LIVER CIRRHOSIS PowerPoint PPT Presentation

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Causes of cirrhosis CommonAlcoholHepatitis B D Hepatitis C Autoimmune hepatitis Others Biliary cirrhosis: primary, secondaryHereditary haemochromatosis Hepatic venous congestion Wilson's disease Drugs (e.g. methotrexate) a1-Antitrypsin deficiency Cystic fibrosis

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1. LIVER CIRRHOSIS Cirrhosis results 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 and function. This derangement produces the clinical features of portal hypertension and impaired liver cell function.

2. Causes of cirrhosis Common Alcohol Hepatitis B D Hepatitis C Autoimmune hepatitis Others Biliary cirrhosis: primary, secondary Hereditary haemochromatosis Hepatic venous congestion Wilson's disease Drugs (e.g. methotrexate) a1-Antitrypsin deficiency Cystic fibrosis Idiopathic (cryptogenic)

3. Pathology The characteristic features of cirrhosis are regenerating nodules separated by fibrous septa and loss of the normal lobular architecture within the nodules . Two types of cirrhosis have been described which give clues to the underlying cause: Micronodular cirrhosis. Regenerating nodules are usually less than 3 mm in size and the liver is involved uniformly. This type is often caused by ongoing alcohol damage or biliary tract disease. Macronodular cirrhosis. The nodules are of variable size and normal acini may be seen within the larger nodules. This type is often seen following previous hepatitis, such as HBV infection. A mixed picture with small and large nodules is sometimes seen.

4. Investigations These are performed to assess the severity and type of liver disease. Liver function. Serum albumin and prothrombin time are the best indicators of liver function: the outlook is poor with an albumin level below 2.8 g/dL. The prothrombin time is prolonged commensurate with the severity of the liver disease . Liver biochemistry. This can be normal depending on the severity of cirrhosis. In most cases there is at least a slight elevation in the serum ALP and serum aminotransferases. In decompensated cirrhosis all biochemistry is deranged. In addition, serum a-fetoprotein if > 400 ng/mL is strongly suggestive of the presence of a hepatocellular carcinoma.

5. viral markers serum autoantibodies . serum immunoglobulins . iron indices and ferritin. copper, caeruloplasmin . a1-antitrypsin . Serum copper and serum a1-antitrypsin should always be measured in young cirrhotics. Total iron-binding capacity (TIBC) and ferritin should be measured to exclude hereditary haemochromatosis;

6. Imaging Ultrasound examination. This can demonstrate changes in size and shape of the liver. Fatty change and fibrosis produce a diffuse increased echogenicity. In established cirrhosis there may be marginal nodularity of the liver surface. The patency of the portal and hepatic veins can be evaluated. It is useful in detecting hepatocellular carcinoma. CT scan .shows hepatosplenomegaly and dilated collaterals seen in chronic liver disease.Contrast-enhanced scans are useful in the detection of hepatocellular carcinoma. Endoscopy is performed for the detection and treatment of varices, and portal hypertensive gastropathy. MRI scan.

7. Liver biopsy This is necessary to confirm the severity and type of liver disease. The core of liver often fragments and sampling errors may occur in macronodular cirrhosis. Special stains may be required for iron and copper, and various immunocytochemical stains can identify viruses, bile ducts and angiogenic structures. Chemical measurement of iron and copper are necessary to confirm diagnosis of iron overload or Wilson's disease.

8. Management Management is that of the complications seen in decompensated cirrhosis. Patients should have 6-monthly ultrasound and serum a-fetoprotein measurements to detect the development of a hepatocellular carcinoma as early as possible. There is no treatment that will arrest or reverse the cirrhotic changes although progression may be halted by correcting the underlying cause . Patients with compensated cirrhosis should lead a normal life. The only dietary restriction is to reduce salt intake. Aspirin and NSAIDs also Alcohol should be avoided.

9. COMPLICATIONS AND EFFECTS OF CIRRHOSIS Portal hypertension The portal vein is formed by the union of the superior mesenteric and splenic veins. The pressure within it is normally 5-8 mmHg Portal hypertension can be classified according to the site of obstruction: prehepatic - due to blockage of the portal vein before the liver intrahepatic - due to distortion of the liver architecture, which can be presinusoidal (e.g. in schistosomiasis) or postsinusoidal (e.g. in cirrhosis) posthepatic - due to venous blockage outside the liver (rare).

10. As portal pressure rises above 10-12 mmHg, the compliant venous system dilates and collaterals occur within the systemic venous system. The main sites of the collaterals are at the gastro-oesophageal junction, the rectum, the left renal vein, the diaphragm, the retroperitoneum and the anterior abdominal wall via the umbilical vein. The collaterals at the gastro-oesophageal junction (varices) are superficial in position and tend to rupture. Portosystemic anastomoses at other sites seldom give rise to symptoms. Rectal varices are found frequently (30%) if carefully looked for and can be differentiated from haemorrhoids, which are lower in the anal canal.

