Fournier Syndrome: Causes, Symptoms, Treatment, Diagnosis, Prevention and Prognosis

Also known as Fournier gangrene, it is an intense pain and sensation in the genitals.

The clinical course generally progresses through the following phases:

  • Prodromal symptoms of fever and lethargy may be present for 2-7 days.
  • Pain and intense genital sensitivity are usually associated with edema of the skin that covers it; Itching may also be present.
  • I am increasing genital pain and sensitivity with progressive erythema of the overlying skin.
  • The dark aspect of the overlying skin; is subcutaneous crepitus.
  • Gangrene is evident from a part of the genitals; purulent drainage of wounds.

At the beginning of the course of the disease, the pain may be disproportionate to the physical findings. The pain may disappear as the nerve tissue becomes necrotic as gangrene develops.

The systemic effects of this process vary from local sensitivity without toxicity to septic shock. The greater the degree of necrosis, the deeper the systemic effects are.

Fournier’s gangrene was identified for the first time in 1883 when the French venereologist Jean Alfred Fournier described a series in which five healthy young men suffered a rapidly progressive infection of the penis and scrotum without apparent cause.

This condition, known as Fournier’s gangrene, is defined as polymicrobial necrotizing fasciitis of the perineal, perianal or genital areas. Unlike the initial description of Fournier, the disease is not limited to young people or men, and now a cause has been identified.

It is known that decreased immunity (for example, diabetes) increases the susceptibility to Fournier gangrene.


Trauma to the genitals, which can cause a breach in the epithelial or urethral mucosa integrity, is a frequently recognized mechanism by which bacteria are introduced, subsequently initiating the infectious process.

Early and aggressive intervention is critical since the condition is associated with a high mortality rate. Surgery is necessary for the definitive diagnosis and excision of the necrotic tissue.

Surgical procedures may include complex closure, suprapubic tube placement, fecal deviation, and debridement. The early administration of broad-spectrum antibiotics is indicated. Finally, any underlying comorbid condition must ultimately be addressed.

In 1764, Baurienne originally described an idiopathic and rapidly progressive process of soft tissue necrosis that led to gangrene of the male genitalia.

However, the disease was named after Jean-Alfred Fournier, a Parisian venereologist, based on a transcript of a clinical conference of 1883 in which Fournier presented a case of perineal gangrene in a healthy young man, adding this to a series compiled from 4 additional points.

He differentiated these cases from perineal gangrene associated with diabetes, alcoholism, or known urogenital traumas, although these are currently recognized risk factors for perineal infection now associated with his name.

This manuscript describing the initial series of fulminating perineal gangrene of Fournier provides a fascinating insight into the social background and practice of medicine at that time.

In anecdotes, Fournier described recognized causes of perineal gangrene, including placing a lover’s ring around the phallus, ligation of the foreskin (used to control enuresis or as an attempt at a birth control technique practiced by a man adulterer to avoid impregnating his married lover).

The placement of foreign bodies such as beans inside the urethra and excessive intercourse in diabetic and alcoholic people.

He calls on doctors to be firm in obtaining a confession of patients for “obscene practices.”

What is Fournier’s syndrome or Fournier’s gangrene?

When many people hear the term “gangrene,” they may think that the toes or fingers are affected by hypothermia, which means their body temperature has decreased and has remained below 95 degrees.

However, with Fournier’s gangrene, his genitals and area are affected. Moreover, hypothermia does not cause it.

Gangrene occurs when the body tissue is dead or dying (known as necrosis) due to a lack of blood flow or bacterial infection.

Fournier’s gangrene involves an infection in the scrotum (including the testicles), the penis, or the perineum. The perineum is the area between the scrotum and the anus of a man; or the space between the anus and the vulva for a woman.

Dead or dying tissue in people with this type of gangrene is often found in the genitals and can extend to the thighs, stomach, and chest.

How common is it?

Fournier’s gangrene is rare. While it is more common in men, women and children can also have it.

