This document provides an overview of necrotizing gangrene of the genitalia and perineum, a life-threatening soft tissue infection. The infection spreads along fascial planes and can be caused by anorectal, genitourinary, or cutaneous infections. Despite treatment including aggressive debridement and antibiotics, patients experience significant morbidity and mortality. Early diagnosis and complete removal of all necrotic tissue are essential for improved outcomes.

1. Necrotizing Gangrene of the Genitalia and Perineum
from Infections in Urology ®
Maxwell V. Meng, MD, Jack W. McAninch, MD, University of California School of Medicine, San
Francisco.
Abstract and Introduction
Abstract
Necrotizing gangrene of the genitalia and perineum is a fulminant, life-threatening infection. The infection
may spread along subcutaneous planes and result in tissue necrosis. Infections are usually
polymicrobial. The organisms most commonly isolated from wound cultures include Bacteroides,
coliforms, Streptococcus, Staphylococcus, and Peptostreptococcus.
Anorectal infections, genitourinary infections, and cutaneous injuries are the most frequent sources of
infection in necrotizing genital gangrene. Despite increased experience in treating this condition, patients
suffer significant morbidity and mortality. Early diagnosis and complete debridement of all necrotic tissue
are essential for improved outcomes.
Introduction
Necrotizing soft-tissue infections of the genitalia and perineum present diagnostic and therapeutic
challenges. Although uncommon, these infections can progress rapidly and cause significant morbidity
and mortality. Therefore, they must be promptly diagnosed and aggressively treated to achieve an
optimal outcome.
The first reported case of such an infection was by Baurienne in 1764.[1] In 1883, the French venereologist
Fournier described a syndrome of abrupt, idiopathic onset of genital gangrene in 5 young, previously
healthy men.[2] Although the condition currently is recognized to afflict an older population of both genders
and has identifiable risk factors, "Fournier's gangrene" still constitutes a urologic emergency. Because of
a greater understanding of the etiology and pathogenesis of this disorder, improved therapy has resulted
in improved outcomes.
Etiology
Fournier was unable to identify the cause of infection in his patients, but the etiology can be discerned in
most cases today (Table). Anorectal infections, genitourinary infections, and cutaneous injuries are the
most frequent sources of infection in necrotizing genital gangrene.[3]
Among gastrointestinal causes (30% to 50%), ischiorectal, perianal, and intrasphincteric abscesses
account for approximately 70%.[4] Nec-rotizing gangrene has also been reported to be secondary to minor
anorectal procedures such as rectal mucosal biopsy, anal dilation, and hemorrhoidectomy as well as
appendicitis, colorectal malignancy, and diverticulitis.[5-7]
Genitourinary foci comprise the second major source of initial infection (20% to 40%); underlying urethral
stricture and periurethral infection are most common.[8] Urologic conditions also associated include
urethral trauma and instrumentation, indwelling urethral catheters, urethral calculi, epididymitis, prostate
biopsy and massage, and bladder cancer extension.[8-10]
Cutaneous injuries and infection account for 20% of cases.[4] Often the dermal source is minor, such as
human and insect bites. Other reported etiologies involving trauma to the superficial soft tissues include
vasectomy, circumcision, genital infections (balanoposthitis), and penile prosthesis insertion.[8,11]

2. Necrotizing gangrene is less common in women. In 1 literature review of 449 cases, 14% involved
women.[8] Typically, abscesses of the vulva or Bartholin's glands initiate the gangrene of the perineum.
Episiotomy, septic abortion, pudendal nerve block, and coital injury are recognized factors in female
necrotizing soft-tissue infections.[12,13]
Additional host factors affect the development of necrotizing gangrene. Increased prevalence of
comorbidities such as diabetes (30% to 60%) and alcoholism (40% to 50%) have been reported.[9,14] It is
postulated that susceptibility to infection from decreased defense mechanisms and impaired active
immune response contribute to the increased incidence. Malnutrition, AIDS, malignancy, renal failure, and
immunosuppressive chemotherapy are other risk factors.[3,15,16] However, outcomes have not correlated
with presence or absence of the comorbid states.[9,14]
Anatomy
The patterns of spread in genital and perineal necrotizing soft-tissue infection can be explained by the
fascial anatomy of the perineum, external genitalia, and abdominal wall. The superficial perineal fascia
(Colles' fascia) is attached laterally to the pubic rami and fascia lata of the thighs, and posteriorly to the
urogenital diaphragm and perineal membrane. The anterior extensions of Colles' fascia include the tunica
dartos of the penis and scrotum and Scarpa's fascia of the anterior abdominal wall. Buck's fascia of the
penis, deep to the tunica dartos, is bound by adherence to the tunica albuginea distally at the coronal
sulcus of the glans and proximally at the crus and suspensory ligament of the penis.[26]
Infections originating in the ano-rectal region first penetrate the sphincteric musculature. Then, the
infection spreads along the perianal region and may extend along Colles' fascia. While lateral spread is
prevented by attachments of Colles' fascia, anterior and superior extension along dartos and Scarpa's
fasciae is unhindered. Alternatively, anorectal infection may spread through the urogenital diaphragm to
the perivesical space, then to the scrotum via the spermatic fascia.
Urethral infections are initially limited by Buck's fascia, surrounding the corpora spongiosum and
cavernosa. Once Buck's fascia is traversed, the infection spreads along the overlying tunica dartos and
the contiguous layers of Scarpa and Colles. In general, necrotizing gangrene of urethral origin does not
spread to the anal triangle, because Colles' fascia is attached to the peri-neal membrane posteriorly;
however, if Colles' fascia or the urogenital diaphragm is violated, the infection can involve the ischiorectal
and perivesical spaces.
Clinical Features
Most cases of necrotizing gangrene, regardless of location, begin insidiously. Patients initially complain of
scrotal discomfort and associated malaise. As the infection worsens, fever and chills develop with genital
skin changes. Scrotal swelling is usually present with erythema and increased pain (Fig. 1). However, the
skin can appear relatively normal, which may account for the delay in presentation after the onset of
symptoms, usually averaging 5 days. In addition, the pain may subside as pressure necrosis and infection
of cutaneous nerves take place. Signs and symptoms frequently found at presentation include pain
(100%), swelling (80% to 100%), fever (60% to 80%), and crepitus (60% to 70%).[7,9,14,27] Systemic
manifestations, such as overt shock and altered mental status, do not often correlate with the physical
findings and must be recognized early.
(click image to zoom) Figure 1. Preoperative photograph of patient with ne
gangrene of perineum demonstrating scrotal edema with minimal skin changes.
Careful history can elucidate the etiology. Symptoms of urgency, frequency, decreased force of stream,
and a history of perineal trauma, instrumentation, or urethral stricture point to a urologic diagnosis.
Because of the increased frequency of gastrointestinal foci, a history of rectal pain and bleeding,
hemorrhoids, and anal fissures can often be elicited. Acute and chronic skin infection of the scrotum or
penis or a history of injection suggest a dermal source. Together with the risk factors discussed above,
the presence of these signs, symptoms, and histories should raise a suspicion of necrotizing soft-tissue
infections.

3. Often nonspecific, abnormal laboratory values are present as the consequence of sepsis. Leukocytosis
>15,000/µL is found at presentation in more than 80% of patients. Anemia frequently develops secondary
to decreased production of RBCs and thrombosis. Hyponatremia, hyperglycemia, hypocalcemia, elevated
creatinine, coagulopathy, and hypoalbuminemia can be present initially and may provide diagnostic clues
to early necrotizing soft-tissue infections.[9,14,28,29]
Due to the nonspecific symptoms, its indolent course, and often unremarkable cutaneous appearance,
necrotizing gangrene of the perineum may be confused with other scrotal and intrascrotal pathology such
as scrotal cellulitis or balanoposthitis. More serious conditions that mimic Fournier's gangrene include
scrotal abscesses or incarcerated hernia. Finally, scrotal or penile gangrene may be primarily due to
vessel occlusion from vasculitis, rather than infection. These conditions include IgE-positive
hypersensitivity vasculitis, poly-arteritis nodosa, and pyoderma gangrenosum.[30,31] It is important to
distinguish these conditions from Fournier's, because appropriate treatment in these patients may include
corticosteroids and local wound care, not radical excision.
