a) Diagnosis

• Ascites: uniform abdominal distension with shifting dullness
• Portal hypertension: splenomegaly and ascites
• Hepatic encephalopathy: asterixis (flapping tremor), likely precipitated by vomiting-related dehydration/electrolyte disturbance, infection, GI bleeding, constipation, etc.
• This is clinically consistent with West Haven grade II hepatic encephalopathy if there is impaired attention, altered behavior, or disorientation on formal assessment. A normal level of consciousness does not exclude it.

b) Investigations

1. Baseline and severity assessment

• CBC with platelet count
• Liver function tests: total/direct bilirubin, AST/ALT, ALP, albumin
• PT/INR
• Renal function tests: urea, creatinine, electrolytes, especially Na+ and K+
• Blood glucose
• Calculate Child-Pugh and MELD-Na scores.

2. Search for encephalopathy precipitants

• Stool/NG aspirate for occult upper GI bleed, and urgent upper GI endoscopy when stable to assess varices
• Blood, urine, and ascitic-fluid cultures if infection is suspected
• Chest radiograph if respiratory infection is possible
• Look for constipation, dehydration, excess diuretics, sedatives, alcohol withdrawal, hypokalemia, hyponatremia, and renal failure.
• Serum ammonia may support the diagnosis if normality is questioned, but its level does not reliably grade hepatic encephalopathy.

3. Ascites evaluation

• Abdominal ultrasound with portal/hepatic-vein Doppler: confirms ascites, assesses nodular liver, portal hypertension, splenomegaly, portal-vein patency, and hepatic-vein obstruction. Ultrasound can detect small volumes of fluid and guide tapping. Yamada's Textbook of Gastroenterology, p. 2099.
• Diagnostic paracentesis, mandatory in new ascites and in a hospitalized decompensated cirrhotic patient. Send ascitic fluid for:
  • Cell count and differential: PMN count of 250 cells/mm³ or greater suggests spontaneous bacterial peritonitis (SBP)
  • Culture, ideally inoculated into blood-culture bottles at bedside
  • Ascitic albumin and total protein, with simultaneous serum albumin to calculate SAAG
  • Cytology if malignancy is possible
  • ADA/AFB tests if tuberculous peritonitis is suspected
  • Amylase if pancreatic ascites is considered.
    Yamada's Textbook of Gastroenterology, pp. 2099-2100.

4. Etiological work-up of chronic liver disease

• Hepatitis B surface antigen and hepatitis C antibody/RNA
• Alcohol-use assessment and nutritional assessment
• Consider autoimmune markers, iron studies, ceruloplasmin, etc., when the clinical setting suggests an alternative or additional liver disease.
• Alpha-fetoprotein and liver ultrasound for hepatocellular carcinoma surveillance.

c) Management of hepatic encephalopathy

1. Stabilize and protect the airway
   • Assess consciousness frequently.
   • If severely drowsy, vomiting, or unable to protect the airway: ICU care and airway protection.
   • Stop alcohol and avoid precipitating drugs, particularly benzodiazepines, opioids, and unnecessary sedatives.
2. Identify and correct the precipitating cause
   • Treat infection, especially SBP.
   • Look for and manage GI bleeding.
   • Correct dehydration, hypokalemia, hyponatremia, alkalosis, hypoglycemia, constipation, renal failure, and excess diuretic use.
   • Perform diagnostic paracentesis promptly to exclude SBP. GI bleeding, hypokalemia, infection, and dehydration are recognized precipitants. ROSEN's Emergency Medicine, section “Hepatic Encephalopathy.”
3. Reduce intestinal ammonia production and absorption
   • Lactulose is first-line. Give orally, via NG tube, or rectally if required, then titrate to 2-3 soft stools daily. Avoid excessive diarrhea because it worsens dehydration and hypokalemia.
   • Add rifaximin for recurrent overt encephalopathy or insufficient response to lactulose.
4. Nutrition and definitive care
   • Do not institute routine protein restriction. Provide adequate calories and protein, preferably with vegetable/dairy protein if poorly tolerated.
   • Give thiamine and other nutritional supplementation in alcohol-associated liver disease.
   • Assess for liver transplantation, as ascites and encephalopathy indicate decompensated cirrhosis.

d) Causes of ascites

1. Portal-hypertensive ascites, usually high SAAG

• Cirrhosis: alcohol-related, viral, metabolic-associated steatotic liver disease, autoimmune, etc. This is the commonest cause.
• Heart failure and constrictive pericarditis
• Budd-Chiari syndrome/hepatic venous outflow obstruction
• Portal-vein thrombosis
• Massive hepatic metastases
• Sinusoidal obstruction syndrome

2. Peritoneal disease, usually low SAAG

• Peritoneal carcinomatosis, including ovarian, gastric, colonic, pancreatic malignancy
• Tuberculous peritonitis
• Other chronic peritoneal infection/inflammation

3. Pancreatic and biliary causes

• Pancreatic ascites due to pancreatic-duct disruption or pseudocyst leakage
• Bile leak

4. Low oncotic pressure or systemic causes

• Nephrotic syndrome
• Protein-losing enteropathy
• Severe malnutrition/hypoalbuminemia
• Renal failure
• Myxedema ascites
• Chylous ascites from lymphatic obstruction, lymphoma, trauma, or infection