Liver cirrhosis: pathophysiology, causes and treatment

By Cristiano Antonino On Feb 21, 2023

Liver cirrhosis is a chronic liver disease characterised by widespread destruction and fibrotic regeneration of liver cells

What is cirrhosis of the liver?

The final stage of liver disease is called cirrhosis.

Cirrhosis is a chronic liver disease characterised by diffuse destruction and fibrotic regeneration of liver cells.

As necrotic tissue gives way to fibrosis, this disease disrupts liver structure and normal vascularisation, impairs blood and lymphatic flow and ultimately causes liver failure.

The prognosis is better in non-cirrhotic forms of liver fibrosis, which cause minimal liver dysfunction and do not destroy liver cells.

The clinical types of liver cirrhosis reflect its different aetiology:

Laennec cirrhosis. This is the most common type and occurs in 30%-50% of cirrhotic patients, up to 90% of whom have a history of alcoholism.

Biliary cirrhosis. Biliary cirrhosis is due to injury or prolonged obstruction.

Postnecrotic cirrhosis. Postnecrotic cirrhosis results from various types of hepatitis.

Pigmentary cirrhosis. Pigmentary cirrhosis may result from disorders such as haemochromatosis.

Cardiac cirrhosis. Cirrhosis of the heart refers to cirrhosis caused by right heart failure.

Idiopathic cirrhosis. Idiopathic cirrhosis has no known cause.

Pathophysiology

Although several factors have been implicated in the aetiology of cirrhosis, alcohol consumption is considered the main causative factor.

Necrosis. Cirrhosis is characterised by episodes of necrosis involving liver cells.

Scar tissue. The destroyed liver cells are gradually replaced by scar tissue.

Fibrosis. There is widespread destruction and fibrotic regeneration of liver cells.

Alteration. As necrotic tissue gives way to fibrosis, the disease alters liver structure and normal vascularisation, impairs blood and lymphatic flow and ultimately causes liver failure.

Various types of cirrhosis of the liver can occur in different types of individuals

The most common, Laennec cirrhosis, occurs in 30%-50% of cirrhotic patients.

Biliary cirrhosis occurs in 15%-20% of patients.

Postnecrotic cirrhosis occurs in 10%-30% of patients.

Pigmentary cirrhosis occurs in 5%-10% of patients.

Idiopathic cirrhosis occurs in about 10% of patients.

The different types of cirrhosis have different causes

Excessive alcohol consumption. Excessive alcohol consumption is the most common cause of cirrhosis, as liver damage is associated with chronic alcohol consumption.

Injury. Prolonged injury or obstruction causes biliary cirrhosis.

Hepatitis. Different types of hepatitis can cause postnecrotic cirrhosis.

Other diseases. Diseases such as haemochromatosis cause pigmentary cirrhosis.

Right heart failure. Cirrhosis, a rare type of cirrhosis, is caused by right heart failure.

Clinical manifestations

The clinical manifestations of the different types of cirrhosis are similar, regardless of the cause.

Gastrointestinal system. Early indicators usually involve gastrointestinal signs and symptoms such as anorexia, indigestion, nausea, vomiting, constipation or diarrhoea.

Respiratory system. Respiratory symptoms occur late as a consequence of liver failure and portal hypertension, such as pleural effusion and limited thoracic expansion due to abdominal ascites, which interfere with the efficiency of gas exchange and lead to hypoxia.

Central nervous system. The signs of hepatic encephalopathy also manifest themselves late in life: lethargy, mental changes, confused speech, asterixis (jerky tremor), peripheral neuritis, paranoia, hallucinations, extreme dullness and, finally, coma.

Haematological: the patient presents bleeding tendencies and anaemia.

Endocrine. Male patients present with testicular atrophy, while female patients may present with menstrual irregularities, gynaecomastia and loss of chest and armpit hair.

Skin. Severe itching, extreme dryness, poor tissue turgor, abnormal pigmentation, spider angiomas, palmar erythema and possibly jaundice are present.

Hepatic. Cirrhosis causes jaundice, ascites, hepatomegaly, leg oedema, hepatic encephalopathy and hepatic renal syndrome.

Complications of cirrhosis include the following:

Portal hypertension. Portal hypertension is the increased pressure in the portal vein that occurs when blood flow encounters increased resistance.

