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PORTAL HYPERTENSION Portal Vein Is Not a True Vein

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PORTAL HYPERTENSION Portal Vein Is Not a True Vein PORTAL HYPERTENSION Portal vein is not a true vein 20 % 80 % • This frequently complicates cirrhosis ,but has other causes. The normal pressure is 5–6 mm Hg. • Clinically significant portal hypertension is present when the gradient exceeds 10 mm Hg and risk of variceal bleeding increases beyond a gradient of 12 mm Hg. • Increased vascular resistance is common in PH. • Causes are classified in accordance with the sites of obstruction to blood flow in the portal venous system. • Extrahepatic portal vein obstruction is the usual source of portal hypertension in childhood and adolescence, while, • cirrhosis causes at least 90% of cases of portal hypertension in adults in developed countries. Prehepatic pre-sinusoidal Intrahepatic pre-sinusoidal Hepatic or Sinusoidal Intrahepatic post-sinusoidal Post-hepatic post-sinusoidal Prehepatic pre-sinusoidal Portal vein thrombosis due to sepsis (umbilical,portal pyaemia) or rocoagulopathy or secondary to cirrhosis Abdominal trauma including surgery Intrahepatic pre-sinusoidal Schistosomiasis Congenital hepatic fibrosis Drugs like Vinyl chloride Sarcoidosis Sinusoidal Cirrhosis Polycystic liver disease Nodular regenerative hyperplasia Metastatic malignant disease Intrahepatic post-sinusoidal Veno-occlusive disease Post-hepatic post-sinusoidal Budd–Chiari syndrome Complications of portal hypertension • Variceal bleeding:oesophageal, gastric,other (rare) • Congestive gastropathy • Hypersplenism • Ascites • Iron deficiency anaemia • Renal failure • Hepatic encephalopathy Clinical features result from portal venous congestion and collateral vessel formation. Splenomegaly is a cardinal finding, and a diagnosis of portal hypertension is unusual when splenomegaly cannot be detected clinically or by ultrasonography. Collateral vessels may be visible on the anterior abdominal wall several radiate from the umbilicus to form a caput medusae. large umbilical collateral vessel has a blood flow sufficient to give a venous hum on auscultation. The most important collateral vessel formation occurs in the oesophagusa nd stomach, and this can be a source of severe bleeding. Rectal varices also cause bleeding . Fetor hepaticus results from portosystemic shunting of blood, which allows mercaptans to pass directly to the lungs. Ascites occurs as a result of renal sodium retentiona The most important consequence of portal hypertension is variceal bleeding, which commonly arises from oesophageal varices located within 3–5 cm of the gastrooesophageal junction, or from gastric varices. Drugs capable of causing mucosal erosion,e.g. as salicylates and NSAIDs, can precipitate bleeding. Variceal bleeding is often severe, and recurrent if preventative treatment is not given. Oesophageal varices Variceal Bleeding Caput Medusae Caput Medusae Haemorrhoids Investigations The diagnosis is often made clinically. Portal venous pressure measurements are rarely needed for clinical assessment or routine management, but can be used to confirm portal hypertension and to differentiate Sinusoidal and pre-sinusoidal forms. Thrombocytopenia is common due to hypersplenism . Leucopenia occurs occasionally but anaemia is seldom attributed directly to hypersplenism; if anaemia is found, a source of bleeding should be sought. The most useful investigation is endoscopy to determine whether gastro- oesophageal varices are present, Once the diagnosis of cirrhosis is made, endoscopy should be performed to screen for oesophageal varices (and repeated every 2 years). Ultrasonography often shows features of portal hypertension, such as splenomegaly and collateral vessels, and can sometimes indicate the cause, such as liver disease or portal vein thrombosis. CT and MRI angiography can identify the extent of portal vein clot and used to identify hepatic vein patency. Management Acute upper gastrointestinal haemorrhage from gastrooesophageal varices is a common manifestation of chronic liver disease.The mortality following a variceal bleed is high in poor liver function.The management of portal hypertension is largely focused on the prevention and/or control of variceal bleeding. However, it should be remembered that bleeding can also result from peptic ulceration, which is more common in patients with liver disease than in the general population. Primary prevention of variceal bleeding If non-bleeding varices are identified at endoscopy, β-adrenoceptor antagonist (β-blocker) therapy with propranolol (80–160 mg/day) or nadolol is effective in reducing portal venous pressure. The efficacy of β-blockers in primary prevention is similar to that of prophylactic banding, which may also considered, particularly in patients that are unable to tolerate β-blocker therapy. Carvedilol, a non-cardioselective vasodilating β-blocker, is also effective. Management of acute variceal bleeding The priority in acute bleeding is to restore the circulation with blood and plasma, not least because shock reduces liver blood flow and causes further deterioration of liver function. The source of bleeding should always be confirmed by endoscopy, because about 20% of patients are bleeding from non-variceal lesions. broad-spectrum antibiotics, such as ciprofloxacin or I.v. cephalosporin, because sepsis is common and treatment with antibiotics has been shown to improve outcomes. The measures used to control acute variceal bleeding include vasoactive medications (e.g. terlipressin), endoscopic therapy (banding or sclerotherapy), balloon tamponade,transjugular intrahepatic portosystemic stentshunting (TIPSS) and, rarely, oesophageal transection. Pharmacological reduction of portal venous pressure. Terlipressin is a synthetic vasopressin analogue that, in contrast to vasopressin, can be given by intermittent injection rather than continuous infusion. It reduces portal blood flow and/or intrahepatic resistance and hence reduces portal pressure. It reduces mortality in the setting of acute variceal bleeding. The dose is 2 mgIV 4 times daily until bleeding stops, and then 1 mg 4 times daily for up to 72 hours. Caution is needed in patients with severe ischaemic heart disease or peripheral vascular disease because of the drug’s vasoconstrictor properties. endoscopic banding TIPS TIPS Emergency management of bleeding • IV fluids (colloid) Extracellular volume replacement • Vasopressor (terlipressin) Reduces portal pressure, acute bleeding and risk of early rebleeding • Prophylactic antibiotics (cephalosporin IV) Reduces incidence of SBP • Emergency endoscopy Confirms variceal rather than ulcer bleed • Variceal band ligation To stop bleeding • Proton pump inhibitor To prevent peptic ulcers • Phosphate enema and/or lactuloseTo prevent hepatic Encephalopathy THANK YOU.
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