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  • See Lawson's notes
  • Probably didn't vomit 2 buckets of blood, but did have a significant hematemesis
  • Cirrhosis: nodular regeneration, fibrosis, irreversible, hepatocellular death, architectural distortion, risk of HCC, portal hypertension,
    • Alcohol: steatosis. Between steatosis and cirrhosis is alcoholic steatohepatitis (acute inflammation; NB - viral hepatitis = chronic inflammation (lymphocytes), around edge of lobule, but steatohepatitis is within the lobule and is neutrophilic). Fat-laden hepatocytes attacked by neutrophils. At this stage, we're still reversible.
    • Hepatitis: chronic injury
  • Antibody +. Antibodies measure exposure to virus and response to virus. Note window period when Ab test negative. Virus eradication can occur in 20% of cases. Those people retain antibody - so we check for RNA (present still in 80%)
  • Hepatitis C treatments - interferon based
  • Hepatitis C in IVDU - around 50%
  • Hepatits C is very resilient and hangs around in the environment unlike HIV
    • Risk from paraphernalia e.g. tourniquets and spoons
    • Source matters: reinfection is possible, and then your treatment might not be useful
  • Other sources of hepatitis: blood transfusion, contaminated barber's equipment, tattooing, vertical trasmission (rare)
  • Alcohol + hepatitis C: 2 substantial sources of injury - compound each other
    • Vomiting due to alcohol can cause rupture of oesophageal varices
    • Hep C treatments are less effective in patients who have cirrhosis
  • Band ligation of oesophageal varices - occludes the vein and the varice undergoes thrombosis -->
  • Location of varices - lower end of oesophages - portal systemic anastamoses
    • Other sites: umbilicus, rectum, can get them virtually anywhere in the abdominal cavity
    • We know about the oesophageal varices because they are much closer to the lumen than elsewhere
  • Eradicating oesophageal varices doesn't get rid of the underling pressure - so other varices will appear. But usually the other sites are without clinical consequence
  • Coagulopathy in hepatitis C - factors 2, 7, 9, 10 are made in the liver and the vitamin K is made in the liver as well
    • Affects prothrombin time and INR
    • Protein C and protein S are antithrombotic, and are also decreased. Therefore DVT, portal vein thrombosis can actually occur in liver disease (actually get clotting problems lol)
    • INR is not an accurate reflection of predisposition to bleeding (in liver disease compared to warfarin) because it's only in vitro
    • Other factors affecting bleeding
      • size - LaPlace's law, T=Pr. (Portal pressure can be measured through the hepatic veins)
  • Cause of portal hypertension: a) anatomic derangement b) vasoactive component (elevated levels of vasoactive peptides in cirrhosis --> reduced flow through the liver at a cellular level)
  • Other portal hypertension signs: ascites, caput medusae, splenomegaly (bloods: decreased platelets because spleen enlarged)
  • Platelet count low because
    • Initial response to bleeding is elevation of platelet count (release from spleen and lungs)
    • Chronic bleed uses up platelet stores because of consumption
    • Malnutrition (B12 and folate)
    • Marrow suppression from alcohol (myelotoxicity) - reversible if you stop drinking
    • Decreased thrombopoietin
  • LFTs
    • AST and ALT high, but they're mid 500s. Normally AST>ALT in alcohol, and only moderately elevated. ALT>AST in other causes (e.g. virus; transaminases will be in the thousands). Paracetamol toxicity - transaminases in 10s of thousands
    • GGT high = alcohol. Inducible enzyme, so elevated in anything that induces liver enzymes (e.g. barbiturates, antiepileptic, alcohol)
    • Other clue about alcohol - mean cell volume (macrocytic anaemia)
  • Enlarged liver because of hepatitis component of illness (fat, inflammation). Cirrhosis will cause it to shrink later
  • Fetor hepaticus - nitrogenous wastes on breath; smells sweet fecal smell; once smelt you'll never forget it. Smells like rotting flowers.
    • Sign of liver failure, as is jaundice
  • Progress
    • Giving vitamin K won't help because the liver isn't working well enough to produce clotting factors. The reason we give it is because we don't know what the vit K level is, and it's not harmful - worth a try.
    • Lots of bleeding, lots of blood products given. Not a unit of blood products costs the system about $1200
    • Minnesota tube
      • 2 balloons: one is a gastric balloon; inflate it, pull up on it, so that the veins on the cardiooesophageal junction are occluded --> stop flow in the varices --> stop bleeding
      • Problem: pressure necrosis of cardio-oesophageal junction. Need to deflate every 24 hours - risk of bleeding during that time
  • Treat her vs not treat her
    • Hasn't reduced alcohol consumption despite many complications so far
    • Not eligible for a transplant while she's actively drinking. She could be in future - complete alcohol cessation for at least 6 months
    • Factors causing liver failure = hep C + alcohol: cirrhosis and a reversible component (steatohepatitis). May be some recovery in liver function long enough for her to sustain for 6 months and get a liver transplant.
    • Hep C is not a contraindication for liver transplant. So they all get recurrent hep C - but you deal with a newly acquired Hep C.
    • Why is intensivist against treatment
      • Ventilation
      • In a nutshell, you are more likely to get out of ICU if you have less systems failing. This lady has respiratory failure (might be due to transfusion, or aspiration pneumonia due to ) and liver failure as well as CNS failure (she has hepatic coma: bled, couldn't metabolise protein --> nitrogenous wastes (false neurotransmitters) --> hepatic encephalopathy). Loose correlation between amount of ammonia and degree of encephalopathy, but it's not ammonia that causes it directly
  • Hepatorenal syndrome: renal failure can occur because there is a pure functional defect because of the severity of liver failure. Probably haemodynamic in origin, because there is effective reduced blood volume, but they have no ATN. Then you can take the kidney out of this patient and give it to someone else and it will work
    • Very poor prognostic sign
    • Liver transplant with hepatorenal syndrome --> kidneys back to normal