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Portal Hypertension12


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Published in: Health & Medicine

Portal Hypertension12

  1. 1. Portal hypertension Wang Wei General Hospital of Tianjin Medical University
  2. 2. Introduction
  3. 3. <ul><li>Portal hypertension is defined as a portal vein pressure greater than 10mmHg (250mm water column) </li></ul><ul><li>Normal portal venous pressure is 5–10mmHg, which is sufficient to maintain a portal flow ( 13-24cm water column). </li></ul><ul><li>Pressure in the portal vein of patients with portal hypertension exceeds 25cm water column. </li></ul>
  4. 4. <ul><li>The phenomenon of increased pressure in this venous circulation produces a wide array of hemodynamic and metabolic consequences, including some of the most lethal and distressing complications. </li></ul><ul><li>Complications : </li></ul><ul><li>Variceal hemorrhage </li></ul><ul><li>Splenomegaly with hypersplenism </li></ul><ul><li>Ascites </li></ul>
  5. 5. Anatomy
  6. 6. <ul><li>The portal venous system drains all blood from the abdominal GI tract, spleen, pancreas, and gallbladder back to the heart through the liver. </li></ul><ul><li>Normally, the portal vein is formed by the union of the superior mesenteric and splenic veins. At the porta hepatis it divides into the right and left branches, which are segmentally distributed intrahepatically. </li></ul>
  7. 8. Anatomic characteristics of portal venous system <ul><li>The liver is a unique organ in that it has a dual blood supply: portal venous and hepatic arterial. The portal vein is formed from the confluence of the superior mesenteric and splenic veins behind the neck of the pancreas and is 6 to 8 cm in length ; </li></ul><ul><li>The portal vein is the valveless vein carrying blood to the liver from the stomach, small intestine, large intestine, pancrea and spleen; </li></ul><ul><li>Both ends of the portal venous system are capillary beds . </li></ul>
  8. 9. Anatomy <ul><li>The tributaries of the portal vein connect with systemic venous system at the following sites: </li></ul><ul><li>Portal vein(PV)connects with the azygos vein and hemiazygos vein by coronary vein and esophageal plexus. </li></ul><ul><li>PV connects with middle and inferior haemorrhoid veins by inferior mesenteric vein and superior haemorrhoid vein . </li></ul><ul><li>PV connects with superior and inferior epigastric vein by obliterated umbilical vein and paraumbilical vein. </li></ul><ul><li>PV,SMV and IMV connect with IVC by retroperitoneal vein. </li></ul>
  9. 10. Anatomy
  10. 11. Etiology <ul><li>From both clinical and pathologic standpoints the causes of portal hypertension may be divided into diseases within the liver and diseases of the blood vessels outside the liver. </li></ul><ul><li>With the exception of the rare splanchnic arteriovenous fistulas, all the conditions cause portal hypertension by producing obstruction to portal blood flow. </li></ul>
  11. 12. Eitology <ul><li>The most common causes of portal hypertension are : </li></ul><ul><li>Postnecrotic cirrhosis due to viral hepatitis is the most common cause of portal hepertension in Asia and Africa. </li></ul><ul><li>Alcoholic cirrhosis is the most common cause of portal hypertension in western countries. </li></ul>
  12. 13. Classification of portal hypertension <ul><li>There are two separate and sometimes overlapping classification systems for the causes of portal hypertension, using either the liver or the hepatic sinusoid as the reference point. </li></ul><ul><li>The former classifies conditions into pre-hepatic, intrahepatic and posthepatic causes, while the latter divides conditions into presinusoidal, sinusoidal and postsinusoidal causes. </li></ul><ul><li>The clinical usefulness of this classification is in separating patients who have normal hepatocellular function from those who have hepatocellular damage . </li></ul>
  13. 15. Fig. 27-1 Etiologies of portal hypertension. These are divided into those associated with normal liver function (presinusoidal) and those associated with liver damage (sinusoidal).
