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6 Fournier's Gangrene

6 Fournier's Gangrene

Chapter 6 6 Fournier’s C.F.Heyns,P.D.Theron

et al. 1983; Hejase et al. 1996). However, the incidence is 6.1 Definition and Historical Perspective 50 rising, most likely due to an increase in the mean age of 6.2 Etiology 50 the population, as well as increased numbers of pa- 6.3 Anatomy 52 tients on immunosuppressive therapy or suffering 6.4 Microbiology 53 from human immunodeficiency virus (HIV) infection, 6.5 Pathogenesis 54 especially in Africa (McKay and Waters 1994; Elem and 6.6 Ranjan 1995; Merino et al. 2001; Heyns and Fisher Clinical Presentation 55 2005). 6.7 Special Investigations 55 6.8 Management 55 6.8.1 Initial and Preoperative Management 56 6.2 6.8.2 Surgery 56 6.8.3 Postoperative Management 57 Etiology 6.8.4 Hyperbaric Oxygen 58 6.8.5 Wound Care 58 Anetiologicalfactororfactorscanbeidentifiedinmore 6.8.6 Reconstructive Surgery 59 than 90% of cases and should be actively sought, be- 6.9 Complications 59 cause it may determine the treatment and prognosis 6.10 Prognosis 59 (Smith et al. 1998; Santora and Rukstalis 2001). In ap- parently idiopathic cases, the cause may have been over- References 59 looked or obscured by the necrotizing disease process. Any process where a virulent, synergistic infection 6.1 gains access to the of the Definition and Historical Perspective may serve as the point of origin. The cause of infection may be from a urogenital, anorectal, cutaneous, or ret- Fournier’s gangrene is a synergistic polymicrobial nec- roperitoneal origin. The urogenital area is the most rotizing fasciitis of the perineum and genitalia. It can common etiologic site, where disease progress to a fulminant soft tissue infection that is at the top of the list (Edino et al. 2005). Knowledge of spreads rapidly along the fascial planes, causing necro- the anatomy of the perineum, urogenital area, and low- sis of the , subcutaneous soft tissue, and , er is necessary to understand the etiology with associated systemic sepsis. If it is not diagnosed and pathogenesis of this fulminant infection. early and treated promptly, significant morbidity with The possible causes of Fournier’s gangrene are listed prolonged hospital stay and even mortality will ensue. in Table 6.1. Infection may originate in any of the listed In 1764, Baurienne described a fulminant gangrene areas, with extension to the fascial planes leading to a ofthemaleperineum.However,JeanAlfredFournier,a proliferating fasciitis (Jones et al. 1979; Karim 1984; French dermatologist and venereologist, became fa- Walker et al. 1984; Walther et al. 1987; Baskin et al. 1990; mous for this notorious condition when, in 1883, he de- Sengoku et al. 1990; Gaeta et al. 1991; Attah 1992; Paty scribed a series of five young men in whom gangrene of and Smith 1992; Theiss et al. 1995; Benizri et al. 1996; the genitalia occurred without any apparent etiologic Hejase et al. 1996; Fialkov et al. 1998; Corman et al. factor. As knowledge of the condition increased over the 1999; Eke 2000; Kilic et al. 2001; Ali 2004; Jeong 2004; years, it became clear that Fournier’s gangrene is most Yeniyol et al. 2004; Edino et al. 2005). commoninoldermen(peakincidenceinthe5th and 6th Although Fournier’s gangrene is predominantly a decades) and that most cases have an identifiable cause. condition of the older male, it may occur at any age, and Fortunately, it is a rare condition, with a reported in- approximately10%ofcasesoccurinfemales(Kilicet cidence of 1/7,500, and accounting for only 1%–2% of al. 2001; Quatan and Kirby 2004). Specific causes in urologic hospital admissions (Bejanga 1979; Bahlmann women include pudendal block or for 6.2 Etiology 51

