Portal Hypertension Mechanisms Pathophysiology by Dr. Aryan
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This document discusses the pathophysiology of portal hypertension. Portal hypertension occurs when there is an elevation in portal venous pressure above 10 mmHg. It can be caused by pre-hepatic issues like portal vein thrombosis, or intrahepatic issues like cirrhosis. The pathophysiology involves increased resistance to portal blood flow from vasoconstriction and fibrosis, as well as increased blood flow from splanchnic vasodilation. This leads to the formation of portosystemic shunts and complications like variceal bleeding, ascites, and hepatic encephalopathy. Management involves general measures during bleeding, pharmacological agents, endoscopic therapy of varices, and procedures like TIPS or transplantation.
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Portal Hypertension Mechanisms Pathophysiology by Dr. Aryan
- 1. PATHOPHYSIOLOGY OF PORTAL HYPERTENSION Presented by: Anish Dhakal Medical Student anishdhakal718@gmail.com 3/29/2018 1
- 2. CONTENTS: Portal hypertension Pathophysiology of portal hypertension Mechanisms/Pathophysiology of clinical signs Clinical manifestations Management options 3/29/2018 2
- 3. NORMAL ANATOMY Portal vein supplies 80% of the blood to the liver. The remaining 20% is supplied by the Hepatic artery 3/29/2018 3
- 4. PORTAL HYPERTENSION • The term “Portal hypertension” was Introduced by Augustin Nicolas Gilbert in 1902 • The normal portal venous pressure is ∼7 mm Hg • An elevation of portal pressure >10 mmHg is called portal hypertension (as high as 60 mm Hg) • Clinical syndrome – 10-12 mm Hg • Variceal bleeding only occurs when pressure rises above 12 mmHg 3/29/2018 4
- 5. CAUSES Pre-hepatic Intrahepatic Posthepatic PREHEPATIC PRESINUSOIDAL •Portal vein or splenic vein thrombosis (sepsis ) •Splenic AV fistula •Massive splenomegaly INTRAHEPATIC PRESINUSOIDAL •Sarcoidosis •Schistosomiasis •Congenital hepatic fibrosis •Myeloproliferative disorders •Nodular regenerative hperplasia •Cirrhosis due to any cause •Nodular regenerative hyperplasia •Metastatic malignant •disease •Budd Chiari syndrome •Right heart failure •Constrictive pericarditis •Web in inferior vena cava. 3/29/2018 5
- 6. • May occur due to • Infection • Portal vein thrombosis • Inflammation (umbilical infection with or without catheterization, acute appendicitis, primary peritonitis, pancreatitis, portal pyemia.) • Hypercoagulable state ( acute dehydration, polycythemia and inherited and acquired deficiencies of anticoagulant proteins (C, S, AT III ) • Trauma to the portal vein • Invasion or compression by tumor or pancreatic mass. 3/29/2018 6
- 8. PATHOPHYSIOLOGY A. Increase resistance to portal flow Release of ET-1, angiotensin, eicosanoids and reduced NO by sinusoidal endothelial cells Contraction of vascular endothelium & smooth muscle cells Disruption of fibrinolytic factors leading to fibrinogenesis which disrupt blood flow by scarring, Parenchymal nodules Increased portal vascular resistance leads to gradual reduction in flow of portal blood to liver Anastomoses between portal and arterial system leads to portosystemic shunting 3/29/2018 8
- 9. PATHOPHYSIOLOGY B. Increase in portal venous blood flow • Arterial vasodilation of splanchnic circulation • Mediators: Prostacyclin, NO, TNF, glucagon Note: NO production is stimulated by decreased clearance of bacterial DNA absorbed from gut 3/29/2018 9
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- 22. CLINICAL PRESENTATION • Sinusoidal and postsinusoidal PH often present with • Hepatomegaly • Ascites • Splenomegaly with stigmata of chronic liver disease. • EHPVO • Usually present at 5-6 yrs of age with hematemesis (+- melena) • Splenomegaly is universal. • Liver is usually normal in size • Ascites is rare in these patients • Child may have variable extent of growth retardation. 3/29/2018 22