The disease is most often found in men between 50 and 60. Men are ten times more likely than women to have Fournier’s gangrene.

Fournier’s gangrene is even rarer in children.

Anatomy of Fournier Syndrome

The complex anatomy of the male external genitalia influences the initiation and progression of Fournier’s gangrene. This infectious process involves the superficial and deep fascial planes of the genitals.

As the microorganisms responsible for the infection multiply, the disease extends along the anatomical fascial planes, often respecting the deep muscle structures and, to varying degrees, the overlying skin, making it difficult to assess the degree of involvement.

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

Skin and superficial fascia:

Because Fournier’s gangrene is predominantly an infectious process of the superficial and deep fascial planes, it is essential to understand the anatomical relationship between the skin and the subcutaneous structures of the perineum and the abdominal wall.

The cephalic skin of the inguinal ligament is supported by Camper’s fascia, which is a layer of fatty tissue of varying thickness and the superficial vessels of the skin that passes through it. Scarpa’s fascia forms another distinct layer deep into Camper’s fascia.

In the perineum, Scarpa’s fascia is mixed with Colles’ fascia (also known as superficial perineal fascia) while continuing with the Dartos fascia of the penis and scrotum.

Several meaningful anatomical relationships must be considered. Potential space between Scarpa’s fascia and the deep fascia of the anterior wall (external abdominal oblique) allows the extension of a perineal infection in the anterior abdominal wall.

Superiorly, the Scarpa and Camper fascia fuse and attach to the clavicles, ultimately limiting the cephalic 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 lower fascia of the urogenital diaphragm and, together with Colles’ fascia, defines the superficial perineal space.

This space contains the membranous urethra, the bulbar urethra, and the bulbourethral glands. In addition, this space is adjacent to the anterior anal wall and the ischiorectal fossae.

Infectious diseases of the male urethra, bulbourethral glands, perineal structures, or rectum can be drained into the superficial perineal space. They can extend into the scrotum or anterior abdominal wall to the level of the clavicles.


Fournier’s gangrene usually occurs because of an infection in or near your genitals. Sources of infection may include:

  • Diseases of the urinary tract.
  • Bladder infections
  • Hysterectomies.
  • Abscesses (swollen body tissue containing pus).

In children, causes may include:

  • Insect bites.
  • Burns
  • Circumcision.

Although they are not considered causes of Fournier’s gangrene, there are other conditions and medications that experts believe may increase the likelihood of contracting this disease, such as:

  • Diabetes.
  • Alcohol abuse.
  • Trauma in the genital area.
  • Steroids
  • Chemotherapy.
  • VIH.
  • Obesity.
  • Cirrhosis (a liver disease).

Doctors can find the cause of Fournier’s gangrene in approximately 90% of cases.


People with Fournier gangrene can have several symptoms, which include:

  • Fever.
  • Pain and swelling in the genitals or anal area.
  • The unpleasant odor comes from the affected skin tissue.
  • Crunchy sound when touching the affected area.
  • Dehydration
  • Anemia.

Examination for Fournier Syndrome

The doctor should pay special attention to the palpation of the genitals and the perineum and the digital rectal examination to evaluate the signs of the disease and look for a possible portal of entry.

Fluctuation, soft tissue crepitus, localized sensibility, or hidden wounds in any site should alert the examiner to possible Fournier gangrene.

The affected region’s skin may be erythematous, edematous, cyanotic, tanned, indurated, blistered, and gangrenous. The appearance of the skin often underestimates the degree of underlying disease.

There may be a smell of feculence due to infection with anaerobic bacteria. Crypt may be present, but its absence does not exclude the presence of Clostridium species or other gas-producing organisms.

Systemic symptoms (e.g., fever, tachycardia, hypotension ) may be present.


The treatment of Fournier’s gangrene involves several modalities. Surgery is necessary for the definitive diagnosis and excision of the necrotic tissue. Previous surgical intervention has been associated with reduced mortality.

