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Portal Hypertension and Bleeding in Cirrhosis PowerPoint Presentation

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Description : This ppt covers latest AASLD guidelines on diagnosis, Management and description on Portal Hypertension and Bleeding in Cirrhosis.

Tags : Portal vein hypertension, Cirrhosis, CLD

Published on : Jul 22, 2023 | Views : 780 | Downloads : 2

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Slide 1-

Yusuf Kagzi Portal Hypertension And Bleeding in Cirrhosis AASLD Guidelines
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Risk Stratification Cirrhosis can be: Compensated >12 yr survival Child Pugh-A Decompensated- clinical decompensation present Ascites, varices hemorrhage, encephalopathy >1.8 yr Child Pugh B and C Advanced CLD: Portal HTN before Dx of cirrhosis
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Portal Hypertension: Main consequence of cirrhosis HVPG >5mmHg is better than liver biopsy to predict complication of cirrhosis/CLD Classification:
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Compensated Cirrhosis Can be of 2 types: Mild PH: HVPG >5 but <10 mmHg Clinically significant PH: > 10 mmHg Increase clinical decompensation risk If Gastro-esoph varices: mean patient has >10 HVPG, determine further worse prognosis in these patients
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2. Decompensated: Clinical signs Other predictors: MELD and Albumin Variceal Hemorrhage- If alone: 20% 5 yr mortality If with other complications: 80% 5 yr mortality
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Epidemiology Predictors of poor outcome Compensated cirrhosis- chances varices will develop at 7-8% every year Decompensated cirrhosis is independent RF for progression Bacterial Infection risk increase when HVPG is >20 Obesity Alcohol use Hep C NASH Always consider wt loss and alcohol cessation in the patients.
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Pathophysiology: Portal Pressure: Increased intrahepatic resistance: d/t fibrous tissue, vascular remodelling Increased hepatic vascular tone: endothelial dysfunction -> reduced NO But nitrates, alpha antagonist should not be used alone as cause sys vasodilation-> dec arterial pressure-> worsen Na retention Use statins as improve endoth dysfunction Increased Splanchnic vasodilation Neoangiogenesis/Collateral-> increase NO production development causes increased gut and splanchnic circulation flow. Vasodilation also occur in sys arterial circulation-> activate vasoconstrictive pathway-> worsen Na retention, Increased Blood volume, and a state of hyperdynamic circulatory state Non selective B-blocker(Carvidelol- more decrease MAP, Propranolol, Nadolol) and Octreotide, somatostatin cause splanchnic vasoconstriction Start NSSBB in clinically signif PH , no role in mild PH
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Diagnosis and Monitoring: Portal HTN: Gradient of Portal vein - Hepatic Vein >5 mmHg Normal 3-5 Mild PHTN >5 - < 10 CSPHTN >10 If >10 + complication: Decompensated - Bleeding risk is clear if: HPVG >12 or GEV present - High risk death if > 16, 1mmhg increase in HPVG means 3% increase in death - Despite it HVPG is so useful it is invasive, require expertise and hence not considered as std of care in every patient
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Non Invasive test to see CSPHTN: Platelet count- low Ultrasound/CT/MRI- report portocollateral circulation US signs: Dilation of portal veins Reduced portal vein velocity Combine both= congestion index Speenomegaly Fibro-Scan: to assess liver stiffness(LS), measures ROC curve >20 kpa LS means CSPHTN >21kpa LS and >10 HVPG= Decompensation New test for sonoelastography methods: SWE(Shear wave elastography) MRE (MR elastography)- measure both liver and spleen stiffness Remember GEV: means CSPHTN
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2. Non Invasive test for GEV Dx: LS and PLC: LS <20 and PLC >150000: <5% risk of varices. Endoscopy can be avoided Who donot meet this criteria: Needs screening endoscopy
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Monitoring of CSPHTN and Varices: Compensated cirrhosis without varices on screening EGD: If ongoing liver injury (obese/alcoholic/hepatitis): repeat every 2yr if CC viral elimination/alcohol abstinence: Do every 3 years: CC with small varices on screening endoscopy: If obese/alcoholic/hepatitis: every year viral elimination/alcohol abstinence: every 2 years CC with or without varices who develop decompensation signs: Repeat Endo at that time
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Management:
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Goals of Care: Compensated: No PH complications HVPG <10: Prevent CSPH HVPG >10 with/without nonbleeding varices: Prevent decompensation Decompensated: >12 HPVG and varices present Acute VH: control bleeding, prevent rebleed Prior VH with no ascites or encephalopathy: Prevent rebleed Prior VH with ascites or encephalopathy: Prevent decompensation and death
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Compensated Cirrhosis + Mild PHTN Goal to prevent CSPHTN Mainstay of therapy to Rx etiology HBV, HCV, alcohol, Iron Statin- antifibrotic, improve endothelial dysfunction, reduce PP No use of Non invasive test to rule out CSPHTN, only way is to do HPVG measurements but not rec clinically NSBBs reduce portal pressure- hence ineffective totally!
