Fournier gangrene pathophysiology

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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]

## Overview

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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.

## Pathophysiology

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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.

### Pathogenesis

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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.

### Common locations

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The common locations of Fournier gangrene are:[2]

* Perineum
* Scrotum
* Penis

### Gross pathology

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

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

### Microscopic histopathological analysis

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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

## References

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1. ↑ 1.0 1.1 1.2 Mallikarjuna MN, Vijayakumar A, Patil VS, Shivswamy BS (2012). "Fournier's Gangrene: Current Practices". ISRN Surg. 2012: 942437. doi:10.5402/2012/942437. PMC 3518952. PMID 23251819.CS1 maint: Multiple names: authors list (link)
2. ↑ 2.0 2.1 2.2 Shyam DC, Rapsang AG (2013). "Fournier's gangrene". Surgeon. 11 (4): 222–32. doi:10.1016/j.surge.2013.02.001. PMID 23578806.
3. ↑ Morua AG, Lopez JA, Garcia JD, Montelongo RM, Guerra LS (2009). "Fournier's gangrene: our experience in 5 years, bibliographic review and assessment of the Fournier's gangrene severity index". Arch Esp Urol. 62 (7): 532–40. PMID 19815967.CS1 maint: Multiple names: authors list (link)
4. ↑ Katib A, Al-Adawi M, Dakkak B, Bakhsh A (2013). "A three-year review of the management of Fournier's gangrene presented in a single Saudi Arabian institute". Cent European J Urol. 66 (3): 331–4. doi:10.5173/ceju.2013.03.art22. PMC 3974467. PMID 24707378.CS1 maint: Multiple names: authors list (link)
5. ↑ Gupta A, Dalela D, Sankhwar SN, Goel MM, Kumar S, Goel A; et al. (2007). "Bilateral testicular gangrene: does it occur in Fournier's gangrene?". Int Urol Nephrol. 39 (3): 913–5. doi:10.1007/s11255-006-9126-1. PMID 17323114.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
6. ↑ Chawla SN, Gallop C, Mydlo JH (2003). "Fournier's gangrene: an analysis of repeated surgical debridement". Eur Urol. 43 (5): 572–5. PMID 12706005.CS1 maint: Multiple names: authors list (link)
7. ↑ Campos JA, Martos JA, Gutiérrez del Pozo R, Carretero P (1990). "Synchronous caverno-spongious thrombosis and Fournier's gangrene". Arch Esp Urol. 43 (4): 423–6. PMID 2383054.CS1 maint: Multiple names: authors list (link)