You should see a doctor immediately. The treatments include:

  • Antibiotics are given intravenously (through your veins).
  • Surgery to remove dead and dying tissue and confirm the diagnosis.

You may also need reconstructive surgery after your infection is under control. Moreover, some people need colostomies (to get rid of the poop) and catheters (to get rid of urine), depending on the area affected.

Some people also need hyperbaric oxygen therapy, which means they are given pure oxygen in a pressurized room.

You can also receive a tetanus shot if you have an injury.

In patients with systemic toxicity, that manifests as hypoperfusion or organic failure.

Aggressive resuscitation to restore perfusion and normal organ function should significantly take precedence over diagnostic maneuvers if these diagnostic studies could compromise resuscitative interventions.

Therefore, treatment in the emergency department of patients with Fournier gangrene includes aggressive resuscitation in anticipation of surgery. Provide airway management, administer supplemental oxygen and establish intravenous access and continuous cardiac monitoring.

Crystalloid replacement is indicated for dehydrated patients who show signs of shock.

The first broad-spectrum antibiotics are indicated. The prophylaxis against tetanus is indicated if there is an injury to the soft tissues.

In addition, all underlying comorbid diseases (e.g., diabetes, alcoholism) must ultimately be addressed. Such conditions are common in these patients and potentially predispose them to Fournier’s gangrene.

The inability to properly manage comorbid conditions can threaten the success of even the most appropriate interventions to resolve the infectious disease.

Antibiotic and antifungal therapy of Fournier Syndrome:

The treatment of Fournier’s gangrene involves the institution of broad-spectrum antibiotic therapy. The spectrum of antibiotics should cover staphylococci, streptococci, the Enterobacteriaceae family of organisms, and anaerobes.

A reasonable empirical regimen could consist of ciprofloxacin and clindamycin. Clindamycin is particularly useful in treating necrotizing soft tissue infections due to its gram-positive and anaerobic activity spectrum.

In animal models of streptococcal infection, clindamycin has produced higher response rates than penicillin or erythromycin, even in deferred treatment.

Other possible options include ampicillin/sulbactam, ticarcillin/clavulanate, or piperacillin/tazobactam combined with aminoglycoside metronidazole or clindamycin. Vancomycin can be used to provide coverage for methicillin-resistant Staphylococcus aureus (MRSA).

In cases associated with sepsis syndrome, treatment with intravenous immunoglobulin (IVIG), which is believed to neutralize superantigens (e.g., Streptotoxins A and B) to mitigate exaggerated cytokine response, is a promising adjuvant for adequate antibiotic coverage and complete surgical debridement.

If initial tissue stains (i.e., potassium hydroxide [KOH]) show fungi, add an empirical antifungal agent such as amphotericin B or caspofungin.

Surgical diagnosis and debridement:

In the case of a presumptive diagnosis based on a clinical examination or diagnostic study, the definitive diagnosis of Fournier gangrene is made by examining the patient under anesthesia, followed by an incision in the area of ​​most significant clinical concern.

If frankly gangrenous tissue is found or the purulence is drained, the diagnosis of Fournier’s gangrene is established.

Occasionally, early-stage Fournier’s disease manifests as severe cellulitis. If an incision is made, the fascia may appear edematous instead of exhibiting the blackish gray appearance of well-established Fournier gangrene.

In this case, obtain an incisional biopsy sample of the deep fascia to evaluate the frozen section to exclude early necrotizing disease.

Extirpating the necrotic tissue:

Once the diagnosis of Fournier gangrene is established, all the necrotic tissue must be removed. In an extensive retrospective review of 379 patients, Sugihara et al. Confirmed the view that early surgical intervention reduces mortality.

Those who underwent an earlier intervention had a lower mortality rate (odds ratio, 0.38) than those whose intervention was delayed three days later.

The skin must be widely opened to expose the full extent of underlying subcranial and fascial tissue necrosis.

All fascial planes that separate easily with a blunt dissection should be considered involved and excised. The dissection should be carried out to include bleeding tissues (i.e., the tissue that is well vascularized).

