Ascites

The abnormal buildup of fluid in the abdomen

Aetiology

  • Cirrhosis is the most common cause in the developed world

Pathophysiology

  1. Portal hypertension increases the production of vasodilators (NO) which act on the splanchnic arteries
    1. Arteries dilate → decreased SVR → decrease in MAP
    2. Causes the activation of RAAS and secretion of ADH → sodium and water retention
  1. Compromised liver function reduces albumin levels, so kidneys detect low plasma volume
    1. Causes the activation of RAAS and secretion of ADH → sodium and water retention
  1. When the vasodilated blood vessels become overwhelmed by all the extra sodium and water, the patient becomes oedematous and ascites form

Clinical presentation

  • S+S of cirrhosis
  • Shifting dullness on examination

Investigations

USS

  • Darkness (fluid)

Serum ascites albumin gradient (SAAG)

  • Obtained by subtracting the ascitic fluid albumin (from paracentesis) from the serum albumin (from blood test)
  • Wide gradient indicates portal hypertension

Management

General considerations

  • No added sodium diet
  • Fluid restriction
  • Improve underlying liver disease
  • Be careful with use of drugs e.g. no NSAIDs, careful with IV drugs (often have high sodium load)

Diuretics

  • Spironolactone first line - blocks aldosterone (RAAS)
  • In recurrent ascites - dual step wise increments of spironolactone and loop diuretic (e.g. furosemide)
  • U+Es should be monitored frequently

Paracentesis

  • Drain inserted into abdomen
  • For patients with large volume of ascites or if their kidneys will not tolerate drainage via diuretics

Trans-jugular intra-hepatic porto-systemic shunt (TIPSS)

  • If paracentesis has to occur too frequently
  • Tract created between the hepatic vein and the portal vein within the liver and stent inserted to keep it open
  • Removes portal hypertension so removes drive towards ascites

Liver transplantation

  • Last line