S5559 From Triad of Trouble to Recovery: Plasmapheresis as Lifeline in G6PD-Mediated Crisis and AKI Triggered by Viral Hepatitis

Introduction: Hepatitis A in rare cases can cause acalculous cholecystitis and accompanying G6PD deficiency can precipitate hemolysis under stress, risking severe jaundice and acute kidney injury. The case describes a male with this complex interplay managed ultimately with therapeutic plasmapheresis. Case Description/Methods: This is case of 23-year man, referred from a peripheral center for persistent jaundice after empiric treatment with broad-spectrum antibiotics (Ceftriaxone, metronidazole, ciprofloxacin) and supportive care for acalculous cholecystitis (based on USG). He had 15-day history of fever, severe epigastric pain, non-bilious emesis and 7 day progressive jaundice. Examination revealed epigastric tenderness without hepatosplenomegaly and nonpalpable gallbladder. No significant past medical history. Family history notable for death of 3 cousins attributed to jaundice. Initial workup revealed white blood cell count 13.9 × 10³/µL, total bilirubin 68.5 mg/dL, SGPT 849 IU/L, SGOT 199 IU/L, creatinine 1.8 mg/dL and urea 88 mg/dL. Serology confirmed acute hepatitis A and ruled out HIV, Leptospira and other hepatitis viruses. Antinuclear antibody and anti-smooth muscle antibodies titers were negative. Repeat labs showed anemia (Hb 5.1 g/dL), LDH 1496 IU/L, reticulocyte count 14%, and G6PD enzyme activity 2.19 U/g Hb, confirming deficiency. Imaging (USG computed tomography (CT) MRCP) showed gallbladder wall thickening with mild pericholecystic fluid indicating acalculous cholecystitis. Kidney function declined evidenced by rising creatinine(3.4 mg/dL) and urea(115 mg/dL). Urinalysis revealed bile pigments and red blood cells but subsequent one showed absence of bilirubin. Within a week he developed confusion and disorientation, raising concern for bilirubin encephalopathy and kernicterus. On admission, he was shifted to only Cefotaxime, ursodeoxycholic acid, rifaximin and supportive treatment. Following renal function decline, all antibiotics were discontinued. Three sessions of plasmapheresis were performed on consecutive days. Subsequently, patient regained full sensorium and orientation, with improved appetite and hepatic and renal parameters. (T. bilirubin 15 mg/dL creatinine 1.36 mg/dL urea 41 mg/dL). Discussion: Hemolysis due to G6PD deficiency along with hepatitis A can significantly elevate bilirubin levels risking precipitation of bile-cast nephropathy and neurologic injury. Delta bilirubin was brought back to normal in days as compared to months naturally. The heroic return of patient to baseline emphasizes on the role of plasmapheresis as a bridge to recovery when conventional therapies fail.