Portal hypertension, varices and bleeding

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  • Created by: z
  • Created 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)
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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
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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 
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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
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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
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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
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