Fournier gangrene pathophysiology

Steven C. Campbell, M.D., Ph.D.; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[1]; Jesus Rosario Hernandez, M.D. [2]

The transmission of pathogens occurs through the following routes:^[1] External trauma, direct spread from a perforated viscus, urogenital organ, perirectal abscess, and decubitus ulcer. 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 liquefactive necrosis at all tissue levels. The development of cutaneous and subcutaneous vascular necrosis leads to local ischemia and further bacterial proliferation. The infection spreads from superficial (colles fascia) and deep fascial planes of genitalia to the overlying skin sparing the muscles. The infection then spreads from colles fascia to the penis and scrotum via Buck's and Dartos fascia or to the anterior abdominal wall via Scarpa's fascia or vice versa. The inferior epigastric and deep circumflex iliac arteries supply the anterior abdominal wall, and the deep external pudendal and internal pudendal arteries supply the scrotal wall. Except for the internal pudendal artery, each of these vessels travels within Camper's fascia and can therefore become thrombosed in the progression of Fournier gangrene. The common locations of Fournier gangrene are^[2] perineum, scrotum, and penis. On gross pathology, the characteristic findings of Fournier gangrene include: Subcutaneous emphysema, swollen scrotal wall, edema, erythema, bullae, skin sloughing. On microscopic histopathological analysis, the characteristic findings of Fournier gangrene are 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, noninflammatory intravascular coagulation and hemorrhage, and myonecrosis.

The transmission of pathogens occurs through the following routes:^[1]

• External trauma (e.g., laceration, abrasion, burn, insect bite)
• Direct spread from a perforated viscus (particularly colon, rectum, or anus) or another surgical procedure (e.g., vasectomy, hemorrhoidectomy)
• Urogenital organ
• Perirectal abscess
• Decubitus ulcer

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 liquefactive necrosis at all tissue levels.

The pathogenesis of Fournier gangrene is the result of an imbalance between host and bacterial factors.^[3][2][1] A decrease in host immunity provides a favorable environment to initiate the infection, while virulence and synergism between multiple bacteria promotes rapid spread of infection.

The aerobic and anaerobic bacteria produce exotoxins and enzymes, such as collagenase, heparinase, and hyaluronidase, which promote the spread of infection. The aerobic bacteria accelerate coagulation by promoting platelet aggregation and complement fixation. The anaerobic bacteria produce collagenase and heparinase that promote the formation of clots leading to Obliterating endarteritis. The development of cutaneous and subcutaneous vascular necrosis leads to local ischemia and further bacterial proliferation.

The infection spreads from superficial (colles fascia) and deep fascial planes of genitalia to the overlying skin sparing the muscles. The infection then spreads from colles fascia to the penis and scrotum via Buck's and Dartos fascia or to the anterior abdominal wall via Scarpa's fascia or vice versa. The inferior epigastric and deep circumflex iliac arteries supply the anterior abdominal wall, and the deep external pudendal and internal pudendal arteries supply the scrotal wall. Except for the internal pudendal artery, each of these vessels travels within Camper's fascia and can therefore become thrombosed in the progression of Fournier gangrene.

The progression of infection to the perineal body, urogenital diaphragm and pubic rami is limited due to perineal fascia.^[4] Because of the direct supply of blood from the aorta, testicular involvement is limited in Fournier gangrene.^[5] However involvement of testis suggests retroperitoneal origin or spread of infection.^[6] Fournier gangrene of the male genetalia spares testes, urethra and deep penile tissues while the skin sloughs off.^[7]

Sepsis and multiorgan failure is the most common cause of death in Fournier gangrene.

The common locations of Fournier gangrene are:^[2]

• Perineum
• Scrotum
• Penis

On gross pathology, the characteristic findings of Fournier gangrene include:

• Subcutaneous emphysema
• Swollen scrotal wall
• Edema
• Erythema
• Bullae
• Skin sloughing

On microscopic histopathological analysis, the characteristic findings of Fournier gangrene are:

• 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