eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections
Clostridial Gas Gangrene
Updated: Jun 23, 2008
Introduction
Background
Clostridial gas gangrene is a highly lethal necrotizing soft tissue infection of skeletal muscle caused by toxin- and gas-producing Clostridium species. The synonym clostridial myonecrosis better describes both the causative agent and the target tissue. Prior to the advent of antibiotics and mobile army surgical hospitals, as many as 5% of battlefield injuries were complicated by this condition. However, the incidence rate dropped to less than 0.01% during the Vietnam War. Presently, 90% of contaminated wounds demonstrate clostridial organisms, but fewer than 2% develop clostridial myonecrosis. This underscores the importance of host and local wound factors in the development of this process, rather than the mere presence of the organisms in the wound.
Pathophysiology
Clostridia are gram-positive, anaerobic, spore-forming bacilli commonly found throughout nature (with the exception of the North African desert). Cultivated rich soil has the highest density of organisms. In addition, clostridia have been isolated from normal human colonic flora, skin, and the vagina. More than 150 Clostridium species have been identified, but only 6 have been demonstrated to be capable of producing the fulminant condition known as clostridial gas gangrene. Usually, more than 1 species is isolated from clinical specimens.
Clostridium perfringens, previously known as Clostridium welchii, is the most common cause of clostridial gas gangrene (80-90% of cases). Other clostridia species responsible for the condition include Clostridium novyi (40%), Clostridium septicum (20%), Clostridium histolyticum (10%), Clostridium bifermentans (10%), and Clostridium fallax (5%).
Infections are characterized by a very low level of host inflammation in response to organism-associated exotoxins. In fact, it is more of a response to the exotoxins than a classic immune response to invading organisms. Purulence is often absent. The process of myonecrosis can spread as fast as 2 cm/h. This results in systemic toxicity and shock that can be fatal within 12 hours. Overwhelming shock with accompanying renal failure usually leads to death.
Infection requires 2 conditions to coexist. First, organisms must be inoculated into the tissues. Second, oxygen tension must be low enough for the organisms to proliferate. These organisms are not strict anaerobes; 30% oxygen tension in the tissues allows for free growth of these bacteria, but 70% oxygen tension restricts their growth. Inoculation of organisms into low oxygen tension tissues is followed by an incubation period that usually ranges from 12-24 hours. However, this period can be as brief as 1 hour or as long as several weeks. The organisms then multiply and produce exotoxins that result in myonecrosis.
Although not very well understood, exotoxins appear to be tissue-destructive soluble antigens produced by clostridia. They include lecithinase, collagenase, hyaluronidase, fibrinolysin, hemagglutinin, and hemolysin toxins. C perfringens produces at least 17 identifiable exotoxins that are used for species typing (eg, type A, type B, type C).
Theta toxin causes direct vascular injury, cytolysis, hemolysis, leukocyte degeneration, and polymorphonuclear cell destruction. These effects on leukocytes may explain the relatively minor host inflammatory response that is observed in tissues of patients with clostridial myonecrosis.
Kappa toxin, also produced by C perfringens, is a collagenase that facilitates the rapid spread of necrosis through tissue planes by destroying connective tissue.
Alpha toxin is produced by most clostridia and has phospholipase C activity. This potent lecithinase causes lysis of red blood cells, myocytes, fibroblasts, platelets, and leukocytes. It also may decrease cardiac inotropy and trigger histamine release, platelet aggregation, and thrombus formation.
Frequency
United States
Approximately 1000 cases of clostridial gas gangrene are reported per year.
International
Although no published data exist, prevalence is most likely higher in countries other than the United States because of lack of access to health care in other parts of the world.
Mortality/Morbidity
If properly treated, the overall mortality rate is 20-30%. If untreated, the process is 100% fatal.
- Spontaneous cases carry a mortality rate of 67-100%.
- With trunk involvement, the mortality rate is higher (60%) than the mortality rate associated with involvement of the extremities, which carries a better prognosis.
- A longer incubation period, presence of significant comorbidities, and development of shock increase the risk of mortality.
Race
No race predilection exists.
Sex
No sex predilection exists.
Age
Age does not seem to be an independent risk factor. However, because elderly individuals more often have significant comorbidities, they are at higher risk for mortality than younger patients.
Clinical
History
Obtaining a thorough medical history is important. It helps the physician identify risk factors that may affect the progression of the disease and the prognosis.
- Pain
- Increasing pain after surgery or trauma
- Out of proportion to physical findings
- Sudden onset
- May be severe
- Prior trauma
- Prior surgery, including abortions
- Diabetes mellitus
- Peripheral vascular disease
- Alcoholism
- Drug abuse
- Advanced age
- Chronic debilitating disease(s)
- Immunocompromised state
- Steroid use
- Malnutrition
- Malignancy
- Acquired immunodeficiency syndrome (AIDS)
Physical
Perform a thorough physical examination before focusing on the involved body part.
- Vital signs - May indicate systemic toxicity and include no or low-grade fever, tachycardia (relative tachycardia), tachypnea, hypotension, or hypoxia
- Edema bullae
- Erythema with purplish black discoloration
- Extreme tenderness
- Brownish skin discoloration (bronzing, brawny) with bullae
- Profuse, "dish-watery," serous drainage from ruptured bullae
- Discharge - May have a peculiar, "mousy," sweet odor
- Minimal crepitant bullae
- Crepitant tissue - May extend well beyond any skin discoloration, edema, or bleb formation
- Mental status - Paradoxically, may be depressed early during the disease course; sensorium then may clear as the disease progresses and the patient is near death
Causes
The disease process must include tissue inoculation and a low oxygen tension environment. More than 50% of cases are preceded by trauma. Other cases occur spontaneously or in patients after operative procedures.