Excised tissue samples will be sent for aerobic and anaerobic cultures and a histological evaluation.

Given the characteristic thrombosis of the nutrient vessels, the skin covering it has an altered blood supply and should be removed if significantly undermined.

The authors strongly recommend radical excisional debridement (see image below) with electrocautery to reduce the considerable loss of operative blood if the area of ​​involvement is extensive.

The testicles are often saved in the necrotizing process. If they are not involved, place the exposed testes in a subcutaneous pocket to avoid drying out.

If a testicle is involved in the necrotic process or its viability is questioned, it will perform an orchiectomy.


Once the infection is eradicated, healthy granulation tissue develops; this means the time to proceed with the reconstruction.

The options for reconstruction include the following:

  • Primary closure of the skin, if possible.
  • Local coverage of skin flap.
  • Split thickness skin grafts.
  • Muscle flaps fill a cavity (e.g., ischiorectal space).

However, skin grafting or flap reconstruction is recommended for defects more significant than 50% of the scrotum or extending beyond the scrotum.

For confined defects involving less than 50% of the scrotum that can not be closed mainly without tension, they recommended reconstruction with a scrotal advance flap or healing by secondary intention.

A two-step technique for treating scrotal defects with total skin loss involving exposed testes. The first step consists of the primary closure with an enveloping skin graft. The second step is to re-approximate the testicles and shape the escort to optimize aesthetics.

Hyperbaric oxygen therapy:

Hyperbaric oxygen therapy (HBO) has been used as adjunct surgical and antimicrobial therapy. Indications include failure of conventional treatment, documented compromise of clostridia or myonecrosis, or deep tissue involvement.

It is postulated that hyperbaric oxygen therapy reduces systemic toxicity, prevents the spread of necrotizing infection, and inhibits the growth of anaerobic bacteria. Hyperbaric oxygen therapy has shown some promising results.

However, there was a trend toward increased mortality in patients undergoing hyperbaric oxygen therapy in one series, although this trend may have been related to selection bias.

The role of hyperbaric oxygen therapy in treating Fournier’s disease should be clarified with a prospective controlled trial.

Decisions regarding hyperbaric oxygen therapy should be made individually, taking into account the patient’s stability. The use of hyperbaric oxygen therapy should not delay surgical debridement.

Fournier’s gangrene is a true surgical emergency. At a minimum, immediate urological consultation or general surgical consultation is mandatory, and administration often requires a multidisciplinary team, including a urologist, a general surgeon, and an intensive care specialist.

Transfer to a tertiary installation may be necessary if these resources are unavailable at the initial installation. Initial debridement can be performed if required before transfer. Arrange for the transfer once the patient has been stabilized and resuscitation efforts have begun.


There are some steps you can take to reduce your chances of getting Fournier’s gangrene:

  • If you have diabetes, control your genitals and surrounding areas for wounds or signs of infection and swelling or drainage.
  • If you are overweight or obese, try to lose some weight.
  • If you smoke or chew tobacco, stop. Tobacco use can damage blood vessels.
  • To reduce the risk of infection, wash open wounds with soap and water and keep them dry and clean until they heal.

Vascular supply to the skin of the lower abdomen and genitals:

The inferior and deep circumflex epigastric iliac arteries branches provide the terrible aspect of the anterior abdominal wall. The components of the external and internal pudendal arteries irrigate the scrotal wall.

Except for the internal pudendal artery, each of these vessels travels within Camper’s fascia and, therefore, can thrombose in the progression of Fournier’s gangrene.

Thrombosis compromises the viability of the skin of the anterior scrotum and the perineum.

Since the internal pudendal artery is not contained within Camper’s fascia, it is less susceptible to thrombosis; therefore, its vascular territory – the posterior face of the scrotal wall – remains viable and can be used in reconstruction after the resolution of the infection.

