Gas gangrene or clostridial myonecrosis is a rare, life-threatening infection of the muscle that is typically associated with recent surgery or trauma. It usually affects older individuals who suffer from vascular insufficiency or who are immunocompromised.
The typical pathogen in gas gangrene is Clostridium perfringens. Atraumatic gas gangrene caused by Clostridium septicum is less common and has a unique association with colon cancer. This condition aggressively spreads through the muscular tissue and often culminates in septic shock. Fatality occurs within 48 hours if left untreated; however, despite emergent treatment, the mortality rate is >50% without any comorbidities.1
Given the propensity for gas gangrene to occur in the extremities, the orthopedic surgeon must be familiar with its presentation, diagnosis, and treatment. This article presents a case of C septicum myonecrosis in a 16-year-old adolescent girl.
A 16-year-old adolescent girl presented to the emergency department with an 18-hour history of malaise and progressive right arm discomfort and swelling. She had developed a small ecchymotic area around the elbow that was expanding rapidly.
Her history was significant for remote self-mutilating behavior. She reported being bitten by a mouse and also scratched by a family cat approximately 1 week previously. She did not seek treatment for either injury.
Physical examination revealed an ill-appearing adolescent girl. She was afebrile and mildly tachycardic. Her initial blood pressure was 106/60 mm Hg, with a repeat measurement of 70/40 mm Hg.
Her right arm was ecchymotic, mottled, and swollen. There were good distal pulses. Subcutaneous crepitance was noted throughout the soft tissue of the right upper extremity. Mottling also was noted in her right lower leg and left thigh. No recent wounds were evident that would have corresponded to an animal bite or self-inflected trauma.
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Figure 1: Preoperative radiograph of the right upper extremity showing air within the muscle of the upper arm and within the pectoralis major crossing over to the chest wall. Figure 2: Photograph showing the appearance of the right upper extremity prior to surgery.
Radiographs of her right upper extremity (Figure 1) revealed gas in the tissue planes throughout the arm with extension into the chest wall. The patient was started on vasopressors and intravenous antibiotics, and then taken to the operating room emergently. The time from the physical examination to operating room was <1 hour.
Initial operative irrigation and debridement began at the right shoulder. The skin and subcutaneous tissue appeared edematous and ischemic (Figure 2). Gas crackling was audible on tissue dissection. The entire shoulder girdle and chest wall were involved. A shoulder disarticulation was performed.
Crepitance was felt in her right lower leg, and a radiograph (Figure 3) showed evidence of involvement of her posterior compartment. This compartment was resected with normal-appearing fascial borders.
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Figure 3: Intraoperative radiograph showing air within the posterior compartment of the right lower extremity.
Further examination revealed blanching and ecchymosis of her left thigh. An intraoperative radiograph revealed the presence of gas gangrene in the gluteus maximus muscle. Operative intervention proceeded with resection of the gluteus maximus.
Her postoperative course was complicated by disseminated intravascular coagulopathy, acute renal failure, and metabolic acidosis. Follow-up radiographs revealed progression of the myonecrosis into her pelvis and left arm. The family decided against additional resective surgery, and the patient died within 24 hours of initial presentation.
The identification and emergent treatment of necrotizing soft-tissue infections is extremely important and often falls on the orthopedic surgeon, especially when isolated to the extremities. Subtle initial presentation and rapid progression of the infection are classic findings of necrotizing soft-tissue infections, particularly with clostridial myonecrosis and necrotizing fasciitis.
Necrotizing soft-tissue infections were first reported by Hippocrates as flesh, sinews, and bones fell away in large quantities...There were many deaths.2 These soft-tissue infections have been labeled as streptococcal gangrene, phagedena, and phagedena gangrenosum, as well as hospital gangrene by a Confederate army surgeon who was the first to report a necrotizing infection in the United States in 1871.3
In 1952, Wilson4 coined the term necrotizing fasciitis, which was used to describe both gas gangrene and other nongas-producing microbes capable of causing rapidly progressive fascial infections. Gas gangrene is noted for its devastating effects on soldiers. During World War I, there was a 5% rate of clostridial myonecrosis complicating wounds, which decreased to 0.7% during World War II, 0.2% during the Korean War, and 0.0002% during the Vietnam War.5-9 This decline is attributed to advances in wound care as well as earlier recognition and treatment of infected wounds.
