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Gas Gangrene

  1. Gas gangrene is caused by exotoxin-producing clostridial species (large, gram-positive, spore-forming bacilli).
  2. These anaerobic organisms normally are found in soil and the gastrointestinal tract. Clostridium perfringens causes 80-95% of cases of gas gangrene.
  3. Spontaneous gas gangrene is caused by hematogenous spread (in immunocompromised or with diabetes). Clostridium septicum is the most common causative organism of spontaneous gas gangrene.
  4. Exotoxin, not bacterial proliferation, is responsible for rapid spread of infection.
  5. Exotoxin causes muscle destruction and creates an anaerobic environment conducive to further bacilli growth.
  6. Products of tissue breakdown (eg, creatine phosphokinase, myoglobin, potassium) cause secondary toxicity.
  7. Mortality from traumatic gas gangrene is greater than 25%.
  8. Mortality from nontraumatic gas gangrene caused by C septicum ranges from 67-100%. 
  1. Pathophysiology:
    An anaerobic, gram-positive, spore-forming bacillus of the genus Clostridium causes gas gangrene.
    1. C perfringens is the most common cause of gas gangrene.
    2. Other common clostridial pathogens causing gas gangrene are Clostridium bifermentans, Clostridium septicum, Clostridium sporogenes, Clostridium novyi, Clostridium fallax, Clostridium histolyticum, and Clostridium tertium.
  2. History:
    Incubation period usually is fewer than 3 days, with rapid onset of symptoms. Infection can advance as   much as 1in/h.
    Pain commonly is out of proportion to physical findings.
    Progression to toxemia and shock can be rapid. 
  3. Physical:
    1. Local swelling and a serosanguineous exudate appear soon after the onset of pain.
    2. The skin characteristically turns to a bronze color, then progresses to a blue-black color with skin blebs and hemorrhagic bullae.
    3. Within hours, the entire region may become markedly edematous.
    4. The wound may be nonodorous or may have a sweet mousy odor.
    5. Crepitus follows gas production; at times, due to brawny edema, crepitus may not be detected with palpation.
    6. Pain and tenderness to palpation disproportionate to wound appearance are common findings.
    7. Tachycardia disproportionate to body temperature is common.
    8. Late signs include hypotension, renal failure, and a paradoxical heightening of mental acuity.
    9. In summary, the typical signs and symptoms are severe pain and tenderness, local swelling to massive edema, skin discoloration with hemorrhagic blebs and bullae, nonodorous or sweet odor, crepitus, fever, relative tachycardia, and altered mental status. 
  4. Lab Studies:
    1. Gram stain of bullae fluid or muscle tissue: Pleomorphic, gram-positive bacilli with a paucity of leukocytes are considered diagnostic.
    2. Complete blood count: hemolysis and anemia secondary to release of toxins.
    3. Liver function tests: Hyperbilirubinemia and liver dysfunction.
    4. Electrolytes: Hyperkalemia can result from cell breakdown.
    5. Renal panel: Kidney dysfunction.
    6. Arterial blood gas: Gas gangrene can cause metabolic acidosis.
    7. Coagulation panel: Coagulopathy and thrombocytopenia can result.
    8. Myoglobin: Myoglobinemia and myoglobinuria dur to cellular breakdown. 
  5. Imaging Studies:
    Plain radiographs may reveal soft tissue gas within the fascial planes.
    Computed tomography demonstrates the extent of tissue involvement. 
  6. Treatment
    Prehospital Care: Oxygenation/ Intravenous (IV) fluids/ Rapid stabilization of patient, because the disease may progress rapidly 
  7. Emergency Department Care: Resuscitation, supplemental oxygen, and aggressive volume expansion may be indicated.
    Use vasoconstrictors only if absolutely necessary; they can decrease perfusion to already ischemic tissue.
    Administer antibiotics.
    Tetanus toxoid and immune globulin may be administered if indicated.
    Surgical debridement is the definitive treatment. 
  8. Surgical Care:
    1. Fasciotomy for compartment syndrome may be necessary immediately.
    2. Daily debridement as needed to remove all necrotic tissue.
    3. Amputation of the extremity may be necessary and life-saving.
    4. Abdominal involvement requires excision of the body wall musculature.
    5. Uterine gas gangrene following septic abortion usually necessitates hysterectomy.
    6. Aggressive surgical debridement and intensive medical therapy are the mainstays of treatment of gas gangrene; however, HBO therapy has become an important adjunct therapy, especially in patients with truncal involvement.

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