Discussion

Chronic alcohol use can disrupt host defense through several complementary mechanisms. Alcohol metabolism generates reactive oxygen species (ROS), which can activate nuclear factor kappa B (NF-κB) and promote inflammatory signaling involved in alcohol-associated liver injury [5]. Chronic alcohol exposure can also disturb the balance between proinflammatory and anti-inflammatory responses within the innate immune system. It impairs neutrophil chemotaxis, phagocytosis, and oxidative burst activity, reducing the ability to contain bacterial infection [5]. Adaptive immunity may also be affected through reduced lymphocyte number and altered dendritic-cell activation of T cells [5]. In addition, chronic alcohol use can alter the intestinal microbiome, favor gram-negative bacterial overgrowth, and impair wound healing through disruption of inflammatory-cell function, collagen production, angiogenesis, and re-epithelialization [5,6].

These mechanisms are clinically relevant to this case because the patient developed a severe enteric soft tissue infection in the setting of prolonged alcohol use, hepatic dysfunction, and possible nutritional compromise. He had thrombocytopenia, hypoalbuminemia, hyperbilirubinemia, elevated transaminases, hepatomegaly, and hepatic steatosis, supporting chronic alcohol-associated hepatic injury. Testing did not identify diabetes mellitus, human immunodeficiency virus infection, the evaluated sexually transmitted infections, or the tested autoimmune conditions as alternative predisposing factors. Although these findings do not establish that alcohol use caused the infection, they support chronic alcohol use disorder as a plausible contributor to impaired host defense and disease severity in this patient.

Syncope was an unusual presenting complaint but was not truly isolated, because the patient also had abdominal pain, tachycardia, leukocytosis, and other evidence of systemic illness. No perineal or genital complaint was documented. Sepsis-associated syncope may result from transient cerebral hypoperfusion related to vasodilation, relative intravascular depletion, or autonomic dysfunction. In this patient, neurologic and cardiac evaluation did not identify an alternative cause, although alcohol intoxication could not be excluded with certainty because a serum ethanol concentration and exact time of last alcohol use were unavailable. Reviews describe early Fournier gangrene presenting with nonspecific pain, systemic toxicity, or minimal local findings before overt tissue changes become apparent [1,9]. CT was therefore critical in identifying perineal soft tissue gas and prompting surgical intervention. Because the detailed initial perineal examination and exact ED-to-CT and CT-to-OR intervals were unavailable, this report cannot determine whether local findings were absent or undocumented or whether a measurable diagnostic delay occurred.

Wound cultures grew K. oxytoca and R. ornithinolytica. _Klebsiella _species are recognized aerobic pathogens in Fournier gangrene [3], whereas R. ornithinolytica is not among the organisms commonly emphasized in the major reviews cited here and was therefore an unusual isolate in this report. Both organisms are compatible with an enteric source arising from the perianal infection. Surgical drainage, initial broad-spectrum antimicrobial therapy, and subsequent culture-directed treatment were followed by normalization of the WBC and platelet counts and stabilization before discharge.

In our patient, we hypothesize that chronic alcohol use was a probable predisposing factor for the development of Fournier gangrene. Although diabetes mellitus is the most commonly reported risk factor, chronic alcohol use disorder has also been identified as an independent contributor to Fournier gangrene through its effects on immune function, nutritional status, and hepatic dysfunction. Reviews of Fournier gangrene consistently identify alcohol misuse, malnutrition, diabetes mellitus, and immunosuppression as important predisposing conditions, supporting chronic alcohol use disorder as a clinically meaningful risk factor in this patient [10]. In a retrospective analysis of 25 patients with Fournier gangrene, alcohol misuse was recognized as one of the major predisposing conditions associated with disease development [11]. Several case reports have also described Fournier gangrene occurring in patients with severe alcohol-associated liver disease. For example, Zenda et al. reported Fournier gangrene in a patient with severe alcoholic hepatitis and concluded that the infection likely developed in the setting of impaired immunologic defenses caused by chronic alcohol consumption and advanced liver dysfunction [12]. In the present case, evaluation did not identify diabetes mellitus, human immunodeficiency virus infection, the evaluated sexually transmitted infections, or the tested autoimmune conditions as alternative predisposing factors. Together with the patient's prolonged alcohol use history and evidence of alcohol-associated liver injury, these findings support chronic alcohol use disorder as a plausible major contributor to the development of Fournier gangrene, although causation cannot be established from a single case.

This report is limited by the retrospective availability of clinical records. Detailed initial perineal, genital, and digital rectal examination findings; exact ED-to-CT and CT-to-OR intervals; serum lactate and C-reactive protein values; complete inputs for retrospective severity scores; detailed examination-under-anesthesia and debridement findings; postoperative wound management; reconstruction; serum ethanol and orthostatic data; and long-term surgical follow-up were unavailable. Consequently, the precise mechanism of syncope and the relative contribution of chronic alcohol use remain probable rather than proven.