What causes ascites?

Causes of Ascites

Cirrhosis is the most common cause of ascites, accounting for approximately 75-85% of cases in Western countries, with the remaining cases caused by malignancy, heart failure, tuberculosis, pancreatic disease, and other miscellaneous conditions. 1

Primary Causes of Ascites

Cirrhosis-Related Ascites (75-85% of cases)

• Cirrhosis leads to portal hypertension and splanchnic arterial vasodilation, causing decreased effective arterial blood volume with activation of sodium-retaining systems (sympathetic nervous system and renin-angiotensin-aldosterone system) 1
• The resulting renal sodium retention leads to expansion of extracellular fluid volume and formation of ascites 1
• Development of ascites in cirrhosis is associated with poor prognosis, reducing 5-year survival from 80% to 30% 1

Non-Cirrhotic Causes (15-25% of cases)

• Malignancy: Peritoneal carcinomatosis, massive liver metastases 1
• Cardiac: Heart failure (distinguishable by elevated jugular venous distention and pro-brain natriuretic peptide levels >6000 pg/mL) 1
• Infectious: Tuberculosis peritonitis 1
• Pancreatic: Pancreatitis with associated ascites 1
• Renal: Nephrotic syndrome 1
• Vascular: Budd-Chiari syndrome, sinusoidal obstruction syndrome 1
• Other: Myxedema, postoperative lymphatic leak, "mixed" ascites (cirrhosis plus another cause) 1

Pathophysiological Mechanisms

Portal Hypertension Pathway

• Portal hypertension is a prerequisite for ascites development in cirrhosis 1
• Increased hydrostatic pressure in the hepatic sinusoids leads to transudation of fluid into the peritoneal space 2
• Portal hypertension contributes to splanchnic vasodilation, further worsening the pathophysiological cascade 1

Sodium and Water Retention Pathway

• Splanchnic arterial vasodilation causes decreased effective arterial blood volume 1
• This triggers activation of:
  • Renin-angiotensin-aldosterone system
  • Sympathetic nervous system
  • Arginine vasopressin release 3
• These systems promote renal sodium and water retention, expanding extracellular fluid volume 4
• Inadequate renal prostaglandin production may contribute to hepatorenal syndrome in advanced cases 3

Diagnostic Approach

Clinical Evaluation

• Physical examination findings include flank dullness and shifting dullness (83% sensitivity, 56% specificity) 1
• Approximately 1500 mL of fluid must be present before flank dullness is detectable 1
• Abdominal ultrasound may be required in obese patients to confirm ascites 1

Ascitic Fluid Analysis

• Diagnostic paracentesis with appropriate fluid analysis is essential for all patients with new-onset ascites 1
• Serum-ascites albumin gradient (SAAG) differentiates portal hypertension-related ascites (≥1.1 g/dL) from other causes with 97% accuracy 1
• Additional tests include neutrophil count, culture, protein concentration, and when indicated: amylase, cytology, and tests for tuberculosis 1

Clinical Implications and Prognosis

• Development of ascites marks a significant decline in prognosis for cirrhosis patients 1
• Approximately 15% of patients with ascites die within 1 year and 44% within 5 years 1
• Patients with ascites are prone to additional complications including spontaneous bacterial peritonitis, electrolyte abnormalities, and hepatorenal syndrome 1
• Patients who develop ascites should be considered for liver transplantation evaluation as it offers the most definitive cure 5

Management Considerations

• Treatment focuses on addressing the underlying cause while managing fluid accumulation 4
• For cirrhotic ascites, sodium restriction and diuretics (spironolactone and furosemide) are first-line therapy 5
• Approximately 10% of patients develop refractory ascites requiring alternative approaches such as large-volume paracentesis with albumin or transjugular intrahepatic portosystemic shunts 4
• Avoid medications that worsen hypotension, such as ACE inhibitors, in cirrhotic patients with ascites 5