Fournier Gangrene

Updated: May 30, 2023

Author: Vernon M Pais, Jr, MD; Chief Editor: Bradley Fields Schwartz, DO, FACS more...

OVERVIEW

Practice Essentials
Fournier gangrene was first identified in 1883, when the French venereologist Jean Alfred
Fournier described a series in which 5 previously healthy young men suffered from a
rapidly progressive gangrene of the penis and scrotum without apparent cause. This
condition, which came to be known as Fournier gangrene, is defined as a polymicrobial
necrotizing fasciitis of the perineal, perianal, or genital areas (see the image below.)

Photomicrograph of Fournier gangrene (necrotizing fasciitis), oil immersion at 1000X magnification. Note the
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 acute inflammatory cells in the necrotic tissue. Bacteria are located in the haziness of their cytoplasm.
Courtesy of Billie Fife, MD, and Thomas A. Santora, MD.

In contrast to Fournier's initial description, the disease is not limited to young people or to
males, and a cause is now usually identified. [1, 2] Impaired immunity (eg, from diabetes) is
known to increase susceptibility to Fournier gangrene. Trauma to the genitalia, which can
cause a breach in the integrity of epithelial or urethral mucosa, is a frequently recognized
mechanism by which bacteria are introduced, subsequently initiating the infectious
process. [3, 4, 5] For more information, see the following Medscape articles:

Testicular Trauma
Scrotal Trauma
Penile Fracture and Trauma
Urethral Trauma

Early, aggressive intervention is critical, as the condition is associated with a high

mortality rate. Surgery is necessary for definitive diagnosis and excision of necrotic tissue.
Along with debridement, surgical procedures may include complex closure, suprapubic
tube placement, and fecal diversion. [6] Early administration of broad-spectrum antibiotics
is indicated. Finally, any underlying comorbid conditions must ultimately be addressed.
See Treatment and Medication.

Background
In 1764, Baurienne originally described an idiopathic, rapidly progressive soft-tissue
necrotizing process that led to gangrene of the male genitalia. However, the disease was
named after Jean-Alfred Fournier, a Parisian venereologist, on the basis of a transcript
from an 1883 clinical lecture in which Fournier presented a case of perineal gangrene in
an otherwise healthy young man, adding this to a compiled series of 4 additional cases. [7]
He differentiated these cases from perineal gangrene associated with diabetes,
alcoholism, or known urogenital trauma, although these are currently recognized risk
factors for the perineal gangrene now associated with his name.

This manuscript outlining Fournier’s initial series of fulminant perineal gangrene provides
a fascinating insight into both the societal background and the practice of medicine at the
time. In anecdotes, Fournier described recognized causes of perineal gangrene, including
placement of a mistress’ ring around the phallus, ligation of the prepuce (used in an
attempt to control enuresis or as an attempted birth control technique practiced by an
adulterous man to avoid impregnating his married lover), placement of foreign bodies
such as beans within the urethra, and excessive intercourse in diabetic and alcoholic
persons. He calls upon physicians to be steadfast in obtaining confession from patients of
“obscene practices.”
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 Anatomy
The complex anatomy of the male external genitalia influences the initiation and
progression of Fournier gangrene. This infectious process involves the superficial and
deep fascial planes of the genitalia. As the microorganisms responsible for the infection
multiply, infection spreads along the anatomical fascial planes, often sparing the deep
muscular structures and, to variable degrees, the overlying skin, making the extent of
involvement difficult to appreciate.

This phenomenon has implications for both initial debridement and subsequent
reconstruction. Therefore, a working knowledge of the anatomy of the male lower urinary
tract and external genitalia is critical for the clinician treating a patient with Fournier
gangrene.

Skin and superficial fascia

Because Fournier gangrene is predominately an infectious process of the superficial and

deep fascial planes, understanding the anatomic relationship of the skin and
subcutaneous structures of the perineum and abdominal wall is important.

