ourniers gangrene (Meleneys synergistic gan-grene,1,2 perineal necrotizing fasciitis3,4) is a fulmi-nant necrotizing infection of the perineum andgenitalia that constitutes a surgical emergency

and can rapidly progress to sepsis and death. Physiciansunfamiliar with this infection will likely misdiagnose it,and those who have seen it will never forget it. Althoughit has been recently dramatized in the lay press as a dis-ease caused by flesh-eating bacteria,5 Fourniers gan-grene has been known since biblical times.3 All physi-cians who work in the acute care setting should be awareof this virulent infection, which is frequently misdiag-nosed as cellulitis with potentially devastating results.This article presents the case of a man with Fourniersgangrene that was initially diagnosed as cellulitis.

CASE PRESENTATION Initial Presentation

A 51-year-old man presented to the emergency de-partment with a 2-day history of scrotal swelling. Hedenied fever, chills, malaise, and other symptoms ex-cept for mild scrotal and left buttock pain. His medicalhistory was negative for drug abuse, steroid use, dia-betes, and other medical conditions except for hyper-tension, but heavy alcohol use was suspected. Edema ofthe scrotum and cellulitis of the perineum were notedduring physical examination. The erythema extendedonto the left buttock, where an extremely induratedarea with skin sloughing was noted medially. No peri-anal or perirectal abscess was found. The results of uri-nalysis were negative, and the leukocyte count was with-in normal limits. The urologist on call admitted thepatient to the hospital with a diagnosis of scrotal celluli-tis. Treatment with levofloxacin was then initiated.

Diagnosis and Subsequent Management

By the following day, the patients physical condi-tion had deteriorated. He exhibited signs of sepsis,with fever, tachycardia, and leukocytosis with left shift.The severity of the scrotal edema and the skin slough-ing on the left buttock had worsened, and the area ofinduration had increased (Figure 1). Consultation wasrequested with the general surgeon on call, who noteda patch of green-black, necrotic skin 1- to 2-cm in size

on the patients medial left buttock, pneumoscrotum(crepitation of the scrotal skin), and a foul odor. Thesurgeon correctly diagnosed the infection as Four-niers gangrene, and the patient underwent immediatesurgery.

Rigid sigmoidoscopy did not reveal an anorectalsource of infection. The frankly necrotic skin was ex-cised, and necrotic, green-grey, gelatinous, subcuta-neous fat was revealed (Figure 2). Malodorous dishwa-tery fluid drained from along the gluteal fascial planes.Wide excision and dbridement of all devitalized tissuefrom the medial buttock into the base of the scrotumwas performed (Figure 3). The subcutaneous necrosiswas much more extensive than the cutaneous necrosis.

After having undergone this procedure, the patientwas treated with triple antibiotic therapy (ampicillin,gentamycin and clindamycin) to cover gram-positive,gram-negative, and anaerobic bacteria. By the next day,the leukocytosis, edema, and cellulitis had begun toresolve. Examination under anesthesia revealed noneed for additional dbridement. Antibiotic treatmentwas continued, and whirlpool therapy was initiated.Gram stain of tissue obtained during the surgical pro-cedure revealed numerous gram-positive and gram-negative bacteria, including Staphylococcus aureus andEscherichia coli.

Case Resolution

By postoperative day 22, the edema had resolved,the wound was healing well, and no sign of surround-ing infection was detected (Figure 4). In the operatingroom, the wound underwent primary closure over aPenrose drain to prevent abscess. The drain was re-moved in 5 days. At the final follow-up evaluation

F

Dr. Stockinger is a staff surgeon in the Department of General Surgery,Naval Medical Center, Portsmouth, VA.

DISCLAIMER: This article was written by CDR Zsolt T. Stockinger, MC,USNR, during his fellowship training in trauma surgery and surgical criti-cal care at Tulane University School of Medicine in New Orleans,Louisiana. The views expressed in this article are those of the author and donot reflect the official policy or position of the US Department of the Navy,the US Department of Defense, or the government of the United States.

www.turner-white.com Hospital Physician September 2004 37

C a s e R e p o r t

Fourniers Gangrene

Zsolt T. Stockinger, MD, FACS

several weeks later, the patient was well and a good cos-metic and functional result had been achieved.

DISCUSSION

Fourniers gangrene is a fulminant soft tissue infec-tion that spreads through the subcutaneous tissueplanes and can rapidly cause death from sepsis, acuterenal failure, diabetic ketoacidosis, or multiple organfailure.24 It occurs with a male-to-female predomi-nance of 10:1.3 The mean age of patients ranges from46 to 56 years,2,4,6,7 although Fourniers gangrene hasbeen reported in children.2 4 Mortality rates range

from 3% to 45%,3,4,6,8 and more than 1700 cases from 5 continents have been reported in the literature.3

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Figure 1. Scrotal edema with skin bronzing and sloughing onthe left medial buttock. The characteristic green-black spot isindicated by the arrow.

Figure 4. Twenty-two days after dbridement. The woundis much smaller after the resolution of edema. Note the flac-cidity of the scrotal skin in comparison with its appearancebefore the first dbridement (Figure 1).

