Gangrene pathophysiology: Difference between revisions

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{{Gangrene}}
{{Gangrene}}
{{CMG}}{{AE}} [[User:Edzelco|Edzel Lorraine Co, D.M.D., M.D.]]
{{CMG}} ; {{AE}} [[User:Edzelco|Edzel Lorraine Co, D.M.D., M.D.]]
==Overview==
There are three types of [[gangrene]] and they have different pathophysiology.
A reduced [[arterial]] [[perfusion]] is observed in [[dry gangrene]] which results in the compensatory [[arteriolar dilation]] , which eventually results in [[distal]] [[edema]], and damage of the [[endothelial tissue]]. <ref name="pmid32809387">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume=  | issue=  | pages=  | pmid=32809387 | doi= | pmc= | url= }} </ref> [[Saprogenic]] [[microorganisms]] such as ''[[Clostridium perfringens]]'' and ''[[Bacillus fusiformis]]'' are the most common organisms observed in [[wet gangrene]] which are responsible for infecting the [[tissues]], thereby producing a putrid smell and [[edema]].  <ref name="pmid29910628">{{cite journal| author=Al Wahbi A| title=Autoamputation of diabetic toe with dry gangrene: a myth or a fact? | journal=Diabetes Metab Syndr Obes | year= 2018 | volume= 11 | issue=  | pages= 255-264 | pmid=29910628 | doi=10.2147/DMSO.S164199 | pmc=5987754 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29910628  }} </ref> ''[[Group A Steptococcus]]'' and [[exotoxins]] from ''[[Clostridium perfringens]]'' are responsible for the local and [[systemic infection]] found 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>
 
==Pathophysiology==
==Pathophysiology==
There are three types of [[gangrene]] and they have different pathophysiology.
===Dry Gangrene===
===Dry Gangrene===
If the blood flow is interrupted for a reason other than severe bacterial infection, the result is a case of dry gangrene. People with impaired peripheral blood flow, such as diabetics, are at greater risk of contracting dry gangrene.The dark coloration is due to liberation of [[hemoglobin]] from hemolyzed red blood cells which is acted upon by [[hydrogen sulfide]] (H<sub>2</sub>S) produced by the bacteria, resulting in formation of black iron sulfide that remains in the tissues<ref>[http://compepid.tuskegee.edu/syllabi/pathobiology/pathology/genpath/chapter3.html chapter 3.html<!-- Bot generated title -->]</ref>.
*A reduced [[arterial]] [[perfusion]] is observed in [[dry gangrene]] which results in the compensatory [[arteriolar dilation]], which eventually results in [[distal]] [[edema]], and damage of the [[endothelial tissue]]. <ref name="pmid32809387">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume=  | issue=  | pages=  | pmid=32809387 | doi= | pmc= | url= }} </ref>
*It is a type of [[coagulative necrosis]] which occurs in [[ischemic tissue]]. <ref> {{cite book | last = Cross | first = Simon | title = Underwood's pathology : a clinical approach | publisher = Churchill Livingstone/Elsevier | location = Edinburgh | year = 2019 | isbn = 9780702072109 }}
*Because there is a decreased supply of [[oxygen]] in the affected [[limb]], [[bacteria]] can not thrive and [[putrefaction]] is limited.
*A dry, shrunken, and reddish-black appearance of the [[limb]] is observed.
*There is a clear demarcation of affected and non-affected parts, and if the affected part is not given an [[urgent]] [[surgical]] [[treatment]], [[autoamputation]] results. <ref name="pmid29910628">{{cite journal| author=Al Wahbi A| title=Autoamputation of diabetic toe with dry gangrene: a myth or a fact? | journal=Diabetes Metab Syndr Obes | year= 2018 | volume= 11 | issue=  | pages= 255-264 | pmid=29910628 | doi=10.2147/DMSO.S164199 | pmc=5987754 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29910628  }} </ref>


===Wet Gangrene===
===Wet Gangrene===
In wet gangrene, the tissue is infected by saprogenic microorganisms (Bac.perfringes, fusiformis, putrificans, etc.), which cause tissue to swell and emit a fetid smell. Wet gangrene usually develops rapidly due to blockage of venous and/or arterial blood flow. The affected part is saturated with stagnant blood which promotes the rapid growth of bacteria. The toxic products formed by bacteria are absorbed causing systemic manifestation of [[septicemia]] and finally death.
*[[Saprogenic]] [[microorganisms]] such as ''[[Clostridium perfringens]]'' and ''[[Bacillus fusiformis]]'' are the most common organisms observed in [[wet gangrene]]. They are responsible for infecting the [[tissues]], thereby producing a putrid smell and [[edema]]. <ref name="pmid29910628">{{cite journal| author=Al Wahbi A| title=Autoamputation of diabetic toe with dry gangrene: a myth or a fact? | journal=Diabetes Metab Syndr Obes | year= 2018 | volume= 11 | issue=  | pages= 255-264 | pmid=29910628 | doi=10.2147/DMSO.S164199 | pmc=5987754 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29910628  }} </ref>
*The pooling and accumulation of [[blood]] in the affected [[tissue]] promotes [[proliferation]] of [[bacteria]].
*An [[edematous]], [[putrid]], [[soft]], and [[dark]] tissue is observed.<ref name="pmid29910628">{{cite journal| author=Al Wahbi A| title=Autoamputation of diabetic toe with dry gangrene: a myth or a fact? | journal=Diabetes Metab Syndr Obes | year= 2018 | volume= 11 | issue=  | pages= 255-264 | pmid=29910628 | doi=10.2147/DMSO.S164199 | pmc=5987754 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29910628  }} </ref>


===Gas Gangrene===
===Gas Gangrene===
Gas gangrene is caused by a bacterial [[exotoxin]]-producing clostridial species, which are mostly found in soil and other anaerobes (e.g. ''[[Bacteroides]]'' and anaerobic [[Streptococcus|streptococci]]). These environmental bacteria may enter the muscle through a wound and subsequently 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.<ref>{{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. |volume=94 |issue=12 |pages=757–9 |year=1995 |month=December |pmid=8541740 |doi= |url=}}</ref>
*''[[Group A Steptococcus]]'' and [[exotoxins]] from ''[[Clostridium perfringens]]'' are responsible for the local and [[systemic infection]] found 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>
*''[[Clostridium perfringens]]'' produces a ''[[Clostridium]]''- [[lecithinase]] called [[Alpha-toxin]] 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>
*Rapid progression to [[shock]] is usually observed.


==References==
==References==
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Latest revision as of 16:45, 28 April 2022

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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

There are three types of gangrene and they have different pathophysiology. A reduced arterial perfusion is observed in dry gangrene which results in the compensatory arteriolar dilation , which eventually results in distal edema, and damage of the endothelial tissue. [1] Saprogenic microorganisms such as Clostridium perfringens and Bacillus fusiformis are the most common organisms observed in wet gangrene which are responsible for infecting the tissues, thereby producing a putrid smell and edema. [2] Group A Steptococcus and exotoxins from Clostridium perfringens are responsible for the local and systemic infection found in gas gangrene.[3]

Pathophysiology

There are three types of gangrene and they have different pathophysiology.

Dry Gangrene

Wet Gangrene

Gas Gangrene

References

  1. 1.0 1.1 "StatPearls". 2022. PMID 32809387 Check |pmid= value (help).
  2. 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. 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.
  4. 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.
  5. 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.