  14. 16. Presinusoidal portal hypertension <ul><li>This may be either extrahepatic or intrahepatic lesion. </li></ul>
  15. 17. Extrahepatic <ul><li>Thrombosis of the extrahepatic portal vein or one of its major tributaries may lead to extrahepatic portal hypertension. Portal vein thrombosis may be seen either: </li></ul><ul><li>• in early life associated with umbilical sepsis </li></ul><ul><li>• in older patients who have a hypercoagulating state eg. polycythemia or a myeloproliferative disorder. </li></ul><ul><li>Isolated splenic vein thrombosis produces left-sided portal hypertension, which involves the spleen and gastric fundus. It is important to identify this because it can be cured by splenectomy </li></ul>
  16. 18. Intrahepatic <ul><li>schistosomiasis and the early stages of primary biliary cirrhosis are pathologic processes that affect the terminal portal venules in the presinusoidal position and result in intrahepatic presinusoidal portal hypertension </li></ul>
  17. 19. Sinusoidal& intrahepatic post sinusoidal obstruction <ul><li>This is caused by cirrhosis, viral hepatitis and ethanol abuse are the most common causes. Less common causes of cirrhosis such as autoimmune liver disease, Wilson’s disease, advanced stages of primary biliary cirrhosis. </li></ul><ul><li>Sinusoidal anatomy is destroyed, regenerative nodules form, fibrosis further obstructs portal venous flow and the normal metabolic processes are disrupted </li></ul>
  18. 20. Postsinusoidal portal hypertension (extrahepatic ) <ul><li>Budd–Chiari syndrome,this is the least common cause of portal hypertension, but may be reversible if identified and treated early. </li></ul>
  19. 21. Pathophysiology of portal hypertension <ul><li>The major theories have been the ‘backward’ and the ‘forward’ flow theories: </li></ul><ul><li>• backward theory postulates that all consequences of portal hypertension result from obstruction to portal venous flow; and </li></ul><ul><li>• forward flow theory postulates that increased inflow to the portal venous system (usually because of splenomegaly) causes the changes that lead to the clinical findings of portal hypertension. </li></ul><ul><li>Current evidence indicates that both theories contribute to the pathophysiology. </li></ul>
  20. 22. pathophysiology of portal hypertension Fig.27.4 Stages in the development of portal hypertension.
  21. 23. Pathophysiology <ul><li>In the resting state, the portal vein carries about 75% of total hepatic blood flow and provides 1/2 of the liver's O 2 supply. </li></ul><ul><li>The portal vein is valveless; thus, pressure in the portal system depends on the product of input from blood flow in the portal vein and total hepatic resistance to outflow. </li></ul>
  22. 24. Pathophysiology <ul><li>The widespread destruction of the hepatic parenchyma in cirrhosis leads to hyperplasia of fibrous tissue and the formation of regenerative nodules; </li></ul><ul><li>As a result, the hepatic blood vessels are compressed and distorted, the branches of the hepatic vein are also affected; </li></ul><ul><li>Hepatic venous outflow obstruction develops, the arteriovenous shunts in the liver also contributes to the portal hypertension. </li></ul>
  23. 25. Pathophysiology <ul><li>In this condition, the pressure in the portal vein rises over 30-50cm water column and lead to an dilation of all the collateral venous connection between the portal and systemic circulations. </li></ul>
  24. 26. portosystemic collaterals <ul><li>• gastroesophageal; </li></ul><ul><li>• hemorrhoidal; </li></ul><ul><li>• periumbilical; </li></ul><ul><li>• retroperitoneal. </li></ul>
  25. 27. Pathophysiology <ul><li>The most prominent collaterals are those veins in the submucosa of the distal esophagus and upper stomach. The increased hydrostatic pressure in the portal vein is responsible for “blowout” rupture of esophageal varices. </li></ul><ul><li>Massive hemorrhage associated with a high mortality of about 60-70% is caused by the rupture of esophageal varices. </li></ul>
  26. 28. Pathophysiology <ul><li>Splenomegaly with hypersplenism: the spleen may be enlarged and may result in the secondary hypersplenism including anemia, leukopenia (WBC<3000/mm 3 ) and thrombocytopenia. </li></ul><ul><li>Ascites develops in association with severe hepatocellular damage and is a manifestation of hepatic decompensation . </li></ul>
  27. 29. Pathogenesis of ascites <ul><li>The increased hydrostatic pressure within the liver may produce the transudation of ascitic fluid into the peritoneal cavity. </li></ul><ul><li>Low osmotic pressure resulting from the lower level of the serum albumin concentration. </li></ul><ul><li>Marked increase of lymphatic leakage from the surface and hilum of the liver. </li></ul><ul><li>Marked salt and water retention due to the secondary hyperaldosteronism. </li></ul>
  28. 30. CLINICAL PRESENTATION Fig. 27-5 Presenting features of portal hypertension.
