Cellulitis pathophysiology
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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 mechanisms. When the immune system cannot respond adequately to the initial bacterial infection, the response can spread systemically through the blood stream.
Pathophysiology
Microorganisms gain initial access into the layers of the skin through the discontinuities and cuts in the skin. The body responds to these microbes as foreign bodies and their detection sets off an inflammatory response. The inflammatory response leads to redness, swelling, pain and itching of the area involved. A local infection leads to inflammation of the area of infection. 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 living on 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.
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.