n CME : Your SA Journal of CPD - Management of chronic liver disease : main article

Volume 23, Issue 8
  • ISSN : 0256-2170



The most ominous complication of portal hypertension is oesophageal variceal bleeding. Patients have a poor long-term prognosis irrespective of treatment and few survive more than 5 years. <br>Patients with cirrhosis should be screened endoscopically to determine the presence and size of varices and the need for therapeutic intervention and surveillance endoscopy. <br>Only 25 - 40% of patients with oesophageal varices will experience variceal bleeding. <br>Endoscopic banding/sclerotherapy together with pharmacological therapy, e.g. octreotide, after adequate resuscitation is the treatment of choice for an acute variceal bleed. <br>Indications for TIPS include: portal hypertensive bleeding, refractory ascites, refractory hepatic hydrothorax and hepatorenal syndrome. <br>Diagnostic paracentesis is indicated in new-onset ascites, admission to hospital, clinical deterioration and fever. <br>An ascitic fluid neutrophil count > 250/mm&lt;sup&gt;3&lt;/sup&gt; is a presumptive threshold for peritonitis. Direct inoculation of 10 ml ascitic acid into blood culture bottles improves the culture yield from 42% to 91%. <br>Splanchnic vasodilatation and subsequent activation of a cascade of vasoconstrictors and antinatriuretic factors is the main pathophysiological factor involved in ascites formation and development of the hepatorenal syndrome. <br>Type I hepatorenal syndrome is characterised by rapidly progressive deterioration in renal function defined by the doubling of the initial serum creatinine to a level greater than 250 mm<sup>3</sup>/ml or 50% reduction in the initial 24-h creatinine clearance to a level lower than 20 ml/min in less than 2 weeks. Type II hepatorenal syndrome is often associated with refractory ascites and is slowly progressive with a moderate reduction in creatinine and glomerular filtration. <br>Management of acute hepatic encephalopathy includes identification and correction of any precipitating factors, restriction of dietary protein and administration of lactulose. <br>Precipitating factors in acute encephalopathy include excess protein, GIT bleeding, ingestion of alcohol and sedatives, overdiuresis, infections and development of hepatocellular carcinoma.

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