Cirrhosis of liver,
Cirrhosis is defined as a diffuse process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal nodule.
Cirrhosis is a gradually progressive wide spread death of liver cells associated with inflammation and fibrosis leading to loss of normal lobular liver architecture.
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- Micro-nodular cirrhosis: The nodules are less than 3-4 mm in diameter characterized by regular connective tissue septa regenerative nodules and involvement of every lobule. Chronic alcoholism is the commonest cause of it.
- Macro-nodular cirrhosis: The nodules measure several centimeters in diameter. Connective tissue septa vary in thickness and nodules show marked differences in size. Chronic active hepatitis is the commonest cause.
- Intermediate mixed form.
- Excessive intake of alcohol
- Post hepatic and post necrotic cirrhosis- hepatitis B, hepatitis C, hepatitis D, may lead to this type of cirrhosis.
- Immunological- Auto immune chronic active hepatitis.
- Primary biliary cirrhosis
- Secondary biliary cirrhosis ( stone, stricture)
- Primary sclerosing cholangitis
- Wilson’s disease
- Glycogen storage disease
After necrosis and disintegration of liver cells the reticular framework collapses thereby portal and central zone are approximated. Fibrous septae develop in the portal zones and proceed towards lobular parenchyma dissecting them into various sizes. In the meantime, some cells regenerate to form nodules of various sizes giving a macroscopic appearance of macronodular, micronodular or mixed type cirrhosis. Gradually portal hypertension develops due to increased intra hepatic vascular resistance. This increased resistance is due to compression of vessel by regenerating nodule, distortion and narrowing of portal vessels by fibrous tissue. Ultimately from portal hypertension, oesophago gastric varices, splenomegaly with or without hypersplenism, ascites and spontaneous bacterial peritonotis develop.
Apart from portal hypertension ascites may develop from other causes also like low COT, increased sodium retention by kidney due to hyperaldosteronism, increased sympathetic activity, altered renal hemodynamics, altered metabolism of prostaglandins, over production of hepatic and splenic lymph giving rise to lymphorroea, non-absorption of water and lymph by the peritoneal lymphatics and impaired renal water excretion by high ADH.
Most common signs and symptoms are as follows-
- Anorexia, nausea, vomiting, flatulence.
- Gradual swelling of the abdomen and feet.
- Gradual weakness, fatigue, muscle cramps and weight loss.
- Malnutrition may be present.
- Hematemasis and malaena
- Upper abdominal discomfort and gaseous abdominal distension.
- Bleeding piles.
- Diarrhea or constipation
- Men-Gynecomastia, testicular atrophy.
- Women- Breast atrophy, irregular menstruation, amenorrhea.
- Hyponatremia- increases loss of sodium.
- Facies-Hepatic facies is present, sunken eyes, prominence of molar bones, mild jaundice, icteroid conjunctiva, muddy complexion of the face and spider telangiectasia.
- Anaemia is present.
- Palmar erythema and spider angioma may be present.
- Oedema is present, pitting in type. This is due to low protein level.
- Cutaneous hemorrhages may be present.
- Fever may be present in 35% of cases due to secondary infection.
- Cyanosis may be present in more than 30% cases due to hypoxemia.
- Abdomen-hepatomegaly, splenomegaly, ascites etc.
- History and physical examination.
- Blood examination shows moderate leucopenia, thrombocytopenia and anaemia.
- Urine shows excess of urobilinogen but bile may be present in biliary cirrhosis.
- Radiological tests
- Plain abdominal x-ray
- Barium contrast or swallow
- Liver function tests
- Plasma bilirubin increased
- Prothrombin time prolonged
- Plasma alkaline phosphate increased in biliary cirrhosis
- SGOT and SGPT levels are elevated.
- Plasma albumin decreased.
- Liver biopsy
- USG is helpful for hepatic enlargement, spleen enlargement, dilated portal vein, ascites.
No treatment can reverse cirrhosis or even ensure that no further progression occurs. Treatment is symptomatic and supportive.
- Rest- rest is advisable when there is hemorrhage, oedema, ascites or other complications.
- Diet- nutritious diet containing more carbohydrate, moderate protein and fat may be given.
- Alcohol must be forbidden.
- Vitamin and other supplements may be required.
- Drugs- Oral thiazide diuretics with potassium supplementation may be may be used. Anti anaemic therapy and blood transfusion should be given if necessary.
- Treatment of complication if any.
- Measured weight and fluid intake and output and record daily.
- Check vital signs 4 hourly and recorded it.
- Liver transplantation may be considered in cases with progressive disease, fulminants hepatic failure or in metabolic defect.
Complications of cirrhosis of liver
- Portal hypertension
- Haetamatemasis and malaena
- Spontaneous bacterial peritonitis
- Hepatic encephalopathy
- Renal encephalopathy
- Renal failure
- Hepatocellular carcinoma