Pathophysiology, Microbiology, and Risk FactorsClostridial myonecrosis refers to fulminant skeletal muscle infection caused by Clostridium species. Commonly called gas gangrene, the infection has a prominent history as a complication of battlefield wounds. Prior to widespread use of antibiotics and improved surgical interventions, clostridial myonecrosis complicated as many as 5% of battlefield injuries in World War II.Clostridia are anaerobic, gram-positive rods found widely in the soil and as a colonizer of humans and animals. Following inoculation, Clostridia multiply in the anaerobic environment created by trauma, impaired blood supply, and foreign bodies. Exotoxins appear to mediate a rapidly spreading myonecrosis, and extensive gas formation is classic. Clostridium perfringens is the most common cause of clostridial myonecrosis, although other Clostridia can also cause the infection. As many as 60% to 85% of infections may additionally involve non-clostridial bacteria.Clostridial myonecrosis can be divided into three categories: posttraumatic, postoperative (non-traumatic), and spontaneous. Causes of post-traumatic clostridial myonecrosis include compound fractures, other potentially contaminated injuries, burns, injections, and decubitus ulcers. Procedures that may be complicated by postoperative clostridial myonecrosis include abdominal surgery, amputations, and other types of surgery. Diabetes, advanced age, immunosuppression, chronic edema, and chronic debilitating illnesses have also been described as risk factors for clostridial myonecrosis. Spontaneous clostridial myonecrosis is usually caused by C. septicum bacteremia, which is associated with lower gastrointestinal (particularly cecal) malignancies, diabetes, and neutropenic colitis.
Clinical PresentationFollowing the initial inoculation or traumatic event, an incubation period of 1 to 4 days is typical, but a range of 1 hour to 6 weeks has been described. Clostridial myonecrosis is classically characterized by a triad of severe pain, tachycardia out of proportion to fever, and crepitus on examination. Early signs in postoperative cases include changes in wound appearance, pain, or onset of systemic toxicity. Signs of progression include edema, bronze purplish or brown skin discoloration, mottling, and bullae with serosanguinous discharge. Hypotension, shock, severe hemolysis, and acute renal failure may occur.*122/348/5*
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