The skin cephalad to the inguinal ligament is backed by Camper fascia, which is a layer of
fat-containing tissue of varying thickness and the superficial vessels to the skin that run
through it. Scarpa fascia forms another distinct layer deep to Camper fascia. In the
perineum, Scarpa fascia blends into Colles fascia (also known as the superficial perineal
fascia), while it is continuous with Dartos fascia of the penis and scrotum (see the image
below).

Fascial envelopment of the perineum (male). Note how Colles fascia completely envelops the scrotum and
penis. Colles fascia is in continuity cephalad to the level of the clavicles. In the inguinal region, this fascial layer
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 is known as Scarpa fascia. Familiarity with this fascial anatomy, along with recognition that necrotizing fasciitis
tends to spread along fascial planes, makes it easy to understand how a process that starts in the perineum
can spread to the abdominal wall, the flank, and even the chest wall.

Several important anatomic relationships should be considered. A potential space

between the Scarpa fascia and the deep fascia of the anterior wall (external abdominal
oblique) allows for the extension of a perineal infection into the anterior abdominal wall.
Superiorly, Scarpa and Camper fascia coalesce and attach to the clavicles, ultimately
limiting the cephalad extension of an infection that may have originated in the perineum.

Colles fascia is attached to the pubic arch and the base of the perineal membrane, and is
continuous with the superficial Dartos fascia of the scrotal wall. The perineal membrane is
also known as the inferior fascia of the urogenital diaphragm and, together with Colles
fascia, defines the superficial perineal space.

This space contains the membranous urethra, bulbar urethra, and bulbourethral glands. In
addition, this space is adjacent to the anterior anal wall and ischiorectal fossae. Infectious
disease of the male urethra, bulbourethral glands, perineal structures, or rectum can drain
into the superficial perineal space and can extend into the scrotum or into the anterior
abdominal wall up to the level of the clavicles.

Vascular supply to the skin of the lower abdomen and genitalia

Branches from the inferior epigastric and deep circumflex iliac arteries supply the lower
aspect of the anterior abdominal wall. Branches of the external and internal pudendal
arteries supply the scrotal wall. With the exception of the internal pudendal artery, each of
these vessels travels within Camper fascia and can therefore become thrombosed in the
progression of Fournier gangrene.

Thrombosis jeopardizes the viability of the skin of the anterior scrotum and perineum.
Since the internal pudendal artery is not contained within Camper fascia, it is less
susceptible to thrombosis; therefore, its vascular territory—the posterior aspect of the
scrotal wall—remains viable and can be used in the reconstruction following resolution of
the infection.

Penis and scrotum

The contents of the scrotum, namely the testicles, epididymides, and cord structures, are
invested by several fascial layers distinct from the Dartos fascia of the scrotal wall. Again,
several important anatomic relationships should be considered.

The most superficial layer of the testis and cord is the external spermatic fascia, which is
continuous with the external aponeurosis of the superficial inguinal ring (external
abdominal oblique). The next deeper layer is the internal spermatic fascia, which is
continuous with the transversalis fascia. A deep fascia termed Buck fascia covers the
erectile bodies of the penis, the corpora cavernosa, and the anterior urethra. Buck fascia
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 fuses to the dense tunica albuginea of the corpora cavernosa, deep in the pelvis.

The fascial layers described in this section do not become involved with an infection of the
superficial perineal space and can limit the depth of tissue destruction in a necrotizing
infection of the genitalia. The corpora cavernosa, urethra, testes, and cord structures are
usually spared in Fournier gangrene, while the superficial and deep fascia and the skin
are destroyed.

Pathophysiology
Localized infection adjacent to a portal of entry is the inciting event in the development of
Fournier gangrene. Ultimately, an obliterative endarteritis develops, and the ensuing
cutaneous and subcutaneous vascular necrosis leads to localized ischemia and further
bacterial proliferation. Rates of fascial destruction as high as 2-3 cm/h have been
described.

