Fournier, Jean-Alfred. Gangrene foudroyante de la verge. Sem Med 1883; 3: 345-8. Translated by Corman AS. Dis Col Rect 1988; 31(12):984-88. The article is difficult to sort out because it is broken up into many anecdotal experiences. Fournier recognizes diabetes, malaria and typhoid as predisposing conditions for perineal gangrene. He describes four cases of idiopathic genital gangrene and adds a fifth from a colleague. The distinguishing feature is the idiopathic nature of the disease, as he elucidates many other cases of genital gangrene with known causes (consistent with a venereologist’s experience in Paris of the 1880’s: “I will add that if it is possible to cause gangrene of the penis by excessive sexual intercourse, then we would see a great deal of this problem in our clinics…”). “In analyzing this story, we could not find any possible explanation for this gangrene…It was truly amazing to see a man lose his penis without really understanding why.” “…I want to state in the name of our Clinic, that there exists a different gangrene of the penis from the other types involving the same organ, and different in these respects: 1. By the absence of any predetermined cause 2. By special symptoms of which the principal ones follow: A gangrenous and sudden beginning; astonishingly rapid extension; always considerable extension; the frequent coexistence of purple discoloration; and finally an excessive morbidity. It is this type of gangrene which, it is no exaggeration to say, should be given the name, fulminant, and it is this description which I propose to dedicate in our next discussion.” Ledingham IM and Tehranis MA. Diagnosis, clinical course and treatment of acute dermal gangrene. Br J Surg 1975; 62: 364-372. Twenty patients with acute dermal gangrene folowing surgery, trauma or sepsis are described. In 12 the skin became gangrenous secondary to a necrotizing process affecting the subdermal fascia, and in 8 the condition arose primarily in the skin. In the first group mortality was high unless radical excision of the necrotic fascia was performed at an early stage; in 3 of the recent patients the overlying skin was removed, defatted and stored for later grafting. In the second group, incision and adequate drainage combined with antibiotics seems to suffice. Hyperbaric oxygen was of dubious value in the first group but appeared to contribute to arrest of the lesion in the second group.” “The multiplicity of terms used to describe variants of the condition further complicates understanding of the clinical problem…[prompting] the authors to simplify the classification of these conditions into two categories…” 1)Necotizing fasciitis (Wilson 1952): “a progressive, usually rapid, necrotizing process affecting the subcutaneous fat, the superficial fascia and the superior surface to the deep fascia. The skin is initially intact but becomes gangrenous secondary to interruption of its deep blood supply.” 2)Progressive bacterial gangrene: “a more slowly progressive lesion affecting the total thickness of skin but not involving deep fascia; pus formation is variable.” Predominantly clostridial infections were excluded. Necotizing fasciitis developed after drainage of ischiorectal sepsis in 6 (50%). Five of the patients had preexisting systemic disease: DM (2), actinomycosis, rheumatoid arthtritis/steroids, and carcinomatosis. Arose as cellulitis progressing to duskiness then blue with blisters. “The fascial involvement was much more extensive than that of the related skin.” Time between initiating factor and the first signs involving skin was 11 days (range 6-31). Most frequent organisms were coliforms, enterococci and strep. Only one instance of hemolytic strep occurred. The authors attribute a shift in isolates (from Meleney’s time) to early use of antibiotics and rapid overgrowth of coliforms (associated with a shift in site from extremities). In three of four cases of radical debridement, skin was banked (4 degrees) for grafting. Mortality 67% (8 of 12) due to PE and toxemia. “On the basis of present experience the best results appear to follow early, multiple and extensive incisions into the affected area with complete excision of the underlying necrotic fascia. Whether the large flaps of skin thus created should simply be reflected or excised and stored is debatable, but if there is any doubt about the adequacy of drainage the latter alternative is preferable and is best done at one operation…The role of hyperbaric oxygen in the treatment of this condition is uncertain…” In progressive bacterial gangrene, no lag time (quiescent period) was noted. Incision and drainage along with hyperbaric oxygen appeared to halt the progression of disease (as opposed to necrotizing fasciitis). Fournier’s gangrene is included in this group. “Recently, the justification for these separate subgroups has been questioned since they are almost certainly at most variants of a single process.” Riseman JA, Zamboni WA, Curtis A. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990; 108(5); 847-850. Group 1 (n=12) patients received standard therapy of debridement and antibiotics while group 2 (n=17) received HBO (90 min at 2.5 atm, every 8 hours the first day then twice daily, average 7.4 treatments total) in addition to surgery and antibiotics. Affected surface areas were similar in size but group 2 had more perineal involvement and shock (27% vs 8%). All group 2 patients had their first dive within 24 hours of admission, five before surgery. Mortality was significantly lower in the HBO group (23% vs 67%, p < 0.02). Group 2 also required less debridements to control the infection (1.2 vs 3.3, p < 0.03). “The addition of HBO therapy to the surgical and antimicrobial treatment of necrotizing fasciitis significantly reduced mortality and wound morbidity (number of debridements) in this study, especially among nonclostridial infections. We conclude that HBO should be used routinely in the treatment of necrotizing fasciitis.” Inclusion of clostridial infections may skew the results. Stephens BJ, Lathrop JC, Rice WT. Fournier’s gagnrene: Historic (1764-1978) versus contemporary (1979-1988) differences in etiology and clinical importance. Am Surgeon 1993; 59: 149-54. In the decade 1979-1988, 449 cases were reported. In the historical period (1764-1978), 386 cases were reported. During the modern period studied, the average age of the patients was 49.8 years; with 14 per cent occurring in females. The most commonly reported etiologies were colorectal (33%), idiopathic (26%), and genitourinary (21%). Mortality associated with colorectal etiology was highest (33%). Female mortality was not significantly greater than male mortality when obstetrical etiology was excluded. Overall mortality was 22%. Compared with the historical figures, the authors concluded that “neither the introduction of antibiotics nor the development of newer ones has reduced mortality significantly. In spite of newer diagnostic techniques, the etiology remains unclear in over one-fourth of cases.” Efem SE. Recent advances in the management of Fournier’s gangrene: preliminary observations. Surgery 1993;113(2): 201-4. Twenty cases were managed with systemic antibiotics and unprocessed honey were compared to 21 cases managed with orthodox (excision, debridement) methods. No deaths and no (excisional) operations occurred in the honey group as opposed to three deaths in the orthodox group. Th authors felt that honey alleviated morbidity faster. The “orthodox” and the honey groups were not managed by the same consultant. The orthodox group was studied retrospectively. “Honey combine all these actions (i.e., wound debridement, topical antibacterial activity, and local generation of oxygen). The action of unprocessed honey on Fourier’s gangrene is simply remarkable. When it is applied on the ulcer, it immediately halts the advancing necrosis. It debrides, sterilized, deodorized, and dehydrates the wound, and it stimulates actual regeneration of scrotal skin by rapid epithelialization. All these changes can be observed within 1 week of topical application of honey.” Laucks SS. Fournier’s Gangrene. Surg Clin North Am 1994; 74 (6): 1339-54 A good, brief description of anatomy is included. “Several named fascial planes, including dartos fascia, Buck’s fascia, and Colles’ fascia, are present in the genital and perineal areas. They are all related by either intermingling of their fibers or immediate physical proximity. The fascial planes of the genitalia continue up onto the anterior abdominal wall as Scarpa’s fascia. Because Fournier’s gangrene begins as a necrotizing infection of the fascia, its direction of spread is determined by these anatomic fascial planes. The outlet of the pelvis is divided into anterior and posterior triangles. Infections of the anterior (urogenital) triangle generally arise in the lower urinary tract, spread to the corpora spongiosum, penetrate the tunica albuginea, and spread to Buck’s fascia. One this plane is readhed, the infection can spread along the fascial planes to the dartos, Colles’, and Scarpa’s fasciae. Infections arising in the posterior (anorectal) triangle penetrate Colles’fascia, then progress anteriorly along the Buck’s, dartos, and Scarpa’s