**4. Diagnosis**

*Pathogenic Bacteria*

**3. Classification**

The acute necrotizing inflammatory process initially affects the deep subcutaneous tissue and the fascia. The most superficial tissues and the skin are affected secondarily, due to vascular injury, thrombosis, and ischemia—resulting from the action of pro-inflammatory cytokines, proteinases, and endothelin. The destruction of subcutaneous nerves occurs in advanced stages. Initially described as a disease of unknown cause, it is now known that an underlying pathological process can be found in most cases of Fournier's gangrene; nonetheless, in a significant number of patients, the cause cannot be determined [15–17]. Therefore, a careful investigation can indicate the point of entry, which is located primarily in the digestive tract, in cutaneous affections, in the urogenital tract, or in cutaneous affections [18]. Eke et al. [16], in 2000, published a series of 1726 cases published cutaneous conditions accounted for 24% of the cases. The agents most associated with NF are group A beta-hemolytic *Streptococcus* and *Staphylococcus aureus*. However, other pathogens have already been linked to this disease, namely, *Clostridium perfringens*, *Peptostreptococcus*, Enterobacteriaceae, Proteus, *Pseudomonas*, and *Klebsiella* [16]. The most commonly observed comorbidity is diabetes mellitus, with a prevalence of 40–60%. Other common comorbidities include hepatic cirrhosis, immunodeficiencies, heart failure, systemic lupus erythematosus, obesity, alcoholism, hypertension, Addison's disease, and peripheral vascular disease. However, NF can

There are two classifications for necrotizing fasciitis. The US Food and Drug Administration (FDA) classifies NF according to its microbiological characteristics: type I, aerobic/anaerobic polymicrobial pattern (streptococci, staphylococci, enterococci, *Bacteroides*); type II, only one agent (*S. aureus* or more commonly group A beta-hemolytic *Streptococcus*) and less aggressive lesions, accounting for 10–15% of the cases; and type III, gastric myonecrosis and necrotizing fasciitis

Féres et al. [21] proposed an anatomic classification. This classification considers two relevant criteria: extension of the necrosis area and correlated it with mortality; these authors defined four groups (increasing mortality), in which group I presented a 12.5% rate, while the mortality rate in group IV was 68.75% (**Table 1**).

*Anatomical classification of the necrosis area and correlation with mortality in Fournier gangrene. Féres* 

present in healthy individuals, without comorbidities [19].

caused by *Clostridium perfringens* (less than 5% of the cases) [20].

**2. Etiology**

**148**

**Table 1.**

*et al. [21].*

The diagnosis is eminently clinical and corroborated by surgical findings, which include low adherence of the subcutaneous tissue, observed to the surgical manipulation, absence of bleeding, and liquefaction of the subcutaneous fat. Due to its severity and speed of evolution, Fournier's gangrene is an emergency. The clinical diagnosis must be suspected of the classic triad, pain, edema, and erythema with fever/tachycardia as soon as possible so that early treatment can be initiated. Necrotizing fasciitis could evolve rapidly with necrotic tissues and hemorrhagic blisters [19]. Patients may present laboratory abnormalities such as elevated serum urea (more than 18 mg/dl), serum creatinine (more than 1.2 mg/dl), leukocytosis (>20,000 WBC/mm3 ), and CPK (more than 600 μ/l) [22].

Furthermore, imaging exams may also be used, such as radiographs (subcutaneous gas formation—low sensitivity and specificity), ultrasonography (has little practical use), computed tomography (lesion extension and gas formation), and magnetic resonance imaging (more accurate but more costly) [23]. CT provides additional information, such as asymmetric thickening of the fascia and changes in subcutaneous fat, as well as the presence of gas and abscesses. MRI, on the other hand, is considered superior to other imaging methods. It has high sensitivity and allows to define the area of necrosis of the fascia and to schedule the surgical procedure. The absence of changes in the deep fascia practically excludes in the diagnosis. It is worth mentioning that the critical condition of the patient often makes transportation impossible to perform the exam, limiting its use.

Culturing the debrided tissue is important in order to guide antibiotic therapy [19]. Biopsy of the fascia is considered the gold standard for diagnosis and should be performed in all patients during debridement, even in those whose macroscopic appearance is normal.
