Portal Hypertension: An Overview

Educational Objectives

The goal of this program is to improve management of portal hypertension. After hearing and assimilating this program, the clinician will be better able to:

1. Identify common causes of portal hypertension.
2. Develop strategies for prophylaxis and management of esophageal and gastric varices in patients with portal hypertension.

Summary

Causes of PHTN: posthepatic — include Budd-Chiari syndrome (hepatic venous outflow tract obstruction [HVOTO]), inferior vena cava obstruction, and many cardiac conditions (eg, constrictive pericarditis, right-sided heart failure); prehepatic — include portal vein thrombosis and splenic vein thrombosis; intrahepatic — subdivided into presinusoidal, (eg, primary biliary cholangitis, primary sclerosing cholangitis, sarcoidosis, schistosomiasis), sinusoidal (eg, cirrhosis), and postsinusoidal (sinusoidal obstruction syndrome)

Hepatic venous pressure gradient (HVPG) and type of PHTN: the HVPG is obtained by subtracting the free hepatic venous pressure from the wedge hepatic venous pressure; the normal value is 3 to 6 mm Hg; patients with prehepatic PHTN or presinusoidal intrahepatic PHTN have normal HVPG readings; patients with cirrhosis and sinusoidal PHTN or sinusoidal obstruction syndrome have a high wedge pressure and a high gradient; measurement may not be possible in patients with HVOTO because radiologists may be unable to wedge the catheter into the hepatic vein because of the venous obstruction; patients with posthepatic PHTN from right-sided heart failure experience high wedge and free pressures, but the gradient remains normal

American Association for the Study of Liver Diseases (AASLD) practice guidance: current guidelines based on Baveno VI criteria (2015) state that patients with liver stiffness <20 kPa and platelet count >150,000/μL have a low probability of high-risk varices and do not need endoscopy; patients who have thrombocytopenia or liver stiffness >20 kPa should undergo endoscopy to screen for varices; patients with compensated cirrhosis (Child-Pugh class A) may have mild PHTN and HVPG between 6 mm Hg and 10 mm Hg or clinically significant PHTN with HVPG >10 mm Hg; patients with signs of decompensation may develop complications (eg, variceal hemorrhage, ascites, encephalopathy) and usually have HVPG >12 mm Hg; late decompensation may lead to recurrent variceal bleeding, refractory ascites, refractory encephalopathy, hyponatremia, or hepatorenal syndrome (HRS); varices tend to form with a HVPG >10 mm Hg; variceal bleeding typically occurs with a HVPG >12 mm Hg, and a HVPG >16 mm Hg is correlated with increased mortality; patients with acute variceal hemorrhage and a HVPG >20 mm Hg are often refractory to endoscopic treatment and require transjugular intrahepatic portosystemic shunt (TIPS)

Varices: in patients with cirrhosis, incidence is 7% to 8% per yr, and the prevalence is 40% to 50%; patients with Child-Pugh class C cirrhosis have a higher prevalence of varices and tend to have larger varices than those with well-compensated Child A cirrhosis; varices can be small (<5 mm diameter) or medium to large (>5 mm diameter), and they may have red wale markings or a fibrin plug (highest-risk stigmata of variceal bleeding); predictors of hemorrhage include variceal size (most important), presence of red wale signs, and higher Child-Pugh scores

Primary prophylaxis for varices: options include a nonselective β-blocker (eg, propranolol, nadolol), an α-blocker that is also a nonselective β-blockers (eg, carvedilol), or primary band ligation; nonselective β-blockers decrease splanchnic vasodilation in cirrhosis, reducing portal venous inflow; carvedilol also decreases intrahepatic resistance and is thus preferred for patients with compensated cirrhosis; as cirrhosis advances, cardiac reserve may decrease and stimulation of sympathetic nervous system activity and the renin-angiotensin-aldosterone system may increase; risk for bacterial translocation and mortality increases over time; β-blockers can be used in medium to large varices (even in early decompensation); however, decrease the dose or temporarily hold β-blockers in patients with refractory ascites and severe circulatory dysfunction (systolic blood pressure <90 mm Hg, serum sodium <130 mEq/L, or HRS); they may be reintroduced if circulatory function improves