Figure 2. Excision of necrotic skin reveals extensive liquefac-tion necrosis of the underlying subcutaneous fat.

Figure 3. Completed dbridement. The involved area ismuch greater than that suggested by skin necrosis.

Pathogenesis

Fourniers gangrene is a polymicrobial infection,3 thesource of which is anorectal in 13% to 50% of cases,3,7,8

genitourinary in 17% to 87%,3,7,8 and cutaneous in 21%to 24%.2,3 It develops after urologic and anorectal proce-dures, including vasectomy.3,4 Thus, it is not surprisingthat the most common etiologic pathogens are com-mensal genitourinary or anorectal bacteria. In decreas-ing incidence, these are E. coli; Proteus, Klebsiella, andBacteroides species; streptococci; and staphylococci.24

Anaerobes are rarely recovered from tissue culture,probably because of inadequate sample collection or theimproper handling of samples.4 The reasons for whichorganisms of normally low virulence produce such anaggressive infection are unclear. However, the frequentcomorbid conditions associated with Fourniers gan-grene, which include diabetes mellitus (21%79% ofcases),3,4,68 immunodeficiency,3,4,7 alcoholism (25%66% of cases),3,4,7,8 intravenous or subcutaneous drugabuse,6 and malnutrition,2,4 may contribute to the rapidprogression of the infection.

A more typical superficial cellulitis is characterizedby spreading erythema with edema but without cellularnecrosis. In Fourniers gangrene, infection leads toobliterative endarteritis and thrombosis of the subcuta-neous vessels.3,4 That thrombosis in turn causes is-chemic necrosis of the overlying skin, the appearanceof which fails to indicate the extent of infection. Thelocalized tissue hypoxia then promotes the growth ofthe anaerobic bacteria usually identified in cases ofFourniers gangrene. Liquefaction necrosis of the sub-cutaneous fat may be caused by toxic bacterial prod-ucts, such as hyaluronidases and collagenases fromstaphylococci and streptococci, coagulases from -hemolytic streptococci, heparinases from some anaero-bic bacteria, and lipopolysaccharides from gram-negativebacteria.2,8 Infection spreads along the subcutaneous andfascial planes, although myonecrosis is rare.3

Although Jean Alfred Fourniers original descrip-tion of the disease that bears his name included onlyscrotal involvement,3 Fourniers gangrene can also in-volve the penis, labia, abdominal wall, thighs, and but-tocks. Because Colles fascia attaches to the perinealbody posteriorly and to the pubic rami laterally, thespread of infection is most likely to occur anteriorlyalong Scarpas or Campers fascia to the abdominalwall and to the scrotum if the source is perianal.2,4,8

The testes are usually uninvolved because their bloodsupply arises separately from the intraabdominal aorta,but the blood supply of the scrotum arises frombranches of the femoral artery.3,8 However, orchiecto-my rates of 10% to 30% have been reported.2,4

Diagnosis

The classic signs of Fourniers gangrene are pain,swelling, and erythema of the scrotum in addition tofever.2,4,8 Patients usually present after 2 to 7 days ofsymptoms.2,4 As the infection progresses, cyanosis, blis-tering, and bronzing of the skin2,4,8 evolve into the for-mation of black or green plaques of frank dermal ne-crosis in up to 100% of cases (Figure 1).9 These plaquesare perhaps the hallmark diagnostic finding of theinfection on physical examination. Pain may diminishafter skin necrosis has occurred.2 Pneumoscrotum hasbeen reported in 18% to 62% of cases.4,8 That findingcan lead to misdiagnosis as gas gangrene, even thoughClostridium perfringens is infrequently isolated from tissuecultures.3 Septic symptoms may be disproportionate tothe appearance of the scrotal skin.4,8

Urinalysis, cystoscopy, anoscopy, or rigid sigmoid-oscopy may be indicated because a genitourinary oranorectal source of infection is often identified.3,8 Asearch for the previously mentioned comorbid condi-tions frequently associated with Fourniers gangrene isalso warranted.2,4 Fourniers gangrene has also beenreported as the initial presentation of HIV infection4

and of diabetes mellitus.2,3

Fourniers gangrene is most frequently misdiag-nosed as strangulated hernia, scrotal cellulitis, or otherintrascrotal pathology (eg, torsion, abscess).2,4 How-ever, pyoderma gangrenosum and dry (noninfectious)gangrene caused by vasculitis are occasionally misdiag-nosed as Fourniers gangrene.2 Cellulitis that does notrespond appropriately to antibiotic treatment is highlysuggestive of Fourniers gangrene8 and should promptearly surgical consultation. A high index of suspicion isrequired for accurate, early diagnosis, which minimizestissue loss and mortality.

