Diagnosis: Advanced Cirrhosis with Decompensation (Likely Alcoholic Liver Disease)
This patient presents with severe jaundice (total bilirubin 9.7 mg/dL), profound hypoalbuminemia (2.3 g/dL), thrombocytopenia (81 K/mm³), macrocytic anemia (MCV 111 fL), and elevated ammonia (71 µmol/L)—a constellation strongly indicating decompensated cirrhosis with portal hypertension. 1
Laboratory Pattern Analysis
The pattern is cholestatic with hepatocellular dysfunction:
Markedly elevated total bilirubin (9.7 mg/dL) with disproportionately elevated alkaline phosphatase (251 IU/L) relative to transaminases (AST 34, ALT 19) indicates cholestatic injury superimposed on chronic liver disease. 1, 2
The AST/ALT ratio of 1.8 strongly suggests alcoholic liver disease as the underlying etiology, as ratios >1.5-2.0 are characteristic of alcohol-related liver injury. 1
Severe hypoalbuminemia (2.3 g/dL) and low total protein (4.7 g/dL) reflect profound synthetic dysfunction, indicating advanced cirrhosis rather than acute hepatitis. 1
Thrombocytopenia (81 K/mm³) and macrocytic anemia (MCV 111 fL) are hallmarks of portal hypertension with hypersplenism and chronic alcohol use. 1
Critical Diagnostic Considerations
The relatively normal transaminases (AST 34, ALT 19) despite severe jaundice exclude acute hepatitis or acute liver failure and point toward chronic cholestatic liver disease with decompensation. 1, 2
Elevated ammonia (71 µmol/L) in the setting of severe hypoalbuminemia and jaundice suggests hepatic encephalopathy risk, though the lab note correctly cautions that ammonia levels correlate poorly with clinical encephalopathy severity. 1
The metabolic alkalosis (CO₂ 34 mmol/L) with hypokalemia (3.4 mmol/L) likely reflects diuretic use or contraction alkalosis from ascites management. 1
Hypocalcemia (7.9 mg/dL) is expected given severe hypoalbuminemia—corrected calcium is likely normal, but ionized calcium should be checked if symptomatic. 1
Immediate Diagnostic Workup
Order abdominal ultrasound within 24-48 hours to:
- Assess for cirrhotic liver morphology (nodular surface, caudate lobe hypertrophy)
- Evaluate for portal hypertension (splenomegaly, ascites, portal vein patency)
- Exclude biliary obstruction (though unlikely given the lab pattern)
- Screen for hepatocellular carcinoma 1, 3
Complete the hepatitis and autoimmune workup:
- Hepatitis B surface antigen, hepatitis B core antibody, hepatitis C antibody
- Antinuclear antibodies (ANA), anti-smooth muscle antibodies (anti-SMA)
- Serum ceruloplasmin and 24-hour urinary copper (Wilson's disease can present with acute-on-chronic liver failure)
- Iron studies and ferritin (hemochromatosis) 1, 2
Obtain prothrombin time/INR immediately to assess coagulopathy severity and calculate prognostic scores (MELD, Child-Pugh). 1
Check fractionated bilirubin (direct/indirect) to confirm conjugated hyperbilirubinemia, which is expected in cholestatic cirrhosis. 3, 2
Obtain detailed alcohol history using validated tools (AUDIT questionnaire) and consider urine or hair ethyl glucuronide (EtG) testing to objectively confirm recent alcohol use. 1
Severity Assessment and Prognostication
Calculate the MELD score using bilirubin (9.7 mg/dL), creatinine (0.62 mg/dL), and INR (pending) to stratify mortality risk and transplant priority. 1
Calculate the Child-Pugh score incorporating bilirubin, albumin, INR, presence of ascites, and encephalopathy grade to classify cirrhosis severity (Class A/B/C). 1
If alcoholic hepatitis is suspected (recent heavy drinking, fever, leukocytosis), calculate the Maddrey Discriminant Function: 4.6 × (PT - control PT) + bilirubin (mg/dL). A score ≥32 indicates severe disease requiring corticosteroid consideration. 1
Management Priorities
Initiate aggressive nutritional support:
