portal hypertension

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ameeth jha    on Jul 19, 2012 Says :

thank u khusbu....
Khushbu    on Jul 18, 2012 Says :

exceptinal ppt on portal hypertension. very useful.
ameeth jha    on Jun 27, 2012 Says :

thank u very much 4 ur appreciation.
panithan    on Jun 23, 2012 Says :

it vary good
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Slide 1 : PORTAL HYPERTENSION DR.AMIT JHA DR.AMBESH DESHAR INTERNS:UNIT II
Slide 2 : INTRODUCTION Portal hypertension is a progressive complication of cirrhosis. Portal hypertension is defined as the elevation of the hepatic venous pressure gradient (HVPG) to >5 mmHg
Slide 3 : Portal pressure increases initially 1.as a consequence of an increased resistance to ?ow mostly due to an architectural distortion of the liver secondary to ?brous tissue and regenerative nodules. 2. there is an active intrahepatic vasoconstriction that accounts for 20%-30% of the increased intrahepatic resistance(that is mostly due to a decrease in the endogenous production of nitric oxide.)
Slide 4 : portal hypertension persists despite the development of the collaterals for 2 reasons: an increase in portal venous in?ow that results from splanchnic arteriolar vasodilatation occurring concomitant with the formation of collaterals; and 2. insuf?cient portal decompression through collaterals as these have a higher resistance than that of the normal liver. i.e. due to both increase in resistance to portal flow and increase in portal blood flow
Slide 5 : HEPATIC VENOUS PRESSURE GRADIENT(HVPG) The normal HVPG is 3-5 mmHg HVPG=WHVP(wedged hepatic venous pressure)-FHVP (free hepatic venous pressure) Since it is a measure of sinusoidal pressure, the HVPG will be elevated in intrahepatic causes of portal hypertension,such as cirrhosis, but will be normal in prehepatic causes of portal hypertension, such as portal vein thrombosis. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm
Slide 6 : Clinical features of PORTAL HYPERTENSION Splenomegaly is a cardinal finding Hypersplenism is common and frequently results in thrombocytopenia.Platelet counts are usually around 100 ×109/l; values below 50 × 109/l are uncommon. Leucopenia occurs occasionally but anaemia can hardly ever be attributed directly to hypersplenism. Collateral vessels may be visible on the anterior abdominal wall and occasionally several radiate from the umbilicus to form a caput medusae. Rarely, a large umbilical collateral vessel has a blood flow sufficient to give a venous hum on auscultation (Cruveilhier-Baumgarten syndrome). The most important collateral vessels occur in the oesophagus and stomach, where they can cause severe bleeding. Rectal varices also cause bleeding and are often mistaken for haemorrhoids, which are no more common in portal hypertension than in the general population. Fetor hepaticus results from portosystemic shunting of blood, which allows mercaptans to pass directly to the lungs.
Slide 7 :
Slide 8 : Classification of Portal Hypertension Extrahepatic post-sinusoidal  Budd-Chiari syndrome Intrahepatic post-sinusoidal Veno-occlusive disease Sinusoidal  Cirrhosis* Cystic liver disease Partial nodular transformation of the liver Metastatic malignant disease Intrahepatic pre-sinusoidal Schistosomiasis* Sarcoidosis Congenital hepatic fibrosis Vinyl chloride Drugs  Extrahepatic pre-sinusoidal Portal vein thrombosis due to sepsis* (umbilical, portal pyaemia) or procoagulopathy (thrombotic diseases, oral contraceptives, pregnancy), or secondary to cirrhosis Abdominal trauma, including surgery Malignant disease of pancreas or liver Pancreatitis Congenital Cardiac causes      Restrictive cardiomyopathy    Constrictive pericarditis    Severe congestive heart failure
Slide 9 : etiology
Slide 10 : PORTOCAVAL ANASTOMOSIS A useful mnemonic is that portal hypertension causes problems in the butt, the gut, and caput.
Slide 11 :
Slide 12 : PORTOCAVAL ANASTOMOSIS
Slide 13 : DIAGNOSIS CLINICALLY in patients with cirrhosis being followed up chronically presence of thrombocytopenia; the appearance of an enlarged spleen; or the development of ascites, encephalopathy and/or esophageal varices with or without bleeding
Slide 14 : DIAGNOSIS The gold standard in the diagnosis of varices is esophagogastroduodenoscopy (EGD). A procedure that may replace EGD is esophageal capsule endoscopy. Two recent pilot studies show that capsule endoscopy is a safe and well-tolerated way to diagnose esophageal varices,although its sensitivity remains to be established. On EGD, esophageal varices should be graded as small or large (>5 mm) SEMIQUALITATIVE MORPHOLOGICAL ASSESSMENT small varices generally de?ned as minimally elevated veins above the esophageal mucosal surface, medium varices de?ned as tortuous veins occupying less than one-third of the esophageal lumen, and Large varices de?ned as those occupying more than one-third of the esophageal lumen Abdominal imaging, either by CT or MRI, can be helpful in demonstrating a nodular liver and in finding changes of portal hypertension with intraabdominal collateral circulation.
