Cirrhosis is the liver’s response to chronic or repeated liver injury from a range of insults, characterised by progressive fibrosis with nodular regeneration. All patients with suspected cirrhosis should be referred to secondary care.
The clinical complications of cirrhosis are due to either reduced synthetic/ metabolic function (e.g. low albumin, coagulopathy, jaundice) or portal hypertension (variceal bleeding, ascites formation, encephalopathy).
In Scotland, the common causes of cirrhosis are alcohol, non-alcoholic fatty liver disease and chronic hepatitis C infection. Other causes include chronic hepatitis B infection, autoimmune conditions (autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis), metabolic disorders (haemochromatosis, Wilson’s disease and alpha-1-antitrypsin deficiency), secondary biliary cirrhosis and toxic liver injury due to medications.
There is an increased risk of cirrhosis in patients who misuse alcohol, have risk factors for viral hepatitis (HBV/HCV infection), those who are obese or have type II diabetes mellitus.
Examination: A clinical examination may be entirely normal or may reveal signs of chronic liver disease, e.g. jaundice, bruising, spider naevi, distended abdominal veins, abdominal distension or peripheral oedema.
Baseline investigations: Patients suspected of having cirrhosis or presenting with abnormal liver function tests should undergo an initial liver screen (refer to guidance on investigation of abnormal liver function tests). Patients with cirrhosis and portal hypertension frequently present with low platelets.
Patients should have an abdominal US to look for evidence of cirrhosis or portal hypertension (e.g. ascites, splenomegaly or varices). The liver may appear normal in patients with early cirrhosis or may show non-specific features such as a coarse liver parenchyma.
GPs should refer patients to secondary care at the Border General who are suspected of having advanced liver fibrosis/cirrhosis. Please follow the abnormal liver function guidelines for further advice.
Referral via SCI Gateway: Borders General Hospital -> Gastroenterology -> Borders General Referral
Patients with liver cirrhosis require initial assessment and long-term follow-up in secondary care.
The following guidance is intended to assist primary care in the shared care of selected complications of liver cirrhosis.
Ascites and Peripheral Oedema
Patients with ascites and/or peripheral oedema should be advised on a low salt diet and treated with spironolactone (50-300mg/ day) + furosemide (40-120mg/ day). Diuretics should be commenced at a low dose and increased incrementally with close monitoring of renal function and electrolytes. Patients with recurrent ascites who are either resistant to or intolerant of diuretics may require admission for paracentesis. Transjugular intrahepatic porto-systemic shunt (TIPSS) or liver transplantation is sometimes considered in selected patients with resistant ascites.
A hepatic hydrothorax (pleural effusion) may develop in patients with ascites due to movement of ascitic fluid into the pleural cavity The principles of management are similar to those used in patients with ascites.
Variceal Bleeding
Varices develop as a consequence of portal hypertension. Patients with significant oesophageal or gastric varices are at risk of variceal bleeding which carries a high mortality. Patients with cirrhosis and suspected upper GI bleeding require urgent hospital admission.
Patients with confirmed cirrhosis should have a screening endoscopy which will be arranged by the GI team. If small oesophageal varices are present, they may be offered annual OGDs for monitoring.
If oesophageal varices are present, then patients will be offered treatment with either non-selective beta-blockade (usually. carvedilol 12.5mg /day) or enrolment in a programme of endoscopic band ligation (“banding”).
Patients with a history of variceal haemorrhage may be enrolled in a banding programme to eradicate their varices and may also be started on a carvedilol.
Hepatic Encephalopathy
Hepatic encephalopathy (HE) can occur spontaneously or be precipitated by infection, electrolyte abnormalities, GI bleeding, medication and constipation. Symptoms include change in sleep patterns, poor concentration, change in personality, slurred speech, movement disorders, progressing to severe confusion and reduced conscious level.
The management of HE involves identification and treatment of the underlying cause. Whenever possible, medication such as sedatives and opiates should be discontinued. Lactulose (10-40ml daily) is used to encourage regular bowel motions (two soft motions per day). In selected patients, the non-absorbable antibiotic, Rifaximin 550mg twice daily is used to alter the gut microflora and is successful in treating chronic encephalopathy/ reducing hospital admissions.
HCC Surveillance
Patients with liver cirrhosis are at increased risk of developing hepatocellular carcinoma (HCC). The risk varies according to the underlying cause of liver disease and severity of cirrhosis. If considered appropriate, patients with liver cirrhosis are offered enrolment into HCC surveillance consisting of 6 monthly liver ultrasound and serum alpha fetoprotein (AFP) measurement, arranged through the secondary care liver clinic.
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