Ramadi Satryo Wicaksono
Department of Internal Medicine, Bangil Regional General Hospital, Pasuruan, Indonesia

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Alcohol-Associated Decompensated Cirrhosis with Ascites and Suspected Hepatic Encephalopathy: A Case Report Johanes Aprilius Falerio Kristijanto; Cicilia Diah Puspitasari; Budi Santoso; Ramadi Satryo Wicaksono; Farida Anggraini Soetedjo; Nur Khamidah
Green Medical Journal Vol 8 No 2 (2026): Green Medical Journal
Publisher : Fakultas Kedokteran Universitas Muslim Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33096/anf65h57

Abstract

Introduction: Alcohol-associated cirrhosis is a preventable cause of advanced liver disease, yet it is frequently first recognized after decompensation. This case underscores the diagnostic value of integrating clinical decompensating features with non-invasive fibrosis indices and ultrasonography in a resource-limited setting. Case Summary: A 51-year-old man with a 20-year history of daily alcohol intake presented with progressive abdominal distension, bilateral leg edema, right hypochondrial pain, nausea, jaundice, weight loss, and recent behavioral change. He had previous hematemesis and melena but had declined esophagogastroduodenoscopy. Examination revealed pallor, scleral icterus, ascites, right hypochondrial tenderness, and peripheral edema. Investigations showed anemia, thrombocytopenia, AST-predominant transaminitis, hypoalbuminemia, mild hyponatremia, and non-reactive HBsAg. APRI and FIB-4 were markedly elevated, and ultrasonography demonstrated a shrunken, coarse, irregular liver with ascites, supporting a diagnosis of presumed alcohol-associated decompensated cirrhosis. Behavioral changes without impaired consciousness were clinically suggestive of early hepatic encephalopathy; however, covert hepatic encephalopathy could not be formally confirmed because psychometric testing was not available. Discussion: Ascites, jaundice, cytopenia, hypoalbuminemia, and neuropsychiatric change indicated advanced decompensation, while suspected portal hypertension remained incompletely characterized because endoscopy was unavailable. Management included dietary sodium and fluid restriction, nutritional support, large-volume paracentesis, albumin infusion, empiric antibiotic therapy, acid suppression, ursodeoxycholic acid, diuretic therapy, lactulose, and a non-selective beta-blocker. Conclusion: This case emphasizes early alcohol-use assessment, abstinence-centered care, timely endoscopic risk stratification, and complication-directed management to reduce preventable deterioration in alcohol-associated decompensated cirrhosis.