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Necrotizing fasciitis of the upper extremity resulting from a water moccasin bite.

ABSTRACT

Aeromonas hydrophila infection has been described as the cause of necrotizing fasciitis in patients with suppressed immune systems, burns, or trauma in an aquatic setting. We report a case in which severe necrotizing fasciitis involving hand, arm, chest, and lateral side of trunk, along with toxic shock, developed after the patient was bitten by a venomous snake. Mixed aerobic and anaerobic bacteria, including A hydrophila, were isolated from the wound culture. The patient was treated with antivenom, a diuretic regimen, broad spectrum antibiotics, and 18 separate surgical procedures. After the application of skin grafts, the wound completely healed. This case illustrates that a venomous snakebite may result in infection with A hydrophila and can cause severe necrotizing fasciitis. Early and aggressive surgical intervention should be implemented as soon as the necrotizing fasciitis is diagnosed.

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NECROTIZING FASCIITIS is a serious invasive soft-tissue infection that is relatively uncommon but often life-threatening. It is usually caused by toxin-producing, virulent bacteria and is characterized by widespread, rapidly developing fascial necrosis with relative sparing of skin and underlying muscle. Although this disease occurs more frequently in diabetics, alcoholics, immunosuppressed patients, drug users, and patients with peripheral vascular disease, it also occurs in young, previously healthy individuals. (1-3) We report an unusual case of necrotizing fasciitis of the upper extremity, possibly caused by A hydrophia infection, in a healthy man after a water moccasin bite on the hand.

CASE REPORT

A 38-year-old white man came to the emergency department at the University of Mississippi Medical Center with a snakebite on the dorsum of his left hand. The injury occurred 7 hours earlier and was presumed to have been inflicted by a water moccasin. The patient initially went to a local emergency room and received a single vial of antivenin injection. On presentation, he was conscious and complained of pain and swelling in the left hand and arm, stating that he was unable to move the affected hand. He experienced a brief period of shortness of breath and chest pain during transportation. The patient's medical history was unremarkable.

On arrival at our medical center, the patient was apprehensive, with blood pressure of 71/30 mm Hg, heart rate 112/min, respiratory rate 30/min, and temperature 97.7[degrees]F. Examination of the wounded left extremity revealed edema with ecchymosis throughout the hand and arm extending up to the shoulder (Fig 1). Capillary refill of the hand was delayed. Compartment pressures ranged from 28 to 32 mm Hg. Laboratory values were white blood cell count 6,100/[mm.sup.3], hematocrit 29%, sodium 140 mEq/L, potassium 3.9 mEq/L, chloride ions 122 mEq/L, blood urea nitrogen (BUN) 22 mg/dL, and creatinine 1.3 mg/dL. The platelet count was 94,000/[mm.sup.3], prothrombin time 18.5 sec, and partial thromboplastin time 48.6 sec. Fibrinogen was measured at 72 mg/dL. Findings on chest radiographs were normal.

The patient was initially treated in the emergency room, receiving 14 additional vials of antivenin and other supportive care. During the first hours of presentation, a plastic surgery consultant assessed the patient at the request of primary service and recommended exploration of the arm, but the primary service physician thought the patient's condition was not stable enough for surgery and the wound was not life-threatening. After being transferred to the intensive care unit the following day, the patient continued to receive antivenin, vasopressors to stabilize blood pressure, and broad spectrum antibiotics to control infection. Blood and platelet transfusions were also given to counteract hypotension and coagulopathy.

Three days after hospitalization, the patient had signs of renal damage, with urine output dropping to 30 mL/hr. The BUN level had risen to 84 mg/dL and the creatinine value to 3.2 mg/dL despite supportive therapy including vasopressors and intravenous fluids. Chest x-ray films also revealed bilateral pleural effusions with signs of pulmonary edema. These conditions continued for 2 weeks.

The day after injury, the condition of the arm had worsened, with increased edema. The arm was tender to palpation and manifested blue streaks up to the elbow with extensive ecchymosis throughout the arm. Further recommendation for surgical exploration was delayed because of the patient's unstable condition. By the third day, the blue discoloration and swelling had extended up to the left side of chest. A necrotic area developed on the extensor surface of the left hand, and an odor was present. The patient was still able to flex and extend the fingers. Computed tomography (CT) disclosed air bubbles in the tissue of the arm, indicating necrotizing fasciitis (Fig 2). He was immediately taken to the operating room for the first debridement of the wound.

