Work overview

Section 02 of 04

Case presentation

Atypical Presentation of Fournier Gangrene as Syncope in a Patient With Chronic Alcohol Use Disorder: A Case Report

Anvitha Kambham, Brendan Masi, Abraham E Libman, Himanshukumar Nayak, and Roxana Lazarescu · 2026

Contents

Section 02 of 04

  1. 01Introduction
  2. 02Case presentation
  3. 03Discussion
  4. 04Conclusions
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Work overview

Section 2 of 4

Case presentation

Anvitha Kambham, Brendan Masi, Abraham E Libman, Himanshukumar Nayak, and Roxana Lazarescu · about 6 minutes

A 63-year-old man with a history of AUD presented to the emergency department (ED) after losing consciousness while standing in a store. He struck his head, reportedly lost consciousness for approximately two minutes, and had bowel incontinence. He reported left-sided abdominal and right upper quadrant pain but denied chest pain, fever, chills, palpitations, shortness of breath, nausea, vomiting, urinary incontinence, tongue biting, or other seizure-like activity. No perineal or genital complaint was documented at presentation. He appeared jaundiced and reported drinking approximately one to two eight-ounce cups of whisky almost every day for 30 years.

In the ED, he met systemic inflammatory response syndrome (SIRS) criteria based on a heart rate greater than 90 beats per minute (bpm) and a white blood cell (WBC) count greater than 12,000/mm3. He was afebrile, had a heart rate of 132 bpm, and had a WBC count of 12.7 × 103/µL. A detailed initial examination of the perineal and genital regions and the findings of any digital rectal examination could not be confirmed from the records available to the authors. Other admission laboratory findings are presented in Table 1. Urinalysis and urine culture were unremarkable. Empiric clindamycin, piperacillin-tazobactam, and vancomycin were initiated. He also received intravenous hydration, thiamine, folic acid, and electrolyte supplementation as needed.

Lab | Patient values on admission | Patient values on discharge | Normal range
WBC | 12.7 ↑ | 8.5 | 4.5–11.0 x 103/µL
RBC count | 4.26 ↓ | — | Male: 4.3–5.9 x 106/µL
Hemoglobin | 13.2 | — | Male: 13.5–17.5 g/dL
Hematocrit | 39.1 | — | Male: 41–53%
MCV | 91.8 | — | 80–100 fL
MCH | 31.0 | — | 26–34 pg
MCHC | 33.8 | — | 32–36 g/dL
RDW | 12.7 | — | 11.5–14.5%
Platelet count | 52 ↓ | 384 | 150–400 x 103/µL
Neutrophils | 84.6 ↑ | 59.9 | 54–62%
Lymphocytes | 6.8 ↓ | — | 25–33%
Monocytes | 5.7 | — | 3–7%
Eosinophils | 0.0 ↓ | — | 1–3%
Basophils | 0.3 | — | 0–0.75%
Immature granulocytes | 2.6 ↑ | — | 0–0.5%
Acetaminophen level | <2.0 | — | Therapeutic: 10–30 µg/mL
Calcium | 7.9 ↓ | 8.5 | 8.4–10.2 mg/dL
Albumin | 2.5 ↓ | 2.7 ↓ | 3.5–5.0 g/dL
Total protein | 5.8 ↓ | 6.8 | 6.0–8.0 g/dL
Sodium | 131 ↓ | 139 | 136–145 mEq/L
Potassium | 3.3 ↓ | 3.9 | 3.5–5.0 mEq/L
Chloride | 92 ↓ | — | 95–105 mEq/L
CO2 | 31 | — | 23–30 mEq/L
BUN | 17 | — | 7–18 mg/dL
Glucose | 132 | 109 | <140 mg/dL, non-fasting
Total bilirubin | 12.9 ↑ | 3.7 ↑ | 0.1–1.0 mg/dL
Direct bilirubin | 10.58 ↑ | 3.27 ↑ | 0.0–0.3 mg/dL
Alkaline phosphatase | 242 ↑ | 597 ↑ | 45–115 U/L
AST | 467 ↑ | 276 ↑ | 10–40 U/L
ALT | 294 ↑ | 292 ↑ | 7–56 U/L
Creatinine | 1.59 ↑ | — | Male: 0.6–1.2 mg/dL
eGFR | 48 ↓ | — | >60 mL/min/1.73 m2

Emergent imaging was obtained. Head CT showed no acute intracranial abnormality, and chest radiography showed no acute pulmonary process. CT of the abdomen and pelvis showed hepatomegaly with diffuse low hepatic attenuation consistent with hepatic steatosis; the liver measured 19.9 cm (Figure 1).

