Portal hypertension, varices and bleeding 0.0 / 5 ? MedicineLiverUniversityAll boards Created by: zCreated on: 23-02-16 15:03 Pathogenesis of portal hypertension 25% hepatic flow comes from portal vein from the GIT (75% direct via hepatic artery) portal hypertension= incr pressure in portal vein pressure=flow x resistance resistance= 70% fixed + 30% dynamic (i.e. amenable to drug manipulation) 2 theories for cause of incr pr: "forward theory"- incr splanchnic flow overcomes massive porto-systmeic flow "backward theory" - incr resistance to outflow get venous and arterial stealing in hyperdynamic circulation (i.e. incr BP and HR) venous steal incr intrahepatic pressure causes decrease in portal vein flow ("backed up") blood flows from portal vein straight into hepatic vein (bypass the liver) via portosystemic collaterals results in hepatic ischaemia arterial steal increased flow to splanchnic arteries vasodilation and blood pooling in gut decreased flow to peripheries, head and neck, kidneys (renal underperfusion) 1 of 6 Natural history of varices and bleeding present in 30-40% of pt w/ cirrhosis in 60% with decompensated cirrhosis risk of bleeding is 30% rebleed irsk up to 70% 1 yr mortality following a bleed up to 40% risk factors for variceal bleeding appearance large size, red signs, active bleeding wall tension portal pressure alcohol intake HCC MELD/SOFA/APACHE score MELD= model for end-stage liver disease looks at bilirubin, creatinine, INR and dialysis 2 of 6 Variceal primary prophylaxis endoscopy for all cirrhotic pt pt w/ medium or large varices should receive primary prophylaxis: Non cardio-selective beta blockers (e.g. carvedilol) (BB) beta 1 blockade: reduced CO beta 2 blockade: reduced splanchnic flow results in reduced portal flow thus reduced portal pr thsu reduced porto-systemic shunting reduces bleeding by 50% and mortality by 25-45% NB carvedilol also reduces intrahepatic resistance and has vasodilating effect (alpha 1 antagonist) Variceal band ligation (VBL) 64% reduction in bleeding 45% reudction in mortality BB vs VBL VBL favoured (slightly) compared to BB in meta-analysis BB a/e: SOB, hypotension, impotence, non fatal VBL a/e ulceration/bleeding, some fatalities BB significantly cheaper 3 of 6 Variceal bleeding: drug/fluid management volume expansion aim to preserve tissue perfusion restrictive transfusion (to get pt Hb to 7-8) in haemodynamcacilly pts little evidence for use of blood products must correct hypovolaemia and promote tissue oxygenation (tissue ox= SaO2 x CO x Hb) antibiotics prophylaxis reduce infection (65%), rebleeding (47%) and mortality (21%) Terlipressin tri-glycl vasopressin analogue 2mg= 21% decr in portal pr for 4 hrs mecahnism of action: V1 R - splanchnic vasoconstriction V2 R - reduce renal free water clearance incr SVRI, incr CV (incr renal perfusion) reduces renin 39% reduced mortality 4 of 6 Variceal bleeding endoscopic management VBL first line for acute bleed (prev. sclerotherapy) multibanders rountinely used good initial control but rebleed in 50% best when combined w/ vasoactice drugs incr control, decr rebleed but NO survival benefit ballon tamponade good initial haemostasis controls oesophageal and gastric varcieal bleeding high rebleed rate and local complications (ischaemia) dangerous if inexperienced user TIPSS (transjugular intrahepatic portosystemic stent-shunt) new and promising artificial stent b/w portal vein and hepatic vein better than VBL/BT for rebleed but no effect on total mortality excellent haemostasis as salvage therapy but high mortality 5 of 6 Variceal secondary prophylaxis drug therapy NSBB reduces bleeding and mortality nitrates (isosorbite mononitrate/ISMN) effective in pts who don't respond to NSBB little benefit of adding VBL NSBB + ISMN as effective as VBL endoscopic tehrapy sclerotherapy is effective but assoc w/ a/e VBL- earlier eradication ,better outcomes, less a/e sclerotherapy and VBL combination not recommended bc lots of a/e 6 of 6
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