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Emergent Treatment of Gas Gangrene

  • Author: Lee Stuart Jacobson, MD, PhD; Chief Editor: Rick Kulkarni, MD  more...
Updated: Feb 19, 2014


Gas gangrene, a subset of necrotizing myositis, is an infectious disease emergency associated with extremely high morbidity and mortality. 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]



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.




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.


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 from traumatic gas gangrene is greater than 25%.

Mortality from nontraumatic gas gangrene caused by C septicum ranges from 67-100%.


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]

Contributor Information and Disclosures

Lee Stuart Jacobson, MD, PhD Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Clinical Fellow in Medicine, Harvard Medical School

Lee Stuart Jacobson, MD, PhD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.


Carlo L Rosen, MD Associate Professor of Medicine, Harvard Medical School; Program Director, Vice Chair for Education, Associate Director of Medical Education, Harvard Affiliated Emergency Medicine Residency Program, Department of Emergency Medicine, Beth Israel Deaconess Medical Center

Carlo L Rosen, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jason K Wong, MD Staff Physician, Department of Emergency Medicine, Jefferson Regional Medical Center

Jason K Wong, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Anil Shukla, MD Staff Physician, Harvard Affiliated Emergency Medicine Residency, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, Society for Academic Emergency Medicine

Disclosure: Received salary from WebMD for employment.


Michelle Ervin, MD Chair, Department of Emergency Medicine, Howard University Hospital

Michelle Ervin, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Wende R Reenstra-Buras, MD, PhD Associate Director of Basic Science Research, Staff Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

N Ewen Wang, MD Consulting Staff, Department of Surgery, Division of Emergency Medicine, Stanford University Hospital

Disclosure: Nothing to disclose.

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Left lower extremity in a 56-year-old patient with alcoholism who was found comatose after binge drinking. Surgical drainage was performed to treat the pyomyositis-related, large, non–foul-smelling (sweetish) bullae. Gram staining showed the presence of gram-positive rods. Cultures revealed Clostridium perfringens. The diagnosis was clostridial myonecrosis.
A patient developed gas gangrene after injecting cocaine. Clostridium septicum was isolated in both blood and wound cultures.
Gas feathering in the arm soft tissue of a patient with gas gangrene.
Extension of gas gangrene to the chest wall despite initial debridement.
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