18. Ascites and hepatorenal syndrome

Last updated on March 12, 2019 at 12:41

Ascites

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 be even 15 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. The common causes are:

  • Right-sided heart failure
  • Cirrhosis
  • Hepatitis
  • Cancer in abdominal organs

It can occur in sinusoidal, postsinusoidal and posthepatic obstructions but not in presinusoidal or prehepatic obstruction.

Pathomechanism: Hepatic sinusoids are very fenestrated. As the pressure increases inside the sinusoids will fluid quickly be forced through the fenestra and into the space of Disse. The fenestration allows proteins to pass through as well, so the fluid forced through the fenestra be protein-rich. The lymphatic vessels drain the extra fluid, but as the disease progresses will the extra fluid be too much for the lymph to drain. The excess fluid appears as droplets on the surface of the liver that drip into the abdominal cavity. The droplets have high oncotic pressure and therefore cause more fluid to move from mesenteric capillaries into the abdominal cavity due to Starling forces.

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.

Other mechanisms play a role as well. As blood is redistributed from the non-splanchnic organs to the splanchnic organs due to mesenteric congestion as explained in topic 17 will the kidney be hypoperfused. This causes activation of RAAS which causes salt and water retention. This expands the plasma volume, which contributes to the extravasation of fluid.

The secondary hyperaldosteronism may cause hypokalaemia and metabolic alkalosis.

Treatment: Sodium restriction and diuretic therapy 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 internal jugular vein. It’s only used for patients who are not candidates for paracentesis, transplant or TIPS. It’s mostly superseded by TIPS.

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.

Pathogenesis: In portal hypertension will there be more vasodilation in the splanchnic circulation due to increased production of vasodilators like NO. This “steals” perfusion from other organs to the abdominal organs, which causes a relative increase of blood in the splanchnic circulation and a relative decrease of blood in the non-splanchnic 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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17. Portal hypertension

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19. Hepatic coma

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