Table 6.1. Causes of Fournier’s gangrene Table 6.2. Underlying disorders in patients with Fournier’s gan- grene Urogenital Urethral stricture mellitus Indwelling transurethral catheter Chronic Prolonged or neglected use of condom catheter Urethral calculi Obesity Urethritis Liver cirrhosis Transurethral surger y Poor personal hygiene Infection of periurethral glands and paraurethral : Urogenital tuberculosis Chronic use Urethral cancer Organ transplantation biopsy for malignancy Prostatic massage HIV/AIDS Prostate abscess Tuberculosis Insertion of penile prosthesis Constriction ring device for management of ED Iatrogenic trauma bial infection (Table 6.2). Fournier’s gangrene is often a Cauterization of genital warts marker of an underlying disease such as diabetes melli- tus, urogenital tuberculosis, syphilis, or HIV. Manipulation of longstanding Noniatrogenic trauma Diabetes mellitus is the most common associated Animal, insect, or human bite underlying systemic disease, affecting two-thirds of pa- Scrotal abscess tients with Fournier’s gangrene. Diabetic patients have Infected a higher incidence of urinary tract infections, due to Hydrocelectomy Vasec tomy cystopathy with urinary stasis (Baskin et al. 1990). Hy- perglycemia decreases cellular immunity by decreasing phagocytic function. It retards chemotaxis of leuko- Anorectal cytes to the site of inflammation, neutrophil adhesion, Ischiorectal or perianal or intersphincteric abscess and intracellular oxidative destruction of pathogens. Rectal mucosal biopsy Wound healing is also retarded due to defective epithe- Banding of hemorrhoids Anal dilatation lialization and collagen deposition (Hejase et al. 1996; Cancer of sigmoid or rectum Nisbet and Thompson 2002). Apart from hyperglyce- Diverticulitis mia, diabetic patients also have microvascular disease, Rectal perforation by foreign body which contributes significantly to the pathogenesis. Al- Ischemic colitis though diabetes mellitus increases the risk for develop- Anal stenosis ment of Fournier’s gangrene, it does not increase the Cutaneous mortality (Baskin et al. 1990; Benizri et al. 1996; Hejase Hidradenitis suppurativa et al. 1996; Yeniyol et al. 2004). Scrotal pressure sore Chronic alcoholism, malnutrition, liver cirrhosis, Post-scrotal surgery wound infection poor personal hygiene, and personal neglect are quite of common in patients with Fournier’s gangrene (Benizri gangrenosum Femoral access for intravenous drug users et al. 1996; Hejase et al. 1996; Yeniyol et al. 2004). Other conditions causing depressed immunity that may pre- Retroperitoneal causes Psoas abscess dispose to the development of Fournier’s gangrene in- Perinephric abscess clude chronic steroid use, organ transplantation, che- Appendicitis and appendix abscess motherapy for malignancies such as leukemia, as well Pancreatitis with retroperitoneal fat necrosis as HIV infection (Paty and Smith 1992; Elem and Ran- Other jan 1995; Heyns and Fisher 2005). repair The rising incidence of HIV is paralleled by a rising Filariasis in endemic areas incidence of Fournier’s gangrene, especially in Africa. Strangulated Richter hernia Fournier’s gangrene may be the first presenting condi- tion in patients with HIV infection (McKay and Waters vaginal delivery, septic abortion, hysterectomy, and 1994; Elem and Ranjan 1995; Roca et al. 1998; Heyns Bartholin and vulval abscess (Roberts and Hester 1972; and Fisher 2005). Risk factors include a CD4 count un- Addison et al. 1984). der 400, chemotherapy for Kaposi’s sarcoma, and fem- A prominent feature of patients with Fournier’s gan- oral access for the administration of intravenous drugs. grene is that most of them have an underlying systemic HIV-positive patients with Fournier’s gangrene pre- disorder causing vascular disease or suppressed immu- sent at a younger age and have a wider spectrum of nity, which increases their susceptibility to polymicro- causative bacteria (McKay and Waters 1994). 52 6Fournier’sGangrene

6.3 theglansandproximallywiththesuspensoryligament Anatomy and crura of the . Camper’s fascia is the loose areolar fascial layer deep The can be divided into anterior and pos- totheskinoftheabdominalwall,butsuperficialto terior triangles by drawing a line between the ischial Scarpa’sfascia.TogetherwithScarpa’sfasciaitiscon- tuberosities with the symphysis and being tinuous with Colles’ fascia inferomedially. the apices (Fig. 6.1). Urogenital causes of Fournier’s Scarpa’s fascia lies deep to Camper’s fascia, covering gangrene lead to initial involvement of the anterior tri- the muscles of the anterior abdominal wall and thorax. angle, whereas anorectal causes primarily involve the It terminates at the level of the clavicles. posterior triangle. The perineal membrane lies deep to Colles’ fascia. It The five fascial planes that can be affected are: Col- is triangular in shape and lies between the pubic rami les’fascia,dartosfascia,Buck’sfascia,Scarpa’sfascia, from the symphysis pubis to the ischial tuberosities. It and Camper’s fascia. has a distinct posterior border, with the central perine- Colles’ fascia is the fascia of the anterior triangle of al tendon in the midline. Colles’ fascia terminates in the perineum. Laterally it is attached to the pubic rami this posterior border. and fascia lata, posteriorly it fuses with the perineal The central perineal tendon (or perineal body) lies membrane and perineal body, and anterosuperiorly between the and bulbar . It serves as an at- it is continuous with Scarpa’s fascia (Smith et al. 1998). tachment for the various perineal muscles and helps to It prevents the spread of infection in a posterior or lat- maintain the integrity of the . eraldirection,butprovidesnoresistancetospreadin Via the internal and external fascial layers of the an anterosuperior direction towards the abdominal spermatic cord, the perineal fascia is continuous with wall. the retroperitoneal fascia. This is a potential path for The fascia is the continuation of Colles’ fascia the spread of infection from the perineum to the peri- over the scrotum and penis. vesical and retroperitoneal areas, and vice versa (Paty Buck’s fascia lies deep to the dartos fascia, covering and Smith 1992; Fialkov et al. 1998). the penile corpora. It fuses distally with the corona of Spread of infection along the fascial planes will fol- low the path of least resistance (Jones et al. 1979). Infec- bulbar urethra tion in the anterior perineal triangle will spread prefer- entially in an anterosuperior direction along Scarpa’s anterior triangle symphysis pubis