- Trauma
- Compound fractures
- Foreign bodies
- Frostbite
- Thermal or electrical burns
- Subcutaneous or intravenous injection of medications or illicit drugs
- Pressure sores
- Motor vehicle crashes
- Postoperative
- Gastrointestinal tract surgery
- Genitourinary tract surgery
- Abortion
- Amputation
- Tourniquets, casts, bandages, or dressings applied too tightly
- Spontaneous
- This also is known as nontraumatic, idiopathic, or metastatic gas gangrene.
- It most often is mixed infection caused by C septicum, C perfringens, and C novyi. Several series report a mortality rate that approaches 100%.
- The gastrointestinal tract is the source of organisms. The organisms escape the bowel by translocation, enter the bloodstream, and seed distant sites where they can cause gas gangrene. This process may also result in a more localized infection that involves the viscera or intra-abdominal compartment.
- Approximately 80% of patients without trauma have an overt or occult malignancy. Of these, approximately 40% are hematologic malignancies and an additional 34% are colorectal.1 Survival from this process should initiate a search for an occult malignancy if none has been documented previously in patients without trauma.
More on Clostridial Gas Gangrene |
 Overview: Clostridial Gas Gangrene |
| Differential Diagnoses & Workup: Clostridial Gas Gangrene |
| Treatment & Medication: Clostridial Gas Gangrene |
| Follow-up: Clostridial Gas Gangrene |
| References |
| Next Page » |
References
San Ildefonso A, Maruri I, Facal C, Casal E. Clostridium septicum infection associated with perforation of colon diverticulum. Rev Esp Enferm Dig. Jun 2002;94(6):361-6. [Medline].
Burke MP, Opeskin K. Nontraumatic clostridial myonecrosis. Am J Forensic Med Pathol. Jun 1999;20(2):158-62. [Medline].
Ellemor DM, Baird RN, Awad MM, Boyd RL, Rood JI, Emmins JJ. Use of genetically manipulated strains of Clostridium perfringens reveals that both alpha-toxin and theta-toxin are required for vascular leukostasis to occur in experimental gas gangrene. Infect Immun. Sep 1999;67(9):4902-7. [Medline].
Feingold DS. Gangrenous and crepitant cellulitis. J Am Acad Dermatol. Mar 1982;6(3):289-99. [Medline].
Hart GB, Lamb RC, Strauss MB. Gas gangrene. J Trauma. Nov 1983;23(11):991-1000. [Medline].
Hatheway CL. Toxigenic clostridia. Clin Microbiol Rev. Jan 1990;3(1):66-98. [Medline].
Hirn M. Hyperbaric oxygen in the treatment of gas gangrene and perineal necrotizing fasciitis. A clinical and experimental study. Eur J Surg Suppl. 1993;1-36. [Medline].
Korhonen K, Klossner J, Hirn M, Niinikoski J. Management of clostridial gas gangrene and the role of hyperbaric oxygen. Ann Chir Gynaecol. 1999;88(2):139-42. [Medline].
Larson CM, Bubrick MP, Jacobs DM, West MA. Malignancy, mortality, and medicosurgical management of Clostridium septicum infection. Surgery. Oct 1995;118(4):592-7; discussion 597-8. [Medline].
McDonel JL. Clostridium perfringens toxins (type A, B, C, D, E). Pharmacol Ther. 1980;10(3):617-55. [Medline].
Present DA, Meislin R, Shaffer B. Gas gangrene. A review. Orthop Rev. Apr 1990;19(4):333-41. [Medline].
Rood JI, Cole ST. Molecular genetics and pathogenesis of Clostridium perfringens. Microbiol Rev. Dec 1991;55(4):621-48. [Medline].
Samlaska CP, Maggio KL. Subcutaneous emphysema. Adv Dermatol. 1996;11:117-51; discussion 152. [Medline].
Stephens MB. Gas gangrene: potential for hyperbaric oxygen therapy. Postgrad Med. Apr 1996;99(4):217-20, 224. [Medline].
Stevens DL, Tweten RK, Awad MM, et al. Clostridial gas gangrene: evidence that alpha and theta toxins differentially modulate the immune response and induce acute tissue necrosis. J Infect Dis. Jul 1997;176(1):189-95. [Medline].
Valentine EG. Nontraumatic gas gangrene. Ann Emerg Med. Jul 1997;30(1):109-11. [Medline].
Weinstein L, Barza MA. Gas gangrene. N Engl J Med. Nov 22 1973;289(21):1129-31. [Medline].
Further Reading
Keywords
clostridial gas gangrene, Clostridium gas gangrene, clostridial myonecrosis, myonecrosis, gangrene, soft tissue infection, Clostridium, Clostridium perfringens, C perfringens, Clostridium welchii, C welchii, Clostridium novyi, C novyi, Clostridium septicum, C septicum, Clostridium histolyticum, C histolyticum, Clostridium bifermentans, C bifermentans, Clostridium fallax, C fallax, battlefield injury, war wound, clostridia, compound fracture, frost bite, frostbite, bed sores, bedsores, pressure sores, burns, burn injury