In the first debridement, the necrotic skin and subcutaneous tissue over the extensor surface of the left hand and forearm were excised. Despite the absence of apparent pus, bubbles and gangrenous appearance were evident in the subcutaneous tissue and fascia. The fascia over the extensor surface was also removed until clear fascia margins were obtained (Fig 3). The muscle underneath was viable except for several small areas of necrosis, which were debrided. The wound was then copiously irrigated and scrubbed with 0.25% acetic acid, chlorhexidine gluconate (Hibiclines), hydrogen peroxide, and saline. In view of the patient's general condition and development of necrotizing fasciitis, further debridements were planned.

Tissue biopsy showed subcutaneous abscess formation, acute inflammation, hemorrhage, and necrosis in the soft tissue and fascia. Tissue culture revealed mixed aerobic and anaerobic bacteria. Aeromonas hydrophila was found along with gram-positive cocci, such as Enterococcus sp, and gram-negative rods, such as Klebsiella oxytoca, Morganella morganii, Citrobacter brakii, and Prevotella sp.

Despite antivenin and antibiotics to control infection (aztreonam, metronidazole, gentamicin, ampicillin, vancomycin, and ciprofloxacin), necrosis of soft tissue and fascia developed rapidly. Edematous and erythematous areas became necrotic throughout the medial aspect of the upper arm over the deltoid and latissimus muscles and down the flank. Inner compartmental necrotic fascia was also present. While continuing to receive antivenin, broad spectrum antibiotics, and regimens for hypotension and renal failure, the patient had consecutive debridements from the day after the first operation to 2 weeks after the snakebite injury. Excision of necrotic skin and fascia extended as far as down as the iliac crest and medially to the vertebral column.

The wound condition improved slowly after debridements. On the sixth day after injury, porcine grafts were used to cover the entire wound, with particular care to place them securely over the extensor tendons. On day 13, some granulation tissue was found under the porcine grafts. On day 16, the previous xenograft was removed. A total of approximately 700 [cm.sup.2] split-thickness skin grafts were transplanted to cover selected areas of the wound. On day 20, a second skin grafting was done with approximately 990 [cm.sup.2]. On day 31, a third skin grafting was done with approximately 2,550 [cm.sup.2].

The wound healed completely after these procedures (Fig 4). The procedures and timing of debridements, xenografting, and skin grafting are shown in the Table. The patient was discharged from the hospital on the 49th day after the snakebite injury. Some contracture of skin grafting on the left arm, elbow, and shoulder was surgically released before discharge and again at 3 months after injury.

DISCUSSION

Between 40,000 and 50,000 snakebites are reported each year in the United States. Of these, about 8,000 bites are inflicted by venomous snake. (4, 5) Toxic effects of venoms occur in the cardiovascular and hematologic systems, the nervous system, and the respiratory system. (6) The water moccasin belongs to the Crotalinae family which, including copperhead and rattlesnake, is the main family of poisonous snake in Mississippi. (7, 8) Crotalid venom alters blood vessel permeability, resulting in loss of plasma and blood into the tissue along with breakdown of red blood cells. This produces edema and ecchymosis that cause local necrosis and infection. (9) A recent study found a 6.6% increased incidence of wound necrosis and 5.5% increased incidence of secondary infection after snakebites. (10) A review of the literature on severe problems of the upper extremity caused by snakebite revealed a report of acute compartmental syndrome of the hand due to the bite of Vipera aspis, (11) but we found no previous report o f necrotizing fasciitis.

Although necrotizing fasciitis can occur in any region of the body, the most common sites are the abdominal wall, perineum, and extremities. (12, 13) Bacteriologically, necrotizing fasciitis is grouped as two entities. (14,15) In the type I form, at least one anaerobic species is present, most commonly Bacteroides, Peptococcus, Fusobacterium, Clostridium, or Corynebacterium. These organisms may be isolated as single agents or in combination with one or more facultative aerobes such as [alpha]-hemolytic streptococci, Escherichia coli, or Enterbacter, Kiebsiella, or Proteus species. The type II form, hemolytic streptococcal gangrene, is caused by group A streptococci, either alone or in combination with other species such as Staphylococcus aureus.