Imaging
Necrotizing gangrene of the genitalia and perineum is primarily a clinical diagnosis. Nevertheless,
imaging modalities that have demonstrated utility in confirming the disease, evaluating extent, and
determining the etiology include radiography, ultrasonography, and computed tomography (CT).[32]
Plain radiographs of the abdomen and pelvis can demonstrate subcutaneous air before crepitus is
palpable (Fig. 2). In addition, plain films may aid in defining an intra-abdominal source of the infection.[33,34]
One retrospective review reported that plain films were more sensitive in detecting soft-tissue gas than
physical examination; gas was visualized in all diabetics with necrotizing gangrene.[25] However, the
absence of subcutaneous air in the perineum or scrotum should not exclude the diagnosis.
(click image to zoom) Figure 2. Plain radiograph of pelvis at presentation, demo
air within soft tissues.
Ultrasonography has also proven useful in cases of necrotizing infections.[35,36] Gas can be detected even
when not clinically evident, and the ultrasonographic appearance is striking -- the air appears as discrete,
bright, hyperechoic areas with posterior acoustic shadowing (Fig. 3). Ultrasound can examine the
scrotum, testes and epididymides, perirectal area, and abdomen, helping to differentiate necrotizing
infections from other causes of scrotal pain. Typically, the testes and intrascrotal structures are normal in
size and architecture within a thickened scrotal wall.[37]
(click image to zoom) Figure 3. Ultrasound of scrotum, demonstrating char
hyperechoic appearance of subcutaneous gas.
CT of the abdomen and pelvis has not been well studied in necrotizing infections; however, it appears to
have potential. One study described characteristic CT findings in necrotizing fasciitis associated with
gangrene of the perineum.[38] The soft tissues are thickened with surrounding fat stranding and gas
dissecting along fascial planes. Delineation of gas margins and identification of infected fluid collections
by CT can suggest the extent of the gangrene. In addition, CT provides excellent anatomic detail of peri-
neal, pelvic, and retroperitoneal structures and may diagnose the initial source of infection. MRI provides
the same advantages as CT with improved soft-tissue resolution and multiplanar images.[39]
Treatment
Necrotizing infection of the genitalia and perineum is a surgical disease where medical therapy has a
limited role. After diagnosis, initial management is aimed at preparation for surgery. Because sepsis may
be present, hemodynamic stabilization via aggressive fluid resuscitation is necessary. In addition,
transfusion of blood products may be required to correct anemia and coagulopathy. Need for invasive
monitoring and ventilatory support should be addressed and promptly administered.

4. Empiric, broad-spectrum antibiotic therapy should be instituted.[27] Typical regimens include penicillin for
streptococci, clostridia, and certain anaerobes, gentamicin for gram-negative rods, and clindamycin for
bacteroides and other anaerobes. More recently, semisynthetic penicillins and third-generation
cephalosporins have emerged as alternatives to aminoglycosides.
Surgical debridement should not be delayed by uncertainty in diagnosis or radiologic studies.
Examination under anesthesia and exploration can be performed easily if any doubt exists. One study
reported the utility of intraoperative frozen section in confirming the early diagnosis of necrotizing
gangrene.[18] These biopsies, although rarely required, also can demonstrate evidence of the vascular
immune disorders that can be misdiagnosed as necrotizing infections.
