Gangrene pathophysiology
Gangrene Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Gangrene pathophysiology On the Web |
American Roentgen Ray Society Images of Gangrene pathophysiology |
Risk calculators and risk factors for Gangrene pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
The three main types of gangrene occur in different mechanisms. 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.[1] In wet gangrene, saprogenic microorganisms (Bacillus fusiformis, or Clostridium perfringens) infect the tissues, thereby causing an emission of a foul odor and edema. [2] Multiplication of exotoxins from Clostridium perfringens and group A steptococcus is responsible for the local tissue destruction and systemic infection in gas gangrene.[3]
Pathophysiology
Dry Gangrene
Wet Gangrene
Gas Gangrene
References
- ↑ "StatPearls". 2022. PMID 32809387 Check
|pmid=
value (help). - ↑ Al Wahbi A (2018). "Autoamputation of diabetic toe with dry gangrene: a myth or a fact?". Diabetes Metab Syndr Obes. 11: 255–264. doi:10.2147/DMSO.S164199. PMC 5987754. PMID 29910628.
- ↑ Lehner PJ, Powell H (1991). "Gas gangrene". BMJ. 303 (6796): 240–2. doi:10.1136/bmj.303.6796.240. PMC 1670510. PMID 1884064.