Necrotizing fasciitis pathophysiology: Difference between revisions
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*Comparatively slow process | *Comparatively slow process | ||
*It is commonly seen in [[immunocompromised]] or those with underlying abdominal pathology | *It is commonly seen in [[immunocompromised]] or those with underlying abdominal pathology | ||
*Synergistic NF develops following complicated abdominal surgery, ischiorectal or perineal abscesses when the gut flora breaches the mucosa entering tissue planes. | *Synergistic NF develops following complicated abdominal surgery, [[abscess|ischiorectal]] or [[abscess|perineal abscesses]] when the gut flora breaches the mucosa entering tissue planes. | ||
Revision as of 16:40, 30 August 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Pathophysiology
All types of necrotizing fasciitis have common pathophysiology but the speed of development and associated clinical features may differ depending on the causative organisms.
Type 1 necrotizing fasciitis (Synergistic NF)
- Comparatively slow process
- It is commonly seen in immunocompromised or those with underlying abdominal pathology
- Synergistic NF develops following complicated abdominal surgery, ischiorectal or perineal abscesses when the gut flora breaches the mucosa entering tissue planes.
“Flesh-eating bacteria” is a misnomer, as the bacteria do not actually eat the tissue. They cause the destruction of skin and muscle by releasing toxins (virulence factors). These include streptococcal pyogenic exotoxins and other virulence factors. S. pyogenes produces an exotoxin known as a superantigen. This toxin is capable of activating T-cells non-specifically. This causes the over-production of cytokines that over-stimulate macrophages. The macrophages cause the actual tissue damage by releasing oxygen free radicals that are normally intended to destroy bacteria but are capable of damaging nearly any macromolecule they contact in the body.