see also:

• liver physiology
• assessment of hepatic function
• liver function tests (LFTs)
• jaundice (icterus)
• hepatomegaly
• hepatosplenomegaly
• liver lesions - hepatic abscesses, cysts and nodules
• steatohepatitis (fatty liver)
• cirrhosis
• portal hypertension
• prescribing drugs in patients with liver impairment
• hepatic encephalopathy
• hepatocellular carcinoma

• liver disease is a common presentation to the ED whether it be an acute hepatitis, a complication of chronic hepatitis / cirrhosis such as portal hypertension, or incidental liver disease findings
• the liver is a common site for metastatic deposits from other organ cancers
• the dual blood supply means that liver infarcts are rare but localised infarcts can occur if a intrahepatic branch of the hepatic artery is compromised
  • an exception is when thrombosis of the hepatic artery in a transplanted liver occurs, this results in infarction and loss of the transplanted liver
• a variety of genetic disorders can also cause hepatic dysfunction:
  • alpha-1 antitrypsin deficiency
    • often Dx in children or adolescents but may be silent until cirrhosis develops in middle age onwards
  • Wilson's disease
  • haemochromatosis
    • fully developed cases have micronodular cirrhosis with 75% having diabetes mellitus and skin pigmentation
    • males 5-7x females and usually present in middle age from the 50's onwards
  • various phenotypes may increase risk of more severe hepatitis in those exposed to hepatitis
  • various genetic causes of jaundice:
    • unconjugated hyperbilirubinaemia:
      • Crigler-Najjar syndrome type I and II
      • Gilbert's - persistent mildly raised unconj. bilirubin
    • conjugated hyperbilirubinaemia:
      • Dubin-Johnson syndrome
      • Rotor syndrome

• see hepatitis
• acute hepatitis outcomes:
  • subclinical only (70% of hepatitis B virus, many other viruses cause raised transaminases without jaundice eg. EBV / glandular fever / infectious mononucleosis)
    • <5% of HBV subclinical infections will go onto chronic viral carrier state and chronic hepatitis
  • jaundice (icterus)
  • resolution (far majority of HAV, 90% of hepatitis B virus, most HEV if not pregnant)
  • acute fulminant hepatitis
    • 12% due to viral infections: < 0.5% of hepatitis B virus, 0.1% fatal acute fulminant hepatitis with hepatitis A, 20% mortality rate with HEV in pregnant women, dengue fever, herpes virus
    • ~15% are unknown cause
    • most of the rest are toxins such as paracetamol (acetaminophen), mushroom poisoning
    • ⇒ acute hepatic encephalopathy within 2-3 weeks of onset (by definition of acute fulminant hepatitis)
  • chronic hepatitis (<5% of HBV, most patients with HCV)
    • ⇒ healthy carrier state (~30% of those with HBV chronic hepatitis)
    • ⇒ cirrhosis (12-20% of those with chronic HBV and in 20-30% of chronic HCV)
      • ⇒ steatorrhoea due to reduced bile acid production capacity
      • ⇒ hypoalbuminaemia due to reduced protein production capacity
      • ⇒ coagulopathy with raised INR due to reduced clotting factor production capacity
      • ⇒ portal hypertension
        • ⇒ oesophageal varices
          • ⇒ upper GIT bleeding
        • ⇒ ascites
      • ⇒ hepatic encephalopathy
    • ⇒ hepatocellular carcinoma - 6-15% of patients with cirrhosis

