Management of Peritoneal Fluid (Ascites)
Perform diagnostic paracentesis immediately on all patients with new-onset ascites to determine the underlying cause, as this is the most rapid and cost-effective diagnostic approach. 1
Initial Diagnostic Workup
Essential first-line tests on ascitic fluid include:
- Cell count with differential to detect infection (polymorphonuclear leukocyte count >250 cells/mm³ indicates spontaneous bacterial peritonitis) 1
- Ascitic fluid albumin and serum albumin to calculate the serum-ascites albumin gradient (SAAG) 1, 2, 3
- Ascitic fluid total protein concentration 1
- If infection is suspected, inoculate ascitic fluid into blood culture bottles at the bedside before starting antibiotics (this increases culture yield from 50% to 80%) 1
SAAG interpretation determines treatment approach:
- SAAG ≥1.1 g/dL indicates portal hypertension with 97% accuracy (cirrhosis, heart failure, portal vein thrombosis) 1, 2, 3
- SAAG <1.1 g/dL indicates non-portal hypertensive causes (peritoneal carcinomatosis, tuberculosis, nephrotic syndrome) 1, 3
Determining the Underlying Cause
Cirrhosis accounts for approximately 85% of ascites cases in Western populations, while 15% have non-hepatic causes including cancer, heart failure, tuberculosis, or nephrotic syndrome. 1
Additional testing based on clinical suspicion:
- Cytology: Order only when peritoneal carcinomatosis is suspected (history of breast, colon, gastric, or pancreatic cancer); sensitivity is 96.7% if three 50 mL samples are sent fresh and processed immediately 1
- Mycobacterial testing: Order only in high-risk patients (recent immigration from endemic areas, HIV/AIDS); ascitic fluid adenosine deaminase (ADA) >32 U/L has 91.7% sensitivity and 92% specificity for tuberculous peritonitis in cirrhotic patients 1
- Secondary peritonitis markers: If perforated viscus suspected, measure ascitic glucose (<50 mg/dL), LDH (higher than serum), CEA (>5 ng/mL), or alkaline phosphatase (>240 U/L) 1
Critical pitfall: Never order serum CA125 in patients with ascites—it is elevated in all patients with ascites regardless of cause and may lead to unnecessary gynecologic surgery, particularly in women with cirrhosis. 1
Treatment for Portal Hypertensive Ascites (SAAG ≥1.1 g/dL)
First-Line Medical Management
Sodium restriction to 2000 mg/day (88 mmol/day) combined with diuretic therapy is the cornerstone of treatment. 2
Diuretic regimen:
- Start spironolactone 100 mg once daily plus furosemide 40 mg once daily 2, 4
- Maximum doses: spironolactone 400 mg/day and furosemide 160 mg/day 2, 4
- In cirrhotic patients, initiate therapy in hospital setting and titrate slowly due to risk of hepatic encephalopathy 4, 5
Monitoring parameters:
- Daily weight at same time each day (after voiding) 2
- Target weight loss: 0.5 kg/day without peripheral edema, or 1 kg/day with peripheral edema 2
- Exceeding these targets risks plasma volume contraction, renal failure, and hyponatremia 2
- Monitor serum electrolytes and creatinine regularly, especially during first weeks of therapy 2
Assessing diuretic response:
- If weight loss inadequate, check 24-hour urinary sodium excretion (target >78 mmol/day) 2
- Alternatively, spot urine sodium-to-potassium ratio >1 correlates with adequate sodium excretion with 90% accuracy 2
- Lack of weight loss despite adequate urinary sodium indicates dietary non-compliance 2
Management of Tense Ascites
For patients with tense, uncomfortable ascites, perform large-volume paracentesis (LVP) for immediate symptom relief, then resume diuretics to prevent reaccumulation. 2
Post-paracentesis albumin administration:
- Give intravenous albumin 8 g per liter of ascitic fluid removed when >5 liters removed 1, 2
- This prevents post-paracentesis circulatory dysfunction, which increases mortality 1
- Administer albumin slowly to avoid cardiac overload in patients with underlying cardiomyopathy 1
Treatment of Underlying Liver Disease
Addressing the underlying cause is critical for ascites control and survival:
- Alcohol-related cirrhosis: Abstinence is essential; Child-Pugh class C patients who stop drinking have 75% 3-year survival versus 0% in those who continue 2
- Hepatitis B cirrhosis: Antiviral treatment can lead to dramatic improvement even in decompensated disease 2
- For irreversible liver disease, refer for liver transplantation evaluation, as development of ascites reduces 5-year survival from 80% to 30% 6
Management of Spontaneous Bacterial Peritonitis
If PMN count ≥250 cells/mm³, administer intravenous albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 in addition to antibiotics. 1
- This combination reduces renal impairment (10% vs 33%) and mortality (22% vs 41%) compared to antibiotics alone 1
Critical Medication Precautions
Avoid medications that worsen ascites or precipitate complications:
- NSAIDs: Reduce urinary sodium excretion and can convert diuretic-sensitive patients to refractory 2
- ACE inhibitors: Worsen hypotension in cirrhotic patients 2
- Fluid restriction: Generally unnecessary unless serum sodium <120-125 mmol/L 2
Recognition of Mixed Ascites
Approximately 5% of patients have two or more causes of ascites (e.g., cirrhosis plus peritoneal carcinomatosis, heart failure plus diabetic nephropathy plus cirrhosis). 1
- In these patients, each individual factor may not be severe enough alone to cause fluid retention, but the sum of predisposing factors leads to sodium and water retention 1
- All underlying causes must be addressed for effective treatment 2
When to Consider Refractory Ascites
Refractory ascites is defined as unresponsive to sodium restriction and high-dose diuretics (spironolactone 400 mg/day plus furosemide 160 mg/day). 2
Management options include: