Necrotizing fasciitis pathophysiology: Difference between revisions

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Revision as of 19:02, 2 September 2016

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

The pathophysiology of necrotizing fasciitis is common to all types of NF but the speed of development and associated clinical features differs depending on the causative organisms.

The transmission of pathogens occurs through the following routes

External trauma
Direct spread from a perforated viscus (particularly colon, rectum, or anus)
Urogenital organ

Following transmission, the bacteria uses the entry site to invade the fascial planes which causes the wide spread necrosis of superficial fascia, deep fascia, subcutaneous fat, nerves, arteries, and veins.
Superficial skin and deeper muscles are typically spared.
In late stages, lesions develop liquefaction necrosis at all tissue levels.

Pathogenesis

The pathogenesis of necrotizing fasciitis is the result of bacterial and host factors.

Type 1 NF

The exact pathogenesis of type 1 necrotizing fasciitis is not fully understood.
It is thought that type 1 NF is caused by polymicrobial species that work together to enhance the spread of infection (Synergistic).

Type 2 NF

Group A streptococcus is the most common causative agent of type 2 NF.
The pathogenesis of type 2 NF is the result of the following process:

Inhibition of phagocytosis of bacteria by hyaluronic acid capsule and M protein
Adherence of bacteria to host cell through adherence factors such as M protein, protein F and lipoteichoic acid
Release of exotoxins (streptococcal pyogenic exotoxins and superantigens) into blood cascading release of cytokines
Activation of inflammatory process which begins to kill bacteria along with injury to the surrounding healthy cells
The inflamed cells release more cytokines that stimulate more inflammatory cells

Virulence Factors of Group A Streptococcus
Inhibition of phagocytosis
Adherance to host cell and release of exotoxins
Activation of host immune response

Gross pathology

On gross pathology the characteristic findings of necrotizing fasciitis include:^[1]

Subcutaneous emphysema
Edema
Erythema
Bulae
Skin sloughing
Dull grey discoloration

Beginning of necrotizing fasciitis^[1]
Necrotizing fasciitis of left leg^[1]

Microscopic histopathological analysis

On microscopic histopathological analysis, the characteristic findings of necrotizing fasciitis are^[1]

Early stages

Obliterative vasculitis with microangiopathic thrombosis
Acute inflammation of subcutaneous tissue
Superficial hyaline necrosis along with edema and inflammation of the dermis and subcutaneous fat
Dense neutrophil-predominant inflammatory infiltrate

Late stages

Noninflammatory intravascular coagulation and hemorrhage
Myonecrosis

References

↑ ^1.0 ^1.1 ^1.2 ^1.3 Librae pathology(2015) https://librepathology.org/wiki/Necrotizing_fasciitis Accessed on September 2,2016

[NF-1] 1.0 ^1.1 ^1.2 ^1.3 Librae pathology(2015) https://librepathology.org/wiki/Necrotizing_fasciitis Accessed on September 2,2016

[1]

@@ Line 26: / Line 26: @@
 :*Inhibition of phagocytosis of bacteria by hyaluronic acid capsule and M protein
 :*Adherence of bacteria to host cell through adherence factors such as M protein, protein F and lipoteichoic acid
-:*Release of exotoxins (streptococcal pyogenic exotoxins and superantigen) into blood cascading release of cytokines
+:*Release of exotoxins (streptococcal pyogenic exotoxins and superantigens) into blood cascading release of cytokines
-:*Activation of inflammatory process which begins to kill bacteria along with injury to surrounding healthy cells
+:*Activation of inflammatory process which begins to kill bacteria along with injury to the surrounding healthy cells
 :*The inflamed cells release more cytokines that stimulate more inflammatory cells
@@ Line 39: / Line 39: @@
 Image:Host_immune_response.PNG|Activation of host immune response
 </gallery>
-“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 [[toxin]]s (virulence factors). These include streptococcal pyogenic exotoxins and [[Streptococcus pyogenes|other virulence factors]]. ''S. pyogenes'' produces an exotoxin known as a [[superantigen]]. This toxin is capable of activating [[T-cell]]s non-specifically. This causes the over-production of [[cytokines]] that over-stimulate [[macrophage]]s. 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.
 ===Gross pathology===