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This is a life-threatening bacterial infection with gangrene which has the following three features:
- Muscle necrosis
- Gas production - usually a mixture of hydrogen, carbon dioxide, nitrogen and oxygen
These can rapidly lead to septicaemia and shock and death.
Types of gas gangrene
Gas gangrene can be broadly grouped into:
- Traumatic or surgical - usually caused by direct inoculation with clostridia (especially C. perfringens) but there are other causes too (see section on Pathogens below).
- Nontraumatic or spontaneous - more rare and most often caused by C. septicum. Seen in the setting of colonic neoplasms, immunosuppression or neutropenia. C. septicum from the gastrointestinal (GI) tract can pass via the blood to muscles (associated with a very poor prognosis). C. septicum is aerotolerant and can infect normal tissue.
Previously common in the setting of war but now much less common.
The vast majority of cases are caused by clostridia, especially C. perfringens.
- Clostridium spp. (found in soil and normal GI tract flora of humans and animals), eg C. perfringens, C. septicum, C. novyi , C. histolyticum
- Bacteroides spp.
- Anaerobic streptococci
In traumatic or surgical gas gangrene the pathogens enter through wounds usually after contact with soil, eg soil contaminated with faeces (not always so). The development of gas gangrene does not simply occur with the presence of Clostridium spp. - the environment has to have enough devitalised tissue present to support anaerobic metabolism. The destruction caused by the pathogen is from the release of exotoxins and not from the bacteria itself. C. perfringens releases alpha toxin - which requires anaerobic surroundings to survive and thrive, and also theta toxin. This explains why hypoxic or poorly perfused tissue is attractive to these organisms. The powerful toxins lead to breakdown of cells, coagulation and microvascular thrombosis and these can consequently add or contribute to rhabdomyolysis and renal failure. The toxins also lead to haemolysis of red blood cells, cardiac depression and shock through vasodilatation.
Risk factors for gas gangrene
- Chronic alcohol abuse
- Trauma, eg burns, crush injuries, open fractures, large muscle involvement, eg thigh
- Diabetes mellitus
- Corticosteroid use
- GI tract malignancy, eg infection of perineum or scrotum from colonic seeding
- Haematological disease with immunosuppression
- Has been reported to follow intramuscular injections
- Features relating to the wound, eg contamination with dirt or shrapnel
- Abortion (especially criminal abortion) and Caesarean section
The incubation period varies from one to several days but symptoms may progress within hours.
- Initially - no skin changes - just pain
- Systemic symptoms, eg fever, dehydration
- Once nerves are damaged, anaesthesia occurs
- Skin changes - cellulitic progressing to dark purple; develop vesicles and bullae
- Subcutaneous air on palpation (may not be present early on)
- Foul-smelling discharge
- Necrotic or haemorrhagic tissue
- Patients may also present in septicaemic shock with tachycardia, hypotension, fever, stupor
- Full blood count
- Renal function
- Liver function
- Creatine kinase
- Specimens from skin for culture, eg vesicle exudate
- Immunological methods - provide more rapid diagnosis
- Blood cultures
- Arterial blood gas - patients may be acidotic
- Urine dipstick - query myoglobinuria
- Plain X rays - will show gas in soft tissues
- Supportive therapy - for example, analgesia, oxygen, intravenous fluids and good nourishment.
- Surgical - radical debridement of necrotic tissue (may require amputation if limb involved).
- Antibiotics - these do not work alone as they are unable to penetrate the necrotic tissue. Cover Gram-negative, Gram-positive and anaerobes, eg combination of penicillin, gentamicin and metronidazole.
- Hyperbaric oxygen therapy - kills anaerobic C. perfringens; however, efficacy not proven.
- Tetanus toxoid may also be indicated.
Mortality approaches 25% in conditions associated with trauma and up to 100% in non-traumatic cases. This can be improved with better and more rapid recognition of the disease followed by early treatment of gas gangrene.
Further reading & references
- Shukla A, Rosen CL, Wong JK, Gas Gangrene; eMedicine, June 2009.
- Chuhan FA; Non-traumatic clostridium infection: report of an unusual case with rapid progression and a paucity of clinical signs in a patient with type 1 diabetes. Emerg Med J. 2006 Nov;23(11):e58.
- Rossitto M, Manfre A, Scalisi M, et al; Multiple treatment of gas gangrene at a rare anatomic location. Case report. Minerva Anestesiol. 2004 Mar;70(3):125-9.
- Halpin TF, Molinari JA; Diagnosis and management of clostridium perfringens sepsis and uterine gas gangrene. Obstet Gynecol Surv. 2002 Jan;57(1):53-7.
- Anesti E, Brooks P, Majumder S; Images in emergency medicine. Gas gangrene. Ann Emerg Med. 2007 Jul;50(1):14, 33.
- Roggentin T, Kleineidam RG, Majewski DM, et al; An immunoassay for the rapid and specific detection of three sialidase-producing clostridia causing gas gangrene. J Immunol Methods. 1993 Jan 4;157(1-2):125-33.
- Wang C, Schwaitzberg S, Berliner E, et al; Hyperbaric oxygen for treating wounds: a systematic review of the literature. Arch Surg. 2003 Mar;138(3):272-9; discussion 280.
- Tetanus, Health Protection Agency
- Janssen E, den Ouden H, van Herwaarden J, et al; Gas gangrene spreading to the bone marrow. Neth J Med. 2006 Jul-Aug;64(7):256-7.
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.
|Original Author: Dr Gurvinder Rull||Current Version: Dr Gurvinder Rull|
|Last Checked: 11/12/2009||Document ID: 2178 Version: 22||© EMIS|