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fifth and sixth decades of life, FG is not a gender- or agespecific disease.4,6 In fact, emerging research has concluded that when women develop FG, the clinical course is often protracted and more critical than in men. As a result, it can manifest as prolonged hospital stays, increased ventilator times, and dependence on dialysis during expanded recovery.3,6 Etiology

Generally arising from the gastrointestinal, genitourinary, and integumentary systems, the spectrum of FG causes is vast, ranging from idiopathic to iatrogenic surgical events.1,2,7-9,11-13 Frequently cited etiologies include appendicitis, diverticulitis, colorectal cancer, complicated nephrolithiasis and its sequelae, and urogenital and perineal abscesses.9,11,14 Trauma from indwelling catheter placement, rectal or prostate biopsies, diathermy for genital warts, constriction rings for erectile dysfunction, coital injury, genital trauma, hemorrhoidectomy, and hysterectomies have also been implicated.9,11,14 Of note, the clinical course of FG is dictated not only by host immune defense and the route of opportunistic infection but also by the organism involved.8 Pathogenesis

Pathogenesis of FG is multifactorial and commonly begins as cellulitis or an untreated purulent infection that progresses through enzymatic and platelet reactions, eventually culminating in microthrombotic changes within local subcutaneous veins.2,4,8 This in turn causes an alteration in the delivery of oxygen to the tissues, which allows for development of irreversible necrosis.2,4 FG is able to progress rapidly in these conditions in which ischemic changes result from microvascular constriction in susceptible disease states.4 FG is frequently a polymicrobial infection, and the microbes most commonly implicated in its development are Escherichia coli and Bacteroides, and clostridial, staphylococcal, and streptococcal species.2,4,7,8 Streptococcal and staphylococcal species are known to produce enzymatic reactions that alter host immunity, resulting in degradation of the host’s connective tissue structures and a more rapidly progressive disease state.8,10 Anaerobic bacteria, though more rare than their aerobic counterparts, thrive in this oxygen-deficient environment and create a synergistic effect that perpetuates the fulminant progression of the disease.10,11 These anaerobic organisms subsequently release their own characteristic enzymes that increase intravascular coagulation, resulting in progressive ischemia.9,10,11 As the infectious process progresses from the initial site of inoculation, FG classically traverses the planes of Colles fascia and the perineum with predictable ease and may ultimately affect the distal thighs and abdominal wall.2,4 Infrequent cases

of extension to the clavicles have been reported in instances when the disease was able to progress undetected until late stages.2,9,11,13 The testicles are often spared in the progression of necrosis due to a separate blood supply from the aorta.9,11 Signs and Symptoms

Associated with a myriad of symptoms, FG can easily remain clinically elusive. It has been reported that patients with FG can present early in the course of the disease with nonspecific symptoms of mild, focal swelling and pain in the groin and perineum.7,8,15 Systemic symptoms of fever and nausea are often lacking in early disease. In late stages, pain often becomes more pronounced; men may complain of swelling, and patients may report systemic symptoms such as fever.7,8,10,15 However, the systemic symptoms are unreliable, with fever being present in 20% of confirmed cases of FG. Its absence therefore does little to rule out early- through late-stage disease.15 Physical Examination

Early stages of FG can begin as a focal area of erythema within the perineum and groin with often limited systemic response. Although tachycardia has been observed, findings most consistent with uncomplicated cellulitis typically are present.7,8,9-11,16 As the disease progresses, it becomes more consistent with expanding erythema, hemorrhagic bullae overlying tense skin with palpable crepitus (when gasproducing organisms are present), pain out of proportion to clinical findings or anesthesia, fever, and signs of septic shock including hypotension and tachycardia (Figures 1A, 1B).2,7-9,13 As with symptoms of FG, these physical examination findings TABLE 1. Risk Factors for Fournier Gangrene1,7,9,15 Advanced age


Alcohol abuse

Lymphoproliferative diseases

Chronic steroid use


Cytotoxic drugs


Defective phagocytosis

Obesity (BMI >30 kg/m2)

Diabetes mellitus

Poor hygiene

Diabetic neuropathy

Tobacco use


Vascular compromise • THE CLINICAL ADVISOR • JUNE 2019 21

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June 2019 Clinical Advisor  

June 2019 Clinical Advisor