PORTAL HYPERTENSION by Dr.Abhijeet Majhi.pptx
- 1.
- 2. ANATOMY ▪ The portalvein drains blood from the small and large intestines, stomach, spleen, pancreas, and gallbladder. ▪ The superior mesenteric vein and the splenic vein unite behind the neck of the pancreas to form the portal vein. ▪ It provides - 75% of hepatic blood flow and 50% of the oxygen delivery ▪ The portal vein trunk is 4.8 to 8.8 Cm long with an average length of 6.4 cm and 0.6 to 1.2 cm wide. with an average width of 0.9 cm.
- 3. ▪ The portaltrunk divides into 2 lobar veins. The right branch drains the cystic vein, and the left branch receives the umbilical and paraumbilical veins that enlarge to form umbilical varices in portal hypertension. ▪ The left gastric vein (gastric coronary vein), which runs along the lesser curvature of the stomach, receives distal esophageal veins, which also enlarge in portal hypertension.
- 5. PORTAL HYPERTENSION ▪ Anincrease in portal vein pressure above the normal level of 5-10 mm Hg. ▪ In established cases of portal hypertension , direct portal pressure measurement may be elevated to 15mm Hg or more. ▪ If pressure >12 mmHg - chances of variceal bleeding ▪ Pressure >15mmHg - vigorous bleeding ▪ Pressure > 20mmHg - continuous bleeding
- 6. PATHOPHYSIOLOGY ▪ Prehepatic ▪ Obstructionof portal vein or splenic vein → ↑ hydrostatic pressure in the tributaries of the obstructed vein ▪ Hepatic ▪ Presinusoidal: obstruction of outflow in portal vein at the porta hepatis or in the portal venules within liver → ↑ hydrostatic pressure in the portal vein and its tributaries ▪ Sinusoidal: ↑ resistance to blood flow in the hepatic sinusoids (e.g., due to hepatic fibrosis and cirrhosis) → ↑ hydrostatic pressure in the hepatic sinusoids → ↑ hydrostatic pressure in the portal vein and its tributaries ▪ Postsinusoidal: obstruction of outflow in the central vein and/or hepatic venules → ↑ hydrostatic pressure in the hepatic sinusoids → ↑ hydrostatic pressure in the portal vein and its tributaries ▪ Posthepatic ▪ Hepatic vein congestion or obstruction of hepatic vein outflow → ↑ hydrostatic pressure in the hepatic sinusoids → ↑ hydrostatic pressure in the portal vein and its tributaries
- 8. CAUSES ▪ PRE-HEPATIC ▪ HEPATIC ▪POST HEPATIC
- 9. PRE-HEPATIC ▪ Due toobstruction somewhere in portal vein or its tributaries. ▪ Causes are- ▪ Cavernomatus transformation of the portal vein ▪ Trauma & extrinsic compression caused by adhesion ▪ Tumors pressing on the portal vein ▪ Isolated splenic vein thrombosis (left-sided portal hypertension) (Easily reversed by splenectomy alone)
- 10. HEPATIC ▪ Due toobstruction in portal venules or sinusoids in liver. ▪ Causes are- ▪ Nutritional cirrhosis ▪ Post necrotic cirrhosis ▪ Biliary cirrhosis ▪ Haemochromatosis ▪ Wilsons disease ▪ Congenital hepatic fibrosis ▪ schistosomiasis
- 11. POST-HEPATIC ▪ Due toobstruction in the hepatic veins draining into the inferior venacava. ▪ Causes are- ▪ Budd chiari syndrome ▪ Failure of the right side of the heart, may be caused by tricuspid valvular incompetence & constrictive pericarditis.
- 12. COLLATERAL CIRCULATION ▪ Theresponse to increased venous pressure is the development of collateral circulation that diverts the obstructed blood flow to the systemic veins. ▪ These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting the portal venous system and the superior and inferior vena cava. ▪ These collateral are- ▪ Collaterals around lower end of oesophagus, when dialated called oesophageal varix causing variceal bleeding. ▪ Collaterals around the lower third of anal canal between the superior haemorrhoidal veins & the middle & inferior haemorrhoidal veins. (rarely dialates and causes haemorrhoids) ▪ Collaterals around the umbilicus between the paraumbilical veins. (Dialation causes caput medusae)
- 14. CLINICAL FEATURES Signs andsymptoms of underlying disease, ▪ Clinical features of cirrhosis (jaundice, scleral icterus, spider angioma, palmar erythema, ascites and encephalopathy) ▪ Clinical features of right-sided heart failure (peripheral pitting edema, abdominal pain and jaundice (from hepatic venous congestion), hepatosplenomegaly) Signs and symptoms of complications: ▪ Gastrointestinal bleeding ▪ Hematemesis and/or melena (e.g., due to esophageal varices or gastric varices) ▪ Hematochezia (e.g., due to hemorrhoidal or anorectal varices) ▪ Caput medusae ▪ Signs of hypersplenism due to congestive splenomegaly (e.g., thrombocytopenia) ▪ Abdominal distention due to ascites ▪ Hepatic encephalopathy
- 15. DIAGNOSTICS ▪ CBC ▪ Thrombocytopenia(most common laboratory finding in portal hypertension) ▪ Anemia related to an underlying condition ▪ Liver Function tests ▪ SGOT & SGPT – markers of hepatocyte injury or necrosis ▪ ↑ Alkaline phosphate – when there is biliary obstruction ▪ ↓ Serum Albumin – liver diseases ▪ Coagulation panel: coagulopathy is a sign of advanced liver disease ▪ Ascitic fluid analysis: high SAAG(serum-ascites albumin gradient) ≥ 1.1 g/Dl ▪ Doppler ultrasound abdomen: Obtain to assess portal circulation. ▪ CT or MRI abdomen (usually for extrahepatic obstruction )
- 16. Cavernous transformation ofthe portal vein (the formation of venous channel within or around a previously thrombosed portal vein)
- 18. TREATMENT ▪ PHARMACOTHERAPY ▪ VARICEALTAMPONADE ▪ ENDOSCOPIC THERAPY ▪ DECOMPRESSIVE SHUNTS ▪ DEVASCULARIZATION OPERATIONS ▪ LIVER TRANSPLANTATION
- 19. PHARMACOTHERAPY ▪ Non selectivebeta blockers: used to prevent hepatic decompensation (e.g., variceal bleeding) ▪ Preferred agent: carvedilol ▪ Alternative agents: propranolol, nadolol ▪ NSBBs inhibit beta-2 adrenergic receptors in the gastrointestinal tract, causing splanchnic vasoconstriction, ↓ portal and collateral blood flow, and subsequent ↓ portal hypertension.
- 20. VARICEAL TAMPONADE ▪ Usedto stabilize a patient with massive bleeding prior to definitive therapy. ▪ Sengstaken-Blakemore tube is usually used for balloon tamponade. Balloons must be checked. The tube is advanced well into the stomach. The gastric balloon is then fully inflated with 300ml air and appropriate traction must be applied. The oesophageal balloon should be inflated to 45 mm Hg only if the gastric balloon does not control the bleeding. Oesophageal suction is continued above the balloons. ▪ Advantage : ▪ Immediate cessation of bleeding in more than 85% of patients ▪ widespread availability of this device ▪ Disadvantages ▪ Recurrent hemorrhage in up to 50% of patients after balloon deflation ▪ Discomfort for the patient ▪ High incidence of serious complications when used incorrectly
- 21. ENDOSCOPIC THERAPY ENDOSCOPIC BANDING ▪Multiband ligators uses elastic bands to ligate the enlarged veins or varices. ▪ ADVANTAGES: fewer side effects, obliterates varices faster, and can be easily applied. ENDOSCOPIC SCLEROTHERAPY ▪ Endoscopic sclerotherapy with injection of a sclerosing solution may be a useful adjunct to complete the obliteration of smaller varices that cannot be banded.
- 22.
- 23. DECOMPRESSIVE SHUNTS ▪ Decompressionis considered second-line treatment ▪ Reserved for patients who rebleed through pharmacologic therapy and endoscopic banding or whose varices remain “high risk.” 1. Radiologically placed shunt - TIPS. 2. Surgical shunts - Total, Partial, and Selective shunts.
- 24. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT(TIPS) ▪ Direct puncture of the internal jugular vein (IJV), ▪ passage of a catheter through the internal jugular vein ending in the right hepatic vein followed by a trans-parenchymal puncture of the liver to cannulate the portal vein. ▪ The catheter is passed into the portal vein ▪ The intraparenchymal track is then dilated and the track stented with an expandable metal stent in the 10 to 12mm diameter range. ▪ The technical success rate is high (>90%) with a low procedural morbidity and mortality (<10%). ▪ Patients are usually in the hospital for 1–2 days and the shunt patency should be documented the day after the procedure with a Doppler ultrasound.
