Clinical management of ascites
Overview
Ascites is a pathological accumulation of fluid in the peritoneal cavity. There are two broad categories of ascites...
- Associated with a normal peritoneum.
- Due to a diseased peritoneum "see table 1".
Causes
Most common cause is portal hypertension secondary to chronic liver disease (> 80% of cases). Other causes include infections (tuberculous peritonitis), intra-abdominal malignancy, inflammatory disorders of the peritoneum and ductal disruptions (chylous, pancreatic, biliary).
Risk factors
- Risk factors for ascites include causes of liver disease such as alcohol consumption, transfusions, tattoos, injection drug use, history of viral hepatitis or jaundice and birth in an area endemic for hepatitis.
- History of cancer or marked weight loss suggests malignancy or fevers suggest infected peritoneal fluid, including bacterial peritonitis (spontaneous or secondary) may lead to ascites.
| Table (1). Causes of ascites | ||
|---|---|---|
| Normal Peritoneum | ||
| Portal hypertension (SAAG ≥ 1.1 g/dL) |
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| Hypoalbuminemia (SAAG < 1.1 g/dL) |
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| Miscellaneous conditions (SAAG < 1.1 g/dL) |
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| Diseased peritoneum (SAAG < 1.1 g/dL) | ||
| Infections |
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| Malignant conditions |
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| Other conditions |
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Assessment
Symptoms and signs
Increasing abdominal girth and abdominal pain are common. In portal hypertension, large abdominal wall veins with cephalad flow; inferiorly directed flow implies hepatic vein obstruction.
- In portal hypertension and chronic liver disease: palmar erythema, cutaneous spider angiomas, gynecomastia and muscle wasting.
- Asterixis secondary to hepatic encephalopathy may be present. In right-sided heart failure or constrictive pericarditis, jugular venous pressure elevated.
- In acute alcoholic hepatitis or Budd-Chiari syndrome: large tender liver.
- In cardiac failure or nephrotic syndrome: anasarca.
- In malignancy: firm lymph nodes in the left supraclavicular region or umbilicus.
Diagnosis
Laboratory investigations
Ascitic fluid cell count: normal cell count is < 500 leukocytes/mcL and < 250 polymorphonuclear neutrophils (PMNs)/mcL. PMN count of > 250/mcL (neutrocytic ascites), with > 75% of all white blood cells (WBCs) being PMNs usually indicates bacterial peritonitis. Ascitic fluid culture and Gram stain in suspected peritonitis. Elevated WBCs with a predominance of lymphocytes occur in tuberculosis or peritoneal carcinomatosis. Cloudy ascitic fluid suggests infection. Milky fluid occurs in chylous ascites. Bloody fluid suggests traumatic paracentesis, malignant ascites. Serum-ascites albumin gradient (SAAG) classifies ascites into portal hypertensive and nonportal hypertensive causes "see table 1".
SAAG is calculated by subtracting the ascitic fluid albumin from the serum albumin. SAAG ≥ 1.1 g/dL suggests underlying portal hypertension. SAAG < 1.1 g/dL implicates nonportal hypertensive causes. ∼4% of patients have "mixed ascites," ie, underlying cirrhosis with portal hypertension complicated by a second cause for ascites (such as malignancy or tuberculosis). SAAG > 1.1 g/dL with a high ascitic fluid total protein (> 2.5 g/dL) occurs in hepatic congestion secondary to cardiac disease or Budd-Chiari syndrome and up to 20% of cases of uncomplicated cirrhosis.
Ascitic fluid amylase is elevated in pancreatic ascites or perforation of the gastrointestinal tract. Ascitic fluid bilirubin concentration is greater than the serum bilirubin in perforation of the biliary tree. Ascitic fluid creatinine is elevated in leakage of urine from the bladder or ureters. Adenosine deaminase may be useful for the diagnosis of tuberculous peritonitis
Imaging studies
Ultrasound and CT imaging is useful in distinguishing between causes of portal and nonportal hypertensive ascites, detecting thrombosis of the hepatic veins (Budd-Chiari syndrome) or portal veins and detecting lymphadenopathy and masses Directing percutaneous needle biopsies of abnormal lymph nodes or solid organic masses.
Diagnostic procedures
Physical examination is insensitive for detecting < 1500 mL of ascites fluid. Abdominal paracentesis is indicated in patients with new-onset ascites to determine etiology (portal vs. nonportal hypertensive), patients admitted to the hospital with cirrhosis and ascites to diagnose bacterial peritonitis and patients with known ascites who deteriorate clinically (fever, abdominal pain, rapid worsening of kidney function, or worsened hepatic encephalopathy).
When fluid volume is small or fluid is loculated, abdominal ultrasound confirms presence of ascites and facilitates paracentesis. Cytologic examination is indicated if peritoneal carcinomatosis is suspected. Laparoscopy permits direct visualization and biopsy of the peritoneum, liver, and some intra-abdominal lymph nodes in suspected peritoneal tuberculosis or malignancy.
Management
Medications
For portal hypertensive ascites, diuretics such as spironolactone, 100 mg/day, and furosemide, 40 mg/day. Dose increased every 5–7 days until diuresis achieved, to maximum of 400 mg/day of aldactone and 160 mg/day of furosemide. Goal is to lose 0.5 kg/day. Careful monitoring of serum sodium, potassium, and creatinine required.
Therapeutic procedures
In ascites caused by portal hypertension, dietary sodium restriction to 1–2 g/day; fluid intake restriction if serum Na < 125 mEq/L. Large-volume paracentesis (4–6 L) is indicated for patients with massive ascites or ascites refractory to diuretics.
Intravenous albumin should be administered with large-volume paracentesis to reduce acute and long-term complications: 10 g albumin/L of ascites removed. Transjugular intrahepatic portosystemic shunt (TIPS) effectively controls 75% of carefully selected patients with portal hypertension and refractory ascites. For additional note, see "Pharmacotherapy of cirrhosis".
References
- Solà E, Solé C, Ginès P. Management of uninfected and infected ascites in cirrhosis. Liver Int. 2016;36 Suppl 1:109-115.
- Pericleous M, Sarnowski A, Moore A, Fijten R, Zaman M. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol. 2016;28(3):e10-e18.