perineal body

urogenital membrane

Fig. 6.1.The pelvic outlet can be divid- posterior triangle ed into anterior and posterior trian- gles by drawing a line between the is- ischial coccyx chial tuberosities with the symphysis tuberosity pubis and coccyx being the apices (© Hohenfellner 2007) 6.4 Microbiology 53

suspensory ligament of penis Scarpa’s fascia

Camper’s fascia

Fig. 6.2.Diagram of a sagittal section Buck’s fascia perineal body showing the fascial planes of the male dartos fascia external genitalia, perineum, and lower Colles’ fascia abdomen (© Hohenfellner 2007) external spermatic fascia fascia, whereas lateral spread will be limited by fusion vessels become thrombosed, facilitating the prolifera- of Colles’ fascia to the ischiopubic rami, and posterior tion of anaerobic bacteria. spread to the anal region will be limited by the termina- Blood supply to the testis, bladder, and rectum origi- tion of Colles’ fascia in the posterior edge of the perine- nates directly from the aorta and not from the perineal al membrane (Fig. 6.2). vasculature, and for this reason they are rarely affected Infection from the perianal region may sometimes in Fournier’s gangrene. If the testes are affected, it may penetrate Colles’ fascia, which is fenestrated at the level be from specific testicular pathology such as epididy- of the bulbocavernosus muscle, leading to spread of in- mo-, or from a retroperitoneal infection fection to the anterior triangle (Tobin and Benjamin spreading along the spermatic fascia, causing throm- 1949). Thus, while anterior triangle infection rarely bosis of the testicular . spreads to the posterior triangle, it is possible for infec- tion to spread from the posterior to the anterior trian- gle and then to the anterior abdominal wall (Jones et al. 6.4 1979; Walker et al. 1984; Laucks 1994). Microbiology In the perineum, the vascular supply to the cutane- ous and subcutaneous tissues is mainly derived from One of the characteristics of Fournier’s gangrene is that the perineal branches of the internal pudendal . it is a polymicrobial infection, with a mean of four dif- The deep circumflex iliac artery and superficial inferior ferent organisms usually cultured (Bahlmann et al. epigastric artery supply blood to the lower abdominal 1983; Baskin et al. 1990). wall. These arteries traverse the various fascial planes, Aerobic, anaerobic, Gram-positive and Gram-nega- supplying nutrients and oxygen to the skin and subcu- tive bacteria, yeasts, and even mycobacteria can be taneous tissues. With the fascial planes infected, these found(Table6.3).Themostcommonlyculturedorgan- 54 6Fournier’sGangrene

