Hepatology

A

• Acute Cholangitis - Antibiotics and ERCP

  Diagnose with fever, jaundice, and cholestasis plus imaging; start broad spectrum antibiotics and arrange early biliary drainage with ERCP based on severity.
• Acute Cholangitis — Antibiotics and Urgent ERCP per Tokyo Guidelines

  Charcot triad (fever, jaundice, RUQ pain) ± hypotension/AMS suggests cholangitis. Start broad-spectrum antibiotics and obtain urgent biliary decompression (ERCP) in moderate-to-severe cases per Tokyo Guidelines; correct coagulopathy and fluids.
• Acute Liver Failure - Initial Management

  Acute liver failure is severe acute hepatic injury with coagulopathy and hepatic encephalopathy in a patient without preexisting cirrhosis. Stabilize airway and glucose, identify acetaminophen and other treatable causes immediately, give N-acetylcysteine when indicated and often in early non-acetaminophen ALF, prevent cerebral edema, avoid unnecessary correction of INR, and contact a transplant center early.
• Acute Liver Failure — N‑Acetylcysteine, Cerebral Edema, and Transplant Criteria

  Rapid hepatic dysfunction with INR ≥1.5 and encephalopathy in a non‑cirrhotic patient. Start IV N‑acetylcysteine even in non‑acetaminophen cases; manage cerebral edema with head elevation and hypertonic saline; avoid hypoxia/hypotension. Apply King’s College criteria early for transplant referral; evaluate etiologies (acetaminophen, viral, autoimmune, ischemic, Wilson).
• Alcoholic Hepatitis - Severity and Steroids

  Alcohol-associated hepatitis is acute jaundice and hepatic inflammation after sustained heavy alcohol exposure, usually on a background of chronic liver disease. Exclude infection and alternative causes, assess severity with MELD and a validated alcohol-hepatitis score, provide aggressive nutrition and alcohol-use treatment, and consider corticosteroids only for severe disease without major contraindications, with early response reassessment.

C

• Cirrhotic Ascites - Initial Management

  New or worsening ascites in cirrhosis requires diagnostic paracentesis, assessment for spontaneous bacterial peritonitis and other precipitants, dietary sodium restriction, and individualized diuretic therapy with spironolactone and furosemide. Large-volume paracentesis is first-line for tense ascites, with albumin replacement after large fluid removal, and refractory ascites should prompt transplant and TIPS evaluation.

D

• Drug Induced Liver Injury - Evaluation

  Drug-induced liver injury is a diagnosis of exclusion based on medication and supplement timing, liver-test pattern, competing etiologies, and improvement after withdrawal. Stop the suspected agent, calculate the R ratio to classify hepatocellular versus cholestatic injury, screen for viral, autoimmune, ischemic, and biliary causes, identify Hy’s law or acute liver failure, and avoid rechallenge unless a specialist determines the benefit clearly outweighs risk.

H

• HBV Reactivation - Screening and Prophylaxis

  HBV reactivation occurs when immunosuppression permits renewed viral replication in a patient with current or prior hepatitis B infection. Screen with HBsAg, total anti-HBc, and anti-HBs before significant immunosuppression, stratify by both serology and regimen, give entecavir or tenofovir prophylaxis for high-risk exposures such as B-cell-depleting therapy, and continue monitoring after immunosuppression ends.
• Hepatic Encephalopathy — Acute Management

  Overt hepatic encephalopathy is a clinical diagnosis of brain dysfunction in advanced liver disease or portosystemic shunting after competing causes of altered mental status are considered. Acute management focuses on airway safety, rapid identification and correction of precipitants, lactulose titrated to soft bowel movements, and rifaximin for recurrent or inadequately controlled disease.
• Hepatic Encephalopathy — Lactulose/Rifaximin, Precipitant Search, and Secondary Prevention

  Neuropsychiatric dysfunction in cirrhosis. Exclude alternative causes, correct precipitants (GI bleed, infection, dehydration), and treat with lactulose titrated to 2–3 soft stools/day plus rifaximin for prevention of recurrence; counsel on protein intake and avoid sedatives.
• Hepatorenal Syndrome - Acute Management

  Hepatorenal syndrome-AKI is functional kidney failure in advanced cirrhosis caused by severe circulatory dysfunction after other causes of AKI have been excluded and volume status addressed. Stop nephrotoxins and diuretics, treat infection and bleeding, give albumin as indicated, and use vasoconstrictor therapy, preferably terlipressin where appropriate, while pursuing liver transplantation.

