The incidence of wound infection following crotalid envenomation

The incidence of wound infection following crotalid envenomation

TheJournalofEmergency Medicine, Vol 11,pp583-586, 1993 THE INCIDENCE Printed in the USA OF WOUND INFECTION Richard F. Clark, MD,*§ FOLLOWING . ...

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TheJournalofEmergency Medicine, Vol 11,pp583-586, 1993

THE INCIDENCE

Printed in the USA

OF WOUND INFECTION

Richard F. Clark,

MD,*§

FOLLOWING

. Copyright 0 1993 Pergamon Press Ltd.

CROTALID

Brad S. Selden, rm,t§ and Brent Furbee,

ENVENOMATION MD*§

‘Department of Emergency Medicine, UCSD Medical Center, San Diego, California, tDepartment of Emergency Medicine, Maricopa Medical Center, Phoenix, Arizona, *Department of Emergency Medicine, Methodist Hospital, Indianapolis, Indiana, and SDepartment of Medical Toxicology, Good Samaritan Regional Medical Center, Phoenix, Arizona Reprint Address: Richard F. Clark, MD, Department of Emergency Medicine, UCSD Medical Center, 225 Dickinson St., #8676, San Diego, CA 92103

venomations includes supportive care and crotalidspecific antivenin (l-4). Although snakes are known to harbor organisms such as Salmonella and Bacteroides in their oral cavities (5-7), recent data suggest that crotalid venom may exhibit antibacterial properties (8). Many sources recommend the routine use of broad spectrum prophylactic antibiotics following crotalid envenomation (l-4), but retrospective reports demonstrate a low incidence of wound infection (WI) (8,9). This traditional use of antibiotics has not been substantiated by any scientific research, and, therefore, may unnecessarily increase the cost of patient care, and may add to morbidity and mortality due to antibiotic side effects (1). We prospectively observed patients with crotalid envenomation to assess the incidence of WI and evaluate the need for prophylactic antibiotics.

0 Abstract -Many sources advocate the empiric use of antibiotics to prevent wound infection (Wl) following crotalid (rattlesnake) envenomations. We undertook a prospective observational study to examine the incidence of infections following crotalid envenomation. We studied crotalid envenomations presenting to our institution with follow-up by direct examination or telephone consultation. All patlents presenting to our institution from June 1990 to October 1991 with history and clinical evidence of crotalid envenomation were included in the analysis. Routine management of crotalid envenomation was undertaken in each case, including the use of antivenin, surgical debridement, and antibiotics only when indicated by signs and symptoms of infection. A total of 54 patients were observed during the study period. Twelve patients received prophylactic antibiotics begun either prior to transfer to our instltutlon or following a surgical procedure, and were evaluated separately. Follow-up was obtained on 32 patients 7 or more days following envenomatlon. Only 1 patient from the study group developed clinical evidence of WI during the study period. We conclude that because of a low incidence of WI in this series, the routine use of prophylactic antibiotics in such patients may not be warranted. 0 Keywords- antibiotics; crotalid envenomation; tion; antivenin; rattlesnake

MATERIALS

AND METHODS

All patients managed by the Toxicology Service of an urban hospital and regional Toxicology Referral Center from June 1990 through October 1991 with clinical (presence of puncture wound) and historical (patient heard rattle or saw the rattlesnake) evidence of crotalid envenomation were studied. Patients presented both primarily to our institution and through referral. Common species of crotalids found in this area are: C. atrox, C. cerastes, and C. scutulatus, but specific identification of the snake in some cases was not possible. Envenomations were graded for severity and categorized as mild, moderate, or severe based upon a

infec-

INTRODUCTION

Crotalid (rattlesnake) venom contains a variety of toxic components. Although tissue necrosis and hemotoxicity are most common, severe systemic effects, including hypotension, pulmonary edema, and neurotoxicity, are reported (1,2). Most authorities agree that the mainstay of treatment for severe en-

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19 February 1993;

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Richard F. Clark, Brad S. Selden, Brent Furbee

Table 1. Ciassitlcation of Severity of Crotaiid Envenomation (10) Mild

-Fang marks or mark present -Edema is limited to the site of envenomation or area adjacent to the site of envenomation, and is not rapidly progressing (limited to hand or foot in distal extremity envenomation) -No systemic effects (normal platelets and fibrinogen)

Moderate

-Edema progressing past area adjacent to bite size (that is, to elbow or knee in distal extremity envenomation) -Mild hemotoxicity: platelet count low but above 80,000/m3, fibrinogen low but above 80 mg/dL, but no bleeding present remote from bite site -Nausea and vomiting

Severe

-Edema rapidly progressing and including entire extremity -Severe hemotoxicity: platelet count less than 80,000/m3, fibrinogen less than 80 mg/dL, or bleeding present remote from bite site -Presence of other systemic symptoms: pulmonary edema, neurotoxicity, hypotension, etc.

widely used system proposed by Picchioni (Table 1) (10). Treatment of individual cases was at the discretion of the individual attending toxicologist, but included supportive care, extremity elevation, liberal analgesics, polyvalent crotalid antivenin, monitoring of compartment pressures, and surgical consultation for debridement when necessary. All patients were continuously assessed for signs of WI while hospitalized, and followed for 7 or more days after the envenomation as an outpatient either by telephone contact with the patient or the patient’s guardian (27 patients), telephone contact with the patient’s personal physician (4 patients), or by direct examination at our institution (10 patients). A “wound infection” was defined as presence of 2 out of the following 3 criteria: onset of new or increasing pain, localized erythema or localized swelling at the bite site, or purulence at the bite site. The presence of fever and one of the above criteria would also satisfy the definition of a WI. These signs were to be independent of or additional to the normal findings of crotalid envenomation (diffuse edema, central ecchymosis, nonpurulent serosanguinous drainage). These signs of infection would be expected to occur after the peak period and initial resolution of envenomation signs and symptoms had begun, with an increasing severity, as would be characteristic of soft tissue infection. Fever was not accepted as a criteria if it occurred in clear temporal conjunction with other signs of serum sickness (urticaria, arthralgias, myalgias, pruritis, onset 5-10 days after treatment with antivenin), which almost invariably occurs after antivenin administration. In addition, a culture of purulent drainage from the bite site reported as positive for any organism other than skin flora in combination with one of the above criteria was considered evidence for a WI. RESULTS

A total of 54 patients were entered into the study. Follow-up was obtained on 41 patients. Thirteen patients with inaccurate or false phone numbers or ad-

dresses were lost to follow-up. None of these patients, however, had developed signs or symptoms of a WI prior to discharge (in hospital observation ranging from 2-4 days). All bites occurred either to the trunk (3 patients) or extremities (38 patients). Nine patients received prophylactic antibiotics either prior to transfer to our institution or following a surgical procedure, and were evaluated separately. Twenty-six patients received some form of prehospital intervention consisting of either placement of a ligature (15 patients), electroshock to the bite (1 patient), cryotherapy (ice immersion, 6 patients), or cutting and sucking of the bite site (4 patients), but only 1 of these patients (a cryotherapy patient) eventually developed a WI.

No Antibiotics Group A total of 32 patients were treated without prophylactic antibiotics (Table 2). Twenty-five patients (78%) were male, with an average age of 25. Seventeen patients (53%) were classified as severe envenomations. Twenty-four patients (749’0) received antivenin in their management. Twelve patients (38%) Table 2. Demographics of Patients With Crotaiid Envenomation Observed in This Series

Total Male Average age “Severe envenomations” Received antivenin Surgical procedure Received steroids Time to presentation (minutes) Received prehospital intervention Clinical evidence of wound infections

No Antibiotics

Received Antibiotics

32 25 (78%) 25 17 (68%) 24 (75%) 12 (36%) 8 (25%) 93

9 7 (78%) 35 4 (44%) 7 (78%) 6 (66%) 3 (33%) 72

21(66%)

