Liver Cirrhosis and Portal Hypertension PDF

Liver cirrhosis and portal hypertension/ Dr. Yousif Al-Jubori LIVER CIRRHOSIS Cirrhosis of the liver is a consequence of chronic hepatic injury, with healing by regeneration and fibrosis, progressing to liver failure. Aetiology: The most common causes of cirrhosis are excess alcohol, and chronic h...

Liver cirrhosis and portal hypertension/ Dr. Yousif Al-Jubori LIVER CIRRHOSIS Cirrhosis of the liver is a consequence of chronic hepatic injury, with healing by regeneration and fibrosis, progressing to liver failure. Aetiology: The most common causes of cirrhosis are excess alcohol, and chronic hepatitis C virus infection. In Egypt, schistosomiasis (bilharziasis) is the most common. Clinical features of cirrhosis: A number of specific clinical signs are seen in cirrhosis. These include: 1. Gynaecomastia. 2. Testicular atrophy. 3. Amenorrhoea. 4. Spider naevi. 5. Finger clubbing. 6. Palmar erythema. Complications of cirrhosis: 1. Impaired metabolism of carbohydrates, proteins, and lipids. 2. Impaired metabolism of bilirubin causes jaundice. 3. Impaired synthesis of albumin, and prothrombin. 4. Portal hypertension: This occurs due to compression of the portal venous vessels in the liver by the scarred hepatic tissue leading to visceral venodilation outside the liver. 5. Ascites: This occurs due to visceral venodilation, and low serum albumin, which is responsible for the blood osmotic pressure. 6. Hepatic encephalopathy: A neuropsychiatric condition is characterized by confusion, flapping tremor and hepatic coma. It occurs because the liver is unable to detoxify the nitrogenous breakdown products of protein metabolism; (conversion of ammonia to urea). 7. Hepatorenal failure: Venodilation of portal circulation results in pooling of blood, and distributive shock, which leads to renal hypoperfusion. This is associated with a high mortality. 8. Malignant change (hepatocellular carcinoma). 1  Liver cirrhosis and portal hypertension/ Dr. Yousif Al-Jubori PORTAL HYPERTENSION Portal circulation: The liver unlike other organs has two blood supplies. One from the hepatic artery and the other from the portal vein. The portal vein returns the blood from the digestive tract and spleen to the liver, where nutrients are metabolized, and toxins are detoxified and filtered there, before the blood returns to the heart. Collateral porto-systemic venous channels: Portal vein obstruction results in the development of collateral channels between the portal and systemic venous circulations. The sites of these channels are: 1. At the lower oesophagus forming oesophageal varices, (most important). 2. At the lower rectum forming ano-rectal varices; (second important). 3. Around the umbilicus forming a caput medusae. 4. Retroperitoneal and diaphragmatic anastomoses. Aetiology of portal hypertension: Portal hypertension results from an obstruction to portal vein. The normal portal vein pressure is between 5 and 10 mmHg. In portal hypertension, this pressure is raised. By far the most common cause of portal hypertension is cirrhosis. Complications of portal hypertension: 1. Bleeding oesophageal varices, bleeding ano-rectal varices, or bleeding duodenal ulcers due to the development of collateral porto-systemic venous channels. 2. Splenomegaly: Progressive splenic enlargement occurs due to portal congestion. This is often associated with anaemia, leucopenia and thrombocytopenia. 3. Ascites (accumulation of fluid in the peritoneal cavity), and leg and foot oedema (accumulation of fluids in the subcutaneous tissues of the leg and foot causes swelling). PREPARATION OF A PATIENT WITH PORTAL HYPERTENSION Preoperative investigations: 1. Serum bilirubin: The degree of jaundice is an important prognostic indicator in cirrhosis. It is mostly the direct type rises, then the indirect type increases when biliary obstruction occurs. 2. Liver enzymes tests are mostly increased; alanine transaminase (ALT), and aspartate transaminase (AST), and alkaline phosphatase. 3. Prolonged prothrombin time. 2  Liver cirrhosis and portal hypertension/ Dr. Yousif Al-Jubori 4. Low serum albumin. 5. Abdominal CT or MR scan gives the best assessment of a focal liver lesion, and splenomegaly. 6. Ultrasound can assess focal liver lesions, and splenomegaly also. 7. Upper GIT endoscopy, which may demonstrate varices. 8. Liver biopsy to determine the cause of cirrhosis. 9. Portal vein pressure measurement above 11 mmHg. is diagnostic (using special catheter in portal vein). Preoperative management: 1. Good rehydration with intravenous fluids. 2. Diet: High carbohydrates with low protein and sodium contents. 3. Albumin for patient with hypo-albuminaemia. 4. Blood in case of anaemia, and platelets concentrate for thrombocytopaenia. 5. Vitamin K for patient with prolonged prothrombin time. 6. Diuretics: Spironolactone for patient with ascites. In case of severe ascites, the patient may need abdominal paracentesis. 7. Dialysis for patient with renal failure. 8. Bleeding oesophageal varices: Endoscopic variceal ligation is safer and more effective than sclerotherapy. 9. Lactulose especially in case of hepatic encephalopathy. Lactulose 50 ml t.d.s. produces osmotic diarrhoea to remove protein and blood (if present) from the bowel and prevents proliferation of ammonia producing organisms. 10.Non selective B-blockers (propranolol, and nadolol): These are the treatment of choice causing visceral venoconstriction and should be continued for the rest of the patient's life. 11.Antibiotics; cephalosporine or ciprofloxacin as prophylaxis against infection. 12.Avoidance of hepatotoxic and nephrotoxic medications; (morphine, halothane, acetaminophen, gentamycin, etc.). 3