Penis and scrotum:

The contents of the scrotum, that is, the testicles, epididymis, and cord structures, are inverted by several different fascial layers of the Dartos fascia of the scrotal wall. Again, several meaningful anatomical relationships must be considered.

The most superficial layer of the testicle and the cord is the external spermatic fascia, which is continuous with the external aponeurosis of the simple inguinal ring (external abdominal oblique).

The next deeper layer is the internal spermatic fascia, which is continuous with the transversalis fascia. A deep fascia called fascia Buck covers the erectile bodies of the penis, the corpora cavernosa, and the anterior urethra.

The fascia of the dollar fuses with the tunica albuginea dense of the corpora cavernosa in the deep part of the pelvis.

The fascial layers described in this section are not affected by the superficial perineal space infection. They can limit the depth of tissue destruction in a necrotizing infection of the genitals.

The corpora cavernosa, the urethra, the testicles, and the structures of the umbilical cord are usually freed in Fournier’s gangrene. At the same time, the superficial and deep fascia and the skin are destroyed.

Pathophysiology of Fournier Syndrome

Localized infection adjacent to an entry portal is the inciting event in the development of Fournier’s gangrene.

Endarteritis obliterans develop, resulting in subcutaneous and cutaneous vascular necrosis, leading to localized ischemia and increased bacterial proliferation. Fascial destruction rates of up to 2-3 cm / h have been described.

Infection of the superficial perineal fascia (Colles’ fascia) can spread to the penis and scrotum through the fascia of Buck and Dartos or to the anterior abdominal wall through Scarpa’s fascia or vice versa.

Colles’ fascia is attached to the perineal body and the urogenital diaphragm posteriorly and the pubic branch laterally, which limits progression in these directions.

Testicular involvement is rare since the testicular arteries originate directly from the aorta and, therefore, have a blood supply separated from the affected region.

The very advanced or fulminating Fournier gangrene can extend from the fascial envelope of the genitals along the perineum, the torso, and, occasionally, in the thighs.

The following are pathognomonic findings of Fournier’s gangrene on the pathological evaluation of the affected tissue:

  • Necrosis of superficial and deep fascial planes.
  • Fibrinoid coagulation of the nutrient arterioles.
  • Infiltration of polymorphonuclear cells.

Identified microorganisms within the tissues involved

The infection represents an imbalance between:

One or more comorbid systemic processes often compromise host immunity.

The virulence of the causative microorganisms: the etiological factors allow the portal to enter the organism in 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.

The virulence of the microorganism results from the production of toxins or enzymes that create an environment conducive to rapid microbial multiplication.

Although Meleney in 1924 attributed necrotizing infections only to streptococcal species, subsequent clinical series have emphasized the multi-organ nature of most cases of the necrotizing disease, including Fournier’s gangrene.

Currently, the recovery of streptococcal species is unusual. In contrast, streptococcal organisms are grown together with five other microorganisms. The following are common causative organisms:

  • Streptococcal species.
  • Staphylococcal species.
  • Enterobacteriaceae.
  • Anaerobic Organisms.
  • Fungi.

Most authorities believe that polymicrobial participation is necessary to create the synergy of enzyme production that promotes Fournier’s gangrene’s rapid multiplication and spread.

For example, a microorganism can produce the enzymes necessary to cause the coagulation of the nutrient vessels. Thrombosis of these nutrient vessels reduces local blood supply; therefore, the tissue oxygen tension decreases.

The resulting tissue hypoxia allows the growth of facultative anaerobes and microaerophilic organisms. These latter microorganisms, in turn, can produce enzymes (for example, Lecithinase and collagenase), which lead to the digestion of fascial barriers, which feed the rapid spread of the infection.

Fascial necrosis and digestion are characteristic of this disease process; This is important because it provides the surgeon with a clinical marker of the degree of tissue involvement.

Specifically, if the fascial plane can be easily separated from the surrounding tissue by blunt dissection, it is likely involved in the ischemic-infectious process; therefore, any dissected tissue must be excised.

