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Portal Hypertension
The portal vein is formed by the superior mesenteric and splenic veins. It drains blood from the intestines, pancreas, colon and rectum. Blood from the portal and hepatic arteries mixes in the liver sinusoids before draining into the hepatic vein and inferior vena cava. Portal hypertension occurs when pressure increases due to increased resistance in the liver from cirrhosis and increased blood flow. It can cause ascites, variceal bleeding, and other complications.
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Portal Hypertension
- 1. Anatomy of Portal Venoussystem
- 2. Portal vein isformed by confluence of the superior mesenteric and splenic veins. Superior mesenteric vein drains blood from small intestines, head of pancreas, ascending colon, and part of transverse colon. Splenic vein drains blood from transverse and descending colon, and superior 2/3rd of rectum bia inferior mesentercic vein.
- 3. • Portal venousand hepatic arterial blood, after mixing in sinusoids, drains via central veins into hepatic vein. • Hepatic vein drains via Inferior vena cava into right heart.
- 4. Porto-caval anastomosis • Portalvein also has several tributaries connecting it to systemic venous system (porto-caval anastomosis) which generally remain closed due to equal pressure on both sides.
- 5. Esophageal anastomsis Portal vein Gastricvein Esophageal vein Azygous/hemiazygous vein Superior vena cava
- 6. Rectal anastomosis Portal vein Inferiormesenteric vein Superior rectal vein Middle/inferior rectal vein Internal iliac veinInferior vena cava
- 7. Umbilical anastomosis Portal vein Umbilicalvein Para-umbilical vein Inferior epigastric vein External iliac vein Inferior vena cava Superior epigastric vein Internal thoracic vein Subclavian veinSuperior vena cava
- 8. Portal hypertension Portalpressure is equivalent to wedged-to-free hepatic vein pressure gradient. Portal hypertension is defined as the elevation of hepatic venous pressure gradient (HPVG) to >5 mmHg. And this increased pressure is contributed to by two simultaneously occurring processes that are, increased resistance to blood flow within liver (cirrhosis and regenerative nodules) and increased blood flow to portal venous system.
- 9. Causes of Portal Hypertension •Pre-hepatic • Intra-hepatic • Post-hepatic
- 10. Pre-hepatic causes • Portalvein occlusion :- thrombosis or external compression • Splenic vein occlusion :- thrombosis or external compression • Increased bloof flow :- splanchnic vasodilation
- 11. Intra-hepatic causes • Pre-sinusoidal: schistosomiasis : early primary biliary cirrhosis : sarcoidosis • Sinusoidal : cirrhosis : non-cirrhotic acute alcoholic hepatitis • Post-sinusoidal : veno-occlusive disease : alcoholic central hyaline necrosis
- 12. Post-hepatic causes • Hepaticvein : thrombosis tumour invasion • Inferior vena cava : tumour invasion : thromobosis • Heart : right sided heart failure : contrictive pericarditis
- 14. Pathophysiology Obstruction to forward venous flow Transferof increased backpressure Portal vein congestion Splenic vein congestion Liver dysfunction Hepatorenal syndrome Reduced detoxificatio n Centrilobular necrosis Portocaval shunting
- 16. Outcomes in liver Centralvein congestion will cause :- centrilobular necrosis and peripheral fatty changes (nutmeg liver). Decreased blood flow to liver will cause reduced detoxification presenting as :-
- 17. – This willcause congestive splenomegaly : asymptomatic or dull aching abdominal pain. – Sequestration of blood cells presenting : cytopenias. SPLENIC VEIN CONGESTION
- 18. Sinistral (left sided/segmental) portal hypertension Pathology Results from occlusion of the splenic vein, usually from pancreatic pathology (e.g. pseudocyst, carcinoma). Clinical presentation Most commonly - asymptomatic. In symptomatic patients, the most common presentation (although rare) is gastrointestinal bleeding Splenomegaly is common (~70%). Cirrhosis and ascites are not common presenting features.
- 19. SMV CONGESTION – Dilatationof superior mesenteric vein and splanchnic circulation will cause transudative shift of fluid from blood into surrounding tisses thus causing ascites.
- 20.
- 21. Ascites Clinical features : Smallamounts : asymptomatic; Larger accumulation : abdominal distension, fullness of the flanks and shifting dullness on percussion. Severe ascites : fluid thrill, eversion of the umbilicus, herniae, Abdominal striae, Divarication of the recti and scrotal oedema may be the presenting features.
- 22. Dilatation causes gastroesophageal varices andhaemorrhage. Dilatation causes haemorrhoids and melena. Reopening of umbilical vein present as caput medusa.