18. Ascites and hepatorenal syndrome

Page created on February 19, 2019. Last updated on May 28, 2021 at 12:31


Ascites is the condition when there is pathologic fluid collection inside the abdominal cavity. It usually presents with increased abdominal girth (circumference), causing the abdominal cavity to be elevated above the thoracic cavity when lying down. The amount of fluid can exceed 10 litres. The fluid can be either transudative or exudative, depending on its albumin content.

It’s commonly associated with cirrhosis but can occur without liver damage as well.

Ascites due to portal hypertension

  • Right-sided heart failure
  • Cirrhosis
  • Constrictive pericarditis
  • Budd Chiari syndrome

Ascites without portal hypertension

  • Peritoneal carcinomatosis
  • Peritoneal tuberculosis
  • Pancreatitis
  • Ileus
  • Nephrotic syndrome

In cases of portal hypertension it can occur in intrahepatic and posthepatic obstructions but not in prehepatic obstruction.

In portal hypertension an increased hydrostatic pressure in the hepatic vessels forces fluid out from the intravascular space into the peritoneal cavity. This happens due to backflow and stasis, but also due to the redistribution of blood from non-spanchnic organs to splanchnic organs which causes renal hypoperfusion, activation of the RAAS system and expanded plasma volume.

In case of hypoproteinaemia will the Starling forces be larger and make the ascites even worse. Because of this will liver failure predispose for ascites formation.

The secondary hyperaldosteronism may cause hypokalaemia and metabolic alkalosis.

In ascites not caused by portal hypertension will the fluid leaking into the peritoenum happen due to a lower osmotic gradient. Examples of this is pancreatitis where pancreatic fluid accumulates in peritoneal cavity or peritoneal tuberculosis where the bacteria produces a lot of protein.

SAAG is a useful diagnostic tool for differentiating cases of ascites caused by portal hypertension and those where we have a normal portal pressure.

SAAG = (albumin levels in serum) – (albumin levels in ascites fluid)

Patients with gradients of 1.1 g/dL or greater have portal hypertension , whereas patients with gradients less than 1.1 g/dL do not.

  • Sodium restriction and diuretic therapy with protein replacement is the standard treatment for ascites.
  • Paracentesis is the procedure where abdominal fluid is drained with a needle or catheter. Paracentesis is usually only indicated when ascites can’t be treated by conservative therapy. It should be performed slowly and with simultaneous albumin infusion to prevent circulatory imbalance. TIPS (see topic 17) may also be performed in cases that are not treated by conservative therapy and paracentesis is contraindicated.
  • A peritoneovenous shunt or LaVeen shunt is a long tube with a one-way valve that drains fluid from the abdominal cavity into the IVC. It’s only used for patients who are not candidates for paracentesis, transplant or TIPS. It’s mostly superseded by TIPS.
  • Immersion: Higher outer hydrostatic pressure may promote a backflow of ascites to ECV and vascular space
Hepatorenal syndrome

Hepatorenal syndrome (HRS) is the development of renal failure in patients with liver failure. At least 10% of patients with cirrhosis and ascites will develop HRS, and the number increases in people with end-stage liver disease. HRS develops because of poor renal perfusion without any structural damage. Later will there be damage to the kidney as well.

In portal hypertension, backflow and stasis of vasodilatory substances like NO  begin to accumulate since the liver cant remove them. This splanchnic vasodilation “steals” perfusion from other organs to abdominal organs causing a relative increase of blood in splanchinc circulation and a relative decrease of blood in the non-splanchinc circulation.

This causes a reduction of effective circulating arterial blood volume, which mimics hypovolaemia. Especially the renal perfusion is decreased.

The decreased renal blood flow activates RAAS, which also activates the sympathetic nervous system. RAAS, SNS and other vasoconstrictors causes vasoconstriction of the renal artery, which further decrease renal perfusion. Up until now has there been no structural damage, just pre-renal azotaemia, but at this point may the renal blood flow be so reduced that tubular hypoxia and structural damage occurs. Chronic kidney failure may develop.

The only treatment is liver transplant. Patients who don’t receive liver transplant at this point have poor prognosis.

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