Causes and pathomechanisms of oesophageal varices development

Portal hypertension is a common clinical syndrome with chronic liver diseases and is characterised by a pathological increase in portal pressure. Moreover, portal hypertension is associated with increased portal blood flow. Increased vascular resistance in portal hypertension is because of an increase in both intrahepatic and portosystemic collateral resistance. Chronic elevations in systemic and splanchnic blood flow have been documented as key elements of hyperdynamic circulatory state of hypertensive animals and humans. Peripheral vasodilatation initiates the development of the classic profile of decreased systemic elevated splanchnic blood flow and elevated cardia index that characterises this state. Portosystemic collaterals develop as a result of portal hypertension. This is the central pathophysiological event that leads to bleeding from oesophagogastric varices and portosystemic encephalopathy. Collateral vessels respond to various vasoconstrictors and vasodilators.--Varices in the distal 5 cm of the distal oesophagus are easily identified by endoscopy because of their superficial location in the lamina propria and therefore are must apt to bleed and why the current practise of endoscopic therapy is likely to be successful in obliterating the varices. In patients with oesophageal varices the dilated deep intrinsic veins displace the superficial venous plexus, assume a supepitheal position and are endoscopically visible as teleangiectasia, cherry red spots, red colour signs, hemocystic spots, red wale markings or varices on varices. As alternative endoscopic way of treatment the paravariceal injection has been propagated by our group thus preserving the pathophysiologic collaterals and preventing early new formation of collaterals and rebleeding. Pathophysiologically the concept of erosion has been abandoned and replaced by the explosion theory: bleeding probably occurs when the expanding force by pressure and flow can no longer be counter-balanced by the variceal wall tension; at this point the varices rupture and bleed. When the varix distension has increased, the radius has increased and the wall thickness decreased. Thus early diagnosis of patients with a high tendency to bleed can easily be made by endoscopy, measuring portal and/or oesophageal-variceal pressure and characteristising the chronic liver disease according to the Child-Pugh-classification.