Operative management consists of radical debridement of all areas with overt necrosis. Recent reports
indicate that incision and drainage are insufficient.[21,40] We have found outcomes to be correlated with
adequacy of initial debridement. Mortality was 100% in 4 patients treated with incision and drainage, but
only 8% in 12 patients undergoing complete debridement.[21] Intraoperative findings include edema,
liquefactive necrosis of the subcutaneous tissues, and watery pus.
Skin changes greatly underestimate the severity of the underlying tissue damage. Thus, extensive
unroofing of the involved areas is needed (Fig. 4). If the fascia separates easily from the skin and
subcutaneous tissues above, necrosis is generally present and debridement is continued. Deep fascia
and muscle are seldom involved. The challenge is to determine tissue viability and the extent of
necessary debridement, maintaining a balance between inadequate excision and preservation of
threatened but nonischemic tissue. Drains can be placed in areas of questionable viability to prevent fluid
collections and early skin closure.
(click image to zoom) Figure 4. Intraoperative photograph after debridement of al
tissue, with extensive skin loss but preservation of testes.
Even after satisfactory initial debridement, subsequent procedures are likely to be necessary; reports
have documented a mean of 2 to 4 procedures per patient.[9,29,41] Reexamination of the wound in the
operating room is helpful to completely evaluate wound progress, comfortably change extensive
dressings, and determine need for further debridement. If the patient does not improve clinically after
initial surgery, with resolving fever and leukocytosis, then inadequate debridement should be suspected.
Diversion, either fecal or urinary, is occasionally required. Controversy exists regarding the need for
colostomy. While some advocate diverting colostomy in most cases of perineal necrotizing gangrene,
others believe this to be unnecessary, even with significant gangrene of perirectal tissues. Generally,
colostomy is indicated if the sphincter is grossly infected, rectal or colonic perforation has occurred,
incontinence is present, or if the rectal wound is large.[42,43]
Criteria for urinary drainage are likewise unclear. Many patients are safely managed with an indwelling
catheter, although some recommend routine suprapubic diversion in all patients. Indications for supra-
pubic catheterizations include stricture disease and urinary extravasation or phlegmon.[7] Intraoperative
cystourethroscopy and retrograde urethrography can be performed to evaluate urethral integrity.
Despite extensive tissue involvement and radical debridement, the testicles are routinely spared. This is
presumed to be due to the copious and independent blood supply. Orchiectomy is performed when
conditions such as scrotal abscesses or severe epididymo-orchitis affect testicular viability. Coverage of
the testes is important to prevent dessication. Initially, moist dressings and gauze impregnated with
petroleum jelly provide sufficient protection. Delayed closure of the scrotum is often an option because of
the redundant nature of scrotal skin. If this is not possible, the testes can be placed in temporary
subcutaneous pouches of the medial thighs or lower abdominal wall for later scrotal reconstruction.[9,44]
The large defects in the scrotum, perineum, and abdominal wall after debridement often necessitate later
reconstruction. We have a significant experience in treatment of genital skin defects and have found
excellent results using skin grafts.[9,44,45] Once the patient has improved and local wound healing is

5. complete, reconstruction can be considered. The testes are covered with meshed, split-thickness skin
grafts, creating a neoscrotum, and the penile shaft is covered with unmeshed split-thickness skin grafts
(Fig. 5). Alternative methods of skin coverage include rotational or free myocutaneous flaps and omental
flaps.[44]
(click image to zoom)Figure 5. (A) Appearance of genitalia after reconstruction of scrotum with
split-thickness skin graft. (B) The penis has been covered with unmeshed, split-thickness skin gra
Other issues in treating patients with perineal necrotizing gangrene include nutritional support and the
potential utility of hyperbaric oxygen and topical agents. Calorie balance is important in critically ill
patients with large open wounds and preexisting malnutrition. Enteral or parenteral supplementation when
the patient has insufficient intake, prolonged intubation, or compromised gastrointestinal function is
beneficial.