Although imaging studies such as plain radio-graphs, computed tomography, and ultrasonographycan reveal tissue gas or edema, those evaluations usual-ly are not necessary in the diagnosis of this infection.2,4

Ultrasonography is probably most useful to rule outother acute scrotal pathologies in questionable cases.2,8

Treatment

At diagnosis, treatment with broad-spectrum par-enteral antibiotics effective against gram-positive, gram-negative, and anaerobic bacteria should be initiated.3 Anappropriate empiric antibiotic regimen could includeampicillin or penicillin G to cover gram-positive bacteria,an aminoglycoside or third-generation cephalosporin tocover gram-negative and coliform organisms, and clin-damycin or metronidazole to cover anaerobic bacteria.6,8

However, the primary treatment remains surgical; in fact,

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the removal of devitalized tissue can alleviate systemictoxicity.3

Delay in surgical treatment is a key factor in mortali-ty.6 Definitive treatment requires prompt, aggressive sur-gical dbridement and removal of all nonviable tissue,which may require multiple surgical procedures.2 4

According to Yaghan et al, Under no circumstanceshould the surgeon worry about the amount of tissueexcised [sic] needed to reach viable margins.4 Becausethe spread of infection is subcutaneous, the dbridedarea is usually greater than that suggested by necroticskin2 (Figures 2 and 3). If the dbridement involves theperianal region, colostomy for fecal diversion may berequired to facilitate wound care.2,3 Urinary diversionby Foley catheter is usually sufficient,4 and dbridementof muscle and deep fascia is not usually required.2

Occasionally, the removal of all scrotal skin will leavethe testes hanging on their spermatic cords like theclappers of a bell,3 or the penis may need to be de-gloved. In such cases, creative reconstruction is re-quired at a later date, but the testes must be protectedfrom desiccation in the interim. This can be accom-plished by creating a temporary or permanent thigh orabdominal wall pouch that is superficial enough toallow the lower temperatures required for spermatoge-nesis; alternatively, wet-to-dry dressings can be used.2,8

Fertility is rarely compromised.3

Regardless of the results of Gram stain or tissue cul-ture, Fourniers gangrene is assumed to be a polymi-crobial infection, and broad-spectrum antibiotic cover-age should be continued postoperatively.3,8 Treatmentto eradicate anaerobic bacteria, which frequently fail togrow in culture, is mandatory. Hyperbaric oxygen hasbeen proposed for the treatment of Fourniers gan-grene,7 possibly because scrotal crepitation erroneouslysuggests clostridial gangrene.3 However, that treatmenthas not been uniformly advocated,3,4 and under no cir-cumstance should its use delay surgical dbridement.2,4

Although extensive dbridement of affected areas isrequired, the apparent degree of tissue loss decreasesas edema resolves (Figures 3 and 4), and wounds areoften left to heal by secondary intention.2,4 In spite ofthis, skin grafting or flap reconstruction is frequentlyrequired,24,8 and lengthy hospitalizations for woundcare and reconstruction are common. Wound careafter the completion of dbridement should follow the

usual surgical principles8 and may involve the use ofwet-to-dry dressings, hydrotherapy, or enzymatic d-bridement.4 Maintenance of positive nitrogen balance,preferably by enteral feeding, is necessary.3

CONCLUSION

Fourniers gangrene is an aggressive necrotizinginfection of the perineum and genitalia that can rapidlyprogress to sepsis and death. Unfamiliarity with this dis-ease results in misdiagnosis and a delay in treatment,which contribute greatly to morbidity and mortality.Fourniers gangrene is often misdiagnosed as scrotal cel-lulitis, strangulated hernia, or other intrascrotal patholo-gy and should be suspected in patients with cellulitis thatdoes not respond appropriately to antibiotic treatment.A green or black patch of necrotic skin is the classic signof this infection. Fourniers gangrene spreads subcuta-neously, and as a result, visible signs of the disease fail toindicate the extent of tissue destruction.

Fourniers gangrene is associated with a mortality rateof 3% to 45%. Because the infection is usually polymicro-bial, treatment with broad-spectrum antibiotics is re-quired to eliminate gram-positive, gram-negative, andanaerobic bacteria. Operative dbridement remains thedefinitive treatment, and surgical consultation should beobtained early to ensure the best possible outcome. HP

REFERENCES1. Meleney FL. Hemolytic streptococcus gangrene. Arch

Surg 1924;9:31731. 2. Smith GL, Bunker CB, Dinneen MD. Fourniers gan-

grene. Br J Urol 1998;81:34755.3. Eke N. Fourniers gangrene: a review of 1726 cases. Br J

Surg 2000;87:71828.4. Yaghan RJ, Al-Jaberi TM, Bani-Hani I. Fourniers gan-

grene: changing face of the disease. Dis Colon Rectum2000;43:13008.

5. Moses AE. Necrotizing fasciitis: flesh-eating microbes[editorial]. Isr J Med Sci 1996;32:7814.

6. Bosshardt TL, Henderson VJ, Organ CH Jr. Necrotizingsoft-tissue infections. Arch Surg 1996;131:84654.

7. Dahm P, Roland FH, Vaslef SN, et al. Outcome analysisin patients with primary necrotizing fasciitis of the malegenitalia. Urology 2000;56:316.

8. Vick R, Carson CC 3rd. Fourniers disease. Urol ClinNorth Am 1999;26:8419.

9. Benizri E, Fabiani P, Migliori G, et al. Gangrene of theperineum. Urology 1996;47:9359.

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