Portal hypertension Current Status. Abraham Shaked MD PhD

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1 Portal hypertension Current Status Abraham Shaked MD PhD

2 Portal Hypertension Defined as an increase in portal vein pressure to exceed 6 mmhg It is the underlying process responsible for the most common complications of cirrhosis: Ascites Variceal bleeding Hepatic encephalopathy

3 Portal circulation

4 Classification of portal hypertension (PHTN) Pre-hepatic PHTN Intrahepatic PHTN Post-hepatic PHTN Portal v thrombosis Presinusoidal Sarcoidosis PBC Schistosomiasis Sinusoidal Cirrhosis Alcoholic Hepatitis Postsinusoidal Sinusoid obstruction syndrome (VOD) Budd-Chiari Syndrome Rt heart failure Constrictive pericarditis IVC web

5 - Fibrosis in the space of Disse - Compression by regenerative nodules and fibrous bands - Swelling of hepatocytes

6 Classification of Chronic Liver Disease Histological F1-F3 F4 (Cirrhosis) Clinical Non-cirrhotic Compensated Compensated Decompensated Symptoms None None (no varices) None (varices present) Ascites, VH, encephalopathy Sub-stage - Stage 1 Stage 2 Stages 3 and 4 Hemodynamic (HVPG, mmhg) >6 >10 >12 Biological Fibrogenesis and Angiogenesis Scar and X-linking Thick (acellular) scar and nodules Insoluble scar Garcia Tsao G et al Hepatology 51:145-9;2010

7 Proportion of Patients Cumulative Proportion of Patients Transitioning from Compensated to Decompensated Stage Over Time Pts at risk months D Amico G et al. J Hepatol. 2006;44:

8 Consequences of PHTN: Ascites and Hepatorenal Syndrome Cirrhosis Portal HTN NO Incr Spl capillary pressure Splanchnic vasodilation Arterial Underfilling Angiotensin II Aldosterone Norepinephrine Incr lymph production Na & Water Retention ADH Renal vasoconstriction Impaired free water excretion Ascites Hypotension Hyponatremia Hepatorenal syndrome

9 Consequences of PHTN: Varices and Hepatic Encephalopathy Most common sites portosystemic collaterals - GE junction and proximal stomach: Gatroesophageal varices - Umbilical vein: Caput medusae - Rectum: Rectal varices Consequences: - Increased pressure in collaterals resulting in rupture: variceal bleeding - Shunting of gut derived toxins (ammonia) away from the liver: hepatic encephalopathy

10 Gastroesophageal varices

11 VARICES INCREASE IN DIAMETER PROGRESSIVELY Natural history of varices in cirrhosis Usually develop as HVPG exceeds mmhg Tend to grow with time No varices Small varices < 5 mm Large varices > 5 mm 7-8%/year 7-8%/year Merli et al. J Hepatol 2003;38:266

12 Risk of Esophageal Varices Bleed Cirrhosis % % % Survive 70 % Rebleed % Die

13 Predictors of variceal bleeding Esophageal varices do not usually bleed until HVPG > 12mmHg Bleeding rate: 5-15% / yr Risk of bleeding increases: - Large Varices - Red marks - Child B/C Mortality of 20 % HVPG > 20 mmhg predicts a higher mortality from variceal bleed (64% at 1 yr)

14 Decompensated Compensated Baveno IV International Consensus Workshop Staging System for Cirrhosis: 1-Year Outcome Probabilities Stage 1 NO VARICES NO ASCITES 1% 7% 4.4% Stage 2 VARICES NO ASCITES 3.4% 6.6% 4% DEATH Stage 3 ASCITES VARICES 20% 7.6% Stage 4 BLEEDING ASCITES 57% D Amico G et al. J Hepatol. 2006;44:

15 NON-SELECTIVE BETA-BLOCKERS PREVENT FIRST VARICEAL HEMORRHAGE Non-Selective Beta-Blockers in primary prophylaxis Bleeding rate Control Beta-blocker Absolute rate (~2 year) difference All varices 25% 15% -10% (11 trials) (n=600) (n=590) (-16 to -5) Large varices 30% 14% -16% (8 trials) (n=411) (n=400) (-24 to -8) Small varices 7% 2% -5% (3 trials) (n=100) (n=91) (-11 to 2) D Amico et al., Sem Liv Dis 1999; 19:475

16 Primary prophylaxis for If there are large varices on EGD - β blockers or EVL variceal bleeding EVL: Q1-2 wks until obliteration, repeat at 1-3 months, then Q 6-12 months Once on β blocker for primary prophylaxis, endoscopy not needed unless there is need to stop βblocker or GI bleed

