In cirrhosis the functional liver tissue is replaced by connective tissue.
Alcohol is the most common cause of liver cirrhosis, but other aetiologies should be excluded.
A patient with liver cirrhosis may be asymptomatic for a long period and the symptoms are often related to hepatic failure.
Proneness to developing an alcoholic liver disease is individual and not predictable.
Aetiology
Alcoholic liver disease
Fatty liver and alcoholic hepatitis are intermediate phases in alcoholic liver cirrhosis. The development is preceded nearly always by continuous consumption of alcohol for years.
The level of high risk in women has been estimated to be over 20 g of absolute alcohol, i.e. approximately 2 units, regularly daily or in total 12-16 units per week. In men, the level of high risk is 40 g per day (approx. 3 units) regularly daily or in total 23-24 units per week.
According to a Finnish dietary recommendation published in 2014, the amount should not exceed 10 g per day (women) or 20 g per day (men).
At an early stage cirrhosis is often asymptomatic. Fatigue, itching, jaundice, and abdominal swelling are late symptoms or are associated with the activity of the underlying disease.
Acute bleeding from oesophageal varices or acute jaundice may also be the first symptom of liver cirrhosis.
Possible findings (often the status is normal)
Small, indurated liver, with the edge possibly palpable in patients who have lost weight
Palpable spleen
Muscle wasting and weight loss
Spider naevi on the upper trunk and the face
Palmar erythema
Gynaecomastia and testicular atrophy
Dilated abdominal surface veins
Ascites
Jaundice
Laboratory investigations
The basic investigations when liver disease is suspected
ESR, basic blood count with platelet count, ALT, AST, alkaline phosphatase, GGT, bilirubin, prothrombin time or INR, albumin, prealbumin, potassium, sodium, creatinine and fasting plasma glucose
A "bright" liver indicates fatty transformation or cirrhosis, but is an unspecific finding.
Fatty transformation is not revealed by ultrasonography until it exceeds 30%.
Spleen enlargement, dilated vessels of the portal system, and visible collaterals suggest portal hypertension.
Even a small amount of ascites can be detected easily.
Retrograde flow or obstruction in the portal vein detected by Doppler ultrasonography is a sign of poor prognosis.
MRI or CT
May provide more indications of liver cirrhosis: structure of the liver, signs of portal hypertension, possible focal lesions.
Elastography (e.g. Fibroscan® )
Non-invasive investigation that can be used to evaluate the level of fibrosis in the liver
Associated with some sources of error.
Liver biopsy
Confirmation of cirrhosis
Stage of fibrosis (regenerative nodules, fibrous septa) may provide indications of the aetiology.
In advanced cirrhosis, biopsy does not always provide additional information to the aetiological investigations.
To be considered whether the biopsy has any influence from the therapeutic viewpoint.
Sources of error
False negative result, because even rather healthy tissue may be found between the cirrhotic areas
False positive resuls: biopsy along the capsule, poor sampling, etc.
Liver biopsy can be performed if INR is < 1.5 and platelet count is > 60.
Treatment of cirrhosis and its complications
Abstinence improves prognosis in alcoholic cirrhosis, but the risk of hepatocellular carcinoma Cancer of the Liver and the Biliary Tract nevertheless remains elevated. A diet rich in energy and protein is needed, because cirrhosis is often associated with malnutrition. Due to catabolism, the patient may even be advised to eat before going to bed.
No antifibrotic medication is available, but the treament of the underlying liver disease may halt the progression of cirrhosis.
The development of liver failure in a patient with liver cirrhosis often results from some complication (bleeding, infection, hypovolaemia for other reasons, etc.), the detection and treatment of which is important, in addition to treating the specific symptoms of liver failure.
Grading of cirrhosis enables the assessment of the severity of the liver damage and its influence on the patient's prognosis. Child-Pugh classification http://www.mdcalc.com/child-pugh-score-for-cirrhosis-mortality/ is the most commonly used. It takes into account liver function (INR, albumin), cholestasis (bilirubin) and symptoms (encephalopathy, ascites).
Portal hypertension
Gastroscopy should be performed on all patients with liver cirrhosis to detect possible oesophageal varices.
If the patient has had a variceal bleeding, a recurrence can be prevented
by ablating the varices by rubber band ligation
by lowering portal pressure with a non-selective beta blocker (propranolol 10-40 mg 2-3 times daily; the heart rate is titrated 25% lower).
in profuse acute bleeding by endoscopic procedures, by somatostatin or its analogue octreotide, by Sengstaken-Blakemore tube
sometimes by transjugular intrahepatic portosystemic shunt (TIPS) or shunt surgery if the forementioned methods fail .
If clear oesophageal varices are detected but the patient has not had variceal bleeding, the first bleeding can be prevented by using a beta blocker (propranolol ).
Ascites
Salt restriction (1-3 g of sodium daily; 1 g of sodium is equal to 2.5 g of table salt)
In therapy-resistant ascites even a large paracentesis (5-10 litres during 6-8 hours) is safe if 6-8 g of albumin is infused intravenously for every removed litre of ascites. The ascites puncture (video Removal of Ascites) may be performed with a needle for percutaneous cystostomy or also with Seldinger's technique.
Coagulation factors need not be corrected in association with the puncture, at least if thrombocyte count is > 50 × 109 /l. Diuretics are paused for 2 days after the puncture.
Complications include spontaneous peritonitis, hyponatraemia and hepatorenal syndrome (control sodium, potassium, diuresis, body weight).
Spontaneous peritonitis is often asymptomatic; the ascitic fluid sample is tested for the following: cell count, glucose, albumin, bacterial stain and culture, sometimes tuberculosis samples.
If the ascites does not respond to therapy consult a surgeon or a radiologist: shunt, TIPS .
Refractory ascites may be an indication for liver transplantation.
In hepatorenal syndrome (HRS), renal failure develops in a patient with severe acute or chronic liver disease.
Exclusion of other renal diseases and assessment of predisposing factors
Stop medications with renal toxicity.
Adequate fluid therapy, correction of hypovolaemia and electrolyte disturbances
The condition is regarded as HRS when ascites formation refractory to treatment has led to the impairment of renal function so that no response is anymore obtained even if hypovolaemia were corrected with albumin infusion.
HRS 1: rapid development of renal failure, associated with acute hepatic failure (also in cirrhosis); the prognosis is poor, only some weeks, mortality rate 80-100%
HRS 2: renal failure develops in a slower pace in a patient with hepatic failure; without liver transplantation, 75% of the patients will die within one year.
Treatment
Correction of hypovolaemia, fluid therapy, intravenous albumin, drainage of ascites
Lactulose should be given 15-30 ml 2-3 times daily aiming at 2-3 loose stools per day. It can also be used prophylactically. Lactitol can be used instead of lactulose.