11. Causes of portal hypertension Prehepatic Portal vein thrombosis Intrahepatic Cirrhosis Hepatitis (alcoholic) Schistosomiasis Myelosclerosis (extramedullary haemopoiesis) Posthepatic Budd-Chiari syndrome Veno-occlusive disease Right heart failure (rare) Constrictive pericarditis

12. Clinical features Patients with portal hypertension are often asymptomatic and the only clinical evidence of portal hypertension is splenomegaly. Clinical features of chronic liver disease are usually present . Presenting features may include: haematemesis or melaena from rupture of gastro-oesophageal varices or portal hypertensive gastropathy ascites Encephalopathy.

13. Variceal haemorrhage Approximately 90% of patients with cirrhosis will develop gastro-oesophageal varices, over 10 years, but only one-third of these will bleed from them. Bleeding is likely to occur with large varices, red signs on varices (diagnosed at endoscopy) and in severe liver disease. Management can be divided into the active bleeding episode, the prevention of rebleeding, and prophylactic measures to prevent the first haemorrhage. Despite all the therapeutic techniques available, the prognosis depends on the severity of the underlying liver disease.

14. Urgent endoscopy Endoscopy should be performed to confirm the diagnosis of varices and to exclude bleeding from other sites (e.g. gastric ulceration). Portal hypertensive (or congestive) gastropathy is the term used for chronic gastric congestion, punctate erythema and gastric erosions and is a source of bleeding. Varices may or may not be present. Propranolol is the best treatment for this. Injection sclerotherapy or variceal banding can be used for treatment.

15. Long-term measures Non-selective beta-blockade. Oral propranolol in a dose sufficient to reduce resting pulse rate by 25% has been shown to decrease portal pressure. Portal inflow is reduced by two mechanisms: by a decrease in cardiac output (1), and by the blockade of 2 vasodilator receptors on the splanchnic arteries, leaving an unopposed vasoconstrictor effect. This has been shown to decrease the frequency of rebleeding, and is as effective as sclerotherapy and ligation as it also prevents bleeding from portal hypertensive gastropathy. It is the treatment of first choice. Endoscopic treatment. The use of repeated courses of banding at 2-weekly intervals leads to obliteration of the varices. This markedly reduces rebleeding, most occurring before the varices have been fully obliterated. Between 30% and 40% of varices return per year, so that follow-up endoscopy with ablation should be performed. Banding is superior to sclerotherapy

16. Ascites Ascites is the presence of fluid within the peritoneal cavity and is a common complication of cirrhosis of the liver. The pathogenesis of the development of ascites in liver disease is controversial, but is probably secondary to renal sodium and water retention. Several factors are involved. Sodium and water retention occur as a result of peripheral arterial vasodilatation and consequent reduction in the effective blood volume. Nitric oxide has been postulated as the putative vasodilator, although other substances (e.g. atrial natriuretic peptide and prostaglandins) may be involved. The reduction in effective blood volume activates various neurohumoral pressor systems such as the sympathetic nervous system and the renin-angiotensin system, thus promoting salt and water retention. Portal hypertension exerts a local hydrostatic pressure and leads to increased hepatic and splanchnic production of lymph and transudation of fluid into the peritoneal cavity. Low serum albumin (a consequence of poor synthetic liver function) may further contribute by a reduction in plasma oncotic pressure.

17. Clinical features The abdominal swelling associated with ascites may accumulate over many weeks or as rapidly as a few days. Precipitating factors include a high sodium diet or the development of a hepatocellular carcinoma or splanchnic vein thrombosis. Mild generalized abdominal pain and discomfort are common but, if more severe, should raise the suspicion of spontaneous bacterial peritonitis . Respiratory distress accompanies tense ascites, and also causes difficulty in eating. The presence of fluid is confirmed by the demonstration of shifting dullness. Many patients will also have peripheral oedema. A pleural effusion (usually on the right side) may infrequently be found and is believed to arise from the passage of ascitic fluid through congenital defects in the diaphragm.



22. Investigations A diagnostic aspiration of 10-20 mL of fluid should be obtained and the following performed: Cell count. A neutrophil count above 250 cells/mm3 is indicative of an underlying (usually spontaneous) bacterial peritonitis. Gram stain and culture - for bacteria and acid-fast bacilli. Protein. The ascitic protein level enables a division into transudative and exudative ascites. Cytology - for malignant cells. Amylase - to exclude pancreatic ascites

23. Management Bed rest alone will lead to a diuresis in a small proportion of people by improving renal perfusion,. By dietary sodium restriction it is possible to reduce sodium intake to 40 mmol in 24 hours and still maintain an adequate protein and calorie intake with a palatable diet. Drugs. Remember, many contain significant amounts of sodium (could be up to 50 mmol daily). Examples include antacids, antibiotics (particularly the penicillins and cephalosporins) and effervescent tablets. Sodium-retaining drugs (non-steroidals, corticosteroids) should be avoided if possible. The diuretic of first choice is the aldosterone antagonist spironolactone, staring at 100 mg daily. Chronic administration produces gynaecomastia; amiloride, 5-15 mg daily, is then substituted.

