eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions

Fournier Gangrene

Thomas Santora, MD, Professor and Vice-Chair for Clinical Affairs, Department of Surgery, Temple University Hospital and School of Medicine
Daniel B Rukstalis, MD, Director of Urological Services, Geisinger Medical Center, Geisinger Medical Group

Updated: Mar 19, 2009

Introduction

Fournier gangrene is a necrotizing infection that involves the soft tissues of the male genitalia. In modern-day vernacular, Fournier gangrene is a specific form of necrotizing fasciitis (see Image 2); the latter is a general term that was introduced by Wilson in 1951¹ to describe a necrotizing infection of soft tissue that involves the deep and superficial fascia, regardless of location.

Photomicrograph of Fournier gangrene (necrotizing fasciitis), oil immersion at 1000X magnification. Note the 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.

Originally, the term Fournier gangrene was used to describe idiopathic gangrene of the genitalia; however, it has also has been used to describe most soft-tissue necrotizing infections of the perineum, independent of cause. Modern-day use of the term Fournier gangrene should be restricted to describe infections that primarily involve the genitalia. The indiscriminate use of this eponym complicates the comparison of results from clinical series and definition of a reliable occurrence rate.

History of the Procedure

In 1764, Baurienne originally described an idiopathic, rapidly progressive soft-tissue necrotizing process that led to gangrene of the male genitalia. However, Jean-Alfred Fournier, a Parisian venereologist who practiced his trade from 1860-1902, is more commonly associated with this disease, which bears his name. A transcript from one of Fournier’s clinical lectures in 1883 presented a case of perineal gangrene in an otherwise healthy young man.² This paper, written initially in French and translated recently by Alexander Corman, provides historical insight into the practice of medicine at the time.

In his presentation, Fournier reviewed the systemic and local factors that predispose to this fulminate process. Although Fournier did not emphasize the role of diabetes in this paper, even then, diabetes was known as the leading predisposing systemic factor. Local factors related to trauma of the genitalia accounted for the vast majority of genital gangrene cases. In anecdotes Fournier described some of the misconceptions of the times that led to this condition, including the practice of nighttime ligation of the prepuce to control enuresis or an attempted birth control technique practiced by an adulterating man to avoid impregnating his married lover.

Since Fournier’s description, subsequent experience has shown that, in most cases, Fournier gangrene has an identifiable cause and that it frequently manifests more indolently. Trauma to the genitalia continues to be a frequently recognized vector for the introduction of bacteria that initiate the infectious process.³ For more information, see the articles Testicular Trauma, Scrotal Trauma, Penile Fracture and Trauma, and Urethral Trauma in eMedicine’s Urology volume.

Frequency

In a review of Fournier gangrene in 1992, Paty and coworkers calculated that approximately 500 cases of the infection have been reported in the literature since Fournier’s 1883 report, yielding a prevalence of 1 case in 7500 persons.⁴ Using Medline and its abstracted journals, other researchers have reported approximately 600 cases of Fournier gangrene in the world literature since 1996.⁵ The frequency of Fournier gangrene has not likely changed appreciably; rather, the apparent increase in the number of cases in the literature most likely results from increased reporting. Fortunately, Fournier gangrene is an uncommon, but not rare, disease. No seasonal variation occurs, and Fournier gangrene is not indigenous to any region of the world, although the largest clinical series originate from the African continent.⁶

Etiology

Although originally described as idiopathic gangrene of the genitalia, Fournier gangrene has an identifiable cause in approximately 95% of cases.⁷ The necrotizing process commonly originates from an infection in the anorectum, the urogenital tract, or the skin of the genitalia.⁸

• Anorectal causes of Fournier gangrene include infection in the perianal glands, manifesting as a consequence of colorectal injury or as a complication of colorectal malignancy,^9,10 inflammatory bowel disease,¹¹ colonic diverticulitis, or appendicitis.
• Urogenital tract causes include infection in the bulbourethral glands, urethral injury, iatrogenic injury secondary to urethral stricture manipulation, or lower urinary tract infection.
• Dermatologic causes include hidradenitis suppurativa, ulceration due to scrotal pressure, trauma, intentional trauma (skin popping or piercing),¹² or complications of surgery.
• Other causes of Fournier gangrene, although less common, include bone marrow malignancy (acute promyelocytic leukemia, acute nonlymphoid leukemia, acute myeloblastic leukemia),^13,14 systemic lupus erythematosus,¹⁵ Crohn disease, and HIV infection.¹⁶ Additionally, Fournier gangrene may result from iatrogenic or traumatic perineal injury.