- High-protein diet (1.2-1.5 g/kg/day) unless encephalopathy worsens
- Thiamine 100 mg IV daily, folate 1 mg daily, multivitamin supplementation
- Screen for fat-soluble vitamin deficiencies (A, D, E, K) given cholestasis 1
Correct electrolyte abnormalities:
- Replete potassium to >4.0 mmol/L (target 4.0-4.5 mmol/L)
- Monitor for hypomagnesemia and hypophosphatemia (common in alcoholic liver disease)
- Correct hypocalcemia if ionized calcium is low or patient is symptomatic 1
Manage complications of portal hypertension:
- Initiate lactulose 15-30 mL PO TID if any signs of encephalopathy develop
- Consider rifaximin 550 mg PO BID as adjunct to lactulose for encephalopathy prophylaxis
- Screen for esophageal varices with upper endoscopy if not previously done
- Initiate non-selective beta-blocker (propranolol or carvedilol) for primary variceal prophylaxis if large varices present 1
Address ascites if present:
- Sodium restriction (<2 g/day)
- Spironolactone 100 mg daily, titrate up to 400 mg daily
- Add furosemide 40 mg daily if inadequate response, titrate to 160 mg daily
- Monitor for spontaneous bacterial peritonitis if ascites present (diagnostic paracentesis) 1
Absolute alcohol abstinence is mandatory:
- Refer to addiction medicine or hepatology for alcohol use disorder treatment
- Consider pharmacotherapy (naltrexone, acamprosate, disulfiram)
- Arrange outpatient addiction counseling and support groups 1
Liver transplant evaluation should be initiated if MELD score ≥15 or Child-Pugh Class B/C, provided the patient achieves 6 months of documented abstinence. 1
Critical Pitfalls to Avoid
Do not attribute the jaundice to Gilbert's syndrome—the severe hypoalbuminemia, thrombocytopenia, and elevated alkaline phosphatase exclude benign unconjugated hyperbilirubinemia. 3, 2
Do not delay imaging to "wait and see"—biliary obstruction (malignancy, choledocholithiasis) must be excluded urgently given the cholestatic pattern, even though cirrhosis is more likely. 1, 3
Do not overlook Wilson's disease—though rare, acute-on-chronic Wilson's can present identically with jaundice, low albumin, hemolysis (elevated indirect bilirubin component), and Coombs-negative anemia. Check ceruloplasmin and urinary copper. 1
Do not assume ammonia elevation mandates lactulose—treat based on clinical encephalopathy grade, not ammonia level alone, as levels correlate poorly with symptoms. 1
Do not prescribe hepatotoxic medications—avoid NSAIDs (renal injury risk), acetaminophen >2 g/day, and any unnecessary drugs. Review all current medications for hepatotoxicity. 1
Do not miss spontaneous bacterial peritonitis—if ascites is present, perform diagnostic paracentesis immediately to exclude infection (absolute neutrophil count >250 cells/mm³). 1
Prognosis and Next Steps
The combination of bilirubin >9 mg/dL, albumin <2.5 g/dL, and thrombocytopenia indicates Child-Pugh Class C cirrhosis with 1-year mortality exceeding 50% without transplantation. 1
If alcoholic hepatitis is confirmed (requires liver biopsy via transjugular route given coagulopathy risk), corticosteroids (prednisolone 40 mg daily for 28 days) should be considered if Maddrey DF ≥32 and no contraindications (active infection, GI bleeding, renal failure). 1
Transjugular liver biopsy may be necessary if diagnostic uncertainty persists after serologic and imaging workup, particularly to differentiate alcoholic hepatitis from other causes or to assess for concurrent hepatocellular carcinoma. 1
Close monitoring is essential:
- Repeat liver chemistries, CBC, and INR every 2-3 days initially
- Daily weights and abdominal girth measurements if ascites present
- Serial mental status assessments for encephalopathy
- Urgent hepatology consultation for co-management and transplant evaluation 1