5 (55%)

1 (3%)

2 (22%)

585

Wound Infections After Crotalid Envenomation

required surgical debridement of the bite site at some time during the progression of the envenomation. Eight patients received systemic corticosteroids at some point for the management of hypersensitivity reactions. Only one patient (3%) in this group developed a WI. This patient sustained a bite to the lower leg, and received cryotherapy before arriving at the hospital. The bite was classified as moderate in severity, and treated supportively without antivenin. Examination prior to discharge from the hospital demonstrated no signs of infection. Follow-up was obtained at 7 days through the patient’s primary physician. He had examined the patient 5 days after the envenomation, and at that time described the site of envenomation as erythematous and swollen. The patient was afebrile. Aspiration of a fluctuant area at the site produced clotted blood and a small amount of purulent material. No culture was obtained, and the patient underwent a short course of oral antibiotics and had no further problems.

and several doses of prophylactic oral antibiotics prior to transfer to our institution. She had no evidence of infection the following day when she was discharged. Follow-up was obtained in 1 week from her primary physician who noted the patient to have a low grade fever, and recorded swelling and erythema of the bite site. No purulent discharge was noted. She was placed on oral antibiotics for 5 days with no further sequelae. The second patient was a 40-year-old male who was transferred from another hospital 48 hours after envenomation. His bite was to the thumb, classified as “moderate,” and never required antivenin. He received 48 hours of intravenous antibiotics prior to transfer, but the examination as recorded at the referring institution was unremarkable for any signs of infection. Although antibiotics were initially discontinued after transfer, the patient developed erythema and swelling of the bite site the following day along with a fever of 39.5OC. There was no purulence noted and no cultures obtained, but the patient was continued on oral antibiotics for 10 days.

Antibiotic Group DISCUSSION Nine patients received some type of prophylactic antibiotics during their management (Table 3). Seven received antibiotics in outlying hospitals prior to transport to our institution, and 2 received prophylactic antibiotics following a surgical procedure at our hospital. The average age of this group was 35, and 4 (44%) were classified as severe envenomations (Table 2). Five of these patients required some type of surgical debridement, and 1 required fasciotomy for elevated intracompartmental pressure after direct envenomation of the lateral lower leg. Seven patients in this group received polyvalent crotalid antivenin. Three of these patients received corticosteroids for hypersensitivity reactions, but none developed an infection. Two patients (22%) in this group developed evidence of WI. The first was a 64-year-old female who presented with a “moderate” envenomation of the lower leg. She was treated with 10 vials of antivenin

Table 3. Variety of Prophylactic Antiblotics Received by Patients Cefazolin Ampicillinlclavulinicacid Cephalexin Ceftriaxone Nafcillin Total

Crotalids are known to harbor potentially infectious microorganisms within their oral cavity, likely related to the feces of their prey (5-7). Among the organisms most commonly isolated from crotalid saliva are Pseudomonas arueginosa, Proteus species, coagulase-negative staphylococci, Clostridium species, and Bacteroides fragiiis (5,6). It is possible that variations in bacterial contamination could occur according to the type and location of prey that are consumed by the snake. “Captive” or “pet” snakes are thought to harbor different and more numerous bacteria than wild or recently caught snakes (11). Bites by these pet snakes, therefore, may more likely become infected. Crotalid venom has been shown to be sterile relative to crotalid saliva (5,6). Infections must, therefore, result from bacterial inoculation at the time of the bite from human skin or snake oral flora. The proliferation of bacteria is then aided by tissue necrosis, edema, and vascular compromise due to proteolytic enzymes and other peptides contained within the venom (2). For these reasons, many authors recommend routine prophylaxis with broad spectrum antibiotics following crotalid envenomation (l-6). Retrospective experience suggests a low incidence of infections after crotalid envenomations (2,8,9). For this reason, we do not routinely administer prophylactic antibiotics to patients bitten by crotalids

