Portal hypertension is high blood pressure in the portal vein system, including the portal vein and its branches. It is defined as a hepatic venous pressure gradient over 5mmHg. Common causes include cirrhosis, chronic hepatitis, portal vein thrombosis, and splenic vein thrombosis. Consequences are ascites, esophageal varices, gastric varices, and splenomegaly. Investigations include blood tests, ultrasound, CT, MRI, endoscopy, and liver biopsy to determine the underlying cause.

1. PORTAL HYPERTENSION
By- Dr. Armaan Singh

2. Portal hypertension is hypertension (high blood
pressure) in the portal vein system, which is
composed of the portal vein, and its branches and
tributaries.
Portal hypertension is defined as elevation of
hepatic venous pressure gradient to >5mmHg.
Generally, in clinical practice the pressure is not
measured directly until the decision to place
a transjugular intrahepatic portosystemic
shunt(TIPS) has already been made. As part of
that procedure, a hepatic vein wedge pressure is
measured with the assumption of no pressure drop
across the liver yielding portal vein pressure.

3. CAUSES OF PORTAL HYPERTENSION
 Congenital atresia or stenosis.
 Portal vein thrombosis (idiopathic, umbilical and portal sepsis,
malignancy, hypercoagulable states, pancreatitis).
 Splenic vein thrombosis.
 Extrinsic compression - eg, tumours.
 Cirrhosis.
 Chronic hepatitis.
 Schistosomiasis.
 Myeloproliferative diseases.
 Idiopathic portal hypertension.
 Granulomata - eg, sarcoid.
 Nodular (nodular regenerative hyperplasia, partial nodular
transformation).
 Toxins (arsenic, vinyl chloride).
 Fibropolycystic disease (including congenital hepatic fibrosis).
 Budd-Chiari syndrome (hepatic vein obstruction).
 Constrictive pericarditis.
 Right heart failure.
 Veno-occlusive disease of the smaller hepatic veins/venules (due to
ingestion of pyrrolizidine alkaloids; antileukaemic drugs, radiation).
 Sclerosing hyaline necrosis.

4. CONSEQUENCES OF PORTAL HYPERTENSION ARE
CAUSED BY BLOOD BEING FORCED DOWN ALTERNATE
CHANNELS BY THE INCREASED RESISTANCE TO FLOW
THROUGH THE SYSTEMIC VENOUS SYSTEM RATHER
THAN THE PORTAL SYSTEM. THEY INCLUDE:
 Ascites (free fluid in the peritoneal cavity).[2]
 Hepatic encephalopathy.
 Increased risk of spontaneous bacterial peritonitis.
 Increased risk of hepatorenal syndrome.
 Splenomegaly (enlargement of the spleen) with a
consequent accumulation of red blood cells, white
blood cells, and platelets,
together leading to
mild pancytopenia.
 Portacaval anastomoses: Esophageal varices, gastric
varices, anorectal varices (not to be confused
with hemorrhoids), and caput medusae.
 Esophageal and gastric varices pose an ongoing risk
of life-threatening hemorrhage,
with hematemesis or melena.

5. INVESTIGATIONS
 Blood tests:
 LFTs, U&Es, glucose, FBC, clotting screen.
 Investigations for liver disease if the cause is not known - eg, ferritin (for
haemochromatosis), hepatitis serology, autoantibodies, alpha-1 antitrypsin (for alpha-1-
antitrypsin deficiency), ceruloplasmin (for Wilson's disease).
 Scans:
 Abdominal ultrasound - for liver and spleen size, ascites, portal blood flow and thrombosis of
the portal or splenic veins.
 Doppler ultrasound - can show direction of flow in blood vessels.
 CT scan, especially spiral CT, may show portal vasculature - can be useful if ultrasound was
inconclusive.
 MRI scan - gives similar information to CT.
 Elasticity measurement (FibroScan®) - a new technique based on the velocity of an elastic
wave via an intercostally placed transmitter. Results correlate with liver stiffness and so
with fibrosis.
 Endoscopy - for oesophageal varices - essential for those with suspected portal hypertension.
Varices indicate portal hypertension, but their absence does not exclude it.
 Portal hypertension measurement:
 Portal pressure is indirectly measured in clinical practice by the hepatic venous pressure
gradient (HVPG).
 Normal HVPG values are <5 mm Hg. HVPG >10 mm Hg predicts the development of
oesophageal varices.
 However, HVPG is moderately invasive and its clinical role is uncertain.
 Liver biopsy - if indicated, may help diagnose the underlying cause.

6. INVESTIGATIONS
 Blood tests:
 LFTs, U&Es, glucose, FBC, clotting screen.
 Investigations for liver disease if the cause is not known - eg, ferritin (for
haemochromatosis), hepatitis serology, autoantibodies, alpha-1 antitrypsin (for alpha-1-
antitrypsin deficiency), ceruloplasmin (for Wilson's disease).
 Scans:
 Abdominal ultrasound - for liver and spleen size, ascites, portal blood flow and thrombosis of
the portal or splenic veins.
 Doppler ultrasound - can show direction of flow in blood vessels.
 CT scan, especially spiral CT, may show portal vasculature - can be useful if ultrasound was
inconclusive.
 MRI scan - gives similar information to CT.
 Elasticity measurement (FibroScan®) - a new technique based on the velocity of an elastic
wave via an intercostally placed transmitter. Results correlate with liver stiffness and so
with fibrosis.
 Endoscopy - for oesophageal varices - essential for those with suspected portal hypertension.
Varices indicate portal hypertension, but their absence does not exclude it.
 Portal hypertension measurement:
 Portal pressure is indirectly measured in clinical practice by the hepatic venous pressure
gradient (HVPG).
 Normal HVPG values are <5 mm Hg. HVPG >10 mm Hg predicts the development of
oesophageal varices.
 However, HVPG is moderately invasive and its clinical role is uncertain.
 Liver biopsy - if indicated, may help diagnose the underlying cause.