Table 6.3. Most common causative organisms Aerobic organisms cause intravascular coagulation Gram-negative by inducing platelet aggregation and complement fixa- E. coli tion, while anaerobes produce heparinase. Vascular Klebsiella pneumoniae thrombosis causes necrosis of tissue and decreased Pseudomonas aeruginosa clearance of toxic bacterial metabolites, with subse- Proteus mirabilis quent proliferation of anaerobic bacteria (Paty and Enterobacteria Smith 1992; Hejase et al. 1996). Gram-positive Hypoxic tissue leads to the formation of oxygen free Beta-hemolytic streptococci radicals (superoxide anions, hydrogen peroxide, hy- faecalis droxyl radicals), which play an important role in the Staphylococcus epidermidis pathogenesis.Theeffectsoffreeradicalsincludecell Anaerobes membrane disruption leading to cell death, decreased Bacteroides fragilis ATP production leading to decreased energy delivery, Peptococcus and DNA damage, which leads to decreased protein Fusobacterium perfringens production (Anderson and Vaslef 1997). Anaerobic organisms secrete various enzymes and Mycobacteria toxins. Lecithinase, collagenase, and hyaluronidase Mycobacterium tuberculosis cause digestion of the fascial planes (Baskin et al. 1990). Ye a s t s They produce insoluble hydrogen and nitrogen, lead- Candida albicans ing to the formation of gas in the subcutaneous tissues, clinically palpable as . Aerobic bacteria pro- isms are Escherichia coli, Bacteroides, beta-hemolytic duce CO2, which is soluble and rarely leads to subcuta- streptococci, Staphylococcus spp., and Proteus.Besides neous gas accumulation. being found in the lumen of the gastrointestinal tract, Endotoxins are released from the cell walls of Gram- these bacteria are also normal commensal flora of the negative bacteria. Macrophage activation and subse- skin folds and hair follicles of the perineum (Benizri et quent complement activation ensues with release of al. 1996; Smith et al. 1998). This mixed spectrum of bac- pro-inflammatory cytokines and eventual develop- teria acts in a synergistic fashion to produce and pro- ment of septic shock (Anderson and Vaslef 1997). mote a fulminant . Depending on the origin of the infection, the various Anaerobic organisms are responsible for the forma- paths of spread can be explained with reference to the tion of subcutaneous gas, which leads to the character- anatomy of the fascial planes and adhesions. istic crepitus often found on palpation. Clostridial in- Infection from a urogenital cause, e.g., a patient with fection, classically associated with gas formation, is not a urethral stricture and urinary tract infection leading commonly encountered, but should be suspected when to a paraurethral abscess, will spread from the corpus there is a colorectal origin (Spirnak et al. 1984; Baskin spongiosum by penetrating the and et al. 1990). Buck’s fascia, and will then spread under the dartos fas- It is extremely important to obtain cultures in order cia and Colles’ fascia to Scarpa’s fascia, thereby involv- to identify the causative organism(s), because this ing the anterior abdominal wall. determines the correct choice of antibiotic treatment. Infection from an anorectal cause, e.g., an ischio- Because of the difficulty of culturing anaerobic or- rectal abscess, will spread from the perirectal tissues ganisms, a subcutaneous aspirate should be obtained, to Colles’ fascia. Because Colles’ fascia is fenestrated, it and at initial debridement a piece of infected tissue allows spread from the perirectal area to the dartos should also be sent for anaerobic culture. Microbio- fascia of the scrotum and penis, and from there the in- logical studies should include acid fast staining for fection can spread to Scarpa’s fascia and the anterior Mycobacterium tuberculosis and culture for fungal in- abdominal wall. Because Colles’ fascia terminates in fection. the perineal membrane, infection from the anterior triangle of the perineum, which contains the bulbar urethra and scrotum, cannot spread to the perirectal 6.5 area, but because Colles’ fascia is fenestrated, the op- Pathogenesis posite is possible, i.e., posterior triangle infections may sometimes spread to the anterior triangle and The pathogenesis of Fournier’s gangrene is character- from there to the anterior abdominal wall. This is im- ized by polymicrobial aerobic and anaerobic infection portant in trying to localize the origin of the initial in- with subsequent vascular thrombosis and tissue necro- fection. sis, aggravated by poor host defense due to one or more Retroperitoneal infection, e.g., from a perinephric underlying systemic disorders. orpsoasabscess,mayspreadalongtheinguinalcanal 6.8 Management 55 and spermatic fascia, which connects to Colles’ fascia lytes, liver function tests, blood glucose, blood gases, deep to the bulbocavernosus muscle. Retroperitoneal group and screen, HIV and VDRL. infection should be considered as a cause of Fournier’s Abnormal findings include anemia, thrombocyto- gangrene if no obvious point of origin can be found. penia, coagulopathy, hyponatremia, and raised urea and creatinine. Hypocalcemia may occur in some cases, subsequent to the chelation of ionized calcium by 6.6 triglycerides liberated by bacterial lipases. Clinical Presentation Leukocytosis with a white cell count above 15,000 mm3 and a left shift is found in more than 90% The diagnosis of Fournier’s gangrene is made on clini- of cases. Neutrophilia indicates overwhelming bacteri- cal grounds. It is usually preceded by prodromal symp- al infection. It is noteworthy that leukocytosis may not toms such as fever, prostration, nausea and vomiting, be present in immunosuppressed patients (Baskin et al. perineal discomfort, and poor glucose control in dia- 1990; Laucks 1994). Anemia may be present as part of betics, for a period ranging from 2 to 9 days (Bahlmann the septic profile. Coagulopathy may be indicated by a et al. 1983; Paty and Smith 1992; Benizri et al. 1996; Edi- raised prothrombin time (PT) and partial thrombo- no et al. 2005). plastin time (PTT), and thrombocytopenia. Raised fi- Genital and perineal discomfort worsens, leading to brinogen levels and positive D-dimers may herald the pain, itching, burning sensation, erythema, swelling, onset of disseminated intravascular coagulation (DIC). and eventual skin necrosis. There may be a purulent Blood and urine cultures, together with wound discharge with a feculent odor. The pain may subside as swabs and tissue specimens for bacterial culture are neural damage develops (Corman et al. 1999). Crepitus very important. The HIV status should be determined may be difficult to elicit, due to pain on palpation, but in all patients, as Fournier’s gangrene may be the pre- is present in up to 50%–60% of cases (Corman et al. senting condition in patients with HIV. 1999; Benizri et al. 1996). Radiologic imaging may be useful if the diagnosis is Clinical signs such as an elevated temperature, in doubt, but it should not delay the surgical manage- tachycardia, tachypnea, ileus, poor glucose control, and ment. An x-ray of the abdomen and may demon- vascular collapse may be found, but are not very consis- strate gas in the subcutaneous fascial layers of the peri- tent, especially with underlying immunosuppressive neum and abdominal wall. disorders. Ultrasound provides superior imaging of the peri- The diagnosis is sometimes delayed due to morbid neum and scrotum. The appearance of hyperacoustic obesity, poor communication (stroke, dementia), or in- shadowsinthefascialplanesisdiagnosticofgasforma- adequate physical examination. In Africa, patients may tion, and it may be more sensitive than clinical evalua- first seek help from a traditional healer, thereby delay- tion for crepitus (Kane et al. 1996). However, in patients ing proper medical attention (Attah 1992). with extreme tenderness on palpation, ultrasound ex- Once there is necrosis of the skin, the underlying amination may be too painful. fascia has already undergone extensive necrosis. This Computerized tomography (CT) is more sensitive in explains the frequent finding of systemic symptoms, demonstrating subcutaneous and retroperitoneal gas which are out of proportion to the visible pathology. and fluid collections, but the use of contrast should be Other symptoms and signs depend on the origin of avoided in patients with renal failure. Magnetic reso- the infection. A history of lower urinary tract symp- nance (MR) is the most sensitive imaging modality for toms may indicate a urethral stricture. Preceding ano- evaluating pathology in soft tissues, but is expensive rectal symptoms such as pain, fissures, or hemorrhoids and not readily available. may indicate an anorectal origin of Fournier’s gan- grene. It is essential that the attending doctor have a high 6.8 index of suspicion in patients presenting with perineal Management discomfort accompanied by systemic symptoms. A missed or delayed diagnosis may have catastrophic ThemaingoalsinthemanagementofFournier’sgan- effects. grene are aggressive resuscitation of the patient, ad- ministration of broad-spectrum antibiotics, and de- bridement of infected and necrotic tissue. Debride- 6.7 ment is paramount, and the aim should be to get the pa- Special Investigations tient to the operating room as soon as possible (Baskin et al. 1990; Smith et al. 1998; Quantan and Kirby 2004). Special investigations to be done include a full blood count, clotting profile, urea, creatinine and electro- 56 6Fournier’sGangrene