Comorbid diseases that compromise the immune system have been implicated as necessary predisposing factors for the development of Fournier gangrene. The following are common predisposing comorbidities:

• Diabetes mellitus (cited most often)¹⁷
• Morbid obesity
• Cirrhosis
• Vascular disease of the pelvis
• Malignancies
• High-risk behaviors (eg, alcoholism, intravenous drug abuse)
• Immune suppression due to systemic disease or steroid administration

Pathophysiology

The following are pathognomonic findings of Fournier gangrene upon pathologic evaluation of the 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 of the above 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.

Microorganism virulence (see Image 1) results from the production of toxins or enzymes that create an environment conducive to rapid microbial multiplication.¹⁸ In a 1924 series of Chinese men with necrotizing infections, Meleney reported that streptococcal species were the predominant organisms recovered from cultures.¹⁹ Meleney attributed the necrotizing infection to this sole genus; however, subsequent clinical series have emphasized the multiorganism nature of most cases of necrotizing infection, including Fournier gangrene.^{20,21,22,23,24} Presently, recovering only streptococcal species is unusual²⁵ ; rather, streptococcal organisms are cultured along with as many as 5 other organisms.

Necrotizing infection results from infection with an extremely virulent microorganism or, most commonly, from a combination of microorganisms acting synergistically in a susceptible immunocompromised host.

The following are common causative microorganisms:

• Streptococcal species
• Staphylococcal species
• Genera of the Enterobacteriaceae family
• Anaerobic organisms
• Fungi

Most authorities believe the polymicrobial nature of Fournier gangrene is necessary to create the synergy of enzyme production that promotes rapid multiplication and spread of the infection.¹⁸ 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 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.

The 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. Far-advanced or fulminate Fournier gangrene can spread from the fascial envelopment of the genitalia throughout the perineum, along the torso, and, occasionally, into the thighs.

Presentation

The hallmark of Fournier gangrene is intense pain and tenderness in the genitalia. The clinical course usually progresses through the following phases:

1. Prodromal symptoms of fever and lethargy, which may be present for 2-7 days
2. Intense genital pain and tenderness that is usually associated with edema of the overlying skin
3. Increasing genital pain and tenderness with progressive erythema (see Image 6) of the overlying skin
   
   

   

   Examination of an anesthetized man with alcoholism and known cirrhosis who presented with exquisite pain limited to the scrotum. Note the erythema of the scrotum and the look of skepticism on the face of one of the surgeons. Courtesy of Thomas A. Santora, MD.

   
   
4. Dusky appearance of the overlying skin; subcutaneous crepitation
5. Obvious gangrene of a portion of the genitalia; purulent drainage from wounds

The systemic effects of this process vary from local tenderness with no toxicity to florid septic shock. In general, the greater the degree of necrosis, the more profound the systemic effects.

A typical patient with Fournier gangrene is an elderly man in his sixth or seventh decade of life with comorbid diseases; females are not immune to this disease but are affected much less frequently.

The following are pitfalls in the clinical detection of Fournier gangrene (see Image 3):

• Incomplete examination of the genitalia
• Patients who are unable to communicate pain
• Morbid obesity

Photograph of a morbidly obese male with long-standing phimosis. This condition led to urinary incontinence, perineal diaper rash–like dermatitis, and urinary tract infection. Ultimately, he presented with exquisite perineal pain. An examination with the patient under anesthesia was necessary to discover the necrotizing infection that appeared to originate in the right bulbourethral gland. Courtesy of Thomas A. Santora, MD.

Relevant Anatomy

The complex anatomy (see Image 5) 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. 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 man with Fournier gangrene.

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 is known as Scarpa fascia. Understanding the tendency of necrotizing fasciitis to spread along fascial planes and the fascial anatomy, one can see how a process that initiates in the perineum can spread to the abdominal wall, the flank, and even the chest wall.

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.

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 it 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. Often, the posterior aspect of the scrotal wall supplied by the internal pudendal artery 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 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.

