Gangrene pathophysiology

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 a type of coagulative necrosis which occurs in ischemic tissue. Closing </ref> missing for <ref> tag

• Saprogenic microorganisms such as Clostridium perfringens and Bacillus fusiformis are the most common organisms observed in wet gangrene. They are responsible for infecting the tissues, thereby producing a putrid smell and edema. ^[2]
• The pooling and accumulation of blood in the affected tissue promotes proliferation of bacteria.
• An edematous, putrid, soft, and dark tissue is observed.^[2]

• Group A Steptococcus and exotoxins from Clostridium perfringens are responsible for the local and systemic infection found in gas gangrene. ^[3]
• Clostridium perfringens produces a Clostridium– lecithinase called Alpha-toxin that contributes to tissue necrosis and systemic hemolysis.^[4][5]
• Rapid progression to shock is usually observed.