17 Management of acute variceal bleeding Resuscitate: - IV access, fluids, blood products - Do not overtransfuse! Target Hb 8 g/dl Prophylactic antibiotics x 7 days IV Octreotide for 3-5 days Endoscopy / EVL as soon as stabilized 10-20% of variceal bleeds are uncontrolled with the above measures: TIPS

18 Villanueva C, et al. N Engl J Med 2013;368:11-21 Survival, According to Transfusion Strategy

19 % Hemoglobin threshold for transfusion: Randomized trial of restrictive versus liberal transfusion strategies for acute upper gastrointestinal bleeding Study Outcomes p=0.02 Death from any cause within 45 days p= Patients with cirrhosis p=0.05 Bleeding from esophageal varices 2 Restrictive Strategy Liberal Strategy p= Balloon therapies 4 TIPS 11 p=0.04 Restrictive strategy: Transfuse when Hg below 7g/dL Liberal strategy: Transfuse when Hg below 9g/dL Blood Transfusion Requirement 15 % Vs.51% P <0.001 Villanueva C, et al. N Engl J Med 2013;368:11-21

20 PROPHYLACTIC ANTIBIOTICS PREVENT EARLY VARICEAL REBLEEDING Probability of Remaining Free of Recurrent Variceal Hemorrhage 1.0 % free of variceal bleed Prophylactic antibiotics (n=59) No antibiotics (n=61) 0 0 Hou M-C et al., Hepatology 2004; 39: Follow-up (months)

21 Gastric Varices Rx same as EV Can be seen in Spl. v. thrombosis

22 Bleeding gastric fundus varices Tend to be larger, more tortuous, deeper vessels than EV: present a challenge for endoscopic therapy Can bleed at lower HVPG Best endoscopic therapy: cyanoacrylate injection, but not widely available and cumbersome Low threshold for TIPS in bleeding GV in the fundus

23 Transjugular Intrahepatic Portosystemic Shunt (TIPS) in the Setting of Intrahepatic and Post-hepatic Portal Hypertension Presinusoidal PBC Sinusoidal HCV, ETOH Post-sinusoidal/Post-hepatic BCS

24

25 Outcomes after early TIPS dose of propranolol use of nitrates use of uncovered stents exclusion of those with advanced liver disease García-Pagán JC et al. N Engl J Med 2010;362:

26 The Blakemore Tube

27 Portal Vein Thrombosis Portal vein thrombosis: Incidence in compensated disease: 0.6% to 5% Incidence in advanced disease: up to 40% Risk factors for PVT: Recurrent liver decompensation History of infection, bleeding, endoscopic treatment Abdominal surgery (eg. splenectomy)

28

29

30

31

32

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34 Ascites Fatigue Poor quality of life Muscle wasting Umbilical hernia rupture Hydrothorax SBP Hepatorenal Syndrome

35 Cirrhotic Ascites Survival Survival (%) Onset Years

36 Management of Ascites First Line Therapy Tense ascites Paracentesis Refractory Ascites 10 % Second Line Therapy Repeated Large volume paracentesis (LVP) TIPS? Early Sodim restriction ( 2 Gm/24 Hrs) and diuretics Non-tense ascites Diuretics: Spironolactone 100 mg/day, furosemide 40 mg/day or bumetanide 1 mg a day. Uptitrate stepwise to spironolactone 400 mg/day, furosemide 160 mg/day or bumetanide 4 mg/day as long as it is tolerated Liver Transplantation Post paracentesis albumin infusion may not be necessary for < 5 liters removed Albumin infusion of 6-8 gm/liter of fluid removed is a consideration for repeated LVP

37 Ascites Survival: Only improved by liver transplant After Liver Transplant Survival (%) Onset Years

38 Surgical Resection of HCC in Cirrhosis (not to be done by the general surgeon) Probability (%) No Portal pressure, Bili <1 Portal pressure, Bili <1 Portal pressure, Bili Months Llovet JM, et al. Hepatology 1999;30: Patients selected by Mazzafero Criteria and Child s A cirrhosis

39 Life with Minimal Residual Liver Reserve Stable 49 yrs with PBC who is on the transplant list with MELD of 14 Underwent emergency repair of incarcerated umbilical hernia (no need for bowel resection) 1 week post-op Severe ascites HRS MELD 29 2 weeks post-op undergoes successful OLT

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