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2. Compensated cirrhosis + CSPHTN(>10mmHg)+ No GEV: New objective is not to prevent varices but to prevent clinical decompensation No evidence of NSBBs effective or not. Hence not rec to use Statins use rec
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3. Compensated cirrhosis + CSPHTN(10-12mmHg)+ GEV: GEV by definition 10-12 mmHg HVPG Main objective: prevent first episode of VH NSSBs s/b started- >10% reduction in HVPG, dec risk of ascites and death Decrease in HR donot correlate with HVPG Ligation and banding only to patient intolerant to meds. Hence, Indication of Primary Px: Patient with med/large varices Small varices with red wale sign Decompensated + small varices
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Prevention of hemorrhage in Med/large varices: Either NSBBs- Carvidelol, Propranolol, Nadolol or EVL (Banding) No need for repeat EGD Disadv: C/I in some patients, discontinuation due s/e like fatigue,SOB Carvidelol has least side effect profile and better tolerated Dosing: - not guided by HR Not guided by HR 3.125 BID to max 5=6.25 mg BID - EVL has more severe side effect and NSBBs has more number of S/E. Also, EVL only act as local Rx but NSBB act on pathophysiology - No benefit of combination Rx of NSSB and EVL - TIPS has high mortality side effect. Never rec in this setting (b) Prevention of hemorrhage in Small varices NSBB is recommended.
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4. Pt presented with Acute Variceal Hemorrhage: Considered as Decompensated Goal: to control bleeding, prevent early recurrance and 6 wk mortality Access circulatory and protect respiration. Volume resuscitation Restrictive pRBC transfusion at Hb threshold of 7g and maintain 7-9. Hb >9g/dl or liberal transfusion increase mortality No role of FFP coagulation correction. INR in cirrhosis is not a reliable indicator Abx prophylaxis: dec risk of bact infection, hemorrhage and death. Prefer Ceftriaxone 1g every 24 hrs for short term of 7 d. IV octreotide bolus 50 mcg f/b 50 mcg/hr for 2-5 days EGD ASAP: Signs see= white nipple. VH s/b the Dx when only variceal lesions are found in EGD. EVL can be done in simultaneous setting. Persisted bleed/ severe Re-bleed- Mx with PTFE covered TIPS Bridge Rx before TIPS: Balloon tamponade endoscopically with metal stents
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Endoscopic Variceal ligation: Banding -Repeat until all are obliterated - Require indefinite EGD monitoring for recurrence Local therapy: - mostly for cardiofundal gastric varices 1. Cyanoacrylate glue 2. Transvenous sclerosant/ embolisation in collaterals- called BRTO(Ballon occluded retrograde transvenous obliteration) TIPS: - in decompensated - hypertensive portal vein to normotensive hepatic vein - No need for other therapies for PH if patient has TIPS -
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5. Recovered from Episode of Acute Esophageal Variceal Bleed c/d secondary prophylaxis In patient with only VH and no other complication: objective is to prevent additional complication and rebleed In patient with VH and decompensation complications: objective is to improve survival Patient who had TIPS done for a/c episode - no need Rx to control PHTN. Hence no NSSB or EVL. Refer for transplant. Screen 6m US for HCC All other patients: 1st line is combination of NSSB + EVL If recurrent: TIPS is recommended
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6. Gastric Varices: -Sarin’s Classification: used for risk stratification and management GOV1: below the cardia and lesser curvature GOV2: extend to fundus - 2nd most high risk for bleed Isolated GV1: only in fundus. - most high risk for bleed Isolated GV 2 : cardio-fundal- check for spleenic vein thrombosis
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Management: Prevention of 1st Hemorrhage from Gastric varices: NSSBs rec Never TIPS or BRTO for varices that not bled Mx of a/c hemorrhage from GV: Volume resuscitation, vasoactive drugs, Abx If massive bleed: Balloon tamponade with Linton Nachlas tube Endoscopic Rx and TIPS: In GOV-1: EVL or cynoacrylate glue inj either which is feasible. TIPS is rec in GOV2 or IGV1. If TIPS not available, cyanoacrylate glue is an option © Prevention of re-bleed: - GOV1: EVL and NSBBs combination is first line - GOV2/ IGV 1: TIPS or BRTO are first line - Cyanoacrylate glue inj in cases when TIPS/BRTO not feasible.
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(6). Ectopic Varices: Source of bleed in case of pre-hepatic portal HTN Dx: CT with contrast in portal venous phase Mx: Endoscopic - Ligation or glue, Endosonographic coil placement, TIPS or BRTO
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(7). Special Populations: Pt with Refractory ascites or after SBP: No absolute C/I to NSSBs Avoid high dose >160mg/d propranolol or >80mg/d nadolol as high risk of post-paracentesis circulatory dysfunction and hepatorenal syndrome In patients with severe circulatory dysfunction: SBP <90, Na <130; NSSBs dose should be reduced or discontinued temporarily Pt with 1st variceal hemorrhage while on primary px on NSSBs or EVL: 1st try combination therapy with both NSSB and EVL Alternate: TIPS Pt with HCC: Has worse bleeding prognosis and high chance Follow same principles as those for patients without HCC
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Thank You!