Fournier’s gangrene, an obliterative endarteritis of the subcutaneous arteries resulting in gangrene of the overlying skin, is a rare but severe infective necrotizing. Profile of patients with Fournier’s gangrene and their clinical evolution. Perfil dos pacientes com gangrena de Fournier e sua evolução clínica. DJONEY RAFAEL. La gangrena de Fournier es una infección grave de la zona genital de los ciertas afecciones corren un mayor riesgo de llegar a tener gangrena de Fournier.
|Published (Last):||15 October 2005|
|PDF File Size:||6.74 Mb|
|ePub File Size:||2.36 Mb|
|Price:||Free* [*Free Regsitration Required]|
The nidus for the synergistic polymicrobial infection is usually located in the genitourinary tract, lower gastointestinal tract or skin. Early diagnosis remains imperative as rapid progression of the gangrene can lead to multiorgan failure and death. The diagnosis is often made clinically, although radiography can be helpful when the diagnosis or the extent of the disease is fisippatologia to discern.
Mainstays of treatment include rapid and aggressive surgical debridement of necrotized tissue, hemodynamic support with urgent cournier with fluids, and broad-spectrum parental antibiotics. After initial radical debridement, open wounds are generally managed with sterile dressings and negative-pressure wound therapy.
In cases of severe perineal involvement, colostomy has been used for fecal diversion or alternatively, the Flexi-Seal Fecal Management System can be utilized to prevent fecal contamination of the wound. After extensive debridement, many ee sustain significant defects of the skin and soft tissue, creating a need for reconstructive surgery for satisfactory functional and cosmetic results.
Similar to other necrotizing soft tissue infections, the inflammation and edema from the polymicrobial infection lead to an obliterative endarteritis of the subcutaneous arteries [ Korkut et al. This impaired blood supply furthers perifascial dissection with spread of bacteria and progression to gangrene of the overlying subcutaneous tissue and skin. Even though FG was first described by Baurienne in [ Nathan, ], it is credited to the French venereologist, Jean Alfred Fournier, who provided a detailed description of the disease in as a fulminant gangrene of the penis and scrotum [ Fournier, ].
Over the years, experience has shown that FG often has an identifiable cause and it frequently manifests indolently. Subjects of both genders and all ages may be affected [ Sorensen et al.
Early diagnosis remains imperative, as the rate of fascial necrosis has been noted as high as 2—3 cm per hour [ Uppot et al. Treatment of FG entails treating sepsis, stabilizing medical parameters and urgent surgical debridement. Interestingly, the mortality has been shown to be higher in technologically advanced countries such as the United States, Canada and Europe than in underdeveloped countries [ Eke, ].
Primarily an infective condition, FG has several predisposing factors and theoretically, any condition that decreases the host immunity may predispose a person to the development of FG.
The relatively high incidence of FG in patients with diabetes has been attributed to their small vessel disease, defective phagocytosis, diabetic neuropathy and immunosuppression, all of which can be exacerbated by poor hygiene when present [ Vick and Carson, ].
Other risk factors include extremes in age, malignancy, chronic steroid use, cytotoxic drugs, lymphoproliferative disease, malnutrition and human immunodeficiency virus HIV infection [ Mallikarjuna et al. FG was initially defined as an idiopathic entity, but recent fourner has shown that less than a quarter of FG cases are now considered idiopathic [ Smith et al.
Colorectal sources include local risiopatologia, abscesses particularly in the perianal, perirectal and ischiorectal regionsanal fissures, colonic perforations, diverticulitis, hemorrhoidectomy and rectal carcinoma [ Ash and Hale, ].
Urologic sources of FG include urethral strictures, chronic urinary tract infection, neurogenic bladder, epididymitis and recent instrumentation [ Amendola et al. In women, additional sites of origin include Bartholin gland or vulvar abscess, episiotomy, hysterectomy and septic abortion [ Morua et al. Insect bites, burns, trauma and circumcision have also been reported as causes of pediatric FG [ Amendola et al.
The predisposing and etiologic factors of FG provide a favorable environment for the infection by decreasing the host immunity and allowing a portal hangrena entry for the microorganism into the perineum.
The incident leading to the inoculation may be so trivial that the patient or physician may fail to notice.
Characteristically, FG exists due to synergism between multiple bacteria that theoretically are not highly aggressive when presented alone. The polymicrobial nature of FG with contributions by both aerobic and anaerobic bacteria is necessary to create the production of various exotoxins and enzymes like collagenase, heparinase, fislopatologia, streptokinase and streptodornase, which promote rapid multiplication and spread of infection. The aerobic bacteria cause platelet aggregation and induce complement fixation, thereby causing acceleration of coagulation.