Etiology of Fournier Syndrome

Although initially described as idiopathic gangrene of the genitals, Fournier’s gangrene has an identifiable cause in 75-95% of cases.

The necrosis process usually originates from an infection in the anorectum, the urogenital tract, or the skin of the genitals.

Anorectal causes of Fournier’s 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, inflammatory bowel disease, colonic diverticulitis, or appendicitis.

The causes of the urogenital tract include infection in the bulbourethral glands, urethral injury, iatrogenic injury secondary to manipulation of urethral stenosis, epididymitis, orchitis, or lower urinary tract infection (for example, in patients with long-term permanent urethral catheters).

Dermatological causes include hidradenitis suppurativa, ulceration due to scrotal pressure, and trauma. The inability to practice adequate perineal hygiene increases the risk in paraplegic patients.

Accidental, intentional, or surgical trauma and the presence of foreign bodies can also cause the disease. The following have been reported in the literature as precipitating factors:

  • Closed thoracic trauma.
  • Surface lesions of soft tissues.
  • Genital piercings.
  • Self-injection of the penis with cocaine.
  • Urethral instrumentation
  • Prosthetic penile implants.
  • Intramuscular injections
  • Enemas of steroids (used for the treatment of radiation proctitis).
  • Rectal foreign body.

In women, septic abortions, vulvar or Bartolina’s gland abscesses, hysterectomy, and episiotomy are documented sources. In men, anal intercourse may increase the risk of perineal infection, either by a traumatism closed in the area or by the spread of rectally transported microbes.

In children, the following have led to the disease:

  • Circumcision.
  • Phimosis.
  • Inguinal hernia strangled.
  • Omphalitis.
  • Insect bites.
  • Trauma.
  • Urethral instrumentation
  • Precocity.
  • Perirectal abscesses
  • Systemic infections
  • Diaper rash.
  • Secondary immunodeficiency.

A case report by Numoto et al. describes Fournier’s gangrene that developed after surgical repair of a strangulated inguinal hernia in a 2-month-old child.

The child was receiving adrenocorticotropic hormone (ACTH) therapy for infantile spasms. The authors suggest that immune suppression of adrenocorticotropic hormone therapy may have contributed to the development of Fournier’s gangrene.

Pathogens of Fournier Syndrome

The wound cultures of patients with Fournier gangrene reveal a polymicrobial infection with an average of 4 isolates per case. Escherichia coli is the predominant aerobic, and Bacteroides is the predominant anaerobic.

Other typical microflora includes the following:

  • Proteo.
  • Staphylococcus.
  • Enterococcus
  • Streptococcus (aerobic and anaerobic).
  • Pseudomonas.
  • Klebsiella.
  • Clostridium.

Rarely has it been reported that Candida albicans are the pathogen in Fournier gangrene cases.

Predisposition to the disease

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

  • Diabetes mellitus (present in up to 60% of cases).
  • Morbid obesity.
  • Alcoholism.
  • Cirrhosis.
  • The extremes of age.
  • Vascular disease of the pelvis.
  • Acute leukemia.
  • Systemic lupus erythematosus.
  • Crohn’s disease .
  • HIV infection.
  • Malnutrition.
  • Iatrogenic immunosuppression (for example, long-term corticosteroid therapy or chemotherapy).

Epidemiology of Fournier Syndrome

Fournier’s gangrene is relatively rare, but the exact incidence of the disease is unknown. In a review of Fournier’s gangrene in 1992, Paty et al.

They estimated that approximately 500 cases of infection had been reported in the literature since the 1883 report of Fournier, yielding a rate of 1 point in 7500 people.

A retrospective review of cases revealed 1726 cases documented in the literature from 1950 to 1999, with an average of 97 points per year reported between 1989 and 1998.

A review of the national data of inpatients from 2004-to 2012 identified 9249 patients with Fournier gangrene.

A review with the US Inpatient Patient Database. In 2009, it was estimated that, among the 25.8 million hospital admissions in 2001 and 2004, Fournier’s gangrene constituted only 0.02% of hospital admissions.