  29. 31. <ul><li>the critical determinant is whether this is compensated or decompensated. </li></ul><ul><li>Ascites and encephalopathy are the two clinical presentations indication of decompensation. </li></ul><ul><li>In contrast, variceal bleeding, splenomegaly and hypersplenism or portal hypertension as an incidental finding are presentations that may be associated with compensated disease and have a very different prognosis. </li></ul>
  30. 32. Diagnosis <ul><li>The diagnosis of portal hypertension depends on: </li></ul><ul><li>Three clinical findings: </li></ul><ul><li>Splenomegaly and hypersplenism </li></ul><ul><li>Hematemesis and melena </li></ul><ul><li>Ascites </li></ul><ul><li>And a past history of hepatitiscirrhosis or chronic alcoholism is also important. </li></ul>
  31. 33. Clinical findings <ul><li>Hematemesis and melena: acute episode of upper gastrointestinal bleeding appears without any pain, the color of the vomited blood is usually fresh red and the volume of hematemesis is large. </li></ul><ul><li>Splenomegaly with hypersplenism: the enlarged spleen may be palpated on abdominal examination. Blood test may reveal anemia, leukopenia (WBC<3000/mm 3 ) and thrombocytopenia. </li></ul>
  32. 34. Clinical findings <ul><li>nonspecific complaints such as weight loss, malaise, and weakness, </li></ul><ul><li>past history of chronic alcoholism, hepatitis, complicated biliary disease, or exposure to hepatotoxins should lead one to include cirrhosis in the differential diagnosis. </li></ul><ul><li>underlying chronic liver disease on physical examination are spider angiomas, palmar erythema, testicular atrophy, and gynecomastia. A palpable spleen in association with these signs suggests portal hypertension. </li></ul><ul><li>signs of hepatic functional decompensation or advanced portal hypertension, such as jaundice, ascites, palpation of a firm irregular liver edge, dilated abdominal wall veins, impairment of mental status or the presence of asterixis (liver flap) . </li></ul>
  33. 35. Laboratory tests <ul><li>Blood test: </li></ul><ul><li>anemia, leukopenia and thrombocytopenia. </li></ul><ul><li>(bleeding, nutritional deficiencies, etc) </li></ul><ul><li>Coagulation may also be impaired. </li></ul><ul><li>(coagulation factors are synthesized in the liver) </li></ul>
  34. 36. Laboratory tests <ul><li>* Liver function test will reveal: </li></ul><ul><li>Serum albumin is often declined (which is a reliable index of chronic liver disease) </li></ul><ul><li>Elevation of hepatocellular enzymes (aspartate aminotransferase and alanine aminotransferase) </li></ul><ul><li>(which means hepatocellular damages) </li></ul><ul><li>High level of total bilirubin (which are also indicators of hepatocellular damages) </li></ul><ul><li>*Hepatitis serology should be obtained in most patients with cirrhosis (HBV,HCV) </li></ul><ul><li>* All newly diagnosed cirrhotic patients should be screened for hepatocellular carcinoma by determination of α-fetoprotein level </li></ul>
  35. 37. Liver Biopsy <ul><li>Percutaneous liver biopsy is a useful technique for establishing the cause of cirrhosis and for assessing activity of the liver disease. It should not be done when either coagulopathy or moderate ascites is present </li></ul><ul><li>Laparoscopic biopsy reduces the false-negative rate for diagnosing cirrhosis as compared with blind biopsy techniques. </li></ul>
  36. 38. the assessment of a patient with suspected chronic liver disease or portal hypertension <ul><li>diagnosis of the underlying liver disease </li></ul><ul><li>estimation of functional hepatic reserve </li></ul><ul><li>definition of portal venous anatomy and hepatic hemodynamic evaluation </li></ul><ul><li>identification of the site of upper gastrointestinal hemorrhage, if present </li></ul>
  37. 39. Assessing of hepatic functional reserve It is the best method to predict operative outcome or assessing long-term prognosis in the unoperated patients , and remains the standard for the initial evaluation of patients. Advanced Minimal None Encephalopathy Moderate Slight None Ascites >6 4–6 1–3 PT time (increased seconds) <2.8 2.8–3.5 >3.5 Albumin (g/dL) >3 2–3 <2 Bilirubin (mg/dL) 3 2 1 No. of Points Factor
