Surg Clin N Am 82 (2002) 1213–1224

Fournier’s gangrene
Emilio Morpurgo, MD, Susan Galandiuk, MD*
Section of Colon and Rectal Surgery, University of Louisville, 550 South Jackson Street,
Louisville, KY 40292, USA

Fournier’s gangrene is a disease characterized by necrotizing fasciitis of

the perineal and genital region, resulting from synergistic polymicrobic in-
fection. Regardless of its primary cause, the clinical presentation varies from
anorectal or genital pain with minimal evidence of cutaneous necrosis, to a
rapidly spreading necrosis of the skin and soft tissue, to systemic sepsis with-
out any apparent source of infection. Fournier’s gangrene is a surgical emer-
gency, and because of the differences in clinical presentation, patients may
be initially encountered in various clinical settings. Because delay in diag-
nosis and treatment of this condition can be fatal, it is important not to
overlook the symptoms, even if nonspecific. Once Fournier’s gangrene is
suspected, prompt treatment is essential. Awareness of this condition is cru-
cial in view of the increasing population of immunosuppressed individuals in
this country and the frequently minimal nature of symptoms in this patient
group.

Anatomy
The infection resulting in Fournier’s gangrene arises in the perianal or
genital areas and rapidly spreads along the fascial planes, usually in a matter
of hours. The most important superficial plane of the perineum is Colles’
fascia, which is continuous with the dartos fascia of the scrotum and penis,
and fuses with the urogenital diaphragm. Colles’ fascia surrounds the penis
and continues superiorly to become the Scarpa’s fascia of the abdomen.
Any infections arising in this perineal area can therefore rapidly involve the
skin of the scrotum, penis, and the superficial plane of the abdominal wall.
Laterally, the spread of infection is limited by the attachments of the Colles’
fascia to the pubic rami and the fascia lata.

* Section of Colon and Rectal Surgery, University of Louisville, 550 South Jackson Street,
Louisville, KY 40292.
E-mail address: s0gala01@gwise.louisville.edu (S. Galandiuk).

0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 5 8 - 0
1214 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

Bucks’ fascia surrounds the deeper aspect of the penis, and an infection
that originates from urethral trauma or from the periurethral glands can
remain limited to the ventral portion of the penis. If Bucks’ fascia is in-
terrupted by injury or infection, the fasciitis can reach the plane of the
dartos and Colles’ fascia, involving the entire perineum and the abdominal
wall.
The posterior aspect of the perineum is limited superiorly by the levator
ani muscles, which fuse with the external anal sphincter. If the sphincteric
apparatus is damaged by the primary cause of the infection or by necrotizing
infection, the infection can spread along the rectum into the presacral space,
the retrovesical space, and the pelvirectal tissue. This can involve the retro-
peritoneal space to the level of the upper abdomen, and in rare cases, even to
the paravertebral region up to the neck [1]. Ultimately, the infection can
penetrate into the peritoneal cavity, eventually causing diffuse peritonitis.

Bacteriology
Fournier’s gangrene is usually caused by a polymicrobial infection from
bacteria that are normally present within the distal rectum and perianal
area (Table 1). These pathogens normally have a low virulence, but in
pathologic conditions with local trauma or infection, often in association
with a systemic comorbid disease, their synergistic action is triggered, and
these bacteria can acquire an extremely destructive, virulent behavior.
In most cases, the infection features a combination of aerobes and anae-
robes, with an average of three bacteria being cultured from each diagnosed
patient [2,3]. In many patients, anaerobes are not always cultured, but this
is probably due to inadequate collection and sample processing [3]. There is
only a small percentage of cases in which no bacteria are identified in the
wound culture [2,4–6].
Because this infection is caused by bacteria that normally populate the
perineal area, most of the wound cultures demonstrate growth of Escheri-
chia coli, staphylocci, streptococci, and Proteus. It does not appear that the
origin of the infection (rectum, urinary, dermal) has any impact on the
specificity of the species cultivated [7]. Rarely, Candida can be responsible
for this disorder [8].

