Emergent Treatment of Gas Gangrene

Updated: Oct 21, 2016
  • Author: Xiao Wang, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Overview

Background

Gas gangrene, a subset of necrotizing myositis, is an infectious disease emergency associated with extremely high morbidity and mortality. Organisms in the spore-forming clostridial species, including Clostridium perfringens, Clostridium septicum, and Clostridium novyi, cause most of the cases . A nonclostridial form is caused by a mixed infection of aerobic and anaerobic organisms. The hallmarks of this disease are rapid onset of myonecrosis with muscle swelling, severe pain, gas production, and sepsis. [1, 2, 3]

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Pathophysiology

Clostridium species are gram-positive, spore-forming, anaerobic rods normally found in soil and the gastrointestinal tract of humans and animals. They most often cause disease in the setting of trauma or surgery but can also occur spontaneously in the absence of definite risk factors or exposures. Not all wounds contaminated with clostridia develop gas gangrene; the myonecrosis seems to only develop when sufficient devitalized tissue is present to support anaerobic metabolism. [2]

Traumatic gas gangrene and surgical gas gangrene occur through direct inoculation of a wound. With a compromised blood supply, the wound has an anaerobic environment that is ideal for C perfringens, the cause of 80-95% of cases of gas gangrene. [4, 5]

Spontaneous gas gangrene is most often caused by hematogenous spread of C septicum from the gastrointestinal tract in patients with colon cancer or other portals of entry. Neutropenic and immunocompromised patients are also at risk. The organism enters the blood via a small break in the gastrointestinal mucosa and subsequently seeds muscle tissue. Unlike C perfringens, C septicum is aerotolerant and can infect normal tissues. [6]

With C perfringens, the local and systemic manifestations of infection are due to the production of potent extracellular protein toxins by the bacteria. These are most notably alpha-toxin (a phospholipase C) and theta-toxin (a thiol-activated cytolysin). These toxins hydrolyze cell membranes, cause abnormal coagulation leading to microvascular thrombosis (further extending the borders of devascularized and thus anaerobic tissue), and have direct cardiodepressive effects. Furthermore, the products of tissue breakdown, including creatine phosphokinase, myoglobin, and potassium, may cause secondary toxicity and renal impairment. [7]

Significant and refractory anemia may also be present in patients with gas gangrene. This effect is a direct consequence of toxin-mediated hemolysis of RBCs when significant amounts of alpha toxin are released into the bloodstream. Alpha toxin has negative inotropic effects on cardiac myocytes contributing to the severe, refractory hypotension seen in some cases of gas gangrene. Theta toxin causes a cytokine cascade, which results in peripheral vasodilation similar to that seen in septic shock. Vaccination of experimental animals against alpha and theta toxins substantially decreases the severity of infection.

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Epidemiology

Frequency

United States

Estimates of incidence of gas gangrene vary; however, with improvements in surgical technique and wound care, cases are relatively rare. Data from 1975 estimate 900-1000 cases per year, or 0.03-5.2% of open wounds, depending on type of wound and treatment. Clostridial contamination of wounds may be common, although in the absence of deep injury or significant devitalized tissue, myonecrosis and productive infection do not typically occur.

International

No data are published, but incidence is probably higher internationally than in the United States. Incidence is highest in areas with poor access to proper wound care. The incidence of surgically acquired infection is higher in areas where sterile technique and surgical hygiene may be imperfect.

Mortality/Morbidity

Mortality from traumatic gas gangrene is greater than 25%.

Mortality from nontraumatic gas gangrene caused by C septicum ranges from 67-100%.

Age

Occurrence is not age specific.

Diabetic peripheral vascular disease and other chronic immunocompromised states that can predispose individuals to gas gangrene are more prevalent in older populations. [8, 9]

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