24. Paracentesis This is used to relieve symptomatic tense ascites. It is also used as a means of rapid therapy in patients with ascites and peripheral oedema, thus avoiding prolonged hospital stay. The main danger of this approach is the production of hypovolaemia as the ascites reaccumulates at the expense of the circulating volume.

25. Spontaneous bacterial peritonitis (SBP) This condition represents one of the more serious complications of ascites and occurs in approximately 8% of cirrhotics with ascites. The infecting organisms are believed to gain access to the peritoneum by haematogenous spread. The most frequently incriminated bacteria are Escherichia coli, Klebsiella and enterococci. The condition should be suspected in any patient with ascites with evidence of clinical deterioration. Features such as pain and pyrexia are frequently absent. Diagnostic aspiration should always be performed in patients with ascites . A raised neutrophil count in ascites is alone sufficient evidence to start treatment immediately. A third-generation cephalosporin, such as cefotaxime or ceftazidime, is used and is modified on the basis of culture results. Recurrence is common (70% within a year) and an oral quinolone, e.g. norfloxacin, 400 mg twice daily is prescribed to prevent it. This also prolongs the survival.

26. Portosystemic encephalopathy The term 'portosystemic encephalopathy' (PSE) refers to a chronic neuropsychiatric syndrome secondary to chronic liver disease. This condition occurs with cirrhosis, but a similar acute encephalopathy can occur in acute fulminant hepatic failure . PSE is seen in patients with portal hypertension that is due to spontaneous 'shunting', or in patients following a portosystemic shunt procedure. Encephalopathy is potentially reversible.

27. Many 'toxic' substances have been suggested as the causative factor, including ammonia, free fatty acids, mercaptans and accumulation of false neurotransmitters (octopamine) or activation of the ?-aminobutyric acid (GABA) inhibitory neurotransmitter system. Increased blood levels of aromatic amino acids (tyrosine and phenylalanine) and reduced branched-chain amino acids (valine, leucine and isoleucine) also occur. Nevertheless, ammonia seems to have a major role, and ammonia-induced alteration of brain neurotransmitter balance is the leading concept of the causation. Ammonia is produced by the breakdown of protein by intestinal bacteria, and a high blood ammonia is seen in most patients.

28. Factors precipitating portosystemic encephalopathy High dietary protein Gastrointestinal haemorrhage Constipation Infection, including spontaneous bacterial peritonitis Fluid and electrolyte disturbance due to: diuretic therapy paracentesis Drugs (e.g. any CNS depressant) Any surgical procedure Progressive liver damage Development of hepatocellular carcinoma

29. Clinical features An acute onset often has a precipitating factor . The patient becomes increasingly drowsy and comatose. Chronically, there is a disorder of personality, mood and intellect, with a reversal of normal sleep rhythm. These changes may be fluctuating and a history from a relative must be obtained. The patient is irritable, confused, disorientated and has slow slurred speech. Signs include: fetor hepaticus (a sweet smell to the breath) a coarse flapping tremor seen when the hands are outstretched and the wrists hyperextended (asterixis) .

30. Immediate management Identify and remove the possible precipitating cause, such as drugs with cerebral depressant properties, constipation or electrolyte imbalance due to overdiuresis. Give purgation and enemas to empty the bowels of nitrogenous substances. Lactulose (10-30 mL three times daily) is an osmotic purgative that reduces the colonic pH and limits ammonia absorption. Give antibiotics. Rifaximin is mainly unabsorbed and well tolerated long term. Metronidazole (200 mg four times daily) is also effective in the acute situation. Neomycin should not be used. Stop or reduce diuretic therapy. Give intravenous fluids as necessary (beware of too much sodium). Treat any infection

31. Renal failure (hepatorenal syndrome) The hepatorenal syndrome occurs typically in a patient with advanced cirrhosis with jaundice and ascites. The urine output is low with a low urinary sodium concentration, a maintained capacity to concentrate urine (i.e. tubular function is intact) and an almost normal renal histology. The renal failure is described as 'functional'. It is sometimes precipitated by overvigorous diuretic therapy, diarrhoea or paracentesis, but often no precipitating factor is found. Advanced cases may progress beyond the 'functional' stage to produce an acute tubular necrosis.

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