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Ascites and Hepatic Hydrothorax

Thomas Strobel

Ascites

Background

  • Associated with a reduction in 5 year survival from 80% to 30%.

  • Most often due to portal hypertension. Less common causes include peritoneal or metastatic cancer, heart failure, tuberculosis, nephrotic syndrome, Budd-Chiari, sinusoidal obstructive syndrome (S.O.S), or complications from procedures and pancreatitis
Grade Definition Treatment
Grade 1 Ascites Only seen on imaging 2g Na restriction
Grade 2 Ascites Moderate, symmetric abdominal distension 2g Na restriction, diuretics
Grade 3 Ascites Marked, tense abdominal distension LVP + Na restriction, diuretics (unless refractory)

Evaluation

  • Bedside ultrasound on admission to confirm presence of ascites

  • Diagnostic paracentesis in all pts with ascites on admission mainly to rule out occult SBP

    • Initial paracentesis or when cause of ascites is uncertain: Total Protein, serum and BF Albumin, cell count w/diff, culture
    • Subsequent/Serial paracenteses: cell count w/diff, culture, protein
    • Always inoculate culture bottles at bedside (VA does not allow bedside innoculation)

  • See Procedure section for guidance on paracentesis.

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

0 1 2
Total Protein Ascites (not serum) SAAG > 1.1 g/dL (Portal HTN ) SAAG \< 1.1 g/dL (Non-portal HTN )
\< 2.5 g/dL Cirrhosis Nephrotic Syndrome Myxedema
> 2.5 g/dL Post-hepatic portal HTN: Cardiac Ascites Budd-Chiari Malignant Ascites Pancreatic Ascites TB

  • Calculate PMNs from fluid (see SBP below)

  • Other tests:

    • Triglycerides: if fluid is milky
    • Cytology: if very concerned for peritoneal carcinomatosis. May need up to 3 separate samples (50ml or more) to be able to detect malignant cells
    • ADA: if concern for peritoneal TB
    • Hematocrit: For bloody appearing fluid (not just serosanguinous) to rule out hemoperitoneum. There needs to be a recent serum HCT for comparison.
    • Amylase: If concerned for pancreatic ascites
    • Glucose, LDH if concern about secondary peritonitis (see below)

Management

  • 2000mg sodium restriction per day for all ascites (Grade 1-3)

  • Diuretics (spironolactone and typically furosemide)

    • Start at 100mg of spironolactone with up titration to 400mg
    • Furosemide is added if insufficient diuresis or if limited by hyperkalemia. Use more loop diuretics in patients with CKD
    • If Urine Na:K ratio <1, indicates insufficient natriuresis. Can ↑ doses to a max of 400:160
    • If poor response can change to torsemide 10mg and ↑ to 40mg max (per single dose)
    • Fluid restriction usually not necessary unless serum sodium <125 mmol/L

  • Large volume paracentesis should be performed for tense ascites or refractory ascites (grade 3), regardless of serum Cr. Pts should be tapped dry with each paracentesis

  • Give 6-8g of albumin per liter of ascites removed, even if < 5L

  • Target weight loss of 0.5 kg/day when diuresing to avoid renal injury

  • Discontinue NSAIDs and ACEI/ARB

Refractory Ascites:

  • Two distinctions:

    • 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 2/2 adverse drug effects (unexplained HE, AKI, K abnormalities, hypoNa, intractable muscle cramps)

  • Management aside from liver transplant:

    • Discontinue diuretics once refractory ascites has been established
    • Consider oral midodrine; can be especially helpful if pt is also hypotensive
    • Serial paracenteses, generally arranged OP with IR
    • Consider TIPS (trans jugular intrahepatic portosystemic shunt; has survival benefit). Following TIPS, cessation or decrease in ascites should occur in 4-6 weeks
    • Consider discontinuing beta blockers in patients with refractory ascites if sBP <90, SCr >1.5, or Na <130

Hepatic Hydrothorax

Background

  • Transudative effusion, typically unilateral (75% right sided); reflects ascitic fluid that passes through defects in the diaphragm. 10% can develop without clinical ascites.

  • Present in 4-12% of cirrhotics and portends a poor prognosis (75% mortality within 90 days)

Evaluation

  • Often suspected clinically, though must exclude pleural/cardiopulmonary process

  • Thoracentesis will demonstrate a transudative effusion and should be evaluated with standard pleural fluid lab tests: cell count, protein, albumin, LDH, culture

    • Other considerations: triglycerides, amylase, hematocrit, cytology

  • Rule out SBE which is diagnosed the same as SBP (PMN>250)

Management

  • Similar management of ascites as noted above

  • AVOID chest-tube placement. associated with increased morbidity and mortality due to extensive loss of fluid, electrolytes and protein as well as increased infection risk

    • PleurX catheters can be considered for palliation (e.g., hospice patients)

  • Refractory Hydrothorax is defined similarly and managed similarly with serial thoracentesis or TIPS.

  • Management of spontaneous bacterial empyema is the same as in SBP (see below)