Although these infections have been reported widely by the media in recent years, they are uncommon in the United States, with only 1000 to 3000 cases reported annually.10 Forty-nine percent of these cases occur after a penetrating trauma, 35% occur after surgery, and 16% occur from atraumatic causes.11
Infection with C septicum may be associated with colorectal or hematological malignancy, diabetes mellitus, and drug-induced immunosuppression. It is hypothesized the bacteria gains access to the bloodstream through a defect in the mucosa of the large bowel. Skeletal muscle then can be contaminated via the bloodstream. The majority of these case reports occur in patients with a gastrointestinal malignancy.
Clostridium is an anaerobic, spore-forming, gram-positive, boxcar-shaped bacillus. The most common isolate is C perfringens, whereas C septicum accounts for 4% to 20% of clostridial infections and usually is responsible for atraumatic causes.12
Clostridiae are extremely pervasive in the environment, with no known living life form being spared from colonization. Necrotic, devitalized tissue is ideal environment for transformation into its virulent form. Rapid and extensive muscle destruction is caused by the production of proteolytic toxins.13 The organism contaminates ischemic tissues and rapidly replicates, causing edema and other signs of infection within 2 to 6 hours. The release of toxins causes further tissue destruction and necrosis, propagating a self-perpetuating infection.14
Without early debridement, progression to septicemia, acute tubular necrosis, disseminated intravascular coagulopathy, shock, and death occur within hours to days. Overall mortality rates range from 25% to 75%.15
Early identification and emergent action is necessary for proper treatment. Timely diagnosis of clostridial myonecrosis is of the utmost importance. It often can be overlooked as a benign soft-tissue infection in the early stage. No specific diagnostic criteria exist; however, a triad of pain out of proportion to the injury, tachycardia unexplained by fever, and crepitus in the soft tissue is strongly suggestive. A history of recent open trauma, surgery, diabetes, or an immunocompromised state is important to elicit.9
Patients may complain of pain and heaviness in the area. Edema soon develops, and the skin, which is initially pale, acquires a bronze hue. By the time blebs and hemorrhagic bullae appear, there is significant underlying soft-tissue necrosis and systemic involvement. Drainage also may be present and may be serous or purulent.16
Treatment of clostridial myonecrosis begins with immediate administration of intravenous penicillin, clindamycin, and a fluoroquinolone or chloramphenicol, followed by surgery. Initial skin incision reveals gas throughout the subcutaneous tissue. The infected muscle has a deep purple presentation, and the line between healthy and infected muscle is easily distinguished.
Debridement of all devitalized tissue down to a well-oxygenated core is imperative. If muscle necrosis has progressed across a joint, disarticulation and muscle resection is necessary to prevent further spread.
Cultures should be obtained to confirm the diagnosis and aid in future antibiotic regimens. Wounds typically are left open for repeat irrigation and debridement within 48 hours.
Postoperatively, patients should be placed in an intensive care unit and closely monitored for disease progression, disseminated intravascular coagulation, renal failure, and acute respiratory distress syndrome. Meticulous fluid management is necessary, and patients often will require vasopressors and dialysis.
The use of hyperbaric oxygen may be considered; however, there are no comparative human studies examining the use of hyperbaric oxygen, surgery, and antibiotics versus surgery and antibiotics alone. Comparative studies on animals have shown decreased mortality rates with the use of hyperbaric oxygen.
