eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions

Fournier Gangrene

Author: Thomas Santora, MD, Professor and Vice-Chair for Clinical Affairs, Department of Surgery, Temple University Hospital and School of Medicine
Coauthor(s): Daniel B Rukstalis, MD, Director of Urological Services, Geisinger Medical Center, Geisinger Medical Group
Contributor Information and Disclosures

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.

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.

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.

   [ CLOSE WINDOW ]

   

   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

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.

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.

• Search for CME/CE on This Topic »

• Fournier Gangrene (Emergency Medicine)
• Necrotizing Fasciitis (Dermatology)
• Necrotizing Fasciitis (Emergency Medicine)

• Is Neonatal Circumcision Clinically Beneficial? Argument Against