Workup

Laboratory Studies

• Complete history and physical examination
  • Direct particular attention to palpation of the genitalia and perineum and to the digital rectal examination.
  • Fluctuance, soft-tissue crepitation, localizing tenderness, or occult wounds in any of these sites should alert the examiner to possible Fournier disease.
• Chemistry panel: Perform these tests to evaluate possible electrolyte disturbances, to look for laboratory evidence of dehydration (elevated BUN/creatinine ratio), and to evaluate for glucose intolerance (due to preexisting diabetes or sepsis-induced metabolic disturbance).
• Blood tests
  • Obtain a complete blood cell count to assess the immunologic stress induced by the infectious process, check the adequacy of the red blood cell mass, and evaluate the potential for sepsis-induced thrombocytopenia.
  • Blood samples should be drawn for culture to assess for septicemia.
  • A coagulation profile (prothrombin time, activated partial thromboplastin time, platelet count, fibrinogen level) is helpful to look for sepsis-induced coagulopathy.
  • Consider type and screen if surgical exploration is undertaken.
• Other: Any test deemed necessary to assess exacerbation of a comorbid condition (eg, ECG and cardiac enzyme evaluation in patients with coronary artery disease) is warranted.

Imaging Studies

• Radiography
  • Radiography should be considered to evaluate for the presence and extent of Fournier disease, especially when the clinical examination findings are inconclusive^26,27 Gas within the soft tissues is detected more commonly with imaging modalities than with the physical examination. (Note that demonstration of soft-tissue gas or detection of subcutaneous crepitation is an absolute indication for surgical exploration.)
  • Plain film radiography should be the initial imaging study. It may reveal moderate-to-large amounts of soft-tissue gas or foreign bodies.
• Ultrasonography²⁸
  • Ultrasonography can be used to detect fluid or gas within the soft tissues. In addition, ultrasonography can be used to assess the blood flow to the testes if testicular torsion is a possibility.
  • The drawback of ultrasonography is the need for direct pressure on the involved tissue; patients with Fournier gangrene probably will not be able to tolerate this procedure.
• CT scanning
  • CT scanning can reveal smaller amounts of soft-tissue gas than plain radiography and can demonstrate fluid collections that track along the deep fascial planes.^29,30
  • CT scanning is readily available in most hospitals and should be considered the diagnostic tool of choice.
• MRI: This study yields greater soft tissue detail than does CT scanning; however, MRI requires greater time and limits monitoring during testing. These logistical challenges, which are not shared by CT scanning, limit the practical usefulness of MRI, especially in patients with critical illness.

Diagnostic Procedures

The diagnostic test of choice for Fournier gangrene is an incisional biopsy, which allows pathological distinction of necrotizing infection from severe cellulitis. The former would benefit from excisional debridement, while the latter rarely requires surgical excision.

The biopsy sample should be taken from the point of maximal tenderness, and it should include skin and superficial and deep fascia. This sample should then be sent for frozen-section analysis to assess for fascial necrosis. Early fascial involvement may appear as edematous fascia to the gross vision of the operating surgeon but may appear as frank necrosis on microscopic analysis.

Histologic Findings

Upon pathologic evaluation of the involved tissue, the pathognomonic findings of Fournier gangrene include (1) necrosis of the superficial and deep fascial planes, (2) fibrinoid coagulation of the nutrient arterioles, (3) polymorphonuclear cell infiltration, and (4) microorganisms identified within the involved tissues.

The characteristic finding that most commonly indicates Fournier disease is fibrinoid thrombosis of the nutrient vessels that supply the superficial and deep fascia. A frequent occurrence is widespread necrosis of the fascia with acute inflammatory cell infiltration, necrotic debris, and frequent demonstration of causative microorganisms within the tissues. This extensive inflammatory process is frequently present deep to intact skin, which is often minimally involved with the inflammatory process until late in the disease.

Treatment

Medical Therapy

Treatment of Fournier gangrene involves several modalities, including restoration of normal organ perfusion. In patients who present with systemic toxicity manifesting as hypoperfusion or organ failure, aggressive resuscitation to return normal organ perfusion and function must take precedence over diagnostic maneuvers, especially if these diagnostic studies could compromise the resuscitative interventions.