fasciae.” Necrosis of the testicles implies thrombosis of the testicular artery and suggests an intra-abdominal or retroperitoneal nidus of infection. Consider imaging and laparotomy. Fecal and urinary diversion are controversial. Some propose colostomy in the face of massive perirectal wound, infected sphincter, rectal/colon perforation, or immunocompromise. Suprapubic catheterization may be advocated in known stricture disease with extravasation and phlegmon. Kaiser RE, Cerra FB. Progressive necrotizing surgical infections—a unified approach. J Trauma 1981; 21(5): 349-55. “A number of authors have described various forms of aggressive necrotizing surgical infections. Included in this group are: necrotizing fasciitis, clostridial cellulitis and myonecrosis, and synergistic necrotizing cellulitis. A great deal of effort has been placed in attempts to classify these infectious entities on the basis of the layers of soft tissue involved, the types of organisms involved, and the necessary surgical treatment required. The entities, however, all seem to be variations of the same disease process. Such classification systems only seem to have produced a pseudoclassification that has provided a great deal of confusion for practicing clinical surgeons who deal with this uncommon set of surgical infections.” Twenty “progressive necrotizing surgical infections” were studied. Group I was treated with a “unified treatment protocol:” early diagnosis, antibiotics and early aggressive excision of all necrotic tissue with control of the source if possible. Mortality was 8.3%. Group II was treated with antibiotics and delayed (1-3 days) surgery (mortality 75%). Group III was treated with antibiotics and incision and drainage (100% mortality). No topical antibiotics were used as the series evolved as the authors felt it obscured exam. The authors concluded “there seems to be no need to classify necrotizing infections into different types. Recognizing them as the same disease process treating them with a unified approach resulted in a significant reduction in mortality.” Discussion by Lewis Flint: “Descriptions based upon bacteriologic data are of necessity after the fact, while a definition based upon the type of tissue involved (subcutaneous tissue, fascia, or muscle) may be misleading, since localization of the infection to a single tissue plane is dependent on the point at which diagnostic and therapeutic intervention takes place. For example, necrotizing fasciitis, allowed to progress, will spread to involve underlying muscle and overlying skin and subcutaneous tissue. As surgeons we continuously seek to refine knowledge, but it is obvious that in classifying soft-tissue infections we have been somewhat like the blind men trying to describe an elephant. Several years ago President-elect Baxter suggested we define soft-tissue infections based on the most satisfactory treatment modality.” Plamer LS, Winter HI, Tolia BM. The limited impact of involved surgace area and surgical debridement on survival in Fournier’s gagnrene. Brit J Urol 1995; 76: 208-212. The authors reviewed the records of 30 patients. The mortality rate was 43%. The mean surface area involved in survivors was 4.3% (range 1-16.5%) which did not differ significantly from nonsurvivors, 7.2% (range 5-20.5%). “Although no linear correlation exited, the quantified extent of disease may affect outcome as patients with 5% of body surface area involved were more likely to succumb to the disease. Finally, the number of surgical debridements, even if first performed within 24 hr of presentation, had no impact on outcome in patients with Fournier’s gangrene.” Kirby RS. Improving outcomes in fournier’s gangrene. BJU 2004; 691-692. A very brief review. The title is a little misleading as nothing new in the way of improving outcomes is offered and the majority of the article is simply a review of the entity. Edlich RF, Winters KL, Britt LD. Massive soft tissue infections: Necrotizing fasciitis and Purpura Fulminans. Journal of Long-term Effects of Medical Implants 2005; 15(1); 57-65. The authors are of the opinion that massive soft tissue infections can be best taken care of at burn centers, particularly those with hyperbaric facilities. The authors emphasize EARLY aggressive debridement and resuscitation. Rapid diagnosis should be made on clinical exam. A gram stain of needle aspirate and the “finger test” can support the diagnosis. The authors also discuss frozen section biopsies of fascia. MRI is recommended. Delay in diagnosis and treatment are correlated with mortality. Early enteral feeding is appropriately stressed.