Pathophysiology of variceal bleeding in cirrhotics

Abstract

SUMMARY
Liver cirrhosis is frequently complicated by the development
of portal hypertension. This syndrome is characterised
by a pathological increase of the portal venous pressure,
which leads to the formation of portal-systemic collaterals.
Among these, gastroesophageal varices are of special
interest, since are responsible for the main complication
of portal hypertension, massive gastrointestinal bleeding.
The development of collaterals is due to different factors,
including the dilation of pre-existing vessels and the
action of angiogenic factors. Once formed, varices tend to
dilate as a function of time, persistence of portal hypertension,
and repeated physiological stimuli such as meals, ethanol
consumption, exercise, and increased intrabdominal
pressure which cause abrupt rises in portal pressure and/
or blood flow. The concept ofvariceal wall tension, which
combines variceal size, variceal wall thickness, and variceal
pressure correlates well with the clinical observation that
increased variceal pressure, increased variceal size and
presence of red colour signs are independent predictors of
the risk ofvariceal bleeding. Tension in the variceal wall is
probably the decisive factor determining variceal bleeding,
as when exceeding the elastic limit of the vessel, the varix
ruptures. Endoscopie and endosonographic examinations
may allow a better assessment ofvariceal pressure, size and
wall thickness, and thus a more accurate evaluation of the
individual risk ofvariceal bleeding in cirrhotic patients.
Key Words: Liver Cirrhosis, Portal hypertension, Gastroeophageal
varices, Variceal size, Variceal wall tension,
Variceal bleeding.