FOURNIER’S GANGRENE

BY

RAJAH AMINA SULEIMAN

INTRODUCTION
 Despite being rare, Fournier’s gangrene was and still
remains a formidable disease with severe complications
and a high level of mortality.
 Fournier gangrene is a specific form of necrotizing
fasciitis, localized on the external genital organs, as well
as in the perianal region, accompanied by thrombosis of
the feeding arteries, leading to gangrene of the skin and
subcutaneous tissue, with manifestations of severe
intoxication and multiple organ failure.
DEFINITION
 Fournier gangrene, is defined as a
polymicrobial necrotizing fasciitis of the perineal,
perianal, or genital areas.
 Fournier's gangrene is a rare and often fulminant
necrotizing fasciitis of the perineum and genital region
frequently due to a synergistic polymicrobial infection. 
NECROTIZING FASCITIS

 Necrotizing fasciitis is a rapidly progressive inflammatory

infection of the fascia, with secondary necrosis of the
subcutaneous tissues. 
 Necrotizing fasciitis (NF), also known as flesh-eating
disease, is a bacterial infection that results in the death of
parts of the body's soft tissue.
HISTORY

 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.
EPIDEMIOLOGY

 Fournier gangrene is relatively uncommon, about one per

62,500 males are affected per year.
 The male-to-female ratio is approximately 10:1. The lower
incidence in females may reflect better drainage of the
perineal region through vaginal secretions.
 It commonly occurs in older men, but it can also occur in
women and children.
ETIOLOGY
Fournier’s gangrene commonly originates from an infection in the
anorectum, the urogenital tract, or the skin of the genitalia.
 Anorectal causes of Fournier gangrene include perianal, perirectal,
and ischiorectal abscesses; anal fissures; anal fistula; and colonic
perforations.
 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)
ETIOLOGY
 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.
 Gynaecological causes
 Infected Bartholin's gland
 Septic abortion
 Episiotomy wound
 Coital injury
 Genital mutilation
RISK FACTORS
 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 Urethral instrumentation
 Prosthetic penile implants
 Intramuscular injections
 Steroid enemas (used for the treatment of radiation proctitis)
 Rectal foreign body 
RISK FACTORS
 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
 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)
 Morbid obesity
 Alcoholism
 Excessive masturbation
RISK FACTORS
 Cirrhosis
 Extremes of age
 Vascular disease of the pelvis
 Malignancy (eg, acute leukemia) 
 Systemic lupus erythematosus 
 Crohn disease
 HIV infection 
 Malnutrition
 Iatrogenic immunosuppression (eg, from long-term
corticosteroid therapy or chemotherapy
COMMON CAUSATIVE MICROORGANISMS

 Streptococcal species
 Staphylococcal species
 Enterobacteriaceae
 Anaerobic organisms
 Fungi
PATHOPHYSIOLOGY
 Bacteremia is considered a starting link in the mechanism of the
development of necrosis of the fascia.
 This initiates the cytokine cascade leading to the damage of the
endothelium
 Which in turn activates by means of thromboplastin, a coagulation
cascade with inhibition of fibrinolysis and the formation of
disseminated microthrombosis of vessels feeding the fascia.
 In addition, damage to the endothelium leads to extravasation of the
liquid part of the blood, swelling of tissues, leukocyte infiltration, all
leading to the ischemic necrosis of the fascia.
PATHOPHYSIOLOGY
 Fournier’s disease proceeds clinically with marked symptoms of
intoxication.
 Local manifestations include ulceration in the prepuce, skin of the
penis, or scrotum.
 Within a few hours, the genitalia hyperemia increases and tissue
necrosis occurs.
 Urination becomes painful and difficult.
 The disease lasts from 5 to 8 days.
 Symptomatology is characterised by common necrosis of the skin,
subcutaneous tissue, muscles, accompanied by the development of
sepsis, multi-organ failure, leading to death.
SIGNS AND SYMPTOMS

 Fever
 General discomfort (malaise)
 Moderate to severe pain and swelling in the genital and
anal areas (perineal)
 Rankness and smell of the affected tissues (fetid
suppuration) leading to full blown (fulminating) gangrene.
 Rubbing the affected area yields the distinct sounds
(crepitus) of gas in the wound 
INVESTIGATIONS
 Complete blood cell count (CBC)
 Arterial blood gas (ABG) sampling
 Blood and urine cultures
 Disseminated intravascular coagulation (DIC) panel
 Cultures of any open wound or abscess
 Plain radiography should be the initial imaging study. It
may reveal moderate-to-large amounts of soft-tissue gas,
foreign bodies, or scrotal tissue edema. 
 CT Scan
MECHANISM OF SPREAD OF INFECTION
 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.
MANAGEMENT
 Broad-spectrum intravenous antibiotics as quickly as possible.
E.g. ciprofloxacin and clindamycin, ampicillin/sulbactam,
ticarcillin/clavulanate, or piperacillin/tazobactam in
combination with an aminoglycoside and metronidazole or
clindamycin.
 Surgical debridement of all affected dead (necrotic) skin and
subcutaneous tissue involved, with repeated removal of wound
margins as necessary. 
 Primary closure of the skin, if possible
 Local skin flap coverage
 Split-thickness skin grafts
 Muscular flaps, which are used to fill a cavity
MANAGEMENT
 Hyperbaric oxygen therapy (HBO) has been used as an adjuvant to
surgical and antimicrobial therapy.
 Indications include failure of conventional treatment, documented
clostridial involvement, or myonecrosis or deep tissue involvement.
 HBO is postulated to reduce systemic toxicity, prevent extension of
necrotizing infection, and inhibit growth of anaerobic bacteria.
 Nursing diagnosis
 • Activity intolerance
 • Anxiety
 • Breakdown in physical activity
 • Breakdown in the caretaking role
 • Breakdown in the continuation of health
 • Breakdown in the intra-family processes
 • Breakdown in the pattern of sleep
 • Breakdown in verbal communications
 • Excessive volume of liquids
 Nursing diagnosis
 • Ineective respiratory patterns
 • Lack of knowledge
 • Lack of self-care syndrome
 • Nutrition exceeding body requirements
 • Risk of aspiration
 • Risk of breakdown of skin unity
 • Risk of infection
 • Risk of situational low self-estee
PROGNOSIS

 The prognosis of the disease is serious and the

lethality reaches 90%.
COMPLICATIONS
Systemic complications
 Renal failure
 Acute respiratory distress syndrome
 Heart failure
 Cardiac arrhythmias
 Septic metastasis
 Urinary tract infection
 Stroke
 Acute thromboembolic disease of lower extremities
COMPLICATIONS
Surgical complications
 Wound infection
 Stoma-related complications
 Prolonged ileus (7 days)
 Eventration or evisceration
Long term complications
 Pain (50% of patients)
 Impaired sexual function (due to penile deviation/torsion, loss of
sensitivity of the penile skin or pain during erection)
 Stool incontinence
 Extensive scarring
 O R
S F G
NK I N
A E N
H
T IS T
L