  38. 40. Special examinations <ul><li>Endoscopes </li></ul><ul><li>In the nonbleeding cases, the manifestation of varices may be observed, The risk of the first variceal bleed may be predicted from: </li></ul><ul><li>variceal size; </li></ul><ul><li>red color signs; </li></ul><ul><li>In the massive bleeding cases, the endoscope is a very useful procedure to determine the site and the cause of upper gastrointestinal hemorrhage. </li></ul>
  39. 41. Special examinations <ul><li>Doppler ultrasonography </li></ul><ul><li>Ultrasound (US) is a safe, economical, and effective method for screening portal hypertension. The size of portal vein, splenic vein and ascites can be measured by ultrasonic scan. </li></ul>
  40. 42. Special examinations <ul><li>Computerized Tomography </li></ul><ul><li>CT scan is not affected by patients body habitus or the presence of bowel gas. Compared with ultrasound scan, CT is more effective. </li></ul><ul><li>With improvement of spiral CT scan and 3-dimensional angiographic reconstructive techniques, portal vasculature may be visualized more accurately. </li></ul>
  41. 43. Special examinations <ul><li>Findings suggestive of portal hypertension indicated by CT scan include the following: </li></ul><ul><li>Nodular liver surface </li></ul><ul><li>Splenomegaly </li></ul><ul><li>Collaterals arising from the portal system are suggestive of portal hypertension. </li></ul>
  42. 45. Special examinations <ul><li>Barium swallow </li></ul><ul><li>To demonstrate the presence of esophageal varices. </li></ul><ul><li>Esophageal varices may be recognized as a tortuous, worm-like appearance of the mucosa on a barium swallow. The three key variables that are predictive of variceal bleeding are Child class, variceal size, and the presence and severity of red wale markings (indicative of epithelial thickness). </li></ul>
  43. 46. Treatment <ul><li>There are three aims or problems requiring treatment by surgical procedure: </li></ul><ul><li>Esophageal varices and variceal bleeding </li></ul><ul><li>Splenomegaly with hypersplenism </li></ul><ul><li>Ascites </li></ul><ul><li>Among these conditions, treatment of bleeding, esophageal varicese is the most important aspect of the therapy of portal hypertension. </li></ul>
  44. 47. <ul><li>Principle for the treatment of esophageal varices and variceal bleeding </li></ul><ul><li>Nonoperative treatments are generally preferred for acutely bleeding patients since they often have high operative risks because of decompensated hepatic function. </li></ul><ul><li>Only treatments associated with minimal morbidity and mortality can be considered for prophylaxis, because many patients will be treated unnecessarily(only one third to one half of patients with varices eventually bleed). </li></ul>
  45. 48. Endoscopic treatments <ul><li>Sclerosants are injected through endoscopic direct into and around the bleeding varix. The subsequent inflammation caused by sclerosants leads to eventual thrombosis and fibrosis of the varix lumen. </li></ul>
  46. 49. Endoscopic treatments <ul><li>A newer and probably safer method of endoscopic therapy is ligation. Each varix can be ligated with a rubber band. </li></ul>
  47. 50. Elective surgery for portal ypertension <ul><li>Indications: elective operations are suitable for patients who have previous haemorrhage history or at great risk of bleeding from esophageal varices without any severe damage of liver function. </li></ul>
  48. 51. Surgical methods: <ul><li>A:Shunts operations:This may be carried out by either radiologic or surgical methods and the aim is to reduce intravariceal pressure to less than 12mmHg </li></ul><ul><li>Nonselective shunts:end-to-side portacaval shunts,side-to-side portacaval shunts, interposition shunts,and splenorenal shunts. </li></ul><ul><li>Selective shunt:distal splenorenal shunts </li></ul><ul><li>Partial shunt: small-diameter interposition portacaval shunt </li></ul><ul><li>B:Nonshunts operations: </li></ul>
  49. 52. Nonselective shunts
  50. 53. TOTAL&PARTIAL PORTOSYSTEMIC SURGICAL SHUNTS Fig.27-15 Partial portosystemic shunt with an 8mm graft between the portal vein and inferior vena cava. Exposure is the same as for the total portacaval shunt. Fig. 27-14 Side-to-side portacaval shunt with direct vein-to-vein anastomosis. The portal vein is dissected from the right side, posterior to the bile duct. The intrahepatic vena cava is fully mobilised. If there is a larger caudate lobe, an interposition graft may be used.