- 25.
- 26. TIPS ▪ It isa temporary procedure ▪ Advantages: ▪ Useful in patients waiting for the transplant ▪ Useful in advanced hepatic functional decompensation who are unlikely to survive for longer duration ▪ Useful for the treatment of medically intractable ascites. ▪ DISADVANTAGES ▪ Shunt stenosis ▪ Shunt thrombosis
- 27. SURGICAL SHUNT OPERATIONS Thereare principally 3 types of shunt operations – 1. Portacaval 2. Lieno-renal 3. Mesenterico-caval Surgical shunts are divided into 2 groups - 1. Non-selective Shunts ▪ End-to-side portacaval shunt ▪ Side to side portocaval shunt 2. Selective shunts ▪ Distal splenorenal shunt
- 28. END-TO-SIDE PORTACAVAL SHUNT ▪In end to side portocaval shunt, portal vein is divided at porta hepatis and the splanchnic end anastomosed to the side of the vena cava. ▪ It does not relieve ascites but will control variceal bleeding. ▪ Complications : portosystemic encephalopathy and accelerated hepatic failure.
- 29. SIDE TO SIDEPORTOCAVAL SHUNT ▪ side-to-side portacaval shunts with direct vein-to-vein or a short interposition graft. ▪ These shunts need to be at least 10 mm in diameter, usually being 12–15 mm, to fully decompress portal hypertension. ▪ These shunts differ from the end-to-side portacaval shunt in the way that the intact upper end of the portal vein serves as a decompressive outflow from the high- pressure–obstructed liver sinusoids. ▪ Hence, in addition to controlling variceal bleeding, these shunts also control ascites.
- 30. LIENO-RENAL SHUNT ▪ Onlyperformed when there is thrombosis affecting the portal vein or where splenomegaly deserves removal of the spleen. ▪ Contraindicated if the splenic vein is less than 1cm in diameter. ▪ The conventional splenorenal shunt consists of anastomosis of the proximal splenic vein to the renal vein. ▪ Splenectomy is performed. ▪ Complications : shunt thrombosis
- 31. SELECTIVE SHUNTS ▪ Selectiveshunts are most commonly the distal splenorenal shunt (DSRS) ▪ Divide the splenic vein at its junction with the superior mesenteric vein, and anastomoses the splenic vein to the left renal vein. ▪ This selectively decompresses gastroesophageal varices.
- 32. MESENTERICO-CAVAL SHUNT ▪ Mesocavalshunt is an anastomosis between the superior end of the divided IVC and the side of the superior mesenteric vein. ▪ In principle, it is hemodynamically similar to the side-to-side PortoCaval Shunts. ▪ In patients with extrahepatic portal hypertension due to occlusion of the Portal vein, this type of shunt is very effective. ▪ However, in adult cirrhotic patients it is doubtful that this procedure represents a first choice. Cirrhotic patients retain salt and water, and division of the IVC may lead to intractable edema of the lower extremities
- 33. MESENTERICO-CAVAL SHUNT ▪ Sometimesa dacron graft may be used to connect the superior mesenteric vein and the inferior vena cava. ▪ The interposition mesocaval H-graft is a relatively minor technical variation of direct Side to Side Portocaval Shunts and, both are hemodynamically identical. ▪ It is technically less difficult to perform than conventional shunts. ▪ The major potential disadvantage is the possibility of thrombosis, particularly of the synthetic prostheses.
- 34. Devascularization Procedures ▪ Sugiuraoperation ▪ These operations approach the problem of variceal bleeding by interrupting inflow to the varices. ▪ The components are splenectomy, gastric and esophageal devascularization. ▪ The effectiveness of these procedures appears to depend on the aggressiveness of the operation. ▪ The advantage of these procedures is that portal hypertension is maintained with portal flow to the cirrhotic liver. ▪ Devascularization can be useful when patients have extensive portal and splenic venous thrombosis and there are no other operative or radiologic options.
- 35. Complications ▪ Life-threatening esophagealvariceal bleeding Portal hypertensive gastropathy A condition caused by cirrhosis (leading to portal hypertension) or portal vein thrombosis diffuse lower gastrointestinal bleeding Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Impaired liver function Hepatic encephalopathy Pulmonary complications of portal hypertension (e.g., hepatopulmonary syndrome, portopulmonary hypertension) Cirrhotic cardiomyopathy