Gas gangrene(Redirected from Myonecrosis)
Gas gangrene (also known as clostridial myonecrosis and myonecrosis) is a bacterial infection that produces gas in tissues in gangrene. This deadly form of gangrene usually is caused by Clostridium perfringens bacteria. About 1,000 cases of gas gangrene are reported yearly in the United States.
|Photograph before right leg amputation (hemipelvectomy) of a patient with gas gangrene. The right thigh is edematous (swollen) and discoloured with necrotic bullae (large blisters). Crepitation is detected on deep palpation. At this juncture, the patient is in shock.|
Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections with C. perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis by specific exotoxins. These microorganisms are opportunistic and, in general, enter the body through significant skin breakage. Gangrenous infection by soil-borne bacteria was common in the combat injuries of soldiers well into the 20th century, because of nonsterile field surgery and the basic nature of care for severe projectile wounds.
Other causes of myonecrosis include envenomation by snakes of the genus Bothrops (family Viperidae), ischemic necrosis, caused by vascular blockage (e.g., diabetes type II), tumours that block or hoard blood supply, and disseminated intravascular coagulation or other thromboses.
Gas gangrene can cause myonecrosis (muscle tissue death), gas production, and sepsis. Progression to toxemia and shock is often very rapid. It can easily be noticed by the large, blackened sores that form, as well as a degree of loud and distinctive crepitus caused by gas escaping the necrotic tissue.
Gas gangrene is caused by exotoxin-producing Clostridium species (most often C. perfringens, and C. novyi, but less commonly C. septicum or C. ramnosum), which are mostly found in soil, but also found as normal gut flora, and other anaerobes (e.g., Bacteroides and anaerobic streptococci). The exotoxin is commonly found in C. perfringens type A strain and is known as alpha toxin. This alpha toxin is a lethal toxin and also known as phospholipase C (lecithinase). It increases vascular permeability and produces necrotizing activity. These environmental bacteria may enter the muscle through a wound and go on to proliferate in necrotic tissue and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time.
A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen, and 16.1% oxygen was reported in one clinical case.
Myonecrosis differs slightly from other types of necrosis. While the underlying causes are almost identical, the type of affected tissue (in particular, muscle tissue) is significantly more important for the patient's general health. Superficial necrosis is unsightly and can lead to unattractive scarring, but otherwise does not affect the patient's likelihood of survival or physical capability to the same extent. However, massive myonecrosis will likely result in the loss of movement of the entire region. If the necrotic damage is allowed to continue throughout an affected limb, then often that entire limb is lost permanently.
It is often difficult to identify the extent of muscle damage, as C. perfringens may be at work in deeper fascial layers below the skin. Unlike other anaerobic infections, discharge in these infections is often not purulent (filled with pus). Instead, the discharge is often described as "sweetly putrid" or "dishwater pus" because it is much thinner than normal pus. This is due to the lysis of neutrophils, a type of white blood cell, caused by the lecithinases and other toxins released by Clostridium species.
Soil-borne anaerobes are particularly well-adapted to surviving harsh conditions. Often, a scarcity of nutrition and competition for resources from numerous other species occurs. Changes in pH and temperature are often significant, also. Bacteria often possess the ability to create exotoxins to assist them in competing with other microbes in their natural environments. When such bacteria are able to enter a living host, they encounter a vast supply of nutrients, warm conditions, and an abundance of water. This enables the microbes to rapidly proliferate, far in excess of the immune system's capability to defend, as prokaryotic bacteria possess a far greater capacity for multiplication than the host's immune system. The combination of bacterial load and ability to multiply is the basis for the microbes' ability to cause massive infection. Alongside such rapid proliferation is a corresponding mass-production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is alpha toxin, which is produced by C. perfringens and is the key virulence factor in its pathogenesis.
Massive infection, gross injury, and depletion of the host's immune capability result in system-wide sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory cytokines, and the distribution of bacterial toxins. Massive infection is likely to result in death from a combination of system-wide septic shock and the unintentionally damaging effects of the immune response. In animals, disability and distress caused by all of these factors markedly increase the chance of predation.
Treatment is usually debridement and excision, with amputation necessary in many cases. Water-soluble antibiotics (such as penicillin) alone are not effective because they do not penetrate ischaemic muscles sufficiently to be effective. Penicillin is effective against C. perfringens. When gas gangrene occurs in such regions as the abdominal cavity, the patient can be treated in a hyperbaric chamber. which contains a pressurized oxygen-rich atmosphere. The oxygen saturates the infected tissues and thereby prevents the growth of the obligately anaerobic clostridia. The growth of C. perfringens is inhibited when the availability of oxygen is equivalent to a partial pressure of around 9–10 kPa (compare to 4–5 kPa in venous blood under normal conditions, with 11–13 kPa in arteries and 21 kPa in air at sea level), so if the treatment is started early, this condition can mostly be cured.
- James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. p. 269. ISBN 0-7216-2921-0.
- Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0.
- Jerrold B. Leikin; Frank P. Paloucek, eds. (2008), "Clostridium perfringens Poisoning", Poisoning and Toxicology Handbook (4th ed.), Informa, pp. 892–893, ISBN 978-1-4200-4479-9
- Pailler JL, Labeeu F (1986). "[Gas gangrene: a military disease?]". Acta Chir. Belg. (in French). 86 (2): 63–71. PMID 3716723.
- Hatheway CL (January 1990). "Toxigenic clostridia" (PDF). Clin. Microbiol. Rev. 3 (1): 66–98. doi:10.1128/CMR.3.1.66. PMC 358141. PMID 2404569.
- Bratton SL, Krane EJ, Park JR, Burchette S (1992). "Clostridium septicum infections in children". Pediatr Infect Dis J. 11 (7): 569–75. doi:10.1097/00006454-199207000-00011. PMID 1528648.
- van der Vorm ER, von Rosenstiel IA, Spanjaard L, Dankert J (April 1999). "Gas gangrene in an immunocompromised girl due to a Clostridium ramosum infection". Clin. Infect. Dis. 28 (4): 923–4. doi:10.1086/517249. PMID 10825071.
- Chang CW, Wang TE, Shih SC, Chang WH, Chen MJ (2008). "Shortness of breath, fever—and pain in both legs". Lancet. 372 (9648): 1518. doi:10.1016/S0140-6736(08)61621-9. PMID 18970978.
- ^ Chi CH, Chen KW, Huang JJ, Chuang YC, Wu MH (1995). "Gas composition in Clostridium septicum gas gangrene". J Formos Med Assoc. 94 (12): 757–9. PMID 8541740.
- Awad MM, Bryant AE, Stevens DL, Rood JI (January 1995). "Virulence studies on chromosomal alpha-toxin and theta-toxin mutants constructed by allelic exchange provide genetic evidence for the essential role of alpha-toxin in Clostridium perfringens-mediated gas gangrene". Mol. Microbiol. 15 (2): 191–202. doi:10.1111/j.1365-2958.1995.tb02234.x. PMID 7746141.
- Gerard J. Tortora; Berdell R. Funke; Christine L. Case (2010), Microbiology: An Introduction (10th ed.), Benjamin Cummings, p. 646, ISBN 978-0-321-55007-1
- Guyton and Hall. Textbook of Medical Physiology, 12th edition, chapter 44, "Physiological issues in deep sea diving and other high-pressure conditions"