Because of the importance of anaerobic organisms in necrotizing infections, hyperbaric oxygen has been
proposed as an adjunctive therapy.[46,47] Although experimental studies have demonstrated increased
leukocyte phagocytic function, fibroblast proliferation, and decreased endotoxin with the use of hyperbaric
oxygen, the clinical evidence supporting its utility is inconclusive. Routine wound care, consisting of saline
or Dakin's soaked dressings, is important after debridement. However, some investigators have proposed
the use of unprocessed honey not only as part of postoperative wound care, but as initial, definitive
therapy.[48,49] The studies, although encouraging, involve small numbers of patients and do not provide
sufficient evidence to pursue nonoperative management of necrotizing infections.
Outcomes
Reported mortality rates from genital and perineal necrotizing soft-tissue infections range from 0% to
80%.[3,7] In 2 series with 57 and 29 patients, mortality was 18% and 21%, respectively.[8,9] One review of
449 cases (1979-1988) reported overall mortality of 22%.[14] Patients were typically hospitalized 40 days.
Determinants of outcome have not been clearly defined. In numerous studies, factors such as age,
source of infection, delay in diagnosis, comorbidities, and extent of infection and debridement are not
consistently associated with prognosis. It is clear, however, that delay in adequate surgical intervention
leads to increased mortality. An objective index has been developed in order to quantify "deviations from
homeostasis," the parameter that best predicts outcome.[29] Variables in the classification system include
signs of sepsis (temperature, heart rate, respiratory rate) and laboratory values (sodium, potassium,
creatinine, hematocrit, WBC count, bicarbonate).
Morbidity from necrotizing infections is significant. Early complications include sepsis, respiratory and
renal failure, and coagulopathy; delayed complications that have been reported include fistulae, infertility,
and urethral strictures.[9,14]
Summary
Necrotizing soft-tissue infections of the genitalia and perineum represent a diverse collection of rapidly
progressive, potentially lethal diseases. Patients at risk include those with increased susceptibility to
infections from gastrointestinal, genitourinary, and cutaneous sources. The clinical picture is not always
clear; therefore, a high index of suspicion must be maintained in order to make an early diagnosis.
Radiologic clues may provide additional information. Prompt surgical excision of necrotic tissue, along
with broad-spectrum antibiotics and aggressive supportive care, is paramount to improved survival.
Despite advances in understanding the disease, imaging techniques, and modern medicine, necrotizing
gangrene of the genitalia and perineum carries significant morbidity and mortality.
Teamwork Is the Key

6. This is an excellent review of a disease entity that continues to perplex and frustrate managing
physicians. Aggressive teamwork is the key to the successful treatment of these patients with complex
problems. The use of a multidisciplinary approach using the expertise of the urologist, the reconstructive
surgeon, and either a general surgeon or colon/rectal surgeon as an operative team is critical to the
successful management. Furthermore, general support through nutrition, intensive care, hyperbaric
oxygen, and infectious disease specialists have all helped lower the mortality rate. The cosmetic
appearance of most of these men is dramatically better today through some of the reconstructive
techniques currently used.
S. Lee Guice III, MD
Department of Urology
Nalle Clinic
Charlotte, N.C.

7. Case Report
Fungal Fournier Gangrene
from Infections in Urology®
Posted 08/12/2003
Scott Rutchik, MD, Melinda Sanders, MD
Abstract and Introduction
Abstract
A diagnosis of Fournier gangrene always calls for prompt medical and often surgical action. The addition
of a fungal infection can only enhance the possibility of increased morbidity. Treatment options for
patients with this rare combination are discussed.
Introduction
Fournier gangrene, a necrotizing fasciitis that originates in the perineum, represents one of the few true
emergencies in urology practice. Typically, the infection involves anaerobic bacteria. Fungal infection,
however, has only been implicated in a single case report in the medical literature.[1] We describe here
perhaps only the second case of Fournier gangrene with a fungal organism.