Slide 15 : EGD also remains the main method for diagnosing variceal hemorrhage. The diagnosis of variceal hemorrhage is made when diagnostic endoscopy shows one of the following: active bleeding from a varix, a “white nipple” overlying a varix, clots overlying a varix, or varices with no other potential source of bleeding.
Slide 16 : Nonselective B-blockers prevent bleeding in more than half of patients with medium or large varices. Therefore, it is recommended that patients with cirrhosis undergo endoscopic screening for varices at the time of diagnosis.
Slide 17 : Gastroesophageal varices are the most relevant portosystemic collaterals because their rupture results in variceal hemorrhage, the most common lethal complication of cirrhosis that result most directly from portal hypertension
Slide 18 : CLASSIFICATION OF GASTRIC VARICES Gastric varices are commonly classi?ed based on their relationship with esophageal varices as well as their location in the stomach. Gastroesophageal varices (GOV) are an extension of esophageal varices and are categorized into 2 types. Type 1 (GOV1) gastric varices, which extend along the lesser curvature They are considered extensions of esophageal varices and should be managed similarly. Type 2 (GOV2) gastric varices extend along the fundus and tend to be longer and more tortuous
Slide 19 : Isolated gastric varices (IGV) occur in the absence of esophageal varices and are also classi?ed into 2 types. Type 1 (IGV1) are located in the fundus and tend to be tortuous and complex, and Type 2 (IVG2) are located in the body, antrum, or around the pylorus. The presence of IGV1 fundal varices requires excluding the presence of splenic vein thrombosis.
Slide 20 : MANAGEMENT OF PORTAL HYPERTENSION PHARMACOLOGICAL THERAPY 1.splanchnic vasoconstrictors (Vasoconstrictors act by producing splanchnic vasoconstriction and reducing portal venous in?ow.) vasopressin and analogues, somatostatin and analogues, nonselective B-blockers 2.venodilators (Venodilators theoretically act by decreasing intrahepatic and/or portocollateral resistance). nitrates
Slide 21 : Endoscopic therapies, such as Sclerotherapy or Endoscopic variceal ligation (EVL), are local therapies that have no effect on either portal ?ow or resistance. Shunting therapy, either Radiological (transjugular intrahepatic portosystemic shunt) or Surgical, by bypassing the site of increased resistance, markedly reduces portal pressure by bypassing the site of increased resistance.eg.distal splenorenal shunt.
Slide 22 : In patients with cirrhosis who do not have varices, nonselective B-blockers cannot be recommended to prevent their development. In patients who have compensated cirrhosis and no varices on the initial EGD, it should be repeated in 3 years. If there is evidence of hepatic decompensation,EGD should be done at that time and repeated annually.
Slide 23 : In patients with cirrhosis and small varices that have not bled but have criteria for increased risk of haemorrhage (Child B/C or presence of red wale marks on varices), nonselective B-blockers should be used for the prevention of ?rst variceal hemorrhage. In patients with cirrhosis and small varices that have not bled and have no criteria for increased risk of bleeding,  B-blockers can be used, although their long-term bene?t has not been established. In patients with small varices that have not bled and who are not receiving B-blockers, EGD should be repeated in 2 years. If there is evidence of hepatic decompensation, EGD should be done at that time and repeated annually In patients with small varices who receive B-blockers, a follow-up EGD is not necessary.
Slide 24 : In patients with medium/large varices that have not bled but are at the highest risk of haemorrhage (Child B/C or variceal red wale markings on endoscopy), Nonselective B-blockers (propranolol or nadolol) or EVL may be recommended for the prevention of ?rst variceal hemorrhage. In patients with medium/large varices that have not bled and are not at the highest risk of hemorrhage (Child A patients and no red signs), Nonselective B-blockers (propranolol, nadolol) are preferred and EVL should be considered in patients with contraindications or intolerance or non-compliance to B-blockers. If a patient is placed on a nonselective B-blocker, it should be adjusted to the maximal tolerated dose; follow-up surveillance EGD is unnecessary. If a patient is treated with EVL, it should be repeated every 1-2 weeks until obliteration with the ?rst surveillance EGD performed 1-3 months after obliteration and then every 6-12 months to check for variceal recurrence. Nitrates (either alone or in combination with B-blockers), shunt therapy, or sclerotherapy should not be used in the primary prophylaxis of variceal hemorrhage.
Slide 25 : Acute GI hemorrhage in a patient with cirrhosis an emergency that requires prompt attention GENERAL MEASURES intravascular volume support and blood transfusions, being careful to maintain a hemoglobin of about 8gm/dL. Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and GI hemorrhage. Oral nor?oxacin (400 mg BID) or intravenous cipro?oxacin (in patients in whom oral administration is not possible) is the recommended antibiotic. In patients with advanced cirrhosis intravenous ceftriaxone (1 g/day) may be preferable particularly in centers with a high prevalence of quinolone-resistant Organisms. SPECIFIC MEASURES Pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) Should be initiated as soon as variceal hemorrhage is suspected and continued for 3-5 days after diagnosis is Con?rmed. EGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage,either with EVL or sclerotherapy.
Slide 26 : TIPS is indicated in patients 1. in whom hemorrhage from esophageal varices cannot be controlled 2. in whom bleeding recurs despite combined pharmacological and endoscopic therapy. Balloon tamponade (SENGSTAKEN-BLACKEMORE TUBE/MINNESOTA TUBE) should be used as a temporizing measure (maximum 24 hours) 1. in patients with uncontrollable bleeding for whom a more de?nitive therapy (e.g., TIPS or endoscopic therapy) is planned. 2. In patients who bleed from gastric fundal varices, endoscopic variceal obturation using tissue adhesives such as cyanoacrylate is preferred, where available. Otherwise, EVL is an option A TIPS should be considered in patients in whom hemorrhage from fundal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy.
Slide 27 : Patients with cirrhosis who survive an episode of active variceal hemorrhage should receive therapy to prevent recurrence of variceal hemorrhage (secondary prophylaxis) Combination of nonselective B-blockers plus EVL is the best option for secondary prophylaxis of variceal hemorrhage. The nonselective B-blocker should be adjusted to the maximal tolerated dose. EVL should be repeated every 1-2 weeks until obliteration with the ?rst surveillance EGD performed 1-3 months after obliteration and then every 6-12 months to check for variceal recurrence. TIPS should be considered in patients who are Child A or B who experience recurrent variceal hemorrhage despite combination pharmacological and endoscopic therapy. In centers where the expertise is available, surgical shunt can be considered in Child A Patients. Patients who are otherwise transplant candidates should be referred to a transplant center for evaluation.
Slide 28 :
Slide 29 : The Role of Transjugular Intrahepatic Portosystemic Shunt (TIPS) in the Management of Portal Hypertension: Update 2009 Thomas D. Boyer1 and Ziv J. Haskal2 The 2009 update of the American Association for the Study of Liver Diseases (AASLD) Practice Guideline “The Role of Transjugular Intrahepatic Portosystemic Shunt (TIPS) in the Management of Portal Hypertension Use of expanded polytetra?uoroethylene (ePTFE)-covered stents is now preferred OVER TIPS
Slide 30 : Creation of a TIPS increases the risk of hepatic encephalopathy but the prophylactic use of nonabsorbable disaccharides or antibiotics does not appear to reduce this risk and is not recommended.
Slide 31 : TIPS versus a surgical shunt(DSRS-distal splenorenal shunt) in the prevention of variceal rebleeding in patients who have failed medical therapy Both were effective in preventing rebleeding (rebleeding incidence in 5.5% of DSRS versus 10.5% of TIPS; not signi?cant) with no difference in encephalopathy or survival.
Slide 32 : A cost analysis showed TIPS to be slightly more cost effective than DSRS at year 5,6 and these two approaches are now considered to be of equal ef?cacy in the prevention of variceal rebleeding.
Slide 33 : Role of TIPS in Budd-Chiari Syndrome One-year and 10-year transplant-free sur- vival was 88% and 69%, respectively, which is better than predicted. TIPS patency was best in those who received a covered stent. The recommendation now is for creation of a TIPS in those who fail to improve with anticoagulation
Slide 34 : The purpose of a TIPS to decompress the portal venous system and therefore prevent rebleeding from varices or stop or reduce the formation of ascites. As to varices it is well established that if the hepatic venous pressure gradient (HVPG) or portal pressure gradient (PPG) after TIPS creation can be reduced to less than 12mmHg then the risk of bleeding will fall signi?cantly. Although the gold standard for prevention of rebleeding remains a HVPG of < 12 mm Hg The optimal PPG that needs to be obtained for the control of refractory cirrhotic ascites is even less clear.In one series, the degree of portal decompression did not correlate with successful treatment of refractory cirrhotic ascites and the authors suggested a PPG of  8mmHg should be the hemodynamic goal.
Slide 35 : Contraindications to Placement of a TIPS ABSOLUTE Primary prevention of variceal bleeding Congestive heart failure (mean pulmonary pressures of more than 45 mm Hg as these patients are not candidates for a liver transplant) Multiple hepatic cysts Uncontrolled systemic infection or sepsis Unrelieved biliary obstruction Severe pulmonary hypertension
Slide 36 : RELATIVE( include anatomic ones that can complicate the creation of the shunt and reduce the technical success) Hepatoma especially if central Obstruction of all hepatic veins Portal vein thrombosis Severe coagulopathy (INR  5) Thrombocytopenia of  20,000/cm3 Moderate pulmonary hypertension
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