Oesophageal varices. Oesophageal varices are dilated tortuous veins in the submucosa of the lower oesophagus.

Hepatic encephalopathy. Hepatic encephalopathy may manifest with deterioration of mental status and dementia or with physical signs such as abnormal involuntary and voluntary movements.

Excess fluid volume. Excess fluid volume occurs due to increased cardiac output and decreased peripheral vascular resistance.

Evaluation and diagnostic results

Laboratory findings and imaging studies characteristic of cirrhosis include:

Liver scan. Liver scan shows abnormal thickening and a liver mass.

Liver biopsy. Liver biopsy is the definitive test for cirrhosis as it detects destruction and fibrosis of liver tissue.

Liver imaging. Computed tomography, ultrasound and magnetic resonance imaging can confirm the diagnosis of cirrhosis by visualising masses, abnormal growths, metastases and venous malformations.

Cholecystography and cholangiography. These two techniques visualise the gallbladder and bile duct system.

Splenoportal venography. Splenoportal venography visualises the portal venous system.

Percutaneous transhepatic cholangiography. This test differentiates intrahepatic from extrahepatic obstructive jaundice and reveals liver pathology and the presence of gallstones.

Complete blood count. A decrease in white blood cells, haemoglobin level and haematocrit, albumin or platelets is observed.

Medical management

Treatment is aimed at removing or alleviating the underlying cause of cirrhosis.

Diet. The patient may benefit from a high-calorie, high-protein diet, as the development of hepatic encephalopathy requires restriction of protein intake.

Sodium restriction is usually limited to 2 g/day.

Fluid restriction. Fluids are limited to 1-1.5 litres/day.

Activity. Rest and moderate exercise is essential.

Paracentesis. Paracentesis can help relieve ascites.

Sengstaken-Blakemore or Minnesota tube. The Sengstaken-Blakemore or Minnesota tube can also help control bleeding by applying pressure to the bleeding site.

Drug therapy

Drug therapy requires particular caution because the cirrhotic liver is unable to detoxify effectively.

Octreotide. If necessary, octreotide may be prescribed for oesophageal varices.

Diuretics. Diuretics may be administered for oedema, but require careful monitoring because fluid and electrolyte imbalance may precipitate hepatic encephalopathy.

Lactulose. Encephalopathy is treated with lactulose.

Antibiotics. Antibiotics are used to reduce intestinal bacteria and ammonia production, one of the causes of encephalopathy.

Surgical management

Surgical procedures for the management of cirrhosis of the liver include:

Transjugular intrahepatic portosystemic shunt (TIPS) procedure. The TIPS procedure is used for the treatment of varices by upper endoscopy with bandaging to relieve portal hypertension.

Nursing management

The nursing management of the patient with liver cirrhosis should focus on promoting rest, improving nutritional status, skin care, reducing the risk of injury, and monitoring and managing complications.

Nursing assessment

The evaluation of the patient with cirrhosis of the liver should include the assessment of:

Bleeding. Check the patient’s skin, gums, faeces and vomit for bleeding.
Fluid retention. To assess fluid retention, weigh the patient and measure abdominal circumference at least once a day.
Mentality. Frequently assess the patient’s level of consciousness and carefully observe changes in behaviour or personality.

Nursing diagnosis

Based on the assessment data, the main nursing diagnoses for the patient are:

Activity intolerance related to tiredness, lethargy and malaise.

Imbalanced nutrition: less than body requirements related to abdominal distension and discomfort and anorexia.

Impairment of skin integrity related to itching from jaundice and oedema.

High risk of injury in relation to altered coagulation mechanisms and altered level of consciousness.

Body image disturbance related to changes in appearance, sexual dysfunction and role functions.

Chronic pain and discomfort related to liver enlargement and ascites.

Excess fluid volume related to ascites and oedema formation.

Disturbed mental processes and potential mental deterioration in relation to abnormal liver function and increased serum ammonia level.

Ineffective breathing in relation to ascites and restriction of chest excursion due to ascites, abdominal distension and fluid in the chest cavity.

Nursing care planning and objectives

Main article: 8 Nursing care plans for cirrhosis of the liver

The main goals for a patient with cirrhosis are:

Decrease fatigue and increase the ability to participate in activities.

