MedStar Georgetown University Hospital Baltimore, MD
Urwah Ahmad, MBBS1, Mishal Ejaz, MBBS1, Rabin Shrestha, MD2 1MedStar Georgetown University Hospital, Baltimore, MD; 2MedStar Franklin Square Medical Center, Baltimore, MD Introduction: Cirrhosis causes immune dysfunction, impairing cell-mediated immunity. This predisposes patients to opportunistic infections such as Cryptococcus neoformans. While cryptococcosis is linked to HIV/AIDS, cirrhosis is an independent risk factor. Diagnosis is often delayed due to nonspecific symptoms and overlap with cirrhosis-related complications. Early recognition is critical as cryptococcal infection in cirrhotics often leads to fulminant, disseminated disease with poor outcomes.
Case Description/
Methods: A 53-year-old man with poorly controlled type 2 diabetes mellitus (HbA1c 8.2%) and alcoholic cirrhosis with paraesophageal varices and chronic thrombocytopenia (~40,000/µL) presented with one week of generalized pain and abdominal discomfort after a fall. On arrival, he was afebrile, tachycardic, and hypertensive. Labs showed sodium 128 mmol/L, total bilirubin 7.8 mg/dL, direct bilirubin 2.85 mg/dL, AST 1038 U/L, ALT 240 U/L, INR 1.8, albumin 2.6 g/dL, lactic acid 3.3 mmol/L, CPK 24,177 U/L, and ammonia 58 µmol/L. CBC revealed thrombocytopenia and 32% bands without leukocytosis.
Right upper quadrant ultrasound showed gallbladder wall thickening without cholecystitis. MRI with MRCP confirmed advanced cirrhosis with portal hypertension and paraesophageal varices, but no biliary obstruction or thrombosis. Empiric vancomycin and piperacillin-tazobactam were started.
By hospital day four, the patient developed acute encephalopathy and agonal breathing requiring intubation and ICU transfer. He became hypotensive needing vasopressors, developed metabolic acidosis (pH 7.14), hyperkalemia (K 7.3 mmol/L), and renal failure needing continuous renal replacement therapy. Hemoglobin dropped from 10 to 5.1 g/dL, INR rose to 3.4, fibrinogen decreased to 120 mg/dL, and ammonia went up to 535 µmol/L. Blood cultures drawn on admission grew yeast after 72 hours. Micafungin was started, but clinical improvement was minimal. Repeat cultures grew Cryptococcus. Micafungin was stopped, and amphotericin B was initiated, leading to clinical improvement. Discussion: Cryptococcosis in cirrhosis is often underdiagnosed due to nonspecific presentations mimicking hepatic encephalopathy or bacterial sepsis. Coagulopathy complicates lumbar puncture and delays CNS evaluation. Micafungin lacks activity against Cryptococcus, highlighting the need for early use of appropriate antifungals like amphotericin B in high-risk cirrhotic patients with unexplained decompensation.
Disclosures: Urwah Ahmad indicated no relevant financial relationships. Mishal Ejaz indicated no relevant financial relationships. Rabin Shrestha indicated no relevant financial relationships.
Urwah Ahmad, MBBS1, Mishal Ejaz, MBBS1, Rabin Shrestha, MD2. P5621 - Fulminant Cryptococcal Fungemia and Multi-Organ Failure in a Cirrhotic Patient: A Diagnostic Challenge, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.