In a meta-analysis by Rudge,17 a total of 1,278 patients were treated with hyperbaric oxygen, antibiotics, and surgery, with an overall survival rate of approximately 80%. Other studies comparing treatment before and after the use of hyperbaric oxygen show a decrease in mortality from 70% to 25%.11 Clostridium septicum appears to be minimally affected by hyperbaric oxygen because of its areotolerance.18
Clostridial myonecrosis is a rare orthopedic condition with high mortality. Early diagnosis and debridement is imperative. A team approach to managing these patients postoperatively is necessary. The use of hyperbaric oxygen can be considered; however, it may not be readily available and its utility is unproven in human studies. Because of the high mortality rate associated with clostridial myonecrosis, one should err on the side of more aggressive resective and ablative surgery.
- Larson CM, Bubrick MP, Jacobs DM, West MA. Malignancy, mortality, and medicosurgical management of Clostridium septicum infection. Surgery. 1995; 118(4):592-598.
- Hippocrates. Epidemics. Vol 1. Jones WHS, trans. London, England: Harvard University Press; 1957.
- Jones J. Observations upon the losses of the Confederate armies from battle, wounds and disease during the American Civil War of 1861-1865, with investigations upon the number and character of disease supervening upon gun shot wounds. Richmond Louisville Medical Journal. 1871; 9:453-480.
- Wilson B. Necrotizing fasciitis. Am Surg. 1952; 18(4):416-431.
- MacLennan JD. Anaerobic infections of war wounds in the Middle East. Lancet. 1943; (2):94-98.
- MacLennan JD. The histotoxic clostridial infections of man. Bacteriol Rev. 1962; (26):177-276.
- Altemeier WA, Furste WL. Gas gangrene. Surg Gynecol Obstet. 1947; (84):507-523.
- Simeone F. Clostridial myositis. In: Symposium on Military Medicine in the Far East Command. Surgeons Circular Letter. Medical Section. 1951; Sept (suppl).
- Brown PW, Kinman PB. Gas gangrene in a metropolitan community. J Bone Joint Surg Am. 1974; 56(7):1445-1451.
- Present DA, Meislin R, Shaffer B. Gas gangrene: a review. Orthop Rev. 1990; 19(4):333-341.
- Hart GB, Lamb RC, Strauss MB. Gas gangrene. J Trauma. 1983; 23(11):991-1000.
- Mayer G, Kang R. Gas gangrene, diabetes, and cholecystitis. Am J Emerg Med. 1985; 3(1):42-45.
- Hart G, Lamb R, Strauss MB. Clostridium species. In: Medical Microbiology. St Louis, MO: Mosby; 2002:714.
- McDonel JL. Clostridium perfringens toxins (type A, B, C, D, E). Pharmacol Ther. 1980; 10(3):617-655.
- Hitchcock CR, Demello FJ, Haglin JJ. Gangrene infection: new approaches to an old disease. Surg Clin North Am. 1975; 55(6):1403-1410.
- Perry B, Waldo F. Gas gangrene and necrotizing fasciitis in the upper extremity. Journal of Surgical Orthopaedic Advances. 2004; 13:57-68.
- Rudge FW. The role of hyperbaric oxygenation in the treatment of clostridial myonecrosis. Mil Med. 1993; 158(2):80-83.
- Hill GB, Osterhout S. Experimental effects of hyperbaric oxygen on selected clostridial species, I: in vitro studies. J Infect Dis. 1972; 125(1):17-25.
Dr Wiersema is from the Great Lakes Orthopedic Center, Munson Medical Center, Traverse City, Michigan; Dr Scheid is from the Department of Orthopedic Trauma, OrthoIndy, Indianapolis, Indiana; and Dr Psaradellis is from the Fox Valley Orthopedic Institute, Geneva, Illinois
Drs Wiersema, Scheid, and Psaradellis have no relevant financial relationships to disclose.
Correspondence should be addressed to: Brent M Wiersema, DO, Great Lakes Orthopedic Center, Munson Medical Center, 4045 W Royal Dr, Traverse City, MI 49684.