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| {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | | {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} |
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| ==Overview==
| | {{SK}} Myonecrosis |
| '''Gas gangrene''' (also known as "Clostridial myonecrosis"<ref name="Andrews">{{cite book |author=James, William D.; Berger, Timothy G.; et al. |title=Andrews' Diseases of the Skin: clinical Dermatology |publisher=Saunders Elsevier |location= |year=2006 |pages= |isbn=0-7216-2921-0 |oclc= |doi= |accessdate=}}</ref>{{rp|269}}, and "Myonecrosis"<ref name="Bolognia">{{cite book |author=Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. |title=Dermatology: 2-Volume Set |publisher=Mosby |location=St. Louis |year=2007 |pages= |isbn=1-4160-2999-0 |oclc= |doi= |accessdate=}}</ref>) is a [[bacteria]]l [[infection]] that produces gas in [[biological tissue|tissue]]s in [[gangrene]]. It is a deadly form of gangrene usually caused by ''[[Clostridium perfringens]]'' bacteria. It is a [[medical emergency]].
| | ==[[Gas gangrene overview|Overview]]== |
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| '''Myonecrosis''' is a condition of [[necrosis|necrotic]] damage, specifically to [[muscle]] tissue. It is often seen in infections with ''[[Clostridium perfringens]]'' or any of myriad soil-borne [[anaerobic bacteria]]. Bacteria cause myonecrosis via specific [[exotoxins]]. These [[microorganism]]s are opportunistic and generally enter the body via significant skin breakage. In wartime particularly, the unhygienic conditions and frequent gross injuries meant that [[gangrene|gangrenous]] infection of soil-borne bacteria was particularly prevalent. Indeed mankind has long suffered the ill-effects of gangrenous infections throughout history.
| | ==[[Gas gangrene pathophysiology|Pathophysiology]]== |
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| Other causes of myonecrosis include [[ischemia|ischemic]] necrosis, caused by vascular blockage (e.g. diabetes type II), [[tumour]]s that block or hoard blood supply and [[disseminated intravascular coagulation]] (DIC) or other [[thrombosis|thromboses]].
| | ==[[Gas gangrene causes|Causes]]== |
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| == Pathophysiology == | | ==[[Gas gangrene differential diagnosis|Differentiating Gas gangrene from other Diseases]]== |
| Gas gangrene is caused by [[exotoxin]]-producing [[Clostridium|Clostridial]] species (most often ''[[Clostridium perfringens]]''), which is mostly found in soil but also found as normal [[gut flora]], and other [[anaerobe]]s (e.g. ''[[Bacteroides]]'' and anaerobic [[Streptococcus|streptococci]]). The exotoxin is commonly found in ''C. perfringens'' type A strain and is known as [[Clostridium perfringens alpha toxin|alpha toxin]]. 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. | |
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| A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen and 16.1% oxygen was reported in one clinical case.<ref>{{note|Chi}}{{cite journal | author=Chi CH, Chen KW, Huang JJ, Chuang YC, Wu MH | title=Gas composition in Clostridium septicum gas gangrene | journal=J Formos Med Assoc | year=1995 | pages=757-9 | volume=94 | issue=12 | id=PMID 8541740}}</ref>
| | ==[[Gas gangrene epidemiology and demographics|Epidemiology and Demographics]]== |
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| Myonecrosis differs slightly from other types of [[necrosis]]. While the underlying causes are almost identical, the type of affected tissue (namely [[muscle]] tissue) is significantly more important for the patient's general health. Superficial necrosis is unsightly, and can lead to unattractive [[scar]]ring but otherwise does not affect the patient's likelihood of survival nor physical capability to the same extent. Conversely, 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.
| | ==[[Gas gangrene natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| Soil-borne [[anaerobe]]s are particularly well adapted to surviving harsh conditions. Often there is a scarcity of nutrition and the presence of numerous other species competing for resources. Changes in [[pH]] and temperature are often significant also. Competing bacteria often also possess the ability to create [[exotoxin]]s that assist them in competing with other microbes in their natural environment. 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, particularly as [[prokaryote|prokaryotic bacteria]] possess a far greater capacity for multiplication than the host's immune system. The combination of [[bacteria]]l 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 produced by ''C. perfringens'' and is responsible for the disease manifestations. This exotoxin is known as [[Clostridium perfringens alpha toxin|alpha toxin]].<ref>Awad, M.M., Bryant, A.E., Stevens, D.L. & Rood, J.I. Virulence studies on chromosomal alpha-toxin and alpha-toxin mutants constructed by allelic exchange provide genetic evidence for the essential role of alpha-toxin in Clostridium perfringens-mediated gas gangrene. ''Mol. Microbiol.'' 15:191−202 (1995).</ref>
| | ==Diagnosis== |
| | [[Gas gangrene history and symptoms|History and Symptoms]] | [[Gas gangrene physical examination|Physical Examination]] | [[Gas gangrene laboratory findings|Laboratory Findings]] | [[Gas gangrene x ray|X Ray]] | [[Gas gangrene CT|CT]] | [[Gas gangrene MRI|MRI]] | [[Gas gangrene ultrasound|Ultrasound]] | [[Gas gangrene other diagnostic studies|Other Diagnostic Studies]] |
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| Following a massive infection, gross injury and depletion of the host's immune capability results in system wide [[sepsis]]. This is partly due to the burden on the immune system, its corresponding release of inflammatory [[cytokine]]s and the distribution of bacterial [[toxin]]s. 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 increases the chance of predation.
