Hypertension is a common disease we all are aware of. Portal hypertension is slightly different from systemic hypertension. For ensuring blood supply to the major organs, our body forms collateral circulation, in a simple way, the connection between veins and capillaries is known as portal circulation.
In the human body, portal circulation is seen in the liver and kidney. The normal portal vein pressure is 5-10 mmHg. When portal pressure exceeds the normal range, more precisely >10 mmHg is known as the portal hypertensive state.
20% of upper gastrointestinal hemorrhage is due to portal hypertensive bleeding. Let’s explore this phenomenon.
Any obstruction in the portal collateral system can lead to portal hypertension.
Even though these many causes can lead to portal hypertension, the main cause behind sinusoidal portal hypertension is found to be cirrhosis, and the main cause of intrahepatic presinusoidal portal hypertension is Schistosomiasis.
As a consequence of these causes, increased portal vascular resistance and increased portal flow occurs, it will result in portal hypertension.
How do we recognize the patient?
Portal hypertension per se doesn’t show any typical symptoms. Usually, the patient is identified by any chance when it is associated with decompensated chronic liver disease and encephalopathy, ascites, or variceal bleeding. Many patients show three primary complications. They are esophageal varices, Splenomegaly, and Ascites. It is known as the triad of portal hypertension. Other symptoms can vary based on the underlying causes.
On examination, we can find audible venous hum in caput medusa, known as Cruvielhier-Baumgarten murmur. The Patient may complain about bleeding episodes in the upper GI, usually in the first 1-2 years after the identification of varices.
The primary complications of portal hypertension are gastroesophageal varices with hemorrhage, ascites, hypersplenism, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatocellular carcinoma.