprick sensation. Many victims are bitten while they sleep and may be unaware of the envenomation until a wound develops. The majority of victims do not see the spider at the time of the bite.22 Typically, the bite progressively begins to itch, tingle, and become ecchymotic, indurated, and edematous within several hours.23 Often within hours, a characteristic bleb or bullae will form. The tissue under a blister is likely to become necrotic, but the extent of necrosis is not predictable. As the ischemia and inflammation progresses, the wound becomes painful and may blanch or become erythematous, forming a ‘target’ or ‘halo’ design. Inflammation, ischemia, and pain increase over the first few days after the bite as enzymes spread. Over hours to weeks, an eschar forms at the site of the bite. Eventually, this eschar sloughs, revealing an underlying ulcer that may require months to heal, usually by secondary intention (Fig. 12-2). On very rare occasions, the ulcer does not heal and may require surgical intervention.
FIGURE 12-2 (A) A 3-year-old girl hospitalized on the third day after a brown recluse spider bite for severe hemolytic anemia, hemoglobinuria, and ecchymosis (note the vast expansion of the ecchymosis secondary to hyaluronidase ‘spreading factor’ in the venom). There is no necrosis or ischemia, but a small bleb/blister is present over the right clavicle that, although not pathognomonic, is often present early in lesion progression. Also note that the cutaneous lesion is mild in comparison with this patient’s systemic presentation. (B) On the 15th day after envenomation, the lesion measures 5 cm × 2 cm. Multiple small areas of necrosis have become apparent in the past week. The largest area indicates the original bite size. The lesion’s edges have begun to involute with healing, and the ischemia is fading. (C) Nine months after the bite, the necrotic wound has healed with no significant scarring.
The need for hospitalization occurs if the patient develops systemic symptoms. Two studies documented that 14% to more than 50% of patients developed systemic symptoms, with fever being the most common symptom.10 Other common symptoms include a maculopapular rash, nausea and vomiting, headache, malaise, muscle/joint pain, hepatitis, pancreatitis, and other organ toxicity. Life-threatening systemic effects include hemolysis (intravascular and/or extravascular), coagulopathy, and multiple organ system failure. Secondary effects include sepsis, necrotizing fasciitis, and shock.24–26 Hemolysis usually manifests within the first 96 hours. However, late presentations can occur. When hemolysis does develop, it can take four to seven days (or longer) to resolve. Complications such as cardiac dysrhythmias, coma, respiratory compromise, pulmonary edema, congestive heart failure, renal failure, and seizures can occur.
The diagnosis of a brown recluse spider envenomation is largely one of exclusion as it is rare to see or identify the spider. While the wound can look classic for an envenomation, other etiologies must be considered (Box 12-2). Certain laboratory findings can be consistent with a brown recluse spider envenomation but are not specific in making the diagnosis (Box 12-3).
Controversy surrounds the treatment of dermal and systemic symptoms of loxoscelism. Medications such as dapsone, nitroglycerin, and tetracycline have been used. Also, hyperbaric oxygen (HBO) therapy has been advocated as has excision of the necrotic wound. However, none of these has proven to be effective in treating or preventing the ulcer development. In South America, an antivenom has been developed and used in the treatment of Loxosceles envenomations. Unfortunately, the usual long delay in seeking medical care often leads to ineffective use of this antivenom.27 An antivenom is not available in North America.
The use of dapsone, a leukocyte inhibitor, has been advocated in case reports and animal studies.28–30 However, other animal studies have shown no benefit from this treatment. In an animal study,31 piglets received venom and were randomized to receive one of four treatments: no treatment, HBO, dapsone, or dapsone with HBO. Neither dapsone, HBO, nor the combination treatment reduced necrosis compared with controls. A second study compared the use of HBO, dapsone, or cyproheptadine against no treatment in decreasing the necrotic wound after envenomation with L. deserta venom. No statistical difference was seen with respect to lesion size, ulcer size, or histopathologic ranking.32 In addition, the use of dapsone is not without risk, especially hypersensitivity reactions.33 Therapeutic doses of dapsone are associated with hemolytic anemia, methemoglobinemia, and other hematologic effects in patients with and without glucose-6-phosphate dehydrogenase deficiency.
Topically applied nitroglycerin as a vasodilator had been advocated but is not effective in preventing necrosis.34 Tetracycline has been shown to be effective. Rabbits were inoculated with Loxosceles venom and randomized to receive topical doxycycline, topical tetracycline, or placebo.35 Those who received topical tetracycline had reduced progression of the dermal lesion. However, treatment was started at six hours after envenomation, which may not be realistic after a human bite. In addition, the agents used for this research study are not commercially available in the United States. Further studies need to be performed before topical tetracycline can be recommended.
HBO has been advocated for treatment to prevent progression of the necrotic wound. The initial use of HBO was based on the belief that tissue hypoxia was partially responsible for the subsequent necrosis seen after a bite. As mentioned previously, no statistical differences were noted in animal studies that compared dapsone and HBO.31,32 Similar results have been seen in animal studies assessing the effect of HBO alone.36,37 However, a randomized, controlled trial of HBO in a rabbit model in which standard HBO was used showed a significantly reduced wound diameter at ten days.38 No significant change in blood flow at the wound center or 1–2 cm from the wound center was seen. HBO is expensive and not without complications. At the present time, much of the literature contradicts the benefit of HBO for brown recluse spider envenomations. As such, it is not currently recommended as a therapy for these bites, but may be helpful in patients with underlying/preexisting vascular compromise such as sickle cell anemia or diabetes.
Early surgical intervention is not helpful because the venom diffuses rapidly throughout the soft tissues surrounding the bite.39 In addition, patients may be more at risk for delayed wound healing and excessive scarring if operation occurs within the first 72 hours of the bite.40,41