Etiology
The most common causes of Fournier’s gangrene are anorectal infec-
tions, genitourinary infections or trauma, or perineal and genital skin inju-
ries (Table 2). Perianal infection is the single most common cause (19% to
50% of cases), either due to a primary infection or secondary to perianal sur-
gery. Because of a better understanding of this condition and to an improve-
ment in the diagnostic tools, the number of cases with an unknown origin
Table 1
Bacteriology of Fournier’s gangrene: percentage of cultures with different bacteria
Percentage of cultures with specific bacteria
Author, No. Percentage Escherichia
year of pts polymicrobial coli Staphylococcus Streptococcus Proteus Klebsiella Pseudomonas Clostridium Enterococcus Bacteroides
Asci, 34 * 79 27 72 27 20 27 – 37 51
1998 [2]
Basoglu, 15 33 53 33 15 – – – 1 – –
1997 [18]
Benizri, 24 – 73 42 63 42 – 10 10 – –
1996 [4]
Enriquez, 28 50 85 15 25 25 – – 10 – 65
1987 [5]
Hollabaugh, 26 100 54 37 41 8 – – 4 20 23
1998 [6]
Korhonen, 33 100 51 15 21 6 – – 30 15 54
1998 [19]
Laor, 30 – 37 33 37 10 16 10 30 23
1995 [45]
Olsofka, 14 75 24 14 21 – – – – – –
1999 [16]
Stephens, 70 – 40 64 – – 40 30 60 – 45
1993 [10]
Yaghan, 10 * 80 60 30 – 60 30 – – –
E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

2000 [3]
* Patient had an average of 3 bacteria cultivated.
1215
1216 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

Table 2
Etiology of Fournier’s gangrene
Etiology (percentage)
Author, year No. pts in series Colorectal Urologic Cutaneous Unknown
Asci, 1998 [2] 55 29 35 29 6
Baskin, 1990 [7] 29 48 21 31 –
Basoglu, 1997 [18] 15 40 26 13 20
Benizri, 1996 [4] 24 58 12 4 25
 Eke, 2000 [9] 1726 21 19 24 36
Enriquez, 1987 [5] 28 50 36 – 14
Hollabaugh, 1998 [6] 26 19 39 – 42
Korhonen, 1998 [19] 33 48 0 3 45
Olsofka, 1999 [16] 14 36 14 20 14
Savino, 1993 [38] 10 50 20 – 30
 Stephens, 1993 [10] 449 33 21 6 26
Yaghan, 2000 [3] 10 40 30 30 0
  Historic series.

have decreased over the years, but still remain significant [9,10]. In cases
when an origin of the infection cannot be determined by the clinical
examination, an abdominal source should be suspected and needs to be
investigated, because this can significantly change the type of clinical
management needed. Possible abdominal sources include appendicitis,
diverticulitis [11], colonic cancer [12,13], Crohn’ s disease [14,15], or incar-
cerated hernias [16]. Kyriakidis [17] reported a case of Fournier’s gangrene
caused by a delayed rupture of an ileal neobladder. Even in the most recent
reports [2,6,18,19], a large number of infections of unknown origin remain.
In some of these cases, the amount of necrosis at presentation renders the
primary cause of the infection impossible to visualize. In these cases, a pri-
mary cutaneous cause may be responsible [3,9]. Frequently, and indepen-
dent of the primary cause, these patients have an associated comorbid
factor (Table 3). Twenty per cent to 70% have diabetes mellitus. Chronic
alcoholism is often present. Diabetic patients carry a higher number of bac-
teria on the skin that predispose them to skin infection [20]. Furthermore,
they have impaired chemotaxis, phagocytosis, and intracellular killing func-
tion. Beyond that, diabetic angiopathy can impair blood circulation in the
affected area, thus facilitating anaerobic infection. Other comorbid condi-
tions are post-transplant [6,21] and postchemotherapy [22–24] immunosup-
pression, and steroid therapy. Patients who are severely immunosuppressed
have a high mortality rate and often have monomicrobic culture of bacteria.
Results of wound culture are usually different from those normally encoun-
tered in nonimmunosuppressed patients [22,24]. Perianal sepsis is common
in patients with human immunodeficiency (HIV) syndrome, especially in
male homosexuals [25]. Fournier’s gangrene can be a severe complication
or the first sign of immunosuppression in patients with previously unknown
HIV syndrome [26,27].
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Table 3
Comorbid conditions in patients with Fournier’s gangrene
Percentage pts. with comorbid conditions
Author, year No. pts in series Diabetes Alcoholism Immunosuppression*
Asci, 1998 [2] 34 32 21 –
Baskin, 1990 [7] 29 41 52 –
Basoglu, 1997 [18] 26 26 – –
Eke, 2000 [9] 1726 20 9 –
Enriquez, 1987 [5] 28 21 4 –
Hejase, 1996 [41] 38 66 66 –
Hollabaugh, 1998 [6] 26 38 35 –
Korhonen, 1998 [19] 33 21 12 6
Olsofka, 1999 [16] 14 31 – –
Savino, 1993 [38] 10 60 20 20
Yaghan 2000 [3] 10 70 – –
* Includes steroids and chemotherapy.