Fungal Fournier Gangrene
from Infections in Urology®
Case Report
A 74-year-old man presented to the urology clinic with a 10-day history of fever accompanied by scrotal
swelling and pain. He had been undergoing treatment from his primary care physician with an oral
fluoroquinolone for presumed epididymo-orchitis. His medical history was significant for poorly controlled
diabetes and severe peripheral vascular disease that had necessitated bilateral above-knee amputations.
Physical examination revealed a hemodynamically stable patient with a tender discolored scrotum and
swelling extending into the suprapubic area with palpable crepitus throughout. A clinical diagnosis of
Fournier gangrene was made, and emergent debridement was undertaken.
The initial incision into the scrotum yielded watery pus with a fungal odor. Approximately 350 mL of pus
was aspirated from the wound. Extensive debridement of the scrotum and base of the penis was
performed, exposing necrosis of the scrotum that tracked into the inguinal and suprapubic area. The right
testicle was absent; the left testicle did not appear to be grossly infected and was spared. The skin over
the suprapubic area appeared viable and was not excised.
A suprapubic tube was placed, and the wound was packed with a sterile dressing. Gram stain of the
wound fluid demonstrated yeast, and intravenous therapy with a third-generation cephalosporin and
fluconazole was begun pending results of final wound cultures. A second debridement procedure was
performed 48 hours later.
Aerobic and anaerobic cultures of material obtained from the primary debridement demonstrated only
Candida albicans; blood cultures were negative. Pathologic examination of the debrided tissue showed
acute suppurative inflammation (Figure). Daily whirlpool therapy was initiated, as were wet-to-dry
dressing changes. The patient was discharged from the hospital on postoperative day 4, with
arrangements made for outpatient wound care.

8. Figure. (click image to zoom) Photomicrograph demonstrates an area of intact
striking underlying edema and inflammation (hematoxylin-eosin, ×200). (Photogra
Walz.)
Discussion
Fournier gangrene is somewhat of a misnomer for this disease, because true myonecrosis is uncommon.
Nonetheless, this does not detract from the seriousness of the illness, because the infection tends to
follow the distribution of Scarpa fascia, thereby allowing for extension as far cephalad as the clavicles and
as far caudad as the fascia lata. Although the disease was classically described in patients with
periurethral abscess, more contemporary presentations occur in the diabetic or immunocompromised
host.[2,3]
Modern interventions have greatly improved the prognosis for patients with Fournier gangrene, but the
disease still is capable of producing grave morbidity, because large areas of tissue debridement may be
required for disease control. Dahm and associates[4] reported a 20% mortality rate in their contemporary
case series, with depth of invasion, extent of infection, and treatment with hyperbaric oxygen observed as
the most important prognostic variables. It should be noted, however, that the use of hyperbaric oxygen is
a controversial treatment for patients with Fournier gangrene, although it may be a useful adjunct to
debridement and antibiotic therapy in severe circumstances.
The extensive tissue infarction and destruction seen in Fournier gangrene is usually the result of
anaerobic bacterial infection. In many cases, this infection may begin as a primary infection with less
virulent organisms, with anaerobic infection occurring as a secondary phenomenon. Thus, initial antibiotic
therapy should consist of broad-spectrum coverage that includes agents active against anaerobes.
Because of the rarity of fungal infection in this scenario, antifungal agents are probably not required in
most cases.
Because our patient's solitary testicle appeared viable at surgery, we believe that the most likely scenario
to explain his clinical course was a misdiagnosed scrotal abscess that was managed with a broad-
spectrum antibiotic, resulting in selection for yeast. Thus, we cannot rule out the possibility that a bacterial
infection had been the initial inciting event. Nevertheless, in this patient, fungal sepsis did not develop,
and he did not require extensive hospitalization, perhaps emphasizing the importance of early recognition
and intervention in the management of all types of Fournier gangrene.