Richard F. Clark, Brad S. Selden, Brent Furbee

presenting to our institution. This observational study reiterates our prior experience in this area, and implies little benefit in the routine administration of antibiotics in these patients. Although 13 patients were lost to long-term follow-up, none of these had developed a WI prior to discharge, and all were instructed to contact the Poison Center if any signs or symptoms of infection should occur. In our limited series, neither the administration of antivenin or corticosteroids, nor prehospital procedures such as incision or suctioning of the wound seemed to affect the rate of infections. The severity of the bite also appeared to have little bearing on the development of WI. It is possible that differences in the species of rattlesnake, as well as whether the snake is a “pet” or wild, could influence the bacterial flora involved in the bites. Interestingly, previous studies have suggested that the low incidence of infections may be a result of antibacterial activity of crotalid venom (8,12,13). Talan and colleagues (8) determined minimal inhibitory

and bactericidal concentrations of crotalid venoms for typical oral crotalid microorganisms and found the venoms to possess a broad spectrum of activity against aerobic gram-positive and -negative bacteria. Thus, even patients exposed to human saliva during mouth suctioning after envenomation may not be more likely to develop WI. Although the mechanism of this bactericidal activity is unclear, it may be oxygen-dependent, since Talan demonstrated that many anaerobic strains of bacteria tend to be resistant to higher concentrations of venom (8).

CONCLUSION We conclude that in this observational series there is a low incidence of WI after crotalid envenomation. Therefore, prophylactic antibiotics are probably unnecessary in these patients. Secondary infections may occur after crotalid envenomations, and antibiotics should be reserved for these cases.

REFERENCES 1. Ellenhorn MJ, Barceloux DG. Medical toxicology. New York: Elsevier; 19881113-27. 2. Wingert WA, Chan L. Rattlesnake bites in southern California and rationale for recommended treatment. West J Med. 1988; 14837-44. 3. Gtten EJ. Venomous animal injuries. In: Rosen P, Baker FJ, Barkin RM. Braen RM. Dailey RH, Levy RC, eds. Emergency medicine, ed 2. St. Louis: C.V. Mosby Co.; 1988:981-1000. 4. Edlich RF. Rodeheaver GT, Thacker JG. Wounds, bites, and stings. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. Norwalk. CT: ADDleton & Lanne: 1988:697-736. 5. Theakstoh RDG; Phillips RE, iooareesuwan S, Echevania P, Makin T, Warrell DA. Bacteriological studies of the venom and mouth cavities of the wild Malaysian pit vipers in southern Thailand. Tram R Society Tropical Med Hygiene. 1990$4:875-9. 6. Goldstein EJC. Citron DM, Gonzalez H, Russell FE, Finegold SM. Bacteriology of rattlesnake venom and implications for therapy. J Infect Dis. 1979;140:818-21. 7. Ledbetter EO, Kutcher AT. The aerobic and anaerobic flora

of rattlesnake fangs and venom. Arch Environ Health. 1969; 19:770-8. 8. Talan DA, Citron DM, Overturf GD, Singer B, Froman P, Goldstein EJC. Antibacterial activity of crotalid venoms against oral snake flora. J Infect Dis. 1991;164:195-8. 9. Burch JM. Agarwal R, Mattox KL, Feliciano DV, Jordan GL. The treatment of crotalid envenomation without antivenom. J Trauma. 1988;28:35-43. 10. Picchioni AL, Hardy DL, Russell FE, et al. American Association of Poison Control Centers Scientific Review Committees nuidelines for snakebite ooisonina. Vet Hum Toxicol. 1984: 26:139-40. 11. Williams FE, Freeman M, Kennedy E. The bacterial flora of the mouths of Australian venomous snakes in captivity. Med J Aust. 1954;2:190-3. 12. Boys F, Beamer P, Smith HM. Antibiotics in tests for toxicity of snake venoms. JAMA. 1960;174:306-7. 13. Stoker JF, Traynor JR. The action of various venoms on Escherichiu coli. J Appl Bacterial. 1986;61:383-8.