Figure 1: Computed tomography of abdomen and pelvis without contrast.Computed tomography (CT) of the abdomen and pelvis without contrast showing hepatomegaly with diffuse low hepatic attenuation consistent with hepatic steatosis; the liver measured 19.9 cm (red arrow).

Figure 1: Computed tomography of abdomen and pelvis without contrast.Computed tomography (CT) of the abdomen and pelvis without contrast showing hepatomegaly with diffuse low hepatic attenuation consistent with hepatic steatosis; the liver measured 19.9 cm (red arrow).

Axial and sagittal images also demonstrated soft tissue gas surrounding the anorectal junction and extending into the perineum, concerning for Fournier gangrene (Figures 2, 3). The exact intervals from ED arrival to CT and from CT to the operating room (OR) could not be confirmed from the records available to the authors.

Figure 2: Axial computed tomography of the abdomen and pelvis.Axial computed tomography (CT) image of the abdomen and pelvis showing soft tissue gas surrounding the anorectal junction and extending into the perineum (red box), concerning for Fournier gangrene.

Figure 2: Axial computed tomography of the abdomen and pelvis.Axial computed tomography (CT) image of the abdomen and pelvis showing soft tissue gas surrounding the anorectal junction and extending into the perineum (red box), concerning for Fournier gangrene.

Figure 3: Sagittal computed tomography of the abdomen and pelvis.Sagittal computed tomography (CT) image of the abdomen and pelvis showing soft tissue gas extending into the perineum (red box), concerning for Fournier gangrene.

Figure 3: Sagittal computed tomography of the abdomen and pelvis.Sagittal computed tomography (CT) image of the abdomen and pelvis showing soft tissue gas extending into the perineum (red box), concerning for Fournier gangrene.

The patient underwent incision and drainage of a perianal abscess, and serosanguineous purulent fluid was sent for culture. The operative information available to the authors did not include detailed findings from examination under anesthesia, the extent or depth of necrotic tissue, the extent of tissue excision or debridement, or whether reconstruction was required. Cultures grew Klebsiella oxytoca (K. oxytoca) and _Raoultella ornithinolytica _(R. ornithinolytica), and Gram staining showed rare Gram-positive cocci in pairs. The infectious diseases and pharmacy teams recommended discontinuing the initial antimicrobial regimen and beginning ceftriaxone and metronidazole.

Neurology and cardiology were consulted to evaluate the syncopal episode. A 12-hour electroencephalogram (EEG) showed no seizure activity, carotid ultrasonography was unremarkable, and electrocardiography (ECG) showed sinus tachycardia. Echocardiography demonstrated a left ventricular ejection fraction (LVEF) of 55%-60% with grade 1 diastolic dysfunction. No primary neurologic or cardiac cause of syncope was identified. Sepsis-associated transient cerebral hypoperfusion related to vasodilation, relative intravascular depletion, or autonomic instability was considered the most likely explanation. However, a serum ethanol concentration, orthostatic vital signs, and the exact time of the patient’s last alcohol use could not be confirmed from the available records; therefore, alcohol intoxication could not be excluded with certainty.

The patient denied a history of anal intercourse or anal penetration. Testing for sexually transmitted infections (STIs), including HIV, syphilis, chlamydia, and gonorrhea, was negative. Hemoglobin A1c was 6.0%. Antinuclear antibody (ANA) testing with reflex to titer and pattern and mitochondrial antibody testing were negative. This evaluation did not identify diabetes mellitus, HIV infection, the tested STIs, or the tested autoimmune conditions as alternative predisposing factors.

At discharge, the WBC count and platelet count had normalized. Liver enzymes, total and direct bilirubin, and alkaline phosphatase remained elevated, as shown in Table 1. The patient was afebrile with a heart rate of 84 bpm, and the remaining documented vital signs were stable. The records available to the authors did not include a detailed wound assessment at discharge, the outpatient wound-care plan, whether repeat debridement or reconstruction was required, or subsequent surgical follow-up. The patient was discharged with planned hepatology follow-up and resources for alcohol cessation. Longer-term clinical and wound outcomes were unavailable.