How should I assess and manage a patient with a distended abdomen and elevated ammonia suggestive of decompensated cirrhosis with ascites and hepatic encephalopathy?

Assessment and Management of Distended Abdomen with Elevated Ammonia in Decompensated Cirrhosis

In a patient with distended abdomen and elevated ammonia, immediately perform diagnostic paracentesis to confirm ascites and rule out spontaneous bacterial peritonitis, while simultaneously initiating treatment for hepatic encephalopathy with lactulose, as these represent two distinct but often co-occurring complications of decompensated cirrhosis requiring urgent parallel management. 1

Initial Assessment

Diagnostic Paracentesis - Mandatory First Step

• Perform diagnostic paracentesis without delay in all cirrhotic patients with ascites on hospital admission or with any clinical deterioration 1
• Obtain ascitic fluid for cell count with differential (neutrophil count >250/mm³ confirms spontaneous bacterial peritonitis), culture, albumin, and total protein 1, 2
• Paracentesis is safe even with coagulopathy; severe hemorrhage occurs in only 0.2-2.2% of procedures with a death rate of 0.02% 1
• The left lower quadrant is the preferred site due to greater depth of ascites and thinner abdominal wall 1

Ammonia Measurement - Diagnostic Limitations

• Measure blood ammonia only if there is diagnostic doubt about hepatic encephalopathy, as a normal value casts doubt on the diagnosis, but an elevated value does not confirm it 1
• Ammonia may be elevated in cirrhotic patients without any encephalopathy, making it unreliable for positive diagnosis 1, 3
• Ensure proper sampling technique: fasting patient, avoid venous stasis, EDTA tube, immediate transport on ice within 60-90 minutes 1
• If ammonia is severely elevated (>100 μmol/L) with minimal liver dysfunction, consider inherited metabolic disorders 1

Clinical Grading of Complications

• Grade ascites: Grade 1 (detected only by imaging), Grade 2 (moderate, visible on inspection), or Grade 3 (massive/tense ascites) 1
• Assess for hepatic encephalopathy clinically through mental status examination, looking for impaired vigilance, attention, and temporal-spatial disorientation 1
• Perform Animal Naming Test: <20 animals named in 1 minute suggests covert hepatic encephalopathy 1

Immediate Management Algorithm

For Ascites Management

Grade 2-3 Ascites (Moderate to Tense):

• If tense ascites (Grade 3): perform therapeutic paracentesis first, then initiate medical therapy 1, 2
• Start spironolactone 100 mg/day as monotherapy for first episode ascites 1, 2
• Increase spironolactone in 100 mg steps every 72 hours to maximum 400 mg/day if inadequate response (defined as <2 kg weight loss per week) 1
• Add furosemide 40 mg/day if no response to spironolactone alone or if hyperkalemia develops, increasing in 40 mg steps to maximum 160 mg/day 1
• For recurrent or long-standing ascites, start combination therapy (spironolactone plus furosemide) from the beginning to shorten time to natriuresis and lower hyperkalemia risk 1

Sodium Restriction:

• Restrict sodium to <5 g/day (approximately 88 mmol/day) 1, 2
• Greater restriction is not recommended as it may worsen malnutrition 2
• Fluid restriction is NOT necessary unless serum sodium drops below 120-125 mmol/L 1

For Hepatic Encephalopathy Management

Identify and Treat Precipitating Factors:

• Check for gastrointestinal bleeding, infection (perform diagnostic paracentesis), dehydration, constipation, and electrolyte abnormalities 1
• Monitor serum sodium closely, as hyponatremia <130 mmol/L is an independent risk factor for hepatic encephalopathy and predicts non-response to lactulose 1
• Discontinue benzodiazepines immediately - they are contraindicated in decompensated cirrhosis 1
• Limit proton pump inhibitors to strict validated indications 1

Pharmacological Treatment:

• Initiate lactulose as first-line therapy for hepatic encephalopathy 1, 4
• Add rifaximin for persistent or recurrent episodes 1, 4
• For severe hyperammonemia refractory to standard therapy, consider ammonia scavengers (glycerol phenylbutyrate, sodium benzoate) or polyethylene glycol 3350 bowel cleansing 5

Critical Monitoring Parameters

Diuretic Therapy Monitoring

• Monitor serum creatinine, sodium, and potassium at least weekly during the first month of diuretic therapy 1
• Target weight loss: 0.5 kg/day without peripheral edema, or 1 kg/day with peripheral edema 1
• Discontinue diuretics temporarily if serum sodium falls below 120-125 mmol/L 1
• Common complications include renal failure, hepatic encephalopathy (from increased renal ammonia production), hypokalemia, hypomagnesemia, and hyperkalemia 1

Signs of Infection Requiring Immediate Action

• Fever, abdominal pain, altered mental status, or unexplained clinical deterioration mandate immediate diagnostic paracentesis and empirical antibiotics 1, 2
• Start ceftriaxone 1 g/24h for up to 7 days in decompensated cirrhosis or quinolone-resistant settings 2
• Antibiotic prophylaxis is essential as infection accelerates disease progression 1

Common Pitfalls to Avoid

• Never use NSAIDs - they reduce urinary sodium excretion, precipitate renal dysfunction, and convert diuretic-sensitive ascites to refractory ascites 1, 2
• Discontinue ACE inhibitors and angiotensin receptor blockers - they worsen hypotension and renal function 2
• Do not rely on ammonia levels to diagnose or monitor hepatic encephalopathy - this is a clinical diagnosis of exclusion 1, 3
• Avoid aggressive fluid resuscitation, which can worsen ascites and precipitate pulmonary edema 6
• Do not restrict fluids routinely - only when serum sodium is severely low (<120-125 mmol/L) 1
• Bed rest is not recommended as it causes muscle atrophy; manage patients as outpatients unless complicated by bleeding, severe encephalopathy, infection, or hypotension 2

When to Escalate Care

• Refer to gastroenterology immediately for any decompensation event, refractory ascites (requiring paracentesis more frequently than every 2 weeks), or need for TIPS evaluation 2
• Consider liver transplantation evaluation for all patients with decompensated cirrhosis 1, 2
• Brain imaging (CT or MRI) is indicated during the first episode of hepatic encephalopathy to exclude intracranial hemorrhage, which is more common in cirrhotic patients 1
• Palliative care referral should be offered to patients with refractory ascites who are not transplant candidates 2

Addressing Underlying Etiology

• Treat the underlying cause of cirrhosis aggressively, as this is the cornerstone of management and can potentially reverse early cirrhosis 2
• For viral hepatitis: initiate direct-acting antivirals (HCV) or entecavir/tenofovir (HBV) even in decompensated cirrhosis 2
• For alcoholic cirrhosis: complete and permanent alcohol cessation may lead to "re-compensation" 2
• Etiologic treatment eases control of ascites in many cases 1