| | ==Treatment== |
| | | [[Gas gangrene medical therapy|Medical Therapy]] | [[Gas gangrene surgery|Surgery]] | [[Gas gangrene primary prevention|Primary Prevention]] | [[Gas gangrene cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Gas gangrene future or investigational therapies|Future or Investigational Therapies]] |
| == Treatment == | |
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| Any significantly massive infection is a medical emergency. In cases of gangrene, the infection is so severe by the time that a diagnosis is made that countering the bacterial load is impossible even with the strongest available [[antibiotic]]s, for example [[gentamycin]] and [[vancomycin]]. [[Antibiotic]]s alone are not effective because they don't penetrate [[ischemic]] [[muscle]]s enough to be effective. However, penicillin is given as an [[adjuvant treatment]] to surgery.
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| There are two major reasons for this; current antibiotics only prevent replication of bacteria and the production of toxins continues in pre-existing bacteria. Also, the extent of injury caused by the infection may leave the muscle tissues so damaged that the body will never be able to replace the lost structures (including vasculature).
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| Often the only available cure is [[amputation]], which physically removes the source of infection. Understandably this is not the favoured option unless circumstances are particularly dire.
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| In addition to surgery and antibiotics, [[hyperbaric oxygen therapy]] (HBOT) is used and acts to inhibit the growth of and kill the anaerobic C. perfringens.
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| [[Image:Hemipelvectomy gas gangrene.jpg|thumb|200px|center|[[Hemipelvectomy]] for gas gangrene]] | |
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| ==Case Studies== | | ==Case Studies== |
| | | :[[Gas gangrene case study one|Case #1]] |
| ===Case #1: Clostridial myonecrosis===
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| ====Clinical Summary====
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| This 68-year-old white male with insulin-dependent diabetes was admitted one day before his death. The chief complaints were the occurrence of chills and fever since passing a kidney stone two days earlier. In the last day, the right leg had become swollen. The most striking physical findings were redness of the right posterior calf and crepitance in both legs. The patient's white blood cell count was found to be 34,000 cells/cmm and the packed red blood cell volume (PCV) was 18%. Within hours, the right calf became tense and the crepitance spread up to the nipple line. The patient vomited, aspirated the vomitus, and died 10 hours after admission.
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| ====Histopathological Findings====
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | |
| <gallery>
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| Image:Myonecrosis 001.jpg|This gross photograph of the lower [[extremity]] was taken at autopsy. Notice the swelling and the area of the primary [[infection]] (arrow).
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| Image:Myonecrosis 002.jpg|This gross photograph shows a close-up view of [[hemorrhagic]] [[bleb]]s (arrows) on the skin. The blebs on the skin are accumulations of gas being discharged into the tissues from the [[Clostridium perfringens]]. This gas produces [[crepitance]].
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| Image:Myonecrosis 003.jpg|This is a low-power photomicrograph of [[muscle]] [[fascicle]]s containing large gas bubbles (arrows). Note that there is no [[inflammatory]] reaction in this section.
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| Image:Myonecrosis 004.jpg|This is a high-power photomicrograph of [[skeletal muscle]]. The muscle cells are hyper[[eosinophil]]ic and most do not contain [[nuclei]], indicating that these cells are dead or dying. The round clear spaces (1) in this tissue correspond to gas accumulations prior to death. In between the bundles of muscle cells, accumulations of small dark blue-staining [[bacteria]]l organisms can be seen (2). Also note that there is no inflammatory response in this tissue.
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| Image:Myonecrosis 005.jpg|This high-power photomicrograph shows the gas accumulation present in the tissue, a [[necrotic]] muscle cell (1), and a mild [[inflammatory]] response (2). There is also a [[thrmobosis|thrombosed]] [[blood vessel]] (3). The blue-staining rods (bacterial organisms) can barely be appreciated at this magnification.
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| Image:Myonecrosis 006.jpg|This higher-power photomicrograph of the previous image provides a clearer view of gas bubbles in the tissue, the necrotic hypereosinophilic muscle cell (1), and the mild inflammatory reaction (2). At this magnification, the bacteria located throughout this section can be better appreciated.
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| Image:Myonecrosis 007.jpg|This is a high-power photomicrograph of a tissue section stained with a tissue [[Gram's stain]] (Brown & Brenn). The [[Gram-positive]] [[bacilli]] can be seen throughout this tissue section.
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| </gallery>
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| == References ==
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| {{Reflist|2}}
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| ==External links==
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| * {{GPnotebook|1664417799}}
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| == Related Chapters == | | == Related Chapters == |
