A cirrhotic patient presents with jaundice, hepatic encephalopathy (ammonia 51 µmol/L), hyponatremia (serum sodium 126 mmol/L), ascites, a right pelvic abscess or hematoma, right upper‑quadrant pain, metabolic acidosis (serum CO₂ 14.6 mmol/L), bilirubin 25 µmol/L, aspartate aminotransferase 100 U/L, albumin 2.7 g/dL, and alkaline phosphatase 153 U/L – what is the most likely diagnosis and how should this be managed acutely?

Acute Management of Decompensated Cirrhosis with Multiple Complications

This patient presents with acute-on-chronic liver failure (ACLF) characterized by jaundice, hepatic encephalopathy, severe hyponatremia, ascites, possible infection (pelvic abscess), and metabolic acidosis—immediate priorities are treating precipitating factors (infection, hyponatremia), managing hepatic encephalopathy, and assessing for liver transplantation.

Most Likely Diagnosis

Acute-on-chronic liver failure (ACLF) with multiple precipitating factors: The constellation of jaundice (bilirubin 25 µmol/L), hepatic encephalopathy (ammonia 51 µmol/L), severe hyponatremia (Na 126 mmol/L), ascites, right pelvic abscess/hematoma, and metabolic acidosis (CO₂ 14.6 mmol/L) represents decompensated cirrhosis with acute deterioration 1, 2. The right pelvic abscess is a critical precipitating factor requiring urgent attention 1.

Key Precipitating Factors Identified

• Infection (pelvic abscess): Bacterial infections precipitate hepatic encephalopathy in approximately 50% of cases and must be treated urgently 1
• Severe hyponatremia (Na 126 mmol/L): Hyponatremia below 130 mmol/L is an independent risk factor for hepatic encephalopathy (OR 2.36) and increases mortality 60-fold 1, 3
• Metabolic acidosis (CO₂ 14.6): Suggests tissue hypoperfusion or renal dysfunction, contributing to encephalopathy 1

Immediate Management Priorities

1. Treat Infection Urgently

• Obtain diagnostic paracentesis immediately to rule out spontaneous bacterial peritonitis (SBP), testing for cell count with differential, serum-ascites albumin gradient, Gram stain, and culture 4, 5
• Start empiric broad-spectrum antibiotics (third-generation cephalosporin such as cefotaxime 2g IV every 8 hours) to cover the pelvic abscess and possible SBP without waiting for culture results 1, 5
• Administer albumin 1.5 g/kg IV on day 1, then 1 g/kg on day 3 if SBP is confirmed, as this reduces mortality and prevents hepatorenal syndrome 6, 4, 5
• Surgical or interventional radiology consultation for drainage of the pelvic abscess if it is confirmed as an abscess rather than hematoma 1

2. Manage Severe Hyponatremia (Na 126 mmol/L)

This patient has hypervolemic hyponatremia due to cirrhosis with ascites—fluid restriction is the cornerstone, NOT hypertonic saline unless life-threatening symptoms develop.

• Implement strict fluid restriction to 1,000–1,500 mL/day as first-line therapy for sodium <130 mmol/L in hypervolemic hyponatremia 1, 3, 4
• Discontinue or reduce diuretics temporarily until sodium improves above 125 mmol/L, as diuretics can worsen hyponatremia 1, 3
• Administer 20% albumin infusion (25-50g IV daily) to improve effective circulating volume and sodium levels in cirrhotic patients 3, 6, 4
• Sodium restriction to 2–2.5 g/day (88–110 mmol/day) is more important than fluid restriction for weight loss, as fluid follows sodium 3, 4
• Monitor sodium every 4–6 hours initially, ensuring correction does not exceed 4–6 mmol/L per day (maximum 8 mmol/L in 24 hours) to prevent osmotic demyelination syndrome 1, 3

Critical pitfall: Hypertonic saline should be avoided in cirrhotic patients unless severe neurological symptoms (seizures, coma) develop, as it worsens ascites and edema 1, 3.

3. Treat Hepatic Encephalopathy

• Lactulose 20–30 mL orally every 2–4 hours until 2–3 soft bowel movements per day are achieved, then adjust to maintenance dosing 1, 7, 5
• Rifaximin 550 mg orally twice daily should be added to lactulose for synergistic effect in reducing ammonia-producing bacteria 1, 7
• Correct hyponatremia aggressively as described above, since sodium <130 mmol/L directly contributes to encephalopathy 1, 3
• Avoid benzodiazepines and opioids as they worsen encephalopathy in decompensated cirrhosis 1, 7
• Ensure adequate protein intake (1.2–1.5 g/kg/day) rather than restricting protein, as malnutrition worsens outcomes 7, 5

4. Manage Ascites and Volume Overload

• Therapeutic paracentesis if tense ascites is causing respiratory compromise or discomfort, removing up to 5 liters initially 4, 5
• Administer albumin 6–8 g per liter of ascites removed if >5 liters are drained to prevent post-paracentesis circulatory dysfunction 6, 4, 5
• Resume diuretics cautiously once sodium improves above 125 mmol/L, starting with spironolactone 100 mg and furosemide 40 mg daily, titrating based on weight loss and electrolytes 4, 5

5. Address Metabolic Acidosis

• Assess for hepatorenal syndrome given low albumin (2.7 g/dL), metabolic acidosis, and possible renal dysfunction 1, 5
• Check serum creatinine, BUN, and urine sodium to differentiate prerenal azotemia from hepatorenal syndrome 1, 5
• Avoid nephrotoxic agents including NSAIDs and aminoglycosides 1, 5
• Consider midodrine and octreotide if hepatorenal syndrome is confirmed, along with albumin infusion 6, 5

Monitoring and Follow-Up

• Serum sodium every 4–6 hours during active correction, then daily once stable 1, 3
• Daily weights, strict intake/output monitoring, and clinical assessment for volume status 4, 5
• Liver function tests (AST, ALT, bilirubin, INR) daily to track hepatic function 1
• Renal function (creatinine, BUN) daily to detect hepatorenal syndrome early 1, 5
• Mental status assessment using West Haven criteria for hepatic encephalopathy grading 1, 7
• Blood cultures and repeat paracentesis if fever persists or clinical deterioration occurs 1, 5

Liver Transplantation Evaluation

All patients with ACLF and refractory complications should be evaluated for liver transplantation urgently, regardless of MELD score 4, 2. This patient has multiple poor prognostic indicators:

• Severe hyponatremia (Na 126 mmol/L) predicts poor transplant-free survival 1, 3
• Hepatic encephalopathy with infection indicates high short-term mortality 1, 2
• Low albumin (2.7 g/dL) and elevated bilirubin suggest advanced liver dysfunction 1, 2
• Metabolic acidosis and possible organ failure (ACLF) carry 30–50% short-term mortality 1, 2

Common Pitfalls to Avoid

• Never use hypertonic saline as first-line therapy for hyponatremia in cirrhosis—it worsens ascites and should be reserved only for seizures or coma 1, 3
• Never correct sodium faster than 4–6 mmol/L per day in cirrhotic patients due to exceptionally high risk of osmotic demyelination syndrome 1, 3
• Never continue diuretics when sodium is <125 mmol/L—this precipitates hepatic coma and worsens hyponatremia 1, 3
• Never delay antibiotics while awaiting culture results in suspected infection—bacterial infections are the most common reversible precipitant of hepatic encephalopathy 1
• Never restrict protein in hepatic encephalopathy—adequate nutrition (1.2–1.5 g/kg/day protein) improves outcomes 7, 5
• Never use fluid restriction alone without addressing sodium restriction and albumin infusion in cirrhotic hyponatremia 3, 4