Pathogenesis

The pathogenesis of Fournier's gangrene is characterized by polymicrobial aerobic and anaerobic infection with subsequent vascular thrombosis and tissue necrosis, aggravated by poor host defense due to one or more underlying systemic disorders.

Aerobic organisms cause intravascular coagulation by inducing platelet aggregation and complement fixation, while anaerobes produce heparinase. Vascular thrombosis causes necrosis of tissue and decreased clearance of toxic bacterial metabolites, with subsequent proliferation of anaerobic bacteria (Paty and Smith 1992; Hejase et al. 1996).

Hypoxic tissue leads to the formation of oxygen free radicals (superoxide anions, hydrogen peroxide, hy-droxyl radicals), which play an important role in the pathogenesis. The effects of free radicals include cell membrane disruption leading to cell death, decreased ATP production leading to decreased energy delivery, and DNA damage, which leads to decreased protein production (Anderson and Vaslef 1997).

Anaerobic organisms secrete various enzymes and toxins. Lecithinase, collagenase, and hyaluronidase cause digestion of the fascial planes (Baskin et al. 1990). They produce insoluble hydrogen and nitrogen, leading to the formation of gas in the subcutaneous tissues, clinically palpable as crepitus. Aerobic bacteria produce CO2, which is soluble and rarely leads to subcutaneous gas accumulation.

Endotoxins are released from the cell walls of Gramnegative bacteria. Macrophage activation and subsequent complement activation ensues with release of pro-inflammatory cytokines and eventual development of septic shock (Anderson and Vaslef 1997).

Depending on the origin of the infection, the various paths of spread can be explained with reference to the anatomy of the fascial planes and adhesions.

Infection from a urogenital cause, e.g., a patient with a urethral stricture and urinary tract infection leading to a paraurethral abscess, will spread from the corpus spongiosum by penetrating the tunica albuginea and Buck's fascia, and will then spread under the dartos fascia and Colles' fascia to Scarpa's fascia, thereby involving the anterior abdominal wall.

Infection from an anorectal cause, e.g., an ischio-rectal abscess, will spread from the perirectal tissues to Colles' fascia. Because Colles' fascia is fenestrated, it allows spread from the perirectal area to the dartos fascia of the scrotum and penis, and from there the infection can spread to Scarpa's fascia and the anterior abdominal wall. Because Colles' fascia terminates in the perineal membrane, infection from the anterior triangle of the perineum, which contains the bulbar urethra and scrotum, cannot spread to the perirectal area, but because Colles' fascia is fenestrated, the opposite is possible, i.e., posterior triangle infections may sometimes spread to the anterior triangle and from there to the anterior abdominal wall. This is important in trying to localize the origin of the initial infection.

Retroperitoneal infection, e.g., from a perinephric or psoas abscess, may spread along the inguinal canal and spermatic fascia, which connects to Colles' fascia deep to the bulbocavernosus muscle. Retroperitoneal infection should be considered as a cause of Fournier's gangrene if no obvious point of origin can be found.

0 0

Post a comment