  51. 54. SELECTIVE VARICEAL DECOMPRESSION Fig. 27-16 Distal splenorenal shunt, with anastomosis of the splenic to the left renal vein. The gastric fundus, esophagus and spleen are decompressed. Portal hypertension and prograde portal flow are maintained.
  52. 55. <ul><li>Advantages and disadvantages of nonselective shunts: </li></ul><ul><li>These operations can effective decompress varices, </li></ul><ul><li>However, these operation may cause frequent postoperative encephalopathy and accelerated hepatic failure. </li></ul>
  53. 56. Selective and partial shunts: <ul><li>Objective of these operations is to : ①effective decompression of varices, ②preservation of hepatic portal perfusion. </li></ul>
  54. 57. Transjugular Intrahepatic Portosystemic Shunt TIPS <ul><li>TIPS is a technique that accomplishes portal decompression without an operation. Because of the complexity of the procedure, an experienced interventional radiologist is required. Access is gained to a major intrahepatic portal venous branch through puncture through a hepatic vein. </li></ul>
  55. 58. <ul><li>Depicted is the procedure for performing TIPS. ( a ) A needle is passed under radiologic guidance from a hepatic vein into a major portal venous branch, and a guide wire is advanced through this needle. ( b ) A balloon is passed over the guide wire, creating a tract in the hepatic parenchyma. ( c ) An expandable stent is placed though this tract. ( d ) The effective result is a nonselective portosystemic shunt </li></ul>
  56. 59. Fig. 27-13 TIPS. The metallic shunt maintains the transparenchymal track, which has been made through the liver between the portal and hepatic veins.
  57. 60. Nonshunt operation <ul><li>Esophagogastric devascularization </li></ul><ul><li>The Objective of this method is to ablation of varices or extensive interruption of collateral vessels connecting the high-pressure portal venous system with varices. </li></ul>Nonshunt operation is the frequently used method at present time Fig. 24.17 Gastroesophageal devascularization interrupts all variceal inflow to most of the stomach and the distal 7cm of the esophagus. Splenectomy and desvascularization of the greater curve of the stomach complete the procedure.
  58. 62. . LIVER TRANSPLANTATION <ul><li>The indication for transplant remains end-stage liver disease, and for Child’s class C patients this treatment has altered the long-term outcome. </li></ul>
  59. 63. Treatment <ul><li>The treatment for Splenomegaly with hypersplenism is Splenectomy </li></ul><ul><li>The treatment for Ascites includs: </li></ul>Dietary salt restriction Diuretic therapy Surgical therapy: peritoneovenous shunt is used in patients with intractable ascites.
  60. 64. Management of massive hemorhage Fig.27-10 Treatment strategies for esophagastric varices.
  61. 65. <ul><li>Treatment of the acute bleeding episode </li></ul><ul><li>Resuscitation: vigorous replacement of blood loss with whole blood transfusion is essential. </li></ul><ul><li>Systemic intravenous administration of vasopressin and somatostatin is prescribed; </li></ul><ul><li>Endoscopic treatments (sclerosis or ligation) is the most commonly used therapy for both management of the acute bleeding episode and prevention of recurrent hemorrhage. </li></ul>
  62. 66. Acute bleeding episode <ul><li>Balloon Tamponade: It is a old method used to treat acute bleeding episode. </li></ul><ul><li>Advantages: immediate cessation of bleeding in more than 85% of patients and widespread availability of this device. </li></ul><ul><li>Disadvantages: high rebleeding rate and high incidence of serious complications. </li></ul><ul><li>Because of more effective treatments for acute varices bleeding, balloon tamponade is infrequently used. </li></ul>
  63. 67. Emergency operation: <ul><li>Emergency surgical intervention may be the treatment of choice in patients whose condition appear to be at the grade A or B of child classification. </li></ul><ul><li>It can rapidly and effectively decompresses the portal venous circulation. </li></ul><ul><li>Disadvantages: operative mortality rates exceed 25% because of hepatic functional decompensation. </li></ul>
  64. 68. Budd-Chiari Syndrome <ul><li>The obstruction is usually due to inflammatory or neoplastic thrombosis or fibrosis of the hepatic veins and, sometimes, of the adjacent inferior vena cava; </li></ul><ul><li>The etiology of the process is often obscure; </li></ul><ul><li>Marked hepatomegaly and massive ascites are the most striking clinical findings in patients with portal hypertension. </li></ul>
  65. 69. Thank you!