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Clostridial Myonecrosis (Gas Gangrene) PDF Print E-mail

Pathophysiology and Hyperbaric Effects

Gas gangrene, or Clostridial myosistis and myonecrosis, is an invasive clostridial infection of muscle, characterized by toxemia, extensive edema, massive death of tissue, and a variable degree of gas production. Gas gangrene is either an endogenous infection, caused by contamination from a clostridial focus in the body, or an exogenous infection secondary to trauma. For the induction of gas gangrene, two conditions have to be fulfilled:

I. The presence of clostridial spores; and an area of lowered oxidation-reduction potential caused by circulatory failure in a local area, or

II. Extensive soft tissue damage and necrotic muscle tissue. This condition results in an area with a low oxygen tension where clostridial spores can develop into their vegetative form. Much of the disease process seen in gas gangrene is due to clostridial toxins. Nine clostridial exotoxins have been implicated in the local and systemic changes seen in gas gangrene: alpha, theta, kappa, my and pu toxin, fibrinolysin, neuraminidase, circulating factor, and bursting factor. The most prevalent is alpha-toxin, the oxygen-stable lecithincase-C, which is hemolytic, tissue necrotizing, and lethal. Alpha toxin can be fixed to susceptible skin cells in 20 to 30 minutes, is detoxified within two hours after its elaboration, and causes active immunity with production of a specific antitoxin. The infection, unfortunately, is so progressive, with continuous production of alpha-toxin that the patient dies before any effective immunity can develop. Local host defense mechanisms are eliminated when the toxin production is sufficiently high. Such an event results in fulminating tissue destruction, an increased volume of hypoxic tissue, and further clostridial growth.

The action of hyperbaric oxygen on Clostridia (and other anaerobes) is based on the formation of oxygen free radicals in the absence of free radical degrading enzymes, such as superoxide dismutases, catalases, and peroxidases. Van Unnink showed that an oxygen tension of 250 mm Hg is necessary to stop alpha-toxin production. Although it does not kill all Clostridia, it is bacteriostatic and bactericidal both in vivo and in vitro. The catalase effects of stimulating necrosis are inhibited by high oxygen concentrations. Demello, et al., demonstrated a reduction in the generation rate of heat-activated spores of Clostridia perfringens. Brummelkamp and Boerema were the first to report the successful use of hyperbaric oxygen therapy (HBOT) at 3 ATA in the management of gas gangrene.

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