Infection of superficial perineal fascia (Colles fascia) may spread to the penis and scrotum
via Buck and Dartos fascia, or to the anterior abdominal wall via Scarpa fascia, or vice
versa. Colles fascia is attached to the perineal body and urogenital diaphragm posteriorly
and to the pubic rami laterally, thus limiting progression in these directions. Testicular
involvement is rare, as the testicular arteries originate directly from the aorta and thus
have a blood supply separate from the affected region. Far-advanced or fulminant
Fournier gangrene can spread from the fascial envelopment of the genitalia throughout
the perineum, along the torso, and, occasionally, into the thighs.

The following are pathognomonic findings of Fournier gangrene upon pathologic

evaluation of involved tissue:

Necrosis of the superficial and deep fascial planes<

Fibrinoid coagulation of the nutrient arterioles
Polymorphonuclear cell infiltration
Microorganisms identified within the involved tissues

Infection represents an imbalance between (1) host immunity, which is frequently

compromised by one or more comorbid systemic processes, and (2) the virulence of the
causative microorganisms. The etiologic factors allow the portal for entry of the
microorganism into the perineum; the compromised immunity provides a favorable
environment to initiate the infection; and the virulence of the microorganism promotes the
rapid spread of the disease. See the image below.
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 Necrotizing infection results when the pathogen is extremely virulent or, most commonly, when a combination
of microorganisms act synergistically in a susceptible immunocompromised host.

Microorganism virulence results from the production of toxins or enzymes that create an
environment conducive to rapid microbial multiplication. [8] Although Meleney in 1924
attributed the necrotizing infections to streptococcal species only, [9] subsequent clinical
series have emphasized the multiorganism nature of most cases of necrotizing infection,
including Fournier gangrene. [10, 11, 12, 13, 14]

Presently, recovering only streptococcal species is unusual. [15] Rather, streptococcal

organisms are cultured along with as many as 5 other organisms.

The following are common causative microorganisms:

Streptococcal species
Staphylococcal species
Enterobacteriaceae
Anaerobic organisms
Fungi

Most authorities believe that polymicrobial involvement is necessary to create the synergy
of enzyme production that promotes rapid multiplication and spread of Fournier gangrene.
[8] For example, one microorganism might produce the enzymes necessary to cause

coagulation of the nutrient vessels. Thrombosis of these nutrient vessels reduces local
blood supply; thus, tissue oxygen tension falls.

The resultant tissue hypoxia allows for the growth of facultative anaerobes and
microaerophilic organisms. These latter microorganisms, in turn, may produce enzymes
(eg, lecithinase, collagenase), which lead to digestion of fascial barriers, thus fueling the
rapid extension of the infection.
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 Fascial necrosis and digestion are hallmarks of this disease process; this is important to
appreciate because it provides the surgeon with a clinical marker of the extent of tissue
involvement. Specifically, if the fascial plane can be separated easily from the surrounding
tissue by blunt dissection, it is quite likely to be involved with the ischemic-infectious
process; therefore, any such dissected tissue should be excised.

Etiology
Although originally described as idiopathic gangrene of the genitalia, Fournier gangrene
has an identifiable cause in 75-95% of cases. [16] The necrotizing process commonly
originates from an infection in the anorectum, the urogenital tract, or the skin of the
genitalia. [17]

Anorectal causes of Fournier gangrene include perianal, perirectal, and ischiorectal

abscesses; anal fissures; anal fistula; and colonic perforations. These may be a
consequence of colorectal injury or a complication of colorectal malignancy, [18, 19]
inflammatory bowel disease, [20] colonic diverticulitis, or appendicitis.