Treatment of Fournier gangrene also involves the institution of broad-spectrum antibiotic therapy. The antibiotic spectrum should cover staphylococci, streptococci, the Enterobacteriaceae family of organisms, and anaerobes. A reasonable empiric regimen might consist of ciprofloxacin and clindamycin. Clindamycin is particularly useful in the treatment of necrotizing soft-tissue infections because of its gram-positive and anaerobic spectrum of activity. In animal models of streptococcal infection, clindamycin has been shown to yield response rates superior to those of penicillin or erythromycin, even in the context of delayed treatment.³¹

If initial tissue stains (ie, KOH stain) show fungi, add an empiric antifungal agent such as amphotericin B or caspofungin. In cases associated with sepsis syndrome, therapy with intravenous immunoglobulin (IVIG), which is thought to neutralize superantigens such as the streptotoxins (A, B) believed to mitigate the exaggerated cytokine response, has been shown to be a good adjuvant to appropriate antibiotic coverage and complete surgical debridement.³²

Hyperbaric oxygen, if available, has shown some promising results.^33,34,35 This therapy needs to be balanced with the stability of the patient. Surgical debridement must not be delayed for consideration of hyperbaric oxygen.

In addition to the above treatment interventions used to address the infectious process, the underlying comorbid conditions that frequently coexist and that potentially predispose to Fournier gangrene must ultimately be addressed. For example, blood sugar needs to be controlled in patients with diabetes, and alcohol withdrawal needs to be addressed in patients with alcoholism. Failure to adequately manage the comorbid conditions may threaten the success of even the most appropriate interventions to resolve the infectious disease.

Surgical Therapy

• Establishing the diagnosis
  • In the event of a presumptive diagnosis based on a clinical examination or diagnostic study, the definitive diagnosis of Fournier gangrene is established by examination with the patient under anesthesia followed by incision into the area of greatest clinical concern.
  • If frankly gangrenous tissue is found or purulence is drained (see Image 7), the diagnosis of Fournier gangrene is established.
    
    

    

    The same patient depicted in Image 6. The scrotum has been opened along the median raphe, which liberated foul-smelling brown purulence and exposed necrotic tissue throughout the mid scrotum. The testicles were not involved. Courtesy of Thomas A. Santora, MD.

    
    
  • Occasionally, early-stage Fournier disease manifests as severe cellulitis. If an incision is made, the fascia may appear edematous rather than the gray-black appearance of well-established Fournier gangrene. In this instance, obtain an incisional biopsy sample of the deep fascia for frozen-section evaluation to eliminate the potential for early necrotizing disease.
• Excising necrotic tissue
  • Once a diagnosis of Fournier gangrene is established, all necrotic tissue must be excised. The skin should be opened widely to expose the full extent of the underlying fascial and subcutaneous tissue necrosis. All fascial planes that separate easily with blunt dissection should be considered involved and therefore excised. The dissection should be carried out to include bleeding tissues (ie, tissue that is well vascularized).
  • Send tissue for aerobic and anaerobic cultures and a histologic assessment.
  • Given the characteristic thrombosis of the nutrient vessels, the overlying skin has impaired blood supply and should be excised if significantly undermined. The authors strongly recommend radical excisional debridement (see Image 4) with electrocautery in order to reduce the considerable operative blood loss if the area of involvement is extensive.
    
    

    

    The same patient depicted in Image 3, following the first radical debridement procedure. A dorsal slit was made in the prepuce to expose the glans penis. Urethral catheterization was performed. Incision into the point of maximal tenderness on the right side of the perineum revealed gangrenous necrosis that involved the anterior and posterior aspects of the perineum, the entirety of the right hemiscrotum, and the posterior medial aspect of the right thigh. The skin and involved fascia were excised from these areas. Reconstruction of this defect was performed in a staged approach. A gracilis rotational muscle flap taken from the right thigh was used to fill the cavity in the posterior right perineum as the first step. The remainder of the defect was covered with split-thickness skin grafts. This patient made a full recovery.

