Cirrhosis
D E FI N I T ION
End-stage of chronic liver damage with replacement of normal liver architecture
with diffuse fibrosis and nodules of regenerating hepatocytes. Decompensated when
there are complications such as ascites, jaundice, encephalopathy or GI bleeding (see Liver
failure).
AE T IOLOGY
Chronic alcohol misuse: Most common UK cause.
Chronic viral hepatitis: Hepatitis B/C are the most common causes worldwide.
Autoimmune hepatitis.
Drugs: e.g. methotrexate, hepatotoxic drugs.
Inherited: a1-Antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia,
cystic fibrosis.
Vascular: Budd–Chiari syndrome or hepatic venous congestion.
Chronic biliary diseases: Primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC),
biliary atresia.
Cryptogenic: In 5–10%.
Non-alcoholic steatohepatitis (NASH) " risk of developing cirrhosis. NASH is associated
with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia
and drugs, e.g. amiodarone, tamoxifen.
Decompensation can be precipitated by infection, GI bleeding, constipation, high-protein
meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein
thrombosis.
E P IDEMIOLOGY
Among the top 10 leading cause of deaths worldwide.
H ISTORY
Early non-specific symptoms: Anorexia, nausea, fatigue, weakness, weight loss.
Symptoms caused by # liver synthetic function: Easy bruising, abdominal swelling, ankle
oedema.
Reduced detoxification function: Jaundice, personality change, altered sleep pattern,
amenorrhoea.
Portal hypertension: Abdominal swelling, haematemesis, PR bleeding or melaena.
EXAMINA T I ON
Stigmata of chronic liver disease: Asterixis (‘liver flap’). Bruises. Clubbing.
Dupuytren’s contracture. Erythema (palmar). Jaundice, gynaecomastia, leukonychia, parotid
enlargement, spider naevi, scratch marks, ascites (‘shifting dullness’ and fluid thrill), enlarged
liver (shrunken and small in later stage), testicular atrophy, caput medusae (dilated superficial
abdominal veins), splenomegaly (indicating portal hypertension).
INVE S T I G A T IONS
Blood: FBC: # Hb, # platelets as a result of hypersplenism. LFTs: May be normal or often
" transaminases, AlkPhos, GGT, bilirubin, # albumin. Clotting: Prolonged PT (# synthesis of
clotting factors). Serum AFP: " In chronic liver disease, but high levels may suggest
hepatocellular carcinoma.
Other investigations: To determine the cause, e.g. viral serology (HBsAg, HBsAb, HCV ab),
a1-antitrypsin, caeruloplasmin (Wilson’s disease), iron studies: serum ferritin, iron, total
iron binding capacity (haemochromatosis), antimitochondrial antibody (PBC), antinuclear
antibodies (ANA), SMA (autoimmune hepatitis).
Ascitic tap: Microscopy, culture and sensitivity, biochemistry (protein, albumin, glucose,
amylase) and cytology. If neutrophils >250/mm3, this indicates spontaneous bacterial
peritonitis (SBP).
Liver biopsy: Percutaneous or transjugular if clotting deranged or ascites present. Histopathology:
Periportal fibrosis, loss of normal liver architecture and nodular appearance.
Grade refers to the assessment of degree of inflammation, whereas stage refers to the
degree of architectural distortion, ranging from mild portal fibrosis to cirrhosis.
Cirrhosis (continued)
Imaging: Ultrasound, CT or MRI (to detect complications of cirrhosis such as ascites,
hepatocellular carcinoma, and hepatic or portal vein thrombosis, to exclude biliary
obstruction), MRCP (if PSC suspected).
Endoscopy: Examine for varices, portal hypertensive gastropathy.
Child–Pugh grading: Class A is score 5–6, Class B is score 7–9, Class C is score 10–15.
MANAGEMENT
Treat the cause if possible, avoid alcohol, sedatives, opiates, NSAIDs and
drugs that affect the liver. Nutrition is very important and if intake is poor, dietitian review
and enteral supplements should be given; nasogastric feeding may be indicated.
Treat the complications:
Encephalopathy: Treat infections. Exclude a GI bleed. Lactulose, phosphate enemas and avoid
sedation.
Ascites: Diuretics (spironolactonefurosemide), dietary sodium restriction (88 meq or
2 g/day), therapeutic paracentesis (with human albumin replacement IV). Monitor
weight daily. Fluid restriction in patients with plasma sodium <120 mmol/L. Avoid
alcohol and NSAIDs.
SBP: Antibiotic treatment (e.g. cefuroxime and metronidazole), prophylaxis against recurrent
SBP with ciprofloxacin.
Surgical: Consider insertion of TIPS to relieve portal hypertension (if recurrent variceal
bleeds or diuretic-resistant ascites) although it may precipitate encephalopathy. Liver
transplantation is the only curative measure.
COMPL I C A T IONS
Portal hypertension with ascites, encephalopathy or variceal haemorrhage,
SBP, hepatocellular carcinoma. Renal failure (hepatorenal syndrome). Pulmonary
hypertension (hepatopulmonary syndrome).
P ROGNOS I S
Depends on the aetiology and complications. Generally poor; overall 5-year
survival is 50%. In the presence of ascites, 2-year survival of 50%.
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