Cellulitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Cellulitis]] results from the activation of the body's inflammatory response to bacterial exposure. | [[Cellulitis]] results from the activation of the body's inflammatory response to bacterial exposure. In the absence of an appropriate immune response to the initial bacterial invasion, the infection can spread systemically through the bloodstream. Certain risk factors predispose an individual to develop cellulitis which includes the breaking of the skin, previous unresolved skin infections, and immunosuppression. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Through breaks and discontinuities in the skin barrier, microorganisms have a portal of entry into the layers of the skin. The body responds to these microbes as foreign bodies and their detection initiates an inflammatory response. This response leads to redness, swelling, pain, and itching of the area involved. A local infection leads to [[inflammation]] of the area involved. With a competent immune system, the spread of the infection is limited. If the immune system fails to curb the initial infection, the infection may become systemic by spreading into adjacent areas. If the infection spreads to the bloodstream, it is called [[Bacteremia]]. | |||
[[Group A streptococcal infection|Group A]] [[streptococcus]] and [[staphylococcus]] <ref name="pmid6768328">{{cite journal| author=Fleisher G, Ludwig S| title=Cellulitis: a prospective study. | journal=Ann Emerg Med | year= 1980 | volume= 9 | issue= 5 | pages= 246-9 | pmid=6768328 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6768328 }} </ref> are the most common causative agents of [[cellulitis]]. These bacteria are part of the normal flora | [[Group A streptococcal infection|Group A]] [[streptococcus]] and [[staphylococcus]] <ref name="pmid6768328">{{cite journal| author=Fleisher G, Ludwig S| title=Cellulitis: a prospective study. | journal=Ann Emerg Med | year= 1980 | volume= 9 | issue= 5 | pages= 246-9 | pmid=6768328 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6768328 }} </ref> are the most common causative agents of [[cellulitis]]. These bacteria are part of the normal flora of the skin but they will cause infection if the skin is broken. Predisposing conditions for [[cellulitis]] include insect bites, animal bites, pruritic skin rash, recent [[surgery]], [[athlete's foot]], [[xeroderma|dry skin]], [[eczema]], burns and [[boil]]s. Another cause may be [[Hemophilus influenza]], especially in cases of facial infections.<ref name="pmid7018329">{{cite journal| author=Fleisher G, Ludwig S, Henretig F, Ruddy R, Henry W| title=Cellulitis: initial management. | journal=Ann Emerg Med | year= 1981 | volume= 10 | issue= 7 | pages= 356-9 | pmid=7018329 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7018329 }} </ref> | ||
In rare cases, the infection causing cellulitis can spread to the deep layer of tissue called the fascial lining. [[Necrotizing fasciitis]], also called "flesh-eating disease" by the media, is an example of a deep-layer infection. It represents an extreme [[medical emergency]]. | In rare cases, the infection causing cellulitis can spread to the deep layer of tissue called the fascial lining. [[Necrotizing fasciitis]], also called "flesh-eating disease" by the media, is an example of a deep-layer infection. It represents an extreme [[medical emergency]] requiring surgical consultation. | ||
==References== | ==References== | ||
Revision as of 11:26, 1 December 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S.
Overview
Cellulitis results from the activation of the body's inflammatory response to bacterial exposure. In the absence of an appropriate immune response to the initial bacterial invasion, the infection can spread systemically through the bloodstream. Certain risk factors predispose an individual to develop cellulitis which includes the breaking of the skin, previous unresolved skin infections, and immunosuppression.
Pathophysiology
Through breaks and discontinuities in the skin barrier, microorganisms have a portal of entry into the layers of the skin. The body responds to these microbes as foreign bodies and their detection initiates an inflammatory response. This response leads to redness, swelling, pain, and itching of the area involved. A local infection leads to inflammation of the area involved. With a competent immune system, the spread of the infection is limited. If the immune system fails to curb the initial infection, the infection may become systemic by spreading into adjacent areas. If the infection spreads to the bloodstream, it is called Bacteremia.
Group A streptococcus and staphylococcus [1] are the most common causative agents of cellulitis. These bacteria are part of the normal flora of the skin but they will cause infection if the skin is broken. Predisposing conditions for cellulitis include insect bites, animal bites, pruritic skin rash, recent surgery, athlete's foot, dry skin, eczema, burns and boils. Another cause may be Hemophilus influenza, especially in cases of facial infections.[2]
In rare cases, the infection causing cellulitis can spread to the deep layer of tissue called the fascial lining. Necrotizing fasciitis, also called "flesh-eating disease" by the media, is an example of a deep-layer infection. It represents an extreme medical emergency requiring surgical consultation.
References
- ↑ Fleisher G, Ludwig S (1980). "Cellulitis: a prospective study". Ann Emerg Med. 9 (5): 246–9. PMID 6768328.
- ↑ Fleisher G, Ludwig S, Henretig F, Ruddy R, Henry W (1981). "Cellulitis: initial management". Ann Emerg Med. 10 (7): 356–9. PMID 7018329.