【正文】 nsion can result from: ?increase in resistance to portal flow and/or ?increase in portal venous inflow MECHANISMS OF PORTAL HYPERTENSION Normal Liver Hepatic vein Sinusoid Portal vein Liver Splenic vein Coronary vein THE NORMAL LIVER OFFERS ALMOST NO RESISTANCE TO FLOW Portal systemic collaterals Distorted sinusoidal architecture leads to increased resistance Portal vein Cirrhotic Liver Splenomegaly ARCHITECTURAL LIVER DISRUPTION IS THE MAIN MECHANISM THAT LEADS TO AN INCREASED INTRAHEPATIC RESISTANCE AN INCREASE IN PORTAL VENOUS INFLOW SUSTAINS PORTAL HYPERTENSION Mesenteric veins ? Flow Splanchnic vasodilatation Distorted sinusoidal architechure Portal vein An Increase in Portal Venous Inflow Sustains Portal Hypertension 20 Small varices Large varices No varices 78%/year 78%/year Varices Increase in Diameter Progressively Merli et al. J Hepatol 2022。 5:419 Varices Present (n=72) Varices Absent (n=15) A THRESHOLD PORTAL PRESSURE OF ~12 mmHg IS NECESSARY FOR VARICES TO FORM Variceal Growth Variceal rupture Portal pressure Resistance to portal flow Cirrhosis Splanchnic arteriolar resistance Portal blood inflow Varices PROGRESSION OF PORTAL HYPERTENSION LEADS TO VARICEAL GROWTH AND VARICEAL RUPTURE Predictors of hemorrhage: ? Variceal size ? Red signs ? Child B/C NIEC. N Engl J Med 1988。 80:1611 T = tp x r w Variceal Wall Tension (T) is a Major Determinant of Variceal Rupture Transmural pressure (tp) Radius (r) Esophagus Varix VARICEAL WALL TENSION IS A MAJOR DETERMINANT OF VARICEAL RUPTURE Prophylaxis of Variceal Hemorrhage Diagnosis of Cirrhosis Endoscopy No Varices Followup EGD in 23 years* Small Varices Followup EGD in 12 years* Medium/Large Varices ?Stepwise increase until maximally tolerated dose ?Continue betablocker (lifelong) No Contraindications Contraindications or Betablocker intolerance Betablocker therapy Endoscopic Variceal Band Ligation *EGD every year in depensated cirrhosis MANAGEMENT ALGORITHM FOR THE PROPHYLAXIS OF VARICEAL HEMORRHAGE SUMMARY Treatment of Acute Variceal Hemorrhage General Management: ? IV access and fluid resuscitation ? Do not overtransfuse (hemoglobin ~ 8 g/dL) ? Antibiotic prophylaxis Specific therapy: ? Pharmacological therapy: terlipressin, somatostatin and analogues, vasopressin + nitroglycerin ? Endoscopic therapy: ligation, sclerotherapy ? Shunt therapy: TIPS, surgical shunt TREATMENT OF ACUTE VARICEAL HEMORRHAGE Endoscopic Variceal Band Ligation ? Bleeding controlled in 90% ? Rebleeding rate 30% ? Compared with sclerotherapy: ?Less rebleeding ?Lower mortality ?Fewer plications ?Fewer treatment sessions ENDOSCOPIC VARICEAL BAND LIGATION Transjugular Intrahepatic Portosystemic Shunt Hepatic vein Portal vein Splenic vein Superior mesenteric vein TIPS THE TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT Management of Acute Variceal Hemorrhage Variceal Hemorrhage Suspected Initial Management NO Rescue TIPS/Shunt surgery Balloon Tamponade YES Early rebleeding? Acute Hemorrhage Controlled? YES 2nd Endoscopy Further bleeding NO Prophylaxis against recurrent hemorrhage MANAGEMENT ALGORITHM IN ACUTE ESOPHAGEAL VARICEAL HEMORRHAGE 30 Evolution of Varices Level of Intervention Management Remendations Cirrhosis with no varices Small varices No hemorrhage Medium / large varices No hemorrhage Variceal hemorrhage Recurrent variceal hemorrhage Preprimary prophylaxis Primary prophylaxis Secondary prophylaxis ? Repeat endoscopy in 23 years ? No specific therapy Small varices ? Repeat endoscopy in 12 years ? No specific therapy ? ? betablocker to prevent enlargement Medium/Large varices ? Nonselective betablockers ? EVL in those intolerant to drugs ? Endoscopic/pharmacologic therapy ? Antibiotics in all patients ? TIPS or shunt surgery as rescue therapy ? Betablockers + nitrates or EVL ? Betablockers + EVL ? ? TIPS or shunt surgery as rescue therapy SUMMARY OF MANAGEMENT OF VARICES AND VARICEAL HEMORRHAGE Ascites and Hepatorenal Syndrome ASCITES AND HEPATORENAL SYNDROME Cirrhosis Activation of neurohumoral systems (renin, angiotensin, aldosterone) Effective arterial blood volume Hepatic venous outflow block Ascites Sinusoidal pressure (HVPG ? 1012 mmHg) Sodium and water retention Arteriolar resistance (vasodilation) PATHOGENESIS OF ASCITES Ultrasound is the Most Sensitive Method to Detect Ascites Liver Ascites ULTRASOUND IS THE MOST SENSITIVE METHOD TO DETECT ASCITES In