Aeromonas species are facultatively anaerobic gram-negative rods found as normal flora in nonfecal sewage and in fresh and brackish water. Aeromonas hydrophila is commonly recovered from skin and soft-tissue infections associated with exposure to contaminated water and water-related injuries. (16) Aeromonas hydrophila soft-tissue infection has been documented as a complication of snakebite. (17) Necrotizing fasciitis from A hydrophila in patients with suppressed immunity, burns, and trauma in an aquatic setting has also been reported. (18,19) In our case, A hydrophila was cultured from the necrotic tissue and was presumed to be the cause of necrotizing fasciitis. The other bacteria cultured from biopsy tissue (Enterococcus, Klebsiella oxytoca, Morganella morganii, Citrobacter brakii, and Prevotella sp) may have been from the wound contamination.

Diagnosis of necrotizing fasciitis is often difficult, and the clinical signs are used to make the diagnosis. Recently, Wall et a1 (20) developed a model to help distinguish between necrotizing fasciitis and nonnecrotizing soft tissue infection. They found that a white blood cell count >15,400/[mm.sup.3] and a serum sodium value <135 mEq/L were predictive, with sensitivity of 90% and specificity of 70%. Our patient, however, did not meet these criteria.

Although early debridement and surgical excision of the site of a venomous snakebite remains a controversial issue, (21,22) it is well known that necrotizing fasciitis must be promptly recognized and aggressively treated, since high rates of morbidity and mortality result if treatment is delayed. Treatment of necrotizing fasciitis is first and foremost surgical, along with antibiotic therapy and supportive care. Optimal surgery includes early debridement of all necrotic tissue and drainage of involved fascial planes via extensive fasciectomy until healthy fascia is encountered. These processes have been associated with improved survival as compared with delayed surgical intervention. (23,24) In this report, the major argument was whether the early radical debridement should be pursued or delayed until stabilization of the patient's renal failure and pulmonary edema. Since organisms and toxins are liberated from the area of necrotizing fasciitis into the bloodstream, serious toxic shock and sepsis may develop. There are reports of metastatic abscess formation in liver, lungs, spleen, brain, and pericardium, as well as multiple organ failure. (12,13,25,26) In our case, the patient's arm was debrided as soon as the CT scan showed air bubbles in the tissue and necrotizing fasciitis was suspected. With multiple debridements and high-close broad spectrum antibiotics, the infection was controlled and localized without systemic complications.

This clinical case illustrates that a venomous snakebite with possible A hydrophila infection can cause severe necrotizing fasciitis. In treatment of water moccasin bite, the surgeon should closely monitor the wound and implement early and aggressive surgical intervention as soon as necrotizing fasciitis is suspected.
TABLE.

Chronology of Surgical Therapy

Postinjury Day Surgical Procedure

 3 Debridement, excision of approximately 6% of body
 surface area, fasciotomy
 4 Debridement, removal of necrotic muscle and fascia
 6 Debridement, application of porcine graft
 8 Debridement, removal of porcine graft
 9 Debridement, removal of necrotic muscle and fascia
 10 Debridement, excision over the deltoid down to
 the latissimus areas, 12% of body surface
 11 Debridement, excision extended to iliac crest and
 and vertebral column, 4% of body surface
 12 Debridement, application of porcine graft
 13 Debridement, application of porcine graft
 15 Debridement, application of porcine graft
 16 Debridement, removal of porcine graft, application
 of split-thickness skin graft, 700 [cm.sup.2]
 20 Split-thickness skin graft, 990 [cm.sup.2]
 23 Removal of dressing, application of temporary
 wound dressing
 27 Debridement, application of Biobrane
 31 Debridement, split-thickness skin graft, 2,550
 [cm.sup.2]
 35 Dressing change
 43 Debridement, dressing change, shoulder contracture
 release
 82 Excision of scar tissue and contracture release
 in elbow and shoulder; split-thickness skin
 graft


References

(1.) Pessa ME, Howard RJ: Necrotizing fasciitis. Surg Gynecol Obstet 1985; 161:357-361

(2.) Gonzalez MH: Necrotizing fasciitis and gangrene of the upper extremity. Hand Clin 1998; 14:635-645

(3.) Donaldson PM, Naylor B, Lowe JW, et al: Rapidly fatal necrotising fasciitis caused by Streptococcus pyogenes. J Clin Pathol 1993; 46:617-620

(4.) Forks TP: Evaluation and treatment of poisonous snakebites. Am Fam Physician 1994; 50:123-130

(5.) Kitchens CS: Treatment of pit viper envenomation. J Fta Med Assoc 1996; 83:174-177

(6.) Wingert WA, Wainschel J: Diagnosis and management of envenomation by poisonous snakes. South Med J 1975; 68:1015-1026

