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Drugs & Diseases > Emergency Medicine

EMERGENT TREATMENT OF GAS GANGRENE

Updated: Sep 29, 2023
* Author: Jessica Ward, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III,
MD more...

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Sections
Emergent Treatment of Gas Gangrene

* Sections Emergent Treatment of Gas Gangrene
* Overview

* Background
* Pathophysiology
* Epidemiology
* Prognosis
* Show All
* Presentation

* History
* Physical
* Causes
* Complications
* Show All
* DDx
* Workup

* Laboratory Studies
* Imaging Studies
* Other Tests
* Procedures
* Show All
* Treatment

* Prehospital Care
* Emergency Department Care
* Consultations
* Medical Care
* Prevention
* Further Inpatient Care
* Inpatient & Outpatient Medications
* Transfer
* Show All
* Medication

* Medication Summary
* Antibiotics
* Medicinal gas
* Toxoids
* Immunoglobulins
* Analgesics
* Show All
* Media Gallery
* References

Overview

BACKGROUND

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]

Next: Pathophysiology

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. [3] 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 the vast
majority of cases of gas gangrene. [4] Additionally, while C perfringens cannot
grow in the presence of oxygen, it is relatively resistant to killing by oxygen.
This, along with its extremely rapid doubling time make it highly virulant. [4]
The degredation of host tissues and rapid transport of nutrients into bacterial
cells from the host tissues produces abundant gas from the anaerobic glycolysis
pathway resulting in even more improved conditions for growth. [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 immunocompromised patients, patients who have
undergone prior radiation therapy to the abdomen, and those with vascular
compromise 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. C
perfringens and C histolyticum are more commonly associated with trauma. [6]

With C perfringens, the local and systemic manifestations of infection are due
to the production of potent extracellular protein toxins by the bacteria. [36]
These are most notably alpha-toxin (a phospholipase C) and theta-toxin (a
thiol-activated cytolysin), also known as perfringolysin O (PFO). These toxins
often function synergistically. They 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. The pathogenesis of C perfringens tissue necrosis is characterized by a
lack of acute inflammatory cells such as polymorphonuclear neutrophils (PMNs)
and vascular leukostasis in the tissues, leading to a rapid progression of
infection. In contrast, other soft-tissue infection caused by bacteria such as
Staphylococcus aureus and Streptococcus pneumoniae has a robust presence of PMNs
at the site of infection, leading to minimal tissue destruction. [7]
Furthermore, the products of tissue breakdown seen in C perfringens infection,
including creatine phosphokinase, myoglobin, and potassium, may cause secondary
toxicity and renal impairment. [8]

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.

Previous
Next: Pathophysiology

EPIDEMIOLOGY

FREQUENCY

United States

Estimates of incidence of gas gangrene vary; however, with improvements in
surgical technique and wound care, cases are relatively rare. Data estimate 1000
cases per year in the United States 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 20-30% if early and effective care is
provided.

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. [9, 10]

Previous
Next: Pathophysiology

PROGNOSIS

Clostridial infections are more likely to result in limb loss and mortality than
other soft-tissue infections. If the infection involves the chest wall, the
mortality rate is 2-12 times higher than extremity infections. [6] Early
diagnosis and aggressive treatment of gas gangrene are the keys to decreasing
mortality. Retrospective analysis of all necrotizing soft-tissue infections
indicates that a delay to surgery of greater than 12 hours suggests a 3-fold
increased risk of developing septic shock and a 6-fold increased risk of
mortality. [11]

Clinical Presentation

REFERENCES

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13. Wolf R, Tuzun Y, Davidovici BB. Necrotizing soft tissue infections,
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28. Kaide CG, Khandelwal S. Hyperbaric oxygen: applications in infectious
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MEDLINE Link].

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Media Gallery

* 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.

of 4

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CONTRIBUTOR INFORMATION AND DISCLOSURES

Author

Jessica Ward, MD Resident Physician, Department of Emergency Medicine, Beth
Israel Deaconess Medical Center

Jessica Ward, MD is a member of the following medical societies: American
College of Emergency Physicians, American Medical Association, Society of Women
Engineers

Disclosure: Nothing to disclose.

Coauthor(s)

Carlo L Rosen, MD Associate Professor of Medicine, Harvard Medical School;
Associate Director of Graduate Medical Education, Harvard Affiliated Emergency
Medicine Residency Program, Executive Vice Chair, 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.

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

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of
Surgery, University of South Carolina School of Medicine; Attending Physician /
Clinical Instructor, Compliance Officer, Department of Emergency Medicine,
Prisma Health Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical
societies: American Academy of Emergency Medicine, American College of Emergency
Physicians, American Medical Association, Columbia Medical Society, Society for
Academic Emergency Medicine, South Carolina College of Emergency Physicians,
South Carolina Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor,
consultant or trustee for: Employed contractor - Chief Editor for Medscape.

Additional Contributors

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.

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.

Xiao Wang, MD Resident Physician, Department of Emergency Medicine, Beth Israel
Deaconess Medical Center

Disclosure: Nothing to disclose.

Rodolfo D Loureiro, MD Resident Physician, Department of Emergency Medicine,
Beth Israel Deaconess Medical Center

Rodolfo D Loureiro, MD is a member of the following medical societies: American
College of Emergency Physicians, American Medical Association, Emergency
Medicine Residents' Association, Massachusetts College of Emergency Physicians,
Orange County Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

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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