Ascites and Hepatic Hydrothorax – Lauren Evers Carlini, Thomas Strobel |
Ascites |
Background
- US ~80% due to cirrhosis and associated portal hypertension
- Less common causes: 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 (aerobic, then anaerobic)! Use luer-lock syringe and vacutainer, then hand deliver samples to 4th floor lab to ensure proper/timely delivery
- There is no guideline for INR cutoff for paracentesis, although our procedure team often looks for INR < 3.5 (IR usually doesn’t care about INR)
- Serum-ascites albumin gradient (SAAG) = serum albumin - ascites albumin. SAAG ≥ 1.1 accurately predicts portal hypertension, but this may be due to either cardiac or hepatic causes which can be further evaluated with total protein in the ascites:
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: Total nucleated cells x percent neutrophils
- If ≥> 250, diagnostic of SBP in cirrhosis
- Correction for RBCs: For every 250 RBCs in fluid, subtract 1 PMN
- 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
- Cessation of alcohol, if applicable
- 2000mg sodium restriction per day for all ascites (Grade 1-3)
- Diuretics (spironolactone and typically oral furosemide)
- Start at 100mg of spironolactone with up titration to 400mg
- Furosemide is added if insufficient diuresis or if limited by hyperkalemia
- Can then ↑ to a max of 400:160
- If poor response can change to torsemide 10 and ↑ 40 mg max for cirrhotics
- Fluid restriction usually not necessary unless serum sodium <130 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
- 6-8g of albumin per liter of ascites removed , even if < 5L
-
- So, if 7L removed, you would give 42-56g of albumin
-
- Target weight loss of 0.5kg/day when diuresing to avoid renal injury
Refractory Ascites:
- Two distinctions:
- Diuretic-resistant: lack of response to diuretics (max spironolactone 400mg/lasix160mg), 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 of 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
- If pt with TIPS presents to hospital with accumulation of ascites, can signal that shunt is no longer patent. Obtain RUQ w/doppler or CTA abdomen/pelvis to look for patency. May require IR study if high enough concern
- Medications to avoid or discontinue with refractory ascites:
- ACE/ARB, NSAIDS, β Blockers (if Na <130, systolic <100, MAP <65 or AKI)
Hepatic Hydrothorax |
Background
- transudative effusion, typically unilateral (right sided); reflects ascitic fluid that passes through a small defect in the diaphragm
- present in 5% of cirrhosis with ascites and portends a poor prognosis
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 w/ diff
- Culture (inoculated at the bedside!)
- Protein, albumin, LDH, bilirubin
- Other considerations: triglycerides, amylase, cytology
- Rule out SBE:
- Diagnosed by the following criteria:
- Positive pleural fluid culture, PMN>250
- Negative pleural fluid culture with PMN >500
- No evidence of pneumonia on imaging (to r/o parapneumonic effusion)
- ½ of cases will present with concomitant SBP
- Diagnosed by the following criteria:
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
- Once placed, may be impossible to remove due to constant reaccumulation of fluid
- PleurX catheters can be considered for palliation (e.g., hospice patients)
- Tension hydrothorax with pronounced dyspnea and hemodynamic instability require immediate decompression with thoracentesis
- Refractory Hydrothorax is defined similarly and managed similarly with serial thoracentesis or TIPS. For those who are not candidates, consider:
- Chemical pleurodesis (fraught w/ complications, not commonly performed at VUMC)
- Thoracoscopic mesh repair in patients with clear diaphragmatic deficits, but again, this is not common practice at VUMC
- Management of spontaneous bacterial empyema is the same as in SBP, as noted below