sure (CVP) of 8–12 cm H O should be maintained. The 6.8.1 2 mainstay of management is to optimize oxygen deliv- Initial and Preoperative Management ery by striving to: If there is doubt about the diagnosis of Fournier’s gan- ) Keep oxygen saturation above 90% using an oxy- grene, imaging and laboratory studies may be request- gen mask, continuous positive airway pressure ed, but this should not delay definitive surgical man- (CPAP) or mechanical ventilation agement. ) Optimize cardiac output by improving the heart Thecauseoftheinfectionshouldbeestablished, rate and stroke volume, using sympathomimetics bearing in mind that urogenital causes (urethral stric- and volume expansion ture) and anorectal infections are the most common ) Optimize oxygen transport by using packed red etiological factors. Passing an F16 transurethral cathe- cells to maintain a hemoglobin above 10 g/dl ter should exclude or confirm a urethral stricture, and painful digital rectal examination may indicate an ischiorectal abscess. If rectal examination is too pain- 6.8.2 ful,itcanbeperformedintheoperatingroomwiththe Surgery patient under anesthesia, just before debridement. Aggressive fluid resuscitation with crystalloid or Early and aggressive surgical debridement is essential, colloidfluidsisessentialtooptimizethehemodynamic because it significantly decreases morbidity and mor- status in these volume-depleted, septic patients. tality (Bahlmann et al. 1983). The procedure should be Anemia should be corrected to a hemoglobin great- done under general anesthesia, as the true extent of the er than 10 g/dl. Coagulopathy (raised international infectionisusuallyunknownpreoperatively.Thepa- normalized ratio [INR], PT and PTT, or platelets tient should be placed in a dorsal lithotomy position <100,000) should be diagnosed preoperatively and (Paty and Smith 1992; Smith et al. 1998). The aim of de- platelets should be given intraoperatively if the patient bridement is to remove the origin of the infection as is severely thrombocytopenic. Diabetic patients usual- well as the infected tissues (Quantan and Kirby 2004). ly have severe hyperglycemia, which should be correct- The surgeon as well as the patient should be prepared ed with a glucose-insulin sliding scale. Electrolyte ab- for radical debridement. normalities must be corrected as far as possible, with- A midline perineal and scrotal incision usually gives out incurring unnecessary delay of surgical debride- the best initial exposure (Jones et al. 1979). Debride- ment. ment is extended radially from the skin incision, keep- Antibiotic therapy must be initiated promptly, after ing the anatomy of the fascial planes in mind. Only skin appropriate specimens have been obtained for bacteri- that is clearly necrotic should be excised. Viable skin ological culture. High-dose, broad-spectrum parenter- should be mobilized so that all the underlying necrotic al antibiotics covering Gram-positive and Gram-nega- subcutaneous tissue and fascia can be excised. tive aerobe as well as anaerobe organisms should be A good indication of the extent of the infection is used (Baskin et al. 1990; Paty and Smith 1992; Hejase et where the affected fascia fails to separate from the deep al. 1996; Smith et al. 1998). Aminoglycosides and third- fascia and muscle on blunt dissection (Jones et al. 1979; or fourth-generation cephalosporins are effective Smith et al. 1998; Santora and Rukstalis 2001). The against Gram-negative bacteria, metronidazole against wound edges should bleed like normal tissue, indicat- anaerobic infection, and penicillins against Gram-posi- ing patent nutrient vessels. tive bacteria. Usually combined use of three antibiotics, If no purulent discharge can be milked from the ure- onefromeachofthesegroups,isclinicallyeffective. thra, and an F16 catheter can be passed into the blad- However, to ensure adequate cover against enterococci, der, it is reasonable to assume that the urethra is not the some groups advocate the combined use of the ureido- origin of the infection. However, if it is not possible to penicillin piperacillin with the beta-lactamase inhibi- pass a transurethral catheter easily, a suprapubic cathe- tor tazobactam. It is important to note that antibiotics ter should be inserted (Benizri et al. 1996). Catheteriza- will not penetrate ischemic and necrotic tissues, and tion of the bladder is essential for monitoring fluid therefore serve only as an adjunct to definitive surgical management and for adequate wound care (Laucks management (Baskin et al. 1990). Tetanus toxoid 1994). should also be given to all patients (Laucks 1994). Colostomy is indicated if the anal sphincter is in- The onset of septic shock is heralded by signs such volved, if rectal or colon perforation is present, in im- as altered sensorium, hypotension, hypoperfusion, oli- munocompromised patients with , guria, and lactic acidosis. Multiorgan failure should be andifthereisextensiveinvolvementoftheposterior anticipated and prevented by aggressive fluid manage- perineal triangle (Fig. 6.3). Colostomy allows for better ment and invasive vascular monitoring. A mean arteri- wound care (Paty and Smith 1992; Laucks 1994, Benizri al pressure over 65 mmHg and a central venous pres- et al. 1996). Some authors feel that doing a diverting co- 6.8 Management 57