The anaerobic bacteria promote the formation of clots by producing collagenase and heparinase. Other organisms like Bacteroides inhibit the phagocytosis of aerobic bacteria, aiding in further spread of the infection [ Morua et al. The organisms that tend to be found in FG are species that normally exist below the pelvic diaphragm in the perineum and genitalia [ Eke, ]. The most flsiopatologia isolated aerobic microorganisms are Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureuswhile the fornier commonly isolated anaerobic microorganism is Bacteroides fragilis [ Paty and Smith, ].
In some series, an average of more than three organisms were cultured from each patient [ Addison et al. Group A streptococcal is the most common cause of monomicrobial necrotizing fasciitis [ Ekelius et al.
Although rare, necrotizing fasciitis due to Candida species as well as Lactobacillus gasseri has also been reported [ Tleyjeh et al. The infection in FG tends to spread along the fascial planes with initial involvement of the superficial Colles fascia and deep fascial planes of the genitalia.
Subsequently, there is spread to the overlying skin with sparing of the muscles. The inferior epigastric and deep circumflex iliac arteries supply the lower aspect of the anterior abdominal wall, whereas the external and internal pudendal arteries supply the scrotal wall.
The Fisiopatoogia fascia is attached laterally to the pubic gantrena and fascia lata gqngrena posteriorly to the urogenital diaphragm, thus limiting progression in these directions. In contrast, anorectal sources of infection usually start in the perianal area, a clinical variation that can serve as a guide to localizing the foci of infection [ Smith et al.
Testicular involvement is limited in FG by the fisiopaologia that the blood supply is derived from the aorta, independent from the affected region [ Fsiiopatologia et al. However, involvement of the testis suggests retroperitoneal origin or spread of infection [ Eke, ; Chawla et al. Even though thrombosis of the corpus spongiosum and cavernosum has been reported, corpora involvement is rare while the penile skin sloughs off [ Campos et al.
Usually the infection starts as a cellulitis adjacent to the portal of entry, commonly in the perineum or perineal region, with an insidious presentation. The affected area is often swollen, dusky and covered by macerated skin and presents with a characteristic feculent odor, which is attributed to the role of anaerobes in the infection [ Alonso et al. Patients also may have pronounced systemic signs, usually out of proportion to the local extent of the disease.
Ferreira and colleagues reviewed 43 cases and found the most common presentations were scrotal swelling, ed and pain [ Ferreira et al.
Crepitus of the inflamed tissues is a common feature due to the presence of gas-forming organisms [ Paty and Smith, ]. As the subcutaneous inflammation worsens, necrosis and suppuration of subcutaneous tissues progresses to extensive necrosis [ Laucks li, tournier.
Patients can rapidly deteriorate as sepsis and multiorgan failure, the most common cause of death in these cases, develop [ Sutherland and Meyer, ]. The diagnosis of FG is primarily based on clinical findings of fluctuance, crepitus, localized tenderness and wounds of the genitalia and perineum. Although diagnosis is straightforward when the lesions are found, failure to examine the genitals, especially in the older or obtunded patient, can result in misdiagnosis.
Contemporary diagnosis and management of Fournier’s gangrene
The common laboratory findings are nonspecific and may show anemia, leukocytosis, thrombocytopenia, electrolyte abnormalities, hyperglycemia, elevated serum creatinine level, azotemia and hypoalbuminemia [ Shyam and Rapsang, ]. The diagnosis of FG is primarily clinical, and in most cases imaging is neither necessary nor desirable.
Under no circumstances should surgery be fiurnier significantly for imaging of any kind. However, imaging modalities may be useful in cases when fourbier presentation is atypical or when there is concern regarding the true extent of the disease.
Conventional radiography can be used to detect the presence of soft tissue air in the area overlying the scrotum and perineum before clinical crepitus is detected. In addition to demonstrating significant swelling of the scrotal soft tissue, radiographs may also detect subcutaneous emphysema extending from the scrotum and perineum to the inguinal regions, anterior abdominal wall and thighs.
A significant weakness of radiography in the diagnosis and evaluation of FG is the lack of detection of deep fascial gas [ Wysoki et al. In addition, US can demonstrate paratesticular fluid, which is seen prior to clinical crepitus.
This imaging modality is also useful in differentiating FG from inguinoscrotal hernias.
Overall, US is considered superior to conventional radiography as soft tissue air is more obvious and scrotal contents along with Doppler blood flow can be examined. Computed tomography CT plays an important role in the diagnosis of FG as well as the evaluation of the extent of the disease to guide appropriate surgical treatment. CT findings include asymmetric fascial thickening, fluid collections, abscess formation, fat stranding around involved structures and subcutaneous emphysema [ Rajan and Scharer, ; Sherman et al.