A case of Fournier gangrene was reported in a patient with COVID-19 following prolonged
and repeated ventilation in prone position. [21]

Urogenital tract causes include the following:

Infection in the bulbourethral glands

Urethral injury
Iatrogenic injury secondary to urethral stricture manipulation
Epididymitis
Orchitis
Lower urinary tract infection (eg, in patients with long-term indwelling urethral
catheters)

Dermatologic causes include hidradenitis suppurativa, ulceration due to scrotal pressure,

and trauma. Inability to practice adequate perineal hygiene, such as in paraplegic
patients, results in increased risk.

Accidental, intentional, or surgical trauma [22] and the presence of foreign bodies may also
lead to the disease. The following have been reported in the literature as precipitating
factors:

Blunt thoracic trauma

Superficial soft-tissue injuries
Genital piercings
Penile self-injection with cocaine [23]
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 Urethral instrumentation
Prosthetic penile implants
Intramuscular injections
Steroid enemas (used for the treatment of radiation proctitis)
Rectal foreign body [24]

In women, septic abortions, vulvar or Bartholin gland abscesses, hysterectomy, and

episiotomy are documented sources. A comprehensive literature review of 134 women
with Fournier gangrene reported that perineal abscess was the most common etiology
(n=41, 35%). [2] In men, anal intercourse may increase risk of perineal infection, either
from blunt trauma to the area or by spread of rectally carried microbes.

In children, the following have led to the disease:

Circumcision
Phimosis
Strangulated inguinal hernia
Omphalitis
Insect bites
Trauma
Urethral instrumentation
Prematurity [25]
Perirectal abscesses
Systemic infections
Diaper rash [25]
Secondary immunodeficiency

A case report by Numoto et al describes Fournier gangrene that developed after surgical
repair of a strangulated inguinal hernia in a 2-month-old boy. The boy was receiving
adrenocorticotropic hormone (ACTH) therapy for infantile spasms, and the authors
suggest that immune suppression from the ACTH may have contributed to the
development of Fournier gangrene. [26]

Pathogens

Wound cultures from patients with Fournier gangrene reveal that it is a polymicrobial
infection with an average of 4 isolates per case. Escherichia coli is the predominant
aerobe, and Bacteroides is the predominant anaerobe.

Other common microflora include the following:

Proteus
Staphylococcus
Enterococcus
Streptococcus (aerobic and anaerobic)
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 Pseudomonas
Klebsiella
Clostridium [27]

Rarely, Candida albicans has been reported as the pathogen in cases of Fournier
gangrene. [28, 29, 30]

Predisposition to disease

Any condition that depresses cellular immunity may predispose a patient to the
development of Fournier gangrene. Examples include the following:

Diabetes mellitus (present in as many as 60% of cases) [31, 27]

Morbid obesity
Alcoholism
Cirrhosis
Extremes of age
Vascular disease of the pelvis
Malignancy (eg, acute leukemia) [32, 33]
Systemic lupus erythematosus [34]
Crohn disease
HIV infection [35] ref34}
Malnutrition
Iatrogenic immunosuppression (eg, from long-term corticosteroid therapy or
chemotherapy [36] )

The US Food and Drug Administration (FDA) has noted an increased risk for Fournier
gangrene in patients with type 2 diabetes mellitus treated with sodium-glucose
cotransporter-2 (SGLT2) inhibitors. SGLT2 inhibitors were first approved in 2013, and by
2019, 55 cases of Fournier gangrene had been reported in patients receiving these
agents. By comparison, only 19 cases of Fournier gangrene have been reported over 35
years in patients taking other diabetes drugs. [37]

Details of Fournier gangrene cases associated with SGLT2 inhibitors included the
following [37] :

Patients ranged in age from 33 to 87 years; 39 were men, 16 were women.

Onset of Fournier gangrene after initiation of SGLT2 inhibitors ranged from 5 days to
49 months.
Complications included diabetic ketoacidosis, sepsis, and kidney injury.
Eight patients underwent fecal diversion surgery, two patients required amputation
of a lower extremity due to necrotizing fasciitis, and three patients died.
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