(7.) Thwin MM, Gopalakrishnakone P: Snake envenomation and protective natural endogenous proteins: a mini review of the recent developments (1991-1997). Toxicon 1998; 36:1471-1482

(8.) Burch JM, Agarwal R, Mattox KL, et al: The treatment of crotalid envenomation without antivenin. J Trauma 1988; 28:35-43

(9.) Miller RA, Tu AT: Factors in snake venoms that increase capillary permeability. J Pharm Pharmacol 1989; 41:792-794

(10.) Rojnuckarin P, Mahasandana S, Intragumthornchai T, et al: Prognostic factors of green pit viper bites. Am J Trop Med Hyg 1998; 58:22-25

(11.) Vigasio A, Battiston B, De Filippo C, et al: Compartmental syndrome due to viper bite. Arch Orthop Trauma Surg 1991; 110:175-177

(12.) Umbert IJ, Winkelmann RK, Oliver GF, et al: Necrotizing fasciitis: a clinical, microbiologic, and histopathologic study of 14 patients. J Am Acad Dermatol 1989; 20:774-781

(13.) McHenry CR, Piotrowski JJ, Petrinic D, et al: Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221:558-563

(14.) Galbut DL, Gerber DL, Belgraier AH: Spontaneous necrotizing fasciitis. occurrence secondary to occult diverticulitis. JAMA 1977; 238:2302

(15.) Giuliano A, Lewis F Jr, Hadley K, et al: Bacteriology of necrotizing fasciitis. Am J Surg 1977; 134:52-57

(16.) Gold WL, Salit IE: Aeromonas hydrophila infections of skin and soft tissue: report of 11 cases and review. Chin Infect Dis 1993; 16:69-74

(17.) Jorge MT, Nishioka SD, de Oliveira RB, et al: Aeromonas hydrophila soft-tissue infection as a complication of snake bite: report of three cases. Ann Trop Med Parasitol 1998; 92:213-217

(18.) Minnaganti VR, Patel PJ, Iancu D, et al: Necrotizing fasciitis caused by Aeromonas hydrophila. Heart Lung 2000; 29:306-308

(19.) Furusu A, Yoshizuka N, Abe K, et al: Aeromonas hydrophila necrotizing fasciitis and gas gangrene in a diabetic patient on haemodialysis. Nephrol Dial Transplant 1997; 12:1730-1734

(20.) Wall DB, Klein SR, Black S, et al: A simple model to help distinguish necrotizing fasciitis from nonnecrotizing soft tissue infection. J Am Coll Surg 2000; 191:227-231

(21.) Davidson TM, Schafer SF: Rattlesnake bites, guidelines for aggressive treatment. Postgrad Med 1994; 96:107-114

(22.) Seiler JG III, Sagerman SD, Geller RJ, et al: Venomous snake bite: current concepts of treatment. Orthopedics 1994; 17:707-714

(23.) Voros D, Pissiotis C, Georgantas D, et al: Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infection. Br J Surg 1993; 80:1190-1191

(24.) Ward RG, Walsh MS: Necrotizing fasciitis: 10 years' experience in a district general hospital. Br J Surg 1991; 78:488489

(25.) Stevens DL: Streptococcal toxic shock syndrome associated with necrotizing fasciitis. Annu Rev Med 2000; 5 1:271-288

(26.) Farley DE, Katz VL, Dotters DJ: Toxic shock syndrome associated with vulvar necrotizing fasciitis. Obstet Gynecot 1993; 82:660-662

RELATED ARTICLE: KEY POINTS

* Necrotizing fasciitis is a serious invasive soft-tissue infection that is relatively uncommon but often life-threatening.

* Aeromonas species are facultatively anaerobic, Gram-negative rods found in non-fecal sewage and fresh and brackish water. Aeromonas hydrophila soft-tissue infection can be caused as a complication of snakebite.

* Diagnosis of necrotizing fasciitis is often difficult, and the clinical signs are used to make the diagnosis.

* Early and aggressive surgical intervention should be implemented as soon as the necrotizing fasciitis is diagnosed, along with antivenom and broad spectrum antibiotics.

From the Divisions of Plastic Surgery and Infectious Disease, University of Mississippi Medical Center, Jackson.

Reprint requests to Michael F. Angel, MD, University of Mississippi Medical center, Division of Plastic Surgery, 2500 N State St, Jackson, MS 39216.
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Author:Chapman, Stanley W.
Publication:Southern Medical Journal
Geographic Code:1USA
Date:Sep 1, 2002
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