Maintain a positive nitrogen balance, avoid further loss of muscle mass and meet nutritional requirements.

Reduce the potential for developing pressure ulcers and breaking down skin integrity.

Reduce the risk of injury.

Verbalise feelings consistent with improved body image and self-esteem.

Increase comfort level.

Restore normal fluid volume.

Improve mental state, maintain confidence and ability to cope with cognitive and behavioural changes.

Improve respiratory status.

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Nursing interventions

The patient with cirrhosis needs careful observation, first-class supportive care and sound nutritional advice.

Promoting rest

Position the bed so as to achieve maximum respiratory efficiency; provide oxygen if necessary.

Begin to prevent respiratory, circulatory and vascular disorders.

Encourage the patient to gradually increase activity and plan rest with activity and light exercise.

Improve nutritional status

Provide a nutritious diet rich in protein, supplemented with B-complex vitamins and others, including A, C and K.

Encourage the patient to eat: Provide small, frequent meals, consider the patient’s preferences and provide protein supplements if indicated.

If necessary, provide nutrients via tube or total PN.

Administer water-soluble forms of fat-soluble vitamins A, D and E to patients with fatty stools (steatorrhoea) and give folic acid and iron to prevent anaemia.

Temporarily provide a low protein diet if the patient shows signs of impending or advanced coma; limit sodium if necessary.

Skin care

Change the patient’s position frequently.

Avoid the use of irritating soaps and adhesive tapes.

Provide lotions to soothe irritated skin; take measures to prevent the patient from scratching the skin.

Reducing the risk of injury

Use padded sides if the patient is agitated or restless.

Orient the patient to the time, place and procedures to minimise agitation.

Instruct the patient to ask for assistance to get out of bed.

Carefully assess any injuries for the possibility of internal bleeding.

Provide safety measures to avoid injury or cuts (electric razor, soft toothbrush).

Apply pressure to venipuncture sites to minimise bleeding.

Monitoring and management of complications

Monitor bleeding and haemorrhage.

Closely monitor the patient’s mental status and report changes so that treatment of encephalopathy can be initiated promptly.

Closely monitor serum electrolyte levels and correct them if abnormal.

Administer oxygen in case of oxygen desaturation; monitor for fever or abdominal pain, which may signal the onset of bacterial peritonitis or other infection.

Assess cardiovascular and respiratory status; administer diuretics, implement fluid restriction and improve patient positioning if necessary.

Monitor intake and output, daily weight changes, changes in abdominal girth and oedema formation.

Monitor nocturia and subsequently oliguria, as these states indicate increasing severity of liver dysfunction.

Home management

Prepare for discharge by providing dietary instructions, including exclusion of alcohol.

If indicated, refer to Alcoholics Anonymous, psychiatric assistance, counselling or spiritual counsellor.

Continue sodium restriction; emphasise the importance of avoiding raw shells.

Provide written instructions, teaching, support and reinforcement to the patient and family.

Encourage rest and probably a change in lifestyle (proper, well-balanced diet and elimination of alcohol).

Educate the family about the symptoms of impending encephalopathy and the possibility of haemorrhagic tendencies and infections.

Offer support and encouragement to the patient and provide positive feedback when the patient is successful.

Referring the patient to the home care nurse and assisting him/her in the transition from hospital to home.

Assessment

Expected patient outcomes include:

Decreased fatigue and increased ability to participate in activities.

Maintenance of a positive nitrogen balance, no further loss of muscle mass and fulfilment of nutritional requirements.

Decreased potential for development of pressure ulcers and breakdown of skin integrity.

Reduced risk of injury.

Expressed feelings consistent with improved body image and self-esteem.

Increased comfort level.

Restoration of normal fluid volume.

Improved mental state, maintained confidence and ability to cope with cognitive and behavioural changes.

Improvement of respiratory status.

Discharge and home care guidelines

Discharge education focuses on dietary instructions.

Limitation of alcohol. The most important thing is the exclusion of alcohol from the diet, so the patient may need to be referred to Alcoholics Anonymous, psychiatric care or counselling.

Sodium restriction. Sodium restriction should be continued for a considerable period of time, if not permanently.

Education about complications. The nurse educates the patient and family about symptoms of impending encephalopathy, possible bleeding tendency and susceptibility to infection.