Gangrene pathophysiology: Difference between revisions

	Gangrene Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Gangrene from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
X Ray
CT
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Gangrene pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Gangrene pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Gangrene pathophysiology
CDC on Gangrene pathophysiology
Gangrene pathophysiology in the news
Blogs on Gangrene pathophysiology
Directions to Hospitals Treating Gangrene
Risk calculators and risk factors for Gangrene pathophysiology

Revision as of 23:04, 10 April 2022

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.

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]

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]
It is an example of coagulative necrosis occurring in an ischemic tissue.

In wet gangrene, saprogenic microorganisms (Bacillus fusiformis, or Clostridium perfringens) infect the tissues, thereby causing an emission of a foul odor and edema. ^[2]
The accumulation and pooling of blood in the affected part promotes proliferation of bacteria.
An edematous, putrid, soft and dark tissue is observed.^[2]

@@ Line 10: / Line 10: @@
 ===Dry Gangrene===
-*[[Dry gangrene]] involves a reduction in the [[perfusion]] of the [[arteries]] results in the compensatory dilation of the [[arterioles]], 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>
+*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 an example of [[coagulative necrosis]] occurring in an [[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.