O

• Obstructive Jaundice - Initial Workup

  Obstructive jaundice is conjugated hyperbilirubinemia caused by impaired bile drainage and requires rapid distinction between uncomplicated obstruction and acute cholangitis. Use liver tests and right-upper-quadrant ultrasound first, define anatomy with MRCP or EUS when needed, reserve ERCP primarily for therapeutic drainage or tissue acquisition, and urgently decompress infected obstruction.

S

• Spontaneous Bacterial Peritonitis - Prevention and Prophylaxis

  SBP prophylaxis is reserved for cirrhosis patients at clearly elevated infection risk, particularly after a prior SBP episode, during acute upper GI bleeding, and in selected advanced cirrhosis with low-protein ascites plus renal or hepatic dysfunction. Choose an evidence-based regimen, reassess ongoing indication, and balance benefit against antimicrobial resistance, C. difficile, and drug toxicity.
• Spontaneous Bacterial Peritonitis — Diagnosis & Treatment

  Spontaneous bacterial peritonitis is infection of ascitic fluid without an evident surgically treatable intra-abdominal source, most often in advanced cirrhosis. Diagnosis requires prompt diagnostic paracentesis and is established when the ascitic polymorphonuclear leukocyte count is at least 250 cells/mm3, regardless of whether culture is positive. Treatment should begin immediately with an appropriate third-generation cephalosporin or other locally active regimen, with intravenous albumin for patients at
• Spontaneous Bacterial Peritonitis — Diagnostic Tap, Albumin, and Third-Generation Cephalosporins

  In any cirrhotic with ascites and abdominal pain or encephalopathy, perform diagnostic paracentesis; PMN ≥250 cells/mm³ confirms SBP. Start cefotaxime or ceftriaxone promptly and give albumin on day 1 and 3 to prevent renal failure; begin long-term prophylaxis after recovery when indicated.
• Spontaneous Bacterial Peritonitis — Diagnostic Tap, Ceftriaxone, and Albumin

  In cirrhosis with ascites, perform immediate diagnostic paracentesis. Treat SBP when PMN ≥250/µL with IV third-generation cephalosporin and give IV albumin (day 1: 1.5 g/kg; day 3: 1.0 g/kg) to prevent renal failure. Start lifelong prophylaxis after an episode.

V

• Variceal Upper GI Bleeding — Acute Management

  Acute variceal upper gastrointestinal bleeding is a portal-hypertension emergency, most often due to ruptured esophageal or gastric varices in cirrhosis. Management begins before endoscopy with airway and hemodynamic stabilization, a restrictive red-cell transfusion strategy in most patients, vasoactive therapy, and short-course antibiotic prophylaxis. Upper endoscopy should follow resuscitation promptly, generally within 12 hours, with endoscopic variceal ligation for esophageal varices. Patients at high r
• Variceal Upper GI Bleeding — Octreotide, Antibiotics, Band Ligation, and TIPS

  In cirrhosis with hematemesis/melena, start vasoactive therapy (octreotide) and prophylactic antibiotics immediately, resuscitate with restrictive transfusion, and perform early endoscopy for band ligation. Use balloon tamponade as a bridge if uncontrollable hemorrhage and consider early TIPS for high‑risk or refractory bleeding.
• Variceal Upper GI Bleeding — Vasoactives, Antibiotics, and Band Ligation

  Portal hypertensive bleeding in cirrhosis requires early vasoactive drugs, prophylactic antibiotics, and endoscopic band ligation; use restrictive transfusion strategy and consider TIPS for refractory or high‑risk cases.

W

• Wilson Disease - Clues in Acute Liver Failure

  Wilson disease should be suspected in acute liver failure in a young patient with Coombs-negative hemolytic anemia, disproportionately low alkaline phosphatase relative to bilirubin, and other copper-related clues. Send targeted copper studies without delaying transfer, use plasma exchange as a possible bridge in severe Wilsonian crisis, and pursue emergency liver transplantation because chelation does not rescue Wilson-associated acute liver failure reliably.