The mechanism of the infection is multifactorial and is well explained if

different bacteria contribute to the infection. Bacteroide organisms produce
collagenase and heparinase, whereas aerobic bacteria induce platelet aggre-
gation and complement fixation that in turn can lead to microvascular
thrombosis with subsequent dermal necrosis. Streptococcus and Staphyloco-
ccus contribute to tissue damage with the production of hyaluronidase,
streptokinase, and streptodornase. The action of the phagocytes is severely
impaired within the necrotic, ischemic tissue, leading to spread of the
necrosis [28]. This may explain why necrotic fluid rather than pus is
frequently observed in the wounds of these patients [23].

Clinical presentation
Fournier’s gangrene usually starts with perianal or perineal pain, often
disproportionate with physical findings such as swelling or pruritus in the
affected area. In many cases, the clinical presentation can be less clear and
misleading. Patients may have fever, malaise for a few days [13], nonspecific
abdominal pain [22], general symptoms of infection without any specific sym-
ptoms from the perineal area [23,29], or signs of sepsis with tachycardia, vol-
ume depletion, anemia, increased serum creatinine, and electrolyte imbalance.
The clinical scenario becomes clearer with worsening of the cutaneous
and subcutaneous inflammation and with the presence of the typical skin
necrosis. Black dermal necrosis is rarely the first sign, because it is the result
of the thrombosis of the subcutaneous vessels. It is therefore the cutaneous
manifestation of a more severe underlying infection (Fig. 1A,B) [30]. Crep-
itus is usually present due to the presence of gas-forming bacteria.
Diagnosis is based on clinical examination, during which the origin of
the infection in many patients can be established. Because the delay in the
1218 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

Fig. 1. Cutaneous manifestation of a more severe underlying infection. Patient with perirectal
abscess with spread of infection to the scrotum (patient in lithotomy position) (A) prior to and
(B) after debridement. (Courtesy of Stephen M. Girard, MD, Louisville, KY.)
 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224 1219

treatment has a significant impact on the prognosis [6,13,22,31,32], radiolog-

ical evaluation can speed up the diagnostic process in unclear cases. Scrotal
ultrasound [33] can exclude other causes of an ‘‘acute’’ scrotum, demonstrat-
ing normal testes and the presence of gas in the scrotal skin. Computed tomo-
graphy (CT) scan [34,35] can demonstrate thickening of the fascial planes,
with presence of gas, fat infiltration, and the eventual intra-abdominal or
retroperitoneal progression of the infection (Figs. 2,3). Because prompt and
proper primary debridement positively impacts outcome, a preoperative CT
scan demonstrating involved areas that are not clinically evident can be an
important diagnostic tool [36].

