Liver cirrhosis - complications: esophageal varices, ascites, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, portal encephalopathy (PE).
The main problems with liver cirrhosis are the complications. Let’s address these here.
Esophageal varices
Varices are a direct result of portal hypertension. The most important of these varices are the enlargement of gastric and coronary veins that form gastroesophageal varices. The formation depends on a threshold portal pressure of 10-12 mm Hg, below this, varices do not develop. Once the threshold has been reached, varices can form, typically in the lower ⅓ of the esophagus. These varices are liable to rupture and bleed, causing massive blood loss, hematemesis and high risk of death.
Treatment in the emergency rupture form is a vasoactive drug (terlipressin or octreotide) with antibiotics and urgent variceal ligation or sclerotherapy (injection of sclerosing agents); balloon tamponade, possibly with Sengstaken-Blakemore tube, is only a temporary bridge. Patients with cirrhosis should be regularly monitored for varices with endoscopic examination, short-term antibiotic prophylaxis can be given to help improve patient condition.
Image: “Sengstaken-Blakemore scheme EN” by Olek Remesz (wiki-pl: Orem , commons: Orem ), CC BY-SA 3.0, via Wikimedia Commons.
Ascites
(see below)
Spontaneous bacterial peritonitis
This is the infection of ascitic fluid, in the absence of any particular focus of infection (e.g. perforated bowel). Bacteria is thought to originate from the intestinal lumen to the mesenteric lymph nodes, with impaired local and systemic immune defenses contributing to bacterial translocation. The lack of successful portal system also means that usual transient bacteremia can become more prolonged and colonize ascitic fluid.
Clinical symptoms are that of infection (fever, chills, nausea, vomiting, pain, tenderness, malaise), affected mental status and worsening ascites.
Most common bacterial source is E.coli, followed by Klebsiella, strep and staph.
Treatment is Antibiotics, with third generation cephalosporins as the default (e.g. cefotaxime). SBP occurs in 10-27% of patients with ascites.
Hepatorenal syndrome
Hepatorenal syndrome is an interesting little syndrome that refers to the rapid deterioration in kidney function in individuals with cirrhosis. It usually occurs when there is a sudden drop in liver function and is a relatively common complication. It is best explained by explaining the pathophysiology.
The simplest way to explain this is in a chain:
- Portal hypertension
- Causes release of NO and other vasodilators
- This activates renin-angiotensin-aldosterone system which triggers:
- Renal sodium retention - CAUSING ASCITES
- Renal vasoconstriction - CAUSING HEPATORENAL SYNDROME