Usually a complication of a crushing injury
Infectious disease emergency
Rapid onset of myonecrosis
Mortality in traumatic gas gangrene is >25%
Incubation period is fewer than 3 days with rapid onset of symptoms
Progression of toxemia and shock is rapid.
Caused by clostridium welchii
Exotoxin producing Clostridial species
Large gram positive bacilli, pleomorphic
Spore forming bacilli
Normally found in soil and GI tract and widely distributed in the environment
Thrives in the absence of oxygen
Breed in damaged tissue
Traumatic or post Surgical gas gangrene (Clostridium perfringens)
Contamination may also occur from patient's faecal flora
Spontaneous gas gangrene (Clostridium septicum)
Often in immune compromised host
Associated with hematological and GI malignancies
Drug abuse is a risk factor
Gain access to humans
Direct inoculation into a open wounds due to trauma, bullet wounds, and multiply along with facultative co infecting or colonizing organisms.
Condition consisting of low oxidation reduction potential are necessary for C. perfringens sporulation, followed by rapid division. Gas gangrene is usually a mixed infection aerobic and anaerobic.
Presumably, the other facultative organisms assist in reducing the oxidative-reductive potential.
Invasion and spread in humans
Exotoxin, not bacterial proliferation, is responsible for rapid spread of infection.
Exotoxin causes muscle destruction and creates an anaerobic environment conducive to further bacilli growth.
alpha toxin is produced by the growing C. perfringens, which kill muscle cells and inflammatory cells, alpha toxin's biologic activity is a lecithinase, causing necrosis, and hemolysis.
Beta and epsilon toxins are also necrotizing, and considered major toxins. Subsequently, new necrotic areas will foster growth and spread of the organisms.
Carbohydrate fermentation by C. perfringens is responsible for the gas production (crepitus).
Secondary toxicity. Products of tissue breakdown cause secondary toxicity
WBC's try to attack these organisms.
We have no defense against toxins
Death occurs within about two days if the condition is not treated. Often have shock, jaundice, hemolysis and renal failure along with local findings.
Fowl-smelling serosanguinous discharge
Ischemic appearing muscle tissue
Gas in soft tissue within fascial planes
Systemic secondary to toxins
Fever or hypothermia. Unlike many other infections, hypothermia, or just absence of fever can predominate the clinical course.
Tachycardia is frequently out of proportion to elevation of temperature that is, faster heart rates may not fit with a normal temperature.
Altered level of consciousness
Coagulopathy and thrombocytopenia
Myoglobinemia and Myoglobinuria
Rapid diagnosis is by
Gram stain of bullae fluid or muscle tissue: Paucity of WBC with gram positive bacilli. Inflammatory cells are killed along with muscle cells by alpha toxin.
Pathologic demonstration of myonecrosis : Myoglobinemia and Myoglobinuria
Radiographs showing gas within fascial planes
CBC: Anemia hemolytic secondary to toxins
LFT: Liver dysfunction
Renal panel: Kidney dysfunction
ABG: Metabolic acidosis
Coagulation panel: Coagulopathy and thrombocytopenia
Surgical debridement is the definitive treatment: Emergency consult. Treatment may include fasciotomy, debridement, or amputation.
Hyperbaric oxygen: may be helpful.
IV fluids: Aggressive volume expansion
Antibiotics : Treat mixed infection with Penicillin Sodium and Amino glycosides or Vancomycin.
Appropriate wound care at the time of injury
removal of dead tissue
Prophylactic antibiotics: Benzyl penicillin
The organism is not contagious and does not spread from person to person.
Other clinical infections
Gall bladder with abdominal wall muscle involvement following surgery, uterus (endometrium) are other body sites can be infected by this organism to cause similar disease
Other species of Clostridium
Food poisoning: Botulism