Treatment
Immediate correction of fluid and electrolyte imbalance should be per-
formed, along with the administration of broad-spectrum empiric antibiotic
therapy (penicillins with b lacatamse inhibitor, cabapenems or antibiotic
combinations of penicillins, clindamycin, or metronidazole and aminoglyco-
side) [37]. The primary treatment of Fournier’s gangrene, however, is surgi-
cal. The surgical team must be prepared not only to drain an abscess or to
perform debridement, but also for a major surgical procedure [6,13,30,38].
Careful examination of the patient under general anesthesia is mandatory
to identify the cause of the disease and determine its extent. If a clear peri-
neal cause is not found, an abdominal source should be suspected and an

Fig. 2. Computed tomography scan demonstrating gas (arrows) in scrotum (Courtesy of

Drs. D’Annibale and Fiscon, Hospital of Camposampiero, Padova, Italy.)
1220 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

Fig. 3. Computed tomography scan demonstrating gas (arrow) within the pelvis (Courtesy of
Drs. D’Annibale and Fiscon, Hospital of Camposampiero, Padova, Italy.)

abdominal exploration considered [11,30]. In the minimally invasive surgery

era, laparoscopy, although not reported in literature, can be a useful adjunc-
tive surgical tool. If necrotic testicles are found during debridement, an
abdominal origin should be strongly suspected, because these organs have
an intra-abdominal vascularization and are usually spared if necrosis affects
only the subcutaneous tissue [11]. Surgical debridement should be extended
until well-perfused, viable tissue is identified (see Fig. 1B). Although some
authors claim that minimal debridement may be sufficient [39], one must
remove a large enough portion of the perineal, scrotal, penile, or perianal
skin that viable tissue is found. Tissue that can easily be divided from the
fascial plane has to be completely removed [5,30,31]. Because this type of
infection spreads along the anatomical fascial planes, unnecessary surgical
perforation of these planes should be avoided during debridement to pre-
vent extension of the infection to unaffected areas. This is especially true
if the necrosis remains in the retroperitoneal space, and the peritoneum has
not been violated. Follow-up surgical exploration, with additional debride-
ment if necessary, should be performed 24 to 48 hours after the operation in
order to exclude further extension of the necrosis. Serial re-explorations
should be continued until the infection is well controlled. In most cases,
testes and rectum can be preserved. In some cases, major operations are
required, such as abdominoperineal resection if the rectum is extensively
damaged [11,26,30]. Many surgeons [4,16] believe that colostomy is an inte-
gral part of management of patients requiring extensive debridement. The
 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224 1221

percentage of patients who receive fecal diversion varies among different ser-
ies (Table 4). Colostomy should be performed to protect wounds from fecal
contamination if there is extensive sphincter damage or extensive perineal
debridements. A suprapubic catheter may be required if there is a urologic
etiology of the infection with urethral stricture and urine extravasion [40].
Orchiectomy may be necessary in up to 24% of cases. The testicles can
become necrotic when there is an intra-abdominal source of the infection
[11], or if there is extension of necrosis after extensive debridements [41].
In cases of extensive scrotal skin necrosis, the testes can be protected in
subcutaneous thigh or abdominal skin pockets or with skin flaps
[6,7,19,28,36,38,40]. This will impair subsequent fertility.
Many surgeons believe that hyperbaric oxygen therapy is an effective
adjuvant therapy [4,19,42]. It has been postulated that hyperbaric oxygen
therapy has a direct effect against anaerobic bacteria through the formation
of oxygen free radicals. Furthermore, oxygen improves the action of neutro-
phils that have an increased oxygen consumption during phagocytosis.
Hyperbaric oxygen therapy also has a direct effect on wound healing by
improving fibroblast growth and angiogenesis [42]. The use of hyperbaric
oxygen, however, is controversial. In a series of studies in which hyperbaric
oxygen therapy was not used [2,3,5,10,16,18,38,39,41], the outcomes did not
differ from those in which it was used. Those who strongly advocate the use
of oxygen hyperbaric therapy [4,19] claim that it significantly decreases mor-
tality. Although the use of hyperbaric oxygen therapy has not yet demon-
strated any definitive benefit, its use does have a rationale. It can be used
following adequate debridement, unless real contraindications are present
[42]. Although it has no known deleterious effects, the high associated cost
is often prohibitive.

