80% of cases) and is among the fastest-growing clostridial species, with a generation time,
under ideal conditions, of approximately eight minutes. This organism produces collagenases
and proteases that cause widespread tissue destruction, as well asa-toxin, which have a role in
the high mortality associated with myonecrosis. Thea-toxin causes extensive capillary
destruction and hemolysis, leading to necrosis of the muscle and overlying fascia, skin, and
subcutaneous tissues. Patients complain of sudden onset of pain at the site of trauma or
surgical wounds, which rapidly increases in severity. The skin becomes edematous and tense.
Hemorrhagic bullae are common, as is a thin watery, foul smelling discharge. Examination of
the wound discharge reveals abundant large, boxcar-shaped gram-positive rods with a paucity
of surrounding leukocytes. The usual incubation period between injury and the onset of
clostridial myonecrosis is two to three days, but may be as short as six hours. A definitive
diagnosis is based on the appearance of the muscle on direct visualization by surgical
exposure. Initially, the muscle is pale, edematous, and unresponsive to stimulation. As the
disease process continues, the muscle becomes frankly gangrenous, black, and extremely
friable. This occurs with septicemia and shock. Nearly 15% of patients have positive blood
cultures. Serum creatinine phosphokinase levels are always elevated with muscle involvement.
The mortality rate associated with gas gangrene approaches 60%. Among the signs that predict
a poor outcome are leukopenia, thrombocytopenia, hemolysis, and severe renal failure.
Myoglobinuria is common and can contribute significantly to worsening of renal function.
Frank hemorrhage may be present and is a harbinger of disseminated intravascular
coagulation. Successful treatment of this life-threatening infection depends on early recogni-
tion and debridement of all devitalized and infected tissues. When extremities are involved,
amputation is frequently indicated. The role of hyperbaric oxygen therapy has not been
established (100% oxygen at 3 atm), but it may have a role early in the treatment of seriously ill
patients (19,20). The mainstay of treatment is surgical debridement, and this should not be
delayed. A less life-threatening form of this disease is known as clostridial cellulitis. In this
process, the bacterial tissue invasion is primarily superficial to the fascial layer, without muscle
involvement.C. septicumbacteremia is associated with underlying colon cancer or neutropenic
enterocolitis (21).C. sordellihas been reported to cause rapidly progressive myonecrosis with
fulminant shock syndrome, particularly in obstetric patients. Black tar heroin use has resulted
in the outbreak ofC. botulism, C. tetani, andC. sordelliin IV drug users.
Prompt recognition and treatment, as described earlier, can reduce the associated
morbidity and mortality. High dose of penicillin G is the drug of choice. Protein synthesis
inhibitors such as clindamycin when combined with penicillin has had considerable better
efficacy than penicillin alone.
Nonclostridial Myonecrosis
Nonclostridial myonecrosis encompasses at least five relatively distinct entities that differ from
gas gangrene in their pathogenesis, clinical features, and bacteriology: streptococcal myositis
NF type 2 (see discussion under sect. “Necrotizing Fasciitis”), synergistic nonclostridial anaerobic
myonecrosis NF type 1 (see discussion under sect. “Necrotizing Fasciitis”), anaerobic
streptococcal myonecrosis,Ae. hydrophilamyonecrosis, and infected vascular gangrene.
Anaerobic streptococcal myonecrosis clinically resembles subacute clostridial gas
gangrene. The involved muscles are discolored, in contrast to gas gangrene, early cutaneous
erythema is prominent. If not treated, the infection progresses to gangrene and shock. The
infection is usually mixed; anaerobic streptococci with group AStreptococcusorS. aureus.
Treatment involves the use of high-dose penicillin and antistaphylococcal agent, if indicated,
and surgical debridement.
Rapidly progressive myonecrosis resembling clostridial gangrene but caused byAe.
hydrophilamay occur after injuries sustained in freshwater, or in conjunction with medicinal
leech therapy. Cellulitis often develops within 12 to 24 hours, accompanied by excruciating
pain, marked edema, and bullae. Bacteremia is often documented. Treatment requires prompt
antimicrobial therapy and wide surgical debridement.
Infected vascular gangrene is a focal, usually indolent and primarily ischemic process in
the small muscles of a distal lower extremity already gangrenous from arterial insufficiency.
Diabetic patients are prone to develop this complication, which usually does not extend
Severe Skin and Soft Tissue Infections in Critical Care 307