• viral infection
  • hepatitis A
  • hepatitis B virus
  • hepatitis C virus
  • hepatitis E viruses (HEV)
  • other viruses such as EBV / glandular fever / infectious mononucleosis
• other infections
  • extra-hepatic bacterial infections and sepsis / septicaemia can cause mild transaminitis and variable cholestasis
  • bacterial infections of the liver
    • ascending cholangitis
    • Staph. aureus
    • Salmonella typhi (typhoid enteric fever)
    • secondary or tertiary syphilis
  • parasitic:
    • malaria
    • schistosomiasis
    • strongyloidiasis
    • cryptosporidium
    • visceral leishmaniasis
    • echinococcosis (hydatids)
    • liver flukes
• toxins
  • alcohol
    • the leading cause of liver disease in Western countries
  • overdose of paracetamol (acetaminophen)
  • medications by pattern of injury (most are unpredictable, idiosyncratic reactions):
    • cholestasis: combined oral contraceptive pill (OCP), anabolic steroids, oestrogens
    • cholestatic hepatitis: phenothiazines, many [antibiotics]]
    • hepatocellular necrosis: methyldopa, phenytoin, halothane, isoniazid
    • steatosis: methotrexate, corticosteroids, parenteral nutrition
    • steatohepatitis: amiodarone
    • cirrhosis: methotrexate, isoniazid, enalapril
    • granulomas: sulphonamides, others
    • veno-occlusive disease: chemotherapy for cancers, bush teas
    • Budd-Chiari syndrome (BCS): combined oral contraceptive pill (OCP)
    • sinusoidal dilatation: combined oral contraceptive pill (OCP), others
    • peliosis hepatitis: anabolic steroids, tamoxifen
  • various food toxins:
    • certain mushrooms
    • see also foods as toxins
  • industrial chemicals such as carbon tetrachloride
  • some herbal medicines
• auto-immune
  • idiopathic autoimmune hepatitis:
    • mainly women, esp. northern Europeans
  • concurrent with other autoimmune disorders:
    • systemic lupus erythematosus (SLE), coeliac disease, rheumatoid arthritis, thyroiditis, Sjögren's syndrome (SS), inflammatory bowel disease (IBD)
  • NB. see also the separate entities, primary sclerosing cholangitis / primary biliary cirrhosis
• graft-vs-host disease
  • eg. 10-50 days after bone marrow transplants - may become chronic
• pregnancy
  • pre-eclampsia and eclampsia
  • acute fatty liver of pregnancy (AFLP) - rare condition of 3rd trimester, may be cause hepatic failure - 20-40% have concurrent pre-eclampsia and eclampsia

• mainly due to:
  • Staph. aureus
  • enteric bacteria
  • echinococcosis (hydatids)
  • some amoebae and helminths

• NB. hepatitis may appear normal on USS or it may have a “starry sky” texture due to oedematous parenchyma allowing the portal triads to stand out brightly
• NB. hepatitis may cause GB wall thickening
• cirrhosis
  • develops into nodular and atrophic appearance (esp. R hepatic lobe)
  • on USS:
    • texture becomes heterogeneous and coarse, there may be nodules on the liver surface
  • on contrast CT:
    • nodules may be variable but usually do not significantly enhance with contrast
    • may also have ascites, varices, splenomegaly, carcinoma
• hepatocellular carcinoma
  • may be focal which can invade portal or hepatic veins
  • may be multifocal
  • may be found diffusely in the liver
  • usually is heterogenous in appearance
  • typically enhances more than surrounding liver on IV contrast CT esp. if taken within 20secs of administration (“hepatic arterial phase”)
• cholangiocarcinoma
  • 2nd most common hepatic malignant tumour
• hepatoblastoma
  • most common hepatic tumour of childhood 1-2 per million births
• metastatic tumours
  • most common tumours are colorectal, breast, lung, other GIT, but most can metastasize to the liver
  • most enhance LESS than normal liver on contrast CT scans, but some can be hypervascular and appear bright
  • some can calcify, esp. mucin-producing GIT tumours
  • CT is more sensitive than USS
• benign lesions
  • haemangioma
    • the most common benign tumour seen in the liver
    • mainly in the post. segment of R hepatic lobe and more common in women
    • small ones are usually uniformly hyperechoic on USS
    • have a characteristic image on contrast CT scans with initial peripheral nodular contrast enhancement which becomes more uniform on delayed images
  • hepatic adenoma
    • incidence 1 in 100,000; mostly in woman who have used combined oral contraceptive pill (OCP) and usually regress when OCPs are ceased
    • subcapsular ones have a tendency to rupture causing life threatening haemoperitoneum esp. in pregnancy
    • hypervascular
  • focal nodular hyperplasia
    • mostly in young-middle aged adults
    • hypervascular