Ascites and Hepatic Hydrothorax

Background

• Ascites is most commonly due to portal hypertension and is associated with decreased 5-year survival (≈80% → 30%). 
  • Other causes: malignancy, CHF, TB, nephrotic syndrome, Budd-Chiari, pancreatic disease, and post-procedural complications.

Evaluation

• Ultrasound on admission to confirm presence of ascites 
  • Diagnostic paracentesis for all new ascites or hospital admissions → rule out SBP 
  • Studies sent on initial tap: ascitic fluid total protein, serum and BF Albumin, cell count w/diff, culture (no longer inoculated at bedside) 
  • Add tests only if clinically indicated: HCT (bloody ascites) triglycerides, cytology, AFB/mycobacteria, glucose/LDH (secondary peritonitis) 
• Elevated INR and thrombocytopenia (<50K) are generally NOT contraindications for paracentesis. 

Serum-ascites albumin gradient (SAAG) = serum albumin - ascites albumin 

≥1.1 g/dL → portal HTN 

• Low total protein (<2.5): cirrhosis 
• High protein (≥2.5): cardiac ascites, Budd-Chiari 

<1.1 g/dL → non-portal HTN 

• Malignancy, TB, pancreatic, nephrotic

Management

• 2000mg sodium restriction per day for all ascites (Grade 1-3), no fluid restriction unless HypoNa <125 
• Diuretics (spironolactone and loops) 
  • Start at spironolactone 100mg with up titration to 400mg 
  • Furosemide 40mg up titrated to 160mg is added if insufficient diuresis or if limited by hyperkalemia 
• Avoid ACEi, ARBs and NSAIDs in these patients 

Large Volume Paracentesis (LVP) 

• Defined as paracentesis 5 or more L 
  • Should be performed for grade 3 ascites 
  • Give 6-8g of albumin per liter of ascites removed (e.g., 6L removed, 6*8=48, will give 48g albumin)

Definitions

• Diuretic-resistant: lack of response to diuretics (max spironolactone 400mg/Lasix 160mg), Na restriction and rapid recurrence following paracentesis 
• Diuretic-intractable: unable to tolerate diuretic therapy due to adverse drug effects (unexplained HE, AKI, K abnormalities, hypoNa, intractable muscle cramps) 
• Note: a urine N:K ratio can be obtained to determine if patient is having appropriate natriuresis. (i.e. N:K >1, means appropriate natriuresis/dosing and likely dietary sodium/fluid indiscretion)

Management

• Discontinue diuretics once refractory ascites has been established, but continue Na dietary restriction
• Consider oral midodrine if pt is also hypotensive 
• Serial paracenteses (generally arranged OP with CT/US-guided procedures service) 
• Consider TIPS (trans jugular intrahepatic portosystemic shunt; has survival benefit) for refractory ascites or recurrent ascites (>3 LVPs in one year despite compliance with diet and diuretics). This should be discussed with primary hepatology team. Following TIPS, cessation or decrease in ascites should occur in ~6 weeks 
• Consider discontinuing beta blockers in patients with refractory ascites if SBP <90, SCr >1.5, or Na <130

Hepatic Hydrothorax

• Pleural effusion in a patient with cirrhosis without other cause of cardiopulmonary disease (must rule out other causes), diagnosis of exclusion. 
• Associated with high mortality 
• Caused by passage of ascitic fluid through small diaphragmatic defects into the pleural space 
• Most commonly presents with dyspnea and cough 
• Pleural fluid will have transudative properties

Management

• First line treatment: 2g dietary sodium restriction + diuretic use (same dosing) 
• Therapeutic thoracentesis 
• Avoid chest tube placement (high risk of complications, protein loss, infection) 
• Refractory HH: TIPS, liver transplant (definitive therapy)