In this same database, 66% of hospitals did not report patients with Fournier gangrene, and among high-volume centers, the frequency of admission was only one patient every few months.

The frequency of Fournier’s gangrene probably has not changed appreciably. On the contrary, the apparent increase in the number of cases in the literature is likely to result from an increase in reports.

There is no seasonal variation. Fournier’s gangrene is not native to any region globally, although the most extensive clinical series originates in Africa.

Incidence differences related to sex and age

The typical patient with Fournier gangrene is an older man in his sixth or seventh decade of life with comorbid diseases. The male-female ratio is approximately 10: 1.

The lower incidence in women may reflect better drainage of the perineal region through vaginal secretions.

Men who have sex with men may be at increased risk, especially for infections caused by community-associated methicillin-resistant Staphylococcus aureus (MRSA).

The majority of reported cases occur in patients aged 30-60 years. A literature review found only 56 pediatric cases, with 66% of those in babies under three months.


Significant cutaneous defects of the scrotum, perineum, penis and abdominal wall may require reconstructive procedures; however, the prognosis for patients after the reconstruction of Fournier’s gangrene is usually good.

The scrotum has a remarkable ability to heal and regenerate once infection and necrosis have diminished. However, approximately 50% of men with penile involvement have pain with erection, often related to genital scarring.

Consultation with a psychiatrist can help some patients cope with the emotional stress of an altered body image.

Lymphatic drainage may be affected if extensive soft tissue is lost; therefore, dependent edema and cellulitis may occur. The use of external support may be beneficial in minimizing this postoperative problem.

To date, most studies of Fournier’s gangrene have been retrospective reviews. Therefore, the utility of extracting reliable prognostic information from these studies is minimal.

In 1995, Laor and colleagues presented the severity index of Fournier’s gangrene (FGSI). The severity index of Fournier’s gangrene is based on the deviation of the reference ranges of the following clinical parameters:

  • Temperature.
  • Heart rate.
  • The respiratory frequency.
  • White blood cell count (WBC).
  • Hematocrit.
  • Sodium serum
  • Potassium serum
  • Serum creatinine
  • Serum bicarbonate

Each parameter is assigned a score between 0 and 4, and the highest values ​​indicate a more significant deviation from the normal. The severity index of Fournier’s gangrene represents the sum of all the importance ​​of the parameters.

Labor and colleagues determined that a Fournier gangrene severity index greater than nine correlates with increased mortality. The severity index of Fournier’s gangrene has been validated in several retrospective studies.

In a retrospective review of 20 patients with Fournier’s gangrene, the average Fournier gangrene severity index was 9 in general and 14 for fatal cases.

An increased severity index of Fournier gangrene was predictive of having higher mortality or hospital stay longer than the median (> 25 days) (P = 0.0194).

In 2010, Yilmazlar and his colleagues updated the Fournier gangrene severity index (UFGSI), adding two additional parameters: age and extent of the disease, to further refine the predictive utility of the severity index of Fournier’s gangrene.

These two groups concluded that the risk of mortality, in general, can be directly proportional to the age of the patient and the degree of burden of the disease and systemic toxicity at admission. The factors associated with an improved prognosis include the following:

  • Age less than 60 years.
  • Localized clinical disease
  • Absence of systemic toxicity (for example, low severity of Fournier’s gangrene).
  • Sterile blood cultures.

Factors associated with high mortality include an anorectal source, advanced age, extensive disease (involving the abdominal wall or thighs), shock or sepsis at the time of presentation, renal failure, and hepatic dysfunction.

A Turkish study of 50 patients showed that Acinetobacter baumannii and Klebsiella pneumonia were significantly more common in patients requiring mechanical ventilation. Still, Acinetobacter baumannii was the only microorganism associated with a higher mortality rate.

Death is usually the result of a systemic disease, such as sepsis (usually gram-negative), coagulopathy, acute renal failure, diabetic ketoacidosis, or multiple organ failure.