Fig. 6.3.Extensive debride- ment for necrotizing fasciitis arising from ischio-rectal ar- ea (note transurethral as well as suprapubic catheters, and stoma bag for transverse co- lostomy) lostomy can be delayed until the second-look debride- 6.8.3 ment when the patient is better resuscitated and more Postoperative Management stable, because most acutely ill patients have an ileus for at least 48 h after admission (Bronder et al. 2004). The wound should be inspected daily, and the surgeon The testes, because of their nonperineal blood sup- should have a low threshold for redebridement. A mean ply, are rarely affected, and orchidectomy is required in of 2.5 debridements per patient is reported in the litera- only 10%–20% of cases, if there is extensive involve- ture (Baskin et al. 1990; Corman et al. 1999). Bacterial mentoratesticularcausefortheinfection(Baskinetal. culture results should be checked to make sure that ap- 1990; Okeke 2000). propriate antibiotic therapy is given. If the patient is in During scrotectomy, all necrotic tissues except the renal failure, aminoglycosides should be avoided and a testes and spermatic cords should be debrided. The tes- third- or fourth-generation cephalosporin should be tis can be buried in a lateral thigh pouch or in a subcu- given. taneous abdominal pouch, depending on the extent of Nosocomial infections should be prevented as far as the debridement. This should not be done during the possible. Pulmonary complications (e.g., atelectasis) initial debridement, but during one of the subsequent should be prevented. If postoperative fever persists or procedures, because this decreases the risk of a thigh the patient does not improve clinically, a persistent abscess and extension of the infection. If the testes are source of infection should be suspected. CT or MR im- buried in thigh pouches, they should be placed at dif- aging may demonstrate an intraabdominal or retroperi- ferent levels, eliminating the risk of the testes rubbing tonealinfectivecause.However,evenifthesestudiesare against each other with the patient walking (Laucks negative, there should be a low threshold for reexplora- 1994). Removal of the testes from the pouches and scro- tion and redebridement of the patient under anesthesia. tal reconstruction can be considered later. Maintaining a blood glucose level of 4–6 mmol/l (74–110 mg/dl) optimizes cellular immunity and re- duces morbidity and mortality in the septic patient, re- gardless of whether there was preexisting diabetes or not (Van den Berghe et al. 2001; Fourie 2003). 58 6Fournier’sGangrene

