CIRRHOSIS OF LIVER

Cirrhosis is an irreversible chronic parenchymal disease of the liver resulting from the necrosis of liver cells followed by fibrosis and nodule formation. The liver architecture is diffusely abnormal and this interferes with liver blood flow (causing portal hypertension) and also interferes with hepatic function (resulting in hepatic insufficiency).

ETIOLOGY

Common

Chronic hepatitis due to hepatitis B, C, and D viruses.

Alcohol

Less common

Metabolic disease

Hemochromatosis: Characterized by excessive deposition of iron in the liver.

Wilson’s disease: Characterized by excessive deposition of copper in the liver, mostly in young patients.

Alpha -1 antitrypsin deficiency: results in cirrhosis and emphysema.

Cystic fibrosis

Glycogen storage disease

Biliary obstruction

Primary biliary cirrhosis

Secondary biliary cirrhosis resulting from obstruction of the bile duct due to stricture, stone, or neoplasm.

Primary sclerosing cholangitis.

Drugs

Methyldopa, methotrexate.

Hepatic congestion

Others

Cardiac failure: causing backward pressure for a long period & leads to liver cirrhosis, this is called cardiac cirrhosis.

Budd-Chiari syndrome: Characterized by venous outflow obstruction in the hepatic vein, leading to congestion & cirrhosis.

Cryptogenic: cirrhosis of unknown aetiology.

Autoimmune hepatitis.

Non-specific features

Initially, the features are non-specific e.g.

Weakness, fatigability, weight loss, muscle cramps.

Anorexia, nausea, and occasional vomiting

Abdominal pain due to stretching of the liver capsule

Specific features

The clinical features of cirrhosis are mainly due to

1 . Portal hypertension

2- Hepatic insufficiency

CLINICAL FEATURES OF CIRRHOSIS

Portal hypertension

Splenomegaly

Hypersplenism

Collateral circulation causing variceal bleeding

Ascites

Hepatic insufficiency

Encephalopathy

Jaundice

Palmar erythema and spider nevi

Endocrine abnormalities 

Gynaecomastia

Testicular atrophy

Amenorrhea

Bleeding tendency

Encephalopathy

Skin pigmentation

Dupuytren’s contracture

Hepatopulmonary syndrome

Features of encephalopathy are from restlessness, aggressive outbursts, and drowsiness to coma.

Renal failure (hepatorenal syndrome)

Renal failure develops in advanced cirrhosis mostly with ascites. It is caused by decreased effective blood volume and hypotension as a result of vasodilatation due to the release of nitric oxide from the liver.

INVESTIGATION IN CIRRHOSIS

LFTs raised

Serum albumin is reduced

Prothrombin time becomes prolonged *

Low serum sodium indicates severe liver disease. Hyponatremia is dilutional secondary to a defect in free water clearance (dilutional hyponatremia).

Hyponatremia may be due to excessive diuretic therapy.

FBE – Anemia due to hypersplenism or blood loss.

WBC -count may be decreased due to hypersplenism or increased due to infection or may be normal.

Platelet count is usually low due to hypersplenism.

Imaging

Ultrasound of the upper abdomen may reveal:

Cirrhotic changes in liver

Portal vein dilatation

Splenomegaly

Endoscopy

Esophagogastroscopy to confirm the presence of varices and portal hypertensive gastropathy.

Liver biopsy

A liver biopsy may be needed to confirm the severity and type of liver disease.

To identify the cause

Viral markers

Serum autoantibodies.

Serum immunoglobulins

Serum ceruloplasmin and urinary copper for Wilson’s disease.

Serum alpha 1- antitrypsin should always be done in young cirrhotics.

Serum iron, ferritin, and total iron-binding capacity should be performed to exclude hemochromatosis.

Alpha-fetoprotein: If raised is strongly suggestive of hepatocellular carcinoma.

MANAGEMENT

Referral to gastroeneterologist

There is no treatment that will arrest or reverse cirrhotic changes. Therefore, management is only of the complications.

COMPLICATIONS OF CIRRHOSIS

Variceal haemorrhage

Ascites

Hepatic encephalopathy

Renal failure

Hepatoma