The underlying cause of FG, such as a perianal abscess, a fistulous tract, or an intraabdominal or retroperitoneal infectious process, may also be demonstrated by CT [ Rajan and Scharer, ]. It can help to evaluate both the superficial and the deep fascia, and to differentiate FG from less aggressive entities such as soft-tissue edema or cellulitis, which may appear similar to FG on physical examination. As a whole, CT has greater specificity for evaluating disease extent than does radiography, US or even physical examination [ Rajan and Scharer, ].
Magnetic resonance imaging MRI offers an important diagnostic adjunct in the management of FG as it is more useful than conventional radiography and US for specifying range of infection. Despite timely and aggressive treatment, the mortality rate for FG remains high [ Morpurgo and Galandiuk, ; Sorensen et al. Various comorbidities are known to be associated with FG, of which DM is most common. However, its association with increased mortality is debatable [ Kabay et al.
Similarly, there is uncertainty about the association of age and mortality in FG [ Yeniyol et al. However, two comorbidities associated with increased mortality in FG are ischemic heart disease and hemodialysis-dependent renal failure [ Jeong et al. The presence of severe sepsis on admission has been significantly associated with mortality [ Kara et al.
However, the association between larger gangrenous areas and worse prognosis is not universally accepted [ Clayton et al. Abnormal laboratory parameters at admission have also been noted to have a significant impact on mortality. The laboratory values most often predictive of worse prognosis include increased leukocyte counts, creatinine, creatine kinase, urea, lactate dehydrogenase, alkaline phosphatase, and decreased levels of hematocrit, bicarbonate, sodium, potassium, calcium, total protein and albumin [ Clayton et al.
Using a weighted point system of multiple laboratory markers, the Laboratory Risk Indicator for Necrotizing Fasciitis LRINEC score is often used to stratify patients into low, moderate or high risk for necrotizing soft tissue infections [ Wong et al.
A LRINEC score of more than 6 should raise the suspicion of necrotizing fasciitis among patients with severe soft tissue infections, and a score greater than 8 is strongly predictive of FG. By quantifying the severity of infection using common vital signs temperature, heart rate, respiratory rate and laboratory data serum sodium, serum potassium, serum creatinine, serum bicarbonate, hematocrit and white blood cell countthe FGSI score helps prognosticate progression and predict the mortality.
The degree of deviation from normal is graded from 0 to 4, and individual values are summed to obtain the FGSI score. FGSI has been validated by several studies [ Chawla et al. Kabay and colleagues analyzed patients using this index and showed those with FGSI greater than However, controversy exists regarding the accuracy of FGSI, as Tuncel and colleagues and Janane and colleagues argued the index cannot be relied upon to predict survival [ Tuncel et al.
The management of FG is underscored by three main principles: As the rate of fascial necrosis has been noted as high as 2—3 cm per hour, FG is considered a surgical emergency with prompt, pragmatic and individualized therapy being the cornerstone for effective treatment [ Eke, ; Safioleas et al.
Broad-spectrum parental antibiotic therapy is administered empirically upon diagnosis of FG and then subsequently tailored based on culture results. It is imperative that the antibiotic regimen chosen is effective against staphylococcal, streptococcal and gram-negative bacteria, coliforms, Pseudomonas, Bacteroides and Clostridium [ Mallikarjuna et al. Triple antibiotic therapy consisting of a broad-spectrum penicillin or third-generation cephalosporins, an aminoglycoside e.
Moreover, many have suggested adding penicillin for treatment of streptococci and, in particular, when Clostridia is suspected.
There was a problem providing the content you requested
Alternatively, clindamycin and chloramphenicol can be substituted empirically to facilitate coverage of gram-positive cocci and anaerobes until culture results return [ Martinez-Rodriguez et al.
In patients infected with ce S.
Amphotericin B or caspofungin should be added fournjer the empiric regimen should fungi be detected in tissue cultures [ Pais et al. In addition to broad-spectrum parental fisiopatokogia, early and aggressive surgical debridement has been shown to improve survival in patients presenting with FG as patients often undergo more than one debridement during their hospitalization [ Corman et al.
In a retrospective study of patients presenting with a diagnosis of FG, Proud and colleagues found that there was no statistically significant difference in mortality between patients who underwent debridement before transfer or within 24 h of presentation to those who had not. The authors attributed this seemingly counterintuitive observation to the range in severity of necrotizing soft tissue infections and to the notion that patients are less likely to succumb to localized infections.
Regardless, the authors still advocate rapid and timely surgical debridement [ Proud et al. Since the treatment of FG often requires highly acute and intensive multidisciplinary care, Sorensen and colleagues examined the difference in case severity and management between teaching and nonteaching hospitals.
Overall, the authors analyzed cases of FG at a total of hospitals.