Acute variceal bleeding: admit to the intensive care unit; avoid overtransfusion (maintain hemoglobin levels at 7-8 g/dL); early pharmacotherapy includes intravenous octreotide and antibiotic prophylaxis; perform endoscopy ≤12 hr of admission and perform band ligation for any esophageal varices; a meta-analysis (Bañares et al [2002]) found that endoscopic therapy plus drug therapy is superior to endoscopic therapy alone; for patients refractory to endoscopic therapy, a tube (eg, Minnesota tube, Sengstaken-Blakemore tube) can be used to tamponade bleeding as a bridge to TIPS; the gastric balloon must always be inflated, even for esophageal variceal bleeding; TIPS — is a life-saving measure for patients who are refractory to endoscopic therapy; Garcia-Pagan et al (2010) found that TIPS ≤72 hr of the initial bleed may benefit patients at high risk for failure or rebleeding

Secondary prophylaxis after an index bleed: use band ligation and continue nonselective β-blocker until varices are eradicated; carvedilol is not recommended (insufficient data); propranolol or nadolol are preferred

Gastric varices: are detected at ≈20% of index endoscopies in patients with PHTN (less frequent than esophageal varices); the mortality rate is high; these varices have different venous afferents; classification systems — may be based on the location of the varices (and continuity with the esophagus), endoscopic appearance, or variations in afferent flow; cross-sectional imaging is crucial to assess for evidence of splenic vein thrombosis or shunts (gastrorenal or gastrosplenic); management — varices extending from the esophagus into the cardia are managed similar to esophageal varices; Mishra et al (2011) found that cyanoacrylate was superior to propranolol for high-risk varices; TIPS and balloon-occluded retrograde transvenous obliteration (BRTO) are not recommended for primary prophylaxis; for an acute bleed, use prophylactic antibiotics, vasoactive medications, and potentially endoscopic therapy; before using cyanoacrylate glue, perform an echocardiography to rule out an intracardiac shunt; other options include TIPS (not for left-sided PHTN) or BRTO

Readings

Bañares R, Albillos A, Rincón D, et al. Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a meta-analysis. Hepatology. 2002 Mar;35(3):609-15; García-Pagán JC, Caca K, Bureau C, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010 Jun 24;362(25):2370-9; Jothimani D, Rela M, Kamath PS. Liver cirrhosis and portal hypertension: How to deal with esophageal varices? Med Clin North Am. 2023 May;107(3):491-504; Kaplan DE, Bosch J, Ripoll C, Thiele M, Fortune BE, Simonetto DA, Garcia-Tsao G. AASLD practice guidance on risk stratification and management of portal hypertension and varices in cirrhosis. Hepatology. 2023 Oct 23. doi: 10.1097/HEP.0000000000000647. Epub ahead of print. PMID: 37870298; Li S, Huang P, Jeyarajan AJ, et al. Assessment of non-invasive markers for the prediction of esophageal variceal hemorrhage. Front Med. 2021 December 01;Volume 8. https://doi.org/10.3389/fmed.2021.770836; McConnell MJ, Iwakiri Y. Portal hypertension in alcohol-associated hepatitis. Curr Hepatol Rep. 2023;22(2):67–73; Mishra SR, Sharma BC, Kumar A, Sarin SK. Primary prophylaxis of gastric variceal bleeding comparing cyanoacrylate injection and beta-blockers: a randomized controlled trial. J Hepatol. 2011 Jun;54(6):1161-7. doi: 10.1016/j.jhep.2010.09.031. Epub 2010 Nov 5. PMID: 21145834; Tonon M, Piano S. Cirrhosis and portal hypertension: How do we deal with ascites and its consequences. Med Clin North Am. 2023 May;107(3):505-516; Turco L, Reiberger T, Vitale G, et al. Carvedilol as the new non-selective beta-blocker of choice in patients with cirrhosis and portal hypertension. Liver Int. 2023 Jun;43(6):1183-1194; Wani ZA, Bhat RA, Bhadoria AS, et al. Gastric varices: Classification, endoscopic and ultrasonographic management. J Res Med Sci. 2015 Dec;20(12):1200–1207.

Disclosures

For this program, members of the faculty and planning committee reported nothing relevant to disclose.

Acknowledgements

Dr. Sass was recorded at the 41st Advances in Gastroenterology Conference, held on June 17, 2023, in Atlantic City, NJ, and presented by Sidney Kimmel Medical College at Thomas Jefferson University. For information on future CME activities from this presenter, please visit jefferson.cloud-cme.com. Audio Digest thanks the speakers and Sidney Kimmel Medical College at Thomas Jefferson University for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0.75 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0.75 CE contact hours.

Lecture ID:

GE380201

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.