Table 4
Treatment of Fournier’s gangrene: need for fecal or urinary diversion and/or orchiectomy*
Type of diversion
No. pts Fecal Urinary  Orchiectomy
Author, year in series (% pts) (% pts) (% pts)
Asci, 1998 [2] 55 18 79 32
Baskin, 1990 [7] 29 31 83 10
Basoglu, 1997 [18] 26 33 0 0
Enriquez, 1987 [5] 28 21 14 –
Hejase, 1996 [41] 38 0 60 21
Hollabaugh, 1998 [6] 26 27 62 23
Korhonen, 1998 [19] 33 57 0 9
Olsofka, 1999 [16] 14 57 – 0
Savino, 1993 [38] 10 20 20 10
Yaghan, 2000 [3] 10 0 0 10
* Some patients had more than one procedure.
  Suprapubic catheter.
1222 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224

After surgery, regular daily dressing changes are mandatory, irrigating

with saline or iodine solutions in order to remove necrotic tissue and debris
[43]. Both unprocessed honey and lyophilized collagenase can be used in
postoperative wound treatment. Honey has a proven antibacterial activity.
It can lead to oxygen production, absorbs fluids from the wound, and can
halt the progression of necrosis [41]. Lyophilized collagenase digests necrotic
tissues and may help skin regeneration thus decreasing the need of surgical
debridements [2]. In most cases, adequate healing occurs by simple secon-
dary intention; however, if there have been very extensive debridements,
coverage with split-thickness grafts or myocutaneous flaps may be necessary
in order to prevent excessive scarring retraction [19,28,30,38–41].

Outcome
The mortality rate associated with Fournier’s gangrene ranges from 3%
to 38% (Table 5). Clinical outcome is influenced both by the timing and
adequacy of surgical treatment [13,22,24,31]. Age significantly affects out-
come: patients older than 60 years have a higher mortality rate [4,6,19,
32,44]. The mortality rate is high in immunocompromised patients [22,24].
There is still controversy as to whether the coexistence of diabetes mellitus
influences prognosis [4,7]. We believe that this is a significant negative prog-
nostic factor, because it delays patient presentation. With respect to the site
of origin, patients with an anorectal source tend to have a worse prognosis
as compared to those with a urologic origin [4,7]. Laor and coworkers [45]
have reported a scale based on clinical and laboratory parameters in order
to measure deviation from normal values and predict clinical outcome. In
general, at gangrene onset, those patients who have a major deviation from
the hemodynamic homeostasis [16,45] have a higher mortality rate. Devia-
tion from homeostasis is clearly a reflection of patient age, comorbid condi-
tions, and the delay between the onset of symptoms. Positive blood culture

Table 5
Fournier’s gangrene mortality
Author, year No. pts in series Mortality rate (%)
Asci, 1998 [2] 55 14
Baskin, 1990 [7] 29 21
Basoglu, 1997 [18] 26 20
Benizri, 1996 [4] 24 24
Eke, 2000 [9] 1726 16
Enriquez, 1987 [18] 28 25
Hejase, 1996 [41] 38 3
Hollabaugh, 1998 [6] 26 23
Korhonen, 1998 [19] 33 9
Olsofka, 1999 [16] 14 38
Savino, 1993 [38] 10 10
Stephens, 1993 [10] 449 22
Yaghan, 2000 [3] 10 20
 E. Morpurgo, S. Galandiuk / Surg Clin N Am 82 (2002) 1213–1224 1223

is an adverse prognostic factor, [4,32] with a 100% mortality rate in one

series [4].

Summary
Fournier’s gangrene can still be a life-threatening condition with a high
mortality rate. Diagnosis and treatment should be prompt and adequate.
Radiological studies may help to define the extent of the disease preopera-
tively in cases in which this is unclear. Surgery with extensive debridement
of all necrotic tissue is the mainstay of treatment.

Acknowledgments
We thank Margaret Abby for her assistance in manuscript preparation.

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