Gangrene pathophysiology: Difference between revisions
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===Gas Gangrene=== | ===Gas Gangrene=== | ||
*Multiplication of [[exotoxins]] from ''[[Clostridium perfringens]]'' and [[group A steptococcus]] is responsible for the local [[tissue]] destruction and [[systemic infection]] in [[gas gangrene]].<ref name="pmid1884064">{{cite journal| author=Lehner PJ, Powell H| title=Gas gangrene. | journal=BMJ | year= 1991 | volume= 303 | issue= 6796 | pages= 240-2 | pmid=1884064 | doi=10.1136/bmj.303.6796.240 | pmc=1670510 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1884064 }} </ref> | *Multiplication of [[exotoxins]] from ''[[Clostridium perfringens]]'' and [[group A steptococcus]] is responsible for the local [[tissue]] destruction and [[systemic infection]] in [[gas gangrene]].<ref name="pmid1884064">{{cite journal| author=Lehner PJ, Powell H| title=Gas gangrene. | journal=BMJ | year= 1991 | volume= 303 | issue= 6796 | pages= 240-2 | pmid=1884064 | doi=10.1136/bmj.303.6796.240 | pmc=1670510 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1884064 }} </ref> | ||
*[[Alpha-toxin]] is a | *[[Alpha-toxin]] is a ''[[Clostridium]]''-lecithinase]] produced by ''[[Clostridium perfringens]]'' that contributes to [[tissue necrosis]] and [[systemic]] [[hemolysis]].<ref name="pmid26631369">{{cite journal| author=Yang Z, Hu J, Qu Y, Sun F, Leng X, Li H | display-authors=etal| title=Interventions for treating gas gangrene. | journal=Cochrane Database Syst Rev | year= 2015 | volume= | issue= 12 | pages= CD010577 | pmid=26631369 | doi=10.1002/14651858.CD010577.pub2 | pmc=8652263 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26631369 }} </ref><ref name="pmid15632295">{{cite journal| author=Sakurai J, Nagahama M, Oda M| title=Clostridium perfringens alpha-toxin: characterization and mode of action. | journal=J Biochem | year= 2004 | volume= 136 | issue= 5 | pages= 569-74 | pmid=15632295 | doi=10.1093/jb/mvh161 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15632295 }} </ref> | ||
*Progression of this [[condition]] to [[shock]] is very rapid. | *Progression of this [[condition]] to [[shock]] is very rapid. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
The three main types of gangrene occur in different mechanisms. Dry gangrene involves a reduction in the perfusion of the arteries results in the compensatory dilation of the arterioles, which eventually results in distal edema, and damage of the endothelial tissue.[1] In wet gangrene, saprogenic microorganisms (Bacillus fusiformis, or Clostridium perfringens) infect the tissues, thereby causing an emission of a foul odor and edema. [2] Multiplication of exotoxins from Clostridium perfringens and group A steptococcus is responsible for the local tissue destruction and systemic infection in gas gangrene.[3]
Pathophysiology
The three main types of gangrene occur in different mechanisms.
Dry Gangrene
- Dry gangrene involves a reduction in the perfusion of the arteries results in the compensatory dilation of the arterioles, which eventually results in distal edema, and damage of the endothelial tissue.[1]
- It is an example of coagulative necrosis occurring in an ischemic tissue.
Wet Gangrene
- In wet gangrene, saprogenic microorganisms (Bacillus fusiformis, or Clostridium perfringens) infect the tissues, thereby causing an emission of a foul odor and edema. [2]
- The accumulation and pooling of blood in the affected part promotes proliferation of bacteria.
- An edematous, putrid, soft and dark tissue is observed.[2]
Gas Gangrene
- Multiplication of exotoxins from Clostridium perfringens and group A steptococcus is responsible for the local tissue destruction and systemic infection in gas gangrene.[3]
- Alpha-toxin is a Clostridium-lecithinase]] produced by Clostridium perfringens that contributes to tissue necrosis and systemic hemolysis.[4][5]
- Progression of this condition to shock is very rapid.
References
- ↑ 1.0 1.1 "StatPearls". 2022. PMID 32809387 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 Al Wahbi A (2018). "Autoamputation of diabetic toe with dry gangrene: a myth or a fact?". Diabetes Metab Syndr Obes. 11: 255–264. doi:10.2147/DMSO.S164199. PMC 5987754. PMID 29910628.
- ↑ 3.0 3.1 Lehner PJ, Powell H (1991). "Gas gangrene". BMJ. 303 (6796): 240–2. doi:10.1136/bmj.303.6796.240. PMC 1670510. PMID 1884064.
- ↑ Yang Z, Hu J, Qu Y, Sun F, Leng X, Li H; et al. (2015). "Interventions for treating gas gangrene". Cochrane Database Syst Rev (12): CD010577. doi:10.1002/14651858.CD010577.pub2. PMC 8652263 Check
|pmc=value (help). PMID 26631369. - ↑ Sakurai J, Nagahama M, Oda M (2004). "Clostridium perfringens alpha-toxin: characterization and mode of action". J Biochem. 136 (5): 569–74. doi:10.1093/jb/mvh161. PMID 15632295.