In the acutely ill patient, the development of ileus, responding anaerobic infection. It is important to note stress ulcers, and translocation of gut flora are com- that HBO is only an adjunct and should not delay mon complications. Stress ulcers can be prevented by prompt antibiotic therapy and surgical debridement giving sucralfate (1 g every 6–8 h). Gut integrity can be (Paty and Smith 1992; Laucks 1994; Benizri et al. 1996; maintained by starting early with gastrointestinal feed- Pizzorno et al. 1997; Mindrup et al. 2005). ing and by using enteral rather than parenteral nutri- tion (Anderson and Vaslef 1997). The caloric needs of 6.8.5 25–35 kcal/kg per day and protein of 1.5–2 g/kg per Wound Care dayshouldbemet,especiallyinpatientswithlarge wounds, malnutrition, and those on ventilation (Bas- Care of the debrided wounds should allow for addition- kin et al. 1990; Anderson and Vaslef 1997). al chemical debridement, prevent reinfection and pro- mote natural healing and granulation. Hydrogen peroxide, Eusol, povidone iodine, and so- 6.8.4 dium hypochlorite (Dakin solution) are the agents most Hyperbaric Oxygen often used (Jones et al. 1979; Paty and Smith 1992; Heja- Hyperbaric oxygen (HBO) has been used as an adjunct se et al. 1996; Edino et al. 2005). Eusol (Edinburgh Uni- in the treatment of Fournier’s gangrene. The usual pro- versity solution) is a chlorinated disinfectant included tocolismultiplesessionsat2.5atmfor90minwith100% in the World Health Organization’s “essential therapeu- oxygen inhalation every 20 min (Pizzorno et al. 1997). tic group” of agents. It consists of calcium hypochlorite HBO increases oxygen tension levels in the tissues 1.25 g and boric acid 1.25 g in 100 ml sterile water. Even and has various beneficial effects on wound healing. ifnotcommerciallyavailable,itcanbeeasilyprepared Oxygen free radicals are liberated from hypoxic tissues, by the hospital dispensary, and is an inexpensive and ef- which are directly toxic to anaerobic bacteria. Fibro- fective agent for use in developing countries. Simple ir- blast activity increases, with subsequent angiogenesis rigation with sterile saline solution to keep dressings leading to accelerated wound healing. moist can be very effective in cleansing large open However, HBO is expensive and logistically cumber- wounds. Honey has also been used, because its high os- some. It is contraindicated where closed air spaces in molarity and low pH make it a good desloughing agent, thebodycancausedamageduetoexpansionuponre- while it increases local oxygen concentration and helps turning to normal atmospheric pressure, such as sinus- with wound epithelialization (Hejase et al. 1996). Pseu- itis,otitismedia,asthma,andbullouspulmonarydis- domonas wound infection, characterized by its distinc- ease. Care should be taken with diabetic patients, as hy- tiveodorandgreenresidueonthedressings,canbeef- poglycemia may be exacerbated by HBO. fectively treated with 5% acetic acid dressings. Some authors question the efficacy of empirical Once the patient is stable and in an anabolic state HBO, suggesting that patients should be selected only if with granulating wounds, reconstruction of the denud- thereislargebodysurfaceareainvolvementorpoorly ed areas can be done (Fig. 6.4). Skin grafting should on-