    
    
  • Given the potential fulminant nature of this necrotizing process, consider repeated operative debridement procedures to ensure complete eradication of the infection.
  • Once the results of the tissue cultures are known, alter the antibiotic regimen to cover the causative organisms. Continue antibiotics for 10-14 days or until reconstruction is accomplished.
  • If the perineal involvement is extensive, fecal diversion should be considered at subsequent operative explorations to eliminate the potential for fecal contamination of the wounds. Fecal diversion is usually unnecessary when the necrosis is limited to the genitalia but is mandatory when the perianal area is extensively involved.
  • Urinary diversion is accomplished with a urethral catheter in most cases. Suprapubic cystostomy is used when urethral drainage of the bladder is not possible because of pathology (eg, stricture disease, prostatic hypertrophy).
  • The testicles are often spared in the necrotizing process. If uninvolved, place the exposed testicle in a subcutaneous pocket to prevent desiccation. If a testicle is involved in the necrotic process or its viability is questioned, perform orchiectomy.
  • Once the infection is eradicated, healthy granulation tissue develops; this signifies the time to proceed to reconstruction.
  • Vacuum-assisted closure (VAC) has shown great promise in the hastening wound healing in these patients with Fournier gangrene.³⁶ Application after initial debridement may shorten the hospital stay and may speed up the grafting and flap placement process.
• Options for reconstruction
  • Primary closure of the skin, if possible
  • Local skin flap coverage
  • Split-thickness skin grafts (see Image 8)
    
    

    

    The same patient depicted in Images 6 and 7. Following resolution of the infection, the wound was covered with a split-thickness skin graft. The option of delayed primary closure of this wound was not chosen in this patient because of concern for tension on the closure. Courtesy of Thomas A. Santora, MD.

    
    
  • Muscular flaps, which are used to fill a cavity (eg, ischiorectal space)

Complications

The main complication associated with Fournier disease is unresolved sepsis, often caused by one of the following:

• Unrecognized cause of the infection (eg, perforated peptic ulcer disease, appendicitis, diverticulitis) or extension of the necrotizing process outside the obvious wound (A CT scan is helpful for evaluating these two possibilities.)
• Complication of severe acute illness (eg, line sepsis, bacterial endocarditis, pneumonia)
• The plethora of comorbid conditions (eg, acute myocardial infarction, respiratory failure, pressure ulcerations, delirium) or the bedrest conditions imposed on patients who are acutely ill (eg, pulmonary embolus, deep venous thrombosis, atelectasis, pneumonia)

Outcome and Prognosis

To date, all studies of Fournier gangrene have been in the form of clinical series reviewed retrospectively.^37,38 Therefore, drawing reliable prognostic information from these studies is scientifically unsound. Given that proviso, Laor and colleagues introduced the Fournier Gangrene Severity Index (FGSI) based on deviation from reference ranges of 9 clinical parameters (temperature, heart rate, respiratory rate, white blood cell count, and levels of sodium, potassium, creatinine, hematocrit, sodium bicarbonate). Each parameter was valued between 0 and 4, with the higher value assigned to the greatest deviation from normal. The FGSI represents the sum of all the parameters values. They determined that advanced age (not a factor in the FGSI) and a FGSI greater than 9 correlated with increased mortality.³⁹ Corcoran et al validated the FGSI in a retrospective review of 68 patients.⁴⁰

In summary, the mortality risk may be directly proportional to the age of the patient and the extent of systemic toxicity upon admission (FGSI), as well as to the extent of the local tissue involvement.⁴¹

In some studies, Fournier disease that originates from diseases of the anorectum carries a worse prognosis than cases caused by other factors. In the 600 cases of Fournier gangrene discovered during a Medline search dating back to 1996, 100 deaths occurred (16.5%). In the series that included more than 20 patients, the mortality rate ranged from 4-54%, with most studies reporting mortality rates of 20-30%.^42,43

The prognosis of Fournier disease following reconstruction is usually good. Approximately 50% of men with penile involvement have pain upon arousal. This pain is often related to limited mobility of the genitalia due to scarring. Consultation with a psychiatrist may be beneficial in some patients in order to deal with the emotional stress of an altered body image. If extensive soft tissue is lost, lymphatic drainage may be impaired; thus, dependent edema and cellulitis may result. Use of external support may be beneficial to minimize this postoperative problem.