- 23. INVESTIGATIONS • Complete haemogram- anemia, evidence of hypersplenism • Liver function test • Radiology • Non-invasive • Ultrasound with duplex Doppler • CT scan • MRI • Invasive • Splenoportovenography, • arterioportography, • percutaneous transhepaticportography • Esophago-gastro-duodenal endoscopy 3/29/2018 23
- 24. MANAGEMENT A. General management B. Specific management • Pharmacological therapy • Mechanical therapy • Endoscopic therapy • Surgical therapy C. Management of associated problems 3/29/2018 24
- 25. GENERAL MANAGEMENT • Adequate venous access should be established and iv fluid and /or packed cells infused • Vitamin K, infusion of fresh frozen plasma and/or platelets might be infused to correct coagulopathy • Continuous aspiration of ongoing bleeding to clear stomach by placing NG tube • PPI (Pentoprazole)/H2 receptor antagonist is administered IV to reduce the risk of gastric erosion • Monitor vitals and urine output 3/29/2018 25
- 26. PHARMACOLOGICAL THERAPY • Vasoconstrictive drugs –vasopressin 20U IV over 15 min, glypressin and terlipressin (nitroglycerine can be added) • Cesation of bleeding in 50 – 80 % of cases. • Somatostatin analogs such as octreotide - 1 mcg/kg body wt (max. 100 mcg), followed by 1 mcg/kg/hr as a continuous IV infusion • Used till a bleeding free interval of of 24-48 hours is achieved 3/29/2018 26
- 27. MECHANICAL THERAPY • Inflatable balloons for direct compression of varices. • Commonly used Sengstaken–Blakemore tube 3/29/2018 27
- 28. ENDOSCOPIC THERAPY • Variceal sclerotherapy • Ligation or banding with rubber Surgical therapy • Devascularization or transaction of oesophagus which blocks the blood flow to the varices • Transjugular intrahepatic portalsystemic stent shunt 3/29/2018 28
- 30. MANAGEMENT OF ASSOCIATED PROBLEMS• Hypersplenism- may need splenectomy • Liver transplantation –cirrhosis and hepatic failure Prophylaxis of variceal bleeding • Beta blocker(propranolol,1-2 mg/kg/day) • Heart rate should be monitored 3/29/2018 30
- 31. COMPLICATIONS OF PORTAL HTN • Variceal bleeding (oesophageal, gastric, other) • Ascites • Iron deficiency anaemia • Renal failure • Hepatic encephalopathy • Congestive gastropathy • Hypersplenism 3/29/2018 31
- 32. REFERENCES • Essential pediatrics, OP Ghai, 8th edition • Davidson’s principles and practice of medicine, 19th edition ( Page no. 945 – 947 ) • Bailey and Love, Short Practice of Surgery, 26th Edition. https://www.hindawi.com/journals/ijh/2012/203794/ http://www.ncbi.nlm.nih.gov/books/NBK6973/ , http://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdf s/liver/portal_hypertension.pdf http://www.ncbi.nlm.nih.gov/pubmed/1568769 3/29/2018 32
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Editor's Notes
- The portal vein is formed by the confluence of the Superior mesenteric vein and splenic vein. It collects blood from the GI tract and drains it into the liver. It is not a true vein because it does not conduct blood directly into the heart. It drains blood from the GIT and spleen into the liver
- Vesopressin may induce generalised arterio-veno vaso constriction causing peripheral vascular ischemia, MI or infarction and renal tubular damage, so nitroglysireine is used to attenuate some of these side effects
- TIPS is a minimally invasive means of creating a portosystemic shunt by creating a direct communication between the portal and the hepatic venous systems within the liver. A catheter is introduced through the internal jugular vein and under radiological control, is positioned in the hepatic vein. From here, the portal vein is accessed through the liver, the tract is dilated and and the channel is kept open by placing an expandable metallic stent. This technique is of great value in controlling portal hypertension and variceal bleeding. The shunts remain open in most patients for up to a year, at which point intimal overgrowth leads to thrombosis and occlusion.
- Congestive gastropathy : macroscopic changes of gastric mucosa occurring in portal hypertension that are associated with vascular mucosal and submucosal dilatation and ectasia without significant inflammatory changes