eMedicine Specialties > Emergency Medicine > Infectious Diseases

Gas Gangrene

Author: Anil Shukla, MD, Staff Physician, Harvard Affiliated Emergency Medicine Residency, Beth Israel Deaconess Medical Center
Coauthor(s): Carlo L Rosen, MD, Assistant Professor of Medicine, Harvard Medical School; Program Director, Department of Emergency Medicine, Beth Israel Deaconess Medical Center/ Harvard Affiliated Emergency Medicine Residency program; Jason K Wong, MD, Staff Physician, Department of Emergency Medicine, Jefferson Regional Medical Center
Contributor Information and Disclosures

Updated: Jun 22, 2009

Introduction

Background

Gas gangrene, a subset of necrotizing myositis, is an infectious disease emergency. 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}

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.

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

Clinical

History

History for gas gangrene includes the following:^1,2

• Infection usually results from deep trauma or surgery, although minor procedures, such as intramuscular injection, have been associated with gas gangrene.
• The incubation period is usually less than 24 hours but has been described to be anywhere from 7 hours to 6 weeks, though when symptoms start, clinical deterioration can occur within hours.
• Muscle swelling and severe pain are prominent features. The pain is often out of proportion to physical findings, reflective of the hypoxic state of the muscle tissue, and is key to distinguishing gas gangrene from simple cellulitis.
• Systemic toxicity may cause altered mental status, and the progression to toxemia and shock can be rapid.

Physical

Physical findings of gas gangrene are as follows:^1,2,3,10,11

• Vital signs: Unusually, fever is not a prominent feature of infection and may only be low grade throughout the clinical course. The degree of systemic involvement may produce a spectrum of changes from tachycardia through outright septic shock including hypotension and diaphoresis.
• Overlying skin: Initially, the skin may be normal and then progress through a yellowing or bronzing to bulla formation to patches of green/blue/grey/black necrosis. Serosanguineous drainage may be present, described classically as having a “mousy” or slightly sweet odor.
• Examination: Most notable is extreme pain of the affected area with or without movement and with palpation, which may be out of proportion to the extent of the overlying skin changes. Tense edema with crepitance due to subcutaneous air may be noted and is proportional to the extent of underlying necrosis.
• Vascular examination: Distal pulses may be normal or diminished depending on the extent of local damage.
• Neurologic examination: Decreased pain or anesthesia at the site of infection can indicate that cutaneous nerve endings are being destroyed and that the disease is advanced.

Causes

• Risk factors for gas gangrene^8,12
  • Atherosclerosis
  • Burns
  • Chronic alcoholism

• Corticosteroid use
• Diabetes
• Gastrointestinal malignancy
• HIV/AIDS
• Hypoalbuminemia
• Intravenous drug abuse

• Malnutrition
• Obesity
• Open fractures
• Peripheral vascular disease
• Surgery
• Trauma

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