Fig. 6.4.Well granulated areas ready for skin transplanta- tion References 59 ly be performed if the wounds are clean and healthy, ) Squamous cell carcinoma in the tissue (Chin- with a negative bacterial swab culture. tamani et al. 2004) ) Contractures due to prolonged immobilization ) Depression secondary to dysmorphic body changes 6.8.6 ) Loss of income and disruption of family life due to Reconstructive Surgery prolonged hospitalization Depending on the extent of skin defects, the options in ) Lymphodema of the legs secondary to pelvic de- reconstruction are suturing, split thickness skin graf- bridement and subsequent thrombophlebitis. ting, or myocutaneous vascularized pedicle flaps. Small defects can be closed by primary suturing, es- pecially where only the pliable scrotal skin is involved. 6.10 Split thickness skin grafting is most often used and Prognosis yields acceptable results, even in large defects (Hessel- feldt-Nielsen et al. 1986). Healthy skin from the legs, The reported mortality of Fournier’s gangrene ranges , and arms can be used, in a single or multiple from 0% to 70%, with an average of 20%–30%. The settings. Skin defects on the penile shaft should be lib- factors associated with an adverse outcome are physical erally grafted so as to prevent fibrotic scar formation disability, extent of the infection, delayed treatment, with future erectile problems. poorimmunestatus,diabetesmellitus,oldage,and In extensive defects, especially where tendons are multiorgan failure (Akgun and Yilmaz 2005). Labora- exposed, myocutaneous vascularized flaps should be tory values associated with an increased mortality are used. Medial thigh flaps, e.g., the gracilis myocutaneo- leukocytosis, elevated urea, creatinine, alkaline phos- us pedicle flap, give the best results, because of their phatase (ALP) and lactate dehydrogenase (LD), and a close proximity to the perineum, good mobility, and decrease in the hemoglobin, albumin, bicarbonate, so- hidden donor site (Banks et al. 1986; Paty and dium, and potassium (Laor et al. 1995). Smith 1992; Kayikcioglu 2003). Other flaps using the inferior epigastric arteries can also be considered. In men with underlying urethral stricture disease, References urethroplasty may be extremely difficult or impossible due to extensive loss of penoscrotal skin and even of the Addison WA,Livengood CH 3rd, Hill GB, Sutton GP,Fortier KJ urethra itself. Buccal mucosa may be used to recon- (1984) Necrotizing fasciitis of vulval origin in diabetic pa- tients. Obstet Gynecol 63:473 struct the urethra, but in some cases with extensive tis- Akgun Y, Yilmaz G (2005) Factors affecting mortality in Four- sue loss, a permanent perineal urethrostomy may be nier’s gangrene (in Turkish). Ulus Travma Derg 11:49 the best solution. Ali MZ (2004) Fournier’s gangrene – a rare of hy- drocele aspiration. J Coll Physicians Surg Pak 14:304 Anderson RW, Vaslef SN (1997) Shock. Causes and manage- ment of circulatory collapse. In: Sabiston DC, Lyerly HK 6.9 (eds) Sabiston textbook of surgery – the biological basis of Complications modern surgical practice, 15th edn. WB Saunders Company, Philadelphia, p 68 Nonresolving sepsis may be due to incomplete de- Attah CA (1992) New approach to the management of Four- bridement, a persisting occult source of infection, or a nier’s gangrene. Br J Urol 70:78 Bahlmann JC, Fourie IJ, Arndt TC (1983) Fournier’s gangrene: poor patient immune response. Multiple organ failure necrotising fasciitis of the male genitalia. Br J Urol 55:85 is a feared consequence of unresolved sepsis and most Banks DW, O’Brien DP 3rd, Amerson JR, Hester TR Jr (1986) commonly involves the cardiovascular, pulmonary, Gracilis musculocutaneous flap reconstruction after Four- and renal systems. Coagulopathy, acalculous chole- nier gangrene. 28:275 Baskin LS, Carroll PR, Cattolica EV, McAninch JW (1990) Nec- cystitis, and cerebrovascular accidents have also been rotising soft tissue infections of the perineum and genitalia. reported (Baskin et al. 1990). Myositis and myonecro- Br J Urol 65:524 sis of the upper thigh may occur as a result of sepsis Bejanga BL (1979) Fournier’s gangrene. Br J Urol 51:312 from subcutaneous testicular pouches made during Benizri E, Fabiani P,Migliori G, Chevallier D, Peyrottes A, Rau- the first rather than secondary debridement (Choe coules M, Amiel J, Mouiel J, Toubol J (1996) Gangrene of the perineum. Urology 47:935 et al. 2001). Bronder CS, Cowey A, Hill J (2004) Delayed stoma formation in Late complications include the following: Fournier’s gangrene. Colorectal Dis 6:518 ) Chintamani,ShankarM,SinghalV,SinghJP,BansalA,Saxena Chordee, painful , and erectile dysfunc- S (2004) Squamous cell carcinoma developing in the scar of tion Fournier’s gangrene – case report. BMC Cancer 4:16 ) Infertility as a result of burying the testes in thigh Choe JM, Battino BS, Benedict J, Bell TE (2001) Myositis and pouches (high temperature) myonecrosis of the thigh: an unusual complication of a tes- ticular thigh pouch. J Urol 165:1217 60 6Fournier’sGangrene

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