Medically Fit For Exams
Medically Fit For Exams

Portal Hypertension


  • High blood pressure in the portal system, as a result of increased resistance (in the liver)
  • Have risk of developing varices, which may haemorrhage


Risk factors

  • Alcohol
  • Cirrhosis
  • Liver damage (inc. hepatitis, haemochromatosis, Wilson’s disease)
  • Heart failure
  • Diabetes
  • Schistosomiasis


Differential diagnoses

  • Peptic ulcer
  • Gastric cancer



  • Very common in patients with cirrhosis
  • 30% of patients with compensated, and 60-70% of patients with decompensated cirrhosis at the time of diagnosis also have varices
  • 30% chance of developing varices after 6 years with liver failure
  • Hepatitis B and C are important causes of cirrhosis worldwide
  • Countries with high rates of schistosomiasis infection have cirrhosis related to this
  • More common in men – over 60%



  • Increased vascular resistance to blood flow in the portal system
  • Poisuielle’s Law – resistance is related to radius, viscosity and length
    • Is the radius that is affected in portal hypertension, with decreased width of blood vessels for blood to pass through – leads to ‘backing up’
  • Can be split into pre-hepatic, intra-hepatic and post-hepatic causes
  • Pre-hepatic
    • Splenomegaly, leading to increased flow from the spleen (overwhelming portal system)
    • Thrombotic obstruction
    • Portal vein narrowing before the liver
  • Intra-hepatic (sinusoids are fenestrated vessels where portal vein and arterial blood meet in the liver, separated from space of Disse)
    • Pre-sinusoidal
      • Primary biliary cirrhosis
      • Schistosomiasis
      • Sarcoidosis
    • Sinusoidal
      • Cirrhosis
      • Partial nodular transformation (regeneration)
    • Post-sinusoidal
      • Veno-occlusive disease
      • Budd-Chiari syndrome (obstruction of ascending vena cava between liver and heart)
    • Other – architectural change
      • Massive fatty change
      • Regenerative nodules
  • Varices – collateral blood flow
    • Blood is forced to take another route because pressure and resistance is too high in portal system
    • Use portal-systemic anastomoses – these aren’t usually used
      • Oesophageal varices (left gastric vein and oesophageal vein)
      • Spleen
      • Caput medusae (para-umbilical vein)
      • Anal varices (superior and inferior rectal vein anastomosis)
    • Extra blood flow causes engorgement, and can cause rupture, leading to haemorrhage
      • Oesophageal varices are of particular concern


Clinical features

  • Clinical features relating to cause (eg Dupytron’s contracture, clubbing etc in cirrhosis)
  • Ascites
  • Varices, and variceal bleeding (portosystemic shunts)
    • Haematemesis
    • Malaena
    • Haematochezia (passage of fresh blood) – from colonic shunt (anastomosis)
    • Caput medusa
    • Haemarrhoids (anal varices)
  • Congestive splenomegaly (also a portosystemic shunt)
  • Hepatic encephalitis
    • Lethargy
    • Irritability
    • Change in sleep



  • Cirrhosis/sinusoidal
    • Contraction of smooth muscle and myofibroblasts
    • Disruption of blood flow by scarring and parenchymal nodules
    • Damaged sinusoidal epithelia add to intrahepatic vasoconstriction
      • Reduction in NO production
      • Release of angiotensinogen (RAAS to increase BP)
    • Sinusoidal remodelling between arterial and venous systems causing anastomoses in fibrous septa àimposes arterial pressure on venous system
    • Arterial vasodilation (prehepatic) leads to increased blood flow to liver: hyperdynamic
      • Mostly from splanchnic artery à increased venous efflux into portal venous system
      • Thought to be a result of increased NO levels
        • Increased NO as a result of decrease bacteria clearance in the gut
        • Can be a result of decreased activity of mononuclear phagocytes
        • Or shunting of blood from portal to systemic circulation à phagocytic Kupffer cells are bypassed
        • Antibiotics can be helpful in portal hypertension because increase bacteria clearance and therefore NO lowers and blood supply to the liver reduces



  • Duplex Doppler ultrasonography
    • Portal flow and structural changes
    • Surface nodules
    • Splenomegaly
    • Collateral circulation
  • CT and MRI in cases where ultrasound is inconclusive
  • Angiography in cases of bleeding (can also intervene)
  • PR
  • Endoscopy for oesophageal varices
  • FBC
    • Anaemia
    • Leukopenia
    • Thrombocytopenia
  • LFT
    • Elevated AST and ALT
    • Elevated bilirubin
    • May not show raised enzymes (if liver is ‘burned out’)
    • Raised PT and INR
  • Viral hepatitis serology if cause unknown
  • Hepatic venous pressure gradient can be measure by inserting a catheter



  • Beta blockers for portal hypertension
  • Some evidence statins might help
  • Band ligation for oesophageal varices
  • Transjugular intrahepatic portosystemic shunt (TIPS) for those who don’t respond to/unsuitable for band ligation



  • 40% of patients with advanced cirrhosis get oesophageal varices, and 50% of these get massive haemorrhage and death
  • Prognosis is poor
Portal hypertension.docx
Microsoft Word document [16.2 KB]

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