Future and Controversies

The role of hyperbaric oxygen therapy in the treatment of Fournier disease needs to be clarified with a prospective controlled trial.⁴⁴

The role of topical agents in wound care also requires further investigation. Although reports from Africa extol the beneficial chemical effects of unprocessed honey, the salutatory effect of honey is likely related to its physical property of hyperosmolarity.⁴⁵ Therefore, honey holds little advantage over other hygroscopic agents.⁴⁶ The application of growth hormones and other trophic agents holds the potential to promote faster wound healing. The use of vacuum dressing technologies to hasten the wound closure has only recently been used to treat these wounds.

Multimedia

Media file 1: Necrotizing infection results from infection with an extremely virulent microorganism or, most commonly, from a combination of microorganisms acting synergistically in a susceptible immunocompromised host.

Media file 2: Photomicrograph of Fournier gangrene (necrotizing fasciitis), oil immersion at 1000X magnification. Note the 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.

Media file 3: Photograph of a morbidly obese male with long-standing phimosis. This condition led to urinary incontinence, perineal diaper rash–like dermatitis, and urinary tract infection. Ultimately, he presented with exquisite perineal pain. An examination with the patient under anesthesia was necessary to discover the necrotizing infection that appeared to originate in the right bulbourethral gland. Courtesy of Thomas A. Santora, MD.

Media file 4: The same patient depicted in Image 3, following the first radical debridement procedure. A dorsal slit was made in the prepuce to expose the glans penis. Urethral catheterization was performed. Incision into the point of maximal tenderness on the right side of the perineum revealed gangrenous necrosis that involved the anterior and posterior aspects of the perineum, the entirety of the right hemiscrotum, and the posterior medial aspect of the right thigh. The skin and involved fascia were excised from these areas. Reconstruction of this defect was performed in a staged approach. A gracilis rotational muscle flap taken from the right thigh was used to fill the cavity in the posterior right perineum as the first step. The remainder of the defect was covered with split-thickness skin grafts. This patient made a full recovery.

Media file 5: 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 is known as Scarpa fascia. Understanding the tendency of necrotizing fasciitis to spread along fascial planes and the fascial anatomy, one can see how a process that initiates in the perineum can spread to the abdominal wall, the flank, and even the chest wall.

Media file 6: Examination of an anesthetized man with alcoholism and known cirrhosis who presented with exquisite pain limited to the scrotum. Note the erythema of the scrotum and the look of skepticism on the face of one of the surgeons. Courtesy of Thomas A. Santora, MD.

Media file 7: The same patient depicted in Image 6. The scrotum has been opened along the median raphe, which liberated foul-smelling brown purulence and exposed necrotic tissue throughout the mid scrotum. The testicles were not involved. Courtesy of Thomas A. Santora, MD.

Media file 8: The same patient depicted in Images 6 and 7. Following resolution of the infection, the wound was covered with a split-thickness skin graft. The option of delayed primary closure of this wound was not chosen in this patient because of concern for tension on the closure. Courtesy of Thomas A. Santora, MD.

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Keywords

Fournier gangrene, Fournier's gangrene, genital gangrene, penile gangrene, idiopathic gangrene of the penis and scrotum, spontaneous fulminant gangrene of the scrotum, necrotizing fasciitis of the scrotum, necrotizing fasciitis of the male genitalia, infectious gangrene of the scrotum and penis, scrotal gangrene, synergistic gangrene of the male genitalia, gangrenous erysipelas of the scrotum, streptococcal gangrene of the scrotum, necrotizing fasciitis, genital necrotizing fasciitis, scrotal necrotizing fasciitis, penile necrotizing fasciitis, testicular necrotizing fasciitis, Fournier’s disease, Fournier disease

Contributor Information and Disclosures

Author

Thomas Santora, MD, Professor and Vice-Chair for Clinical Affairs, Department of Surgery, Temple University Hospital and School of Medicine
Thomas Santora, MD is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, American Trauma Society, Association for Academic Surgery, and Eastern Association for the Surgery of Trauma
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel B Rukstalis, MD, Director of Urological Services, Geisinger Medical Center, Geisinger Medical Group
Daniel B Rukstalis, MD is a member of the following medical societies: American Association for the Advancement of Science and American Urological Association
Disclosure: Nothing to disclose.

Medical Editor

Alex Jacocks, MD, Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

David L Morris, MD, PhD, Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting

Chief Editor

Bradley Fields Schwartz, DO, FACS, Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine
Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, and Society of University Urologists
Disclosure: Nothing to disclose.

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