Abstract

Portal hypertension (PH) is defined as an increase of portal venous pressure > 5 mmHg. The gold standard to measure portal venous pressure is the evaluation of hepatic venous pressure gradient (HVPG). Portal venous pressure can be assessed by HVPG, which is measured invasively by a balloon catheter inserted through the right jugular vein and assessed by the difference between free hepatic venous pressure and wedged hepatic venous pressure.A HVPG of 10 mmHg or higher is considered to be clinically significant portal hypertension (CSPH) and is associated with an increased risk of complications like gastrointestinal varices, ascitic decompensation, gastrointestinal hemorrhage from portal hypertensive collaterals and hepatic encephalopathy. Early diagnosis of CSPH is mandatory to optimize patient care and prevent hepatic decompensation(1). As a secondary event, portal hypertension induces splanchnic and systemic arterial vasodilation, leading to the development of a hyperdynamic circulatory syndrome and thereby aggravating and driving clinically detrimental complications(2). The Child–Turcotte–Pugh (CTP) and MELD scores are two of the most commonly used scores in everyday practice for patients with liver cirrhosis (3). A Platelet count-to-spleen diameter ratio (PSDR), platelet count, and spleen diameter have been suggested as possible non-invasive screening tools of EV as they are relatively simple and less expensive. These methods can be used for initiation of treatment with non-selective beta blocker and patient follow up, as well as prioritizing for endoscopy in resource constraint areas(4). Predictive models derived from these parameters were therefore constructed as surrogate tools for the prediction of OV or large OV [10–19]. None of these noninvasive means have been validated in patients with cirrhosis(5). Most of the reported variables are directly or indirectly associated with portal hypertension, such as decreased platelet count, splenomegaly and ascites. However, in patients with liver cirrhosis, the presence of decreased platelet count can be associated with several factors unrelated with portal hypertension, such as shortened platelets mean half life, decreased thrombopoietin production, or mielotoxic effects of alcohol. On the other hand, the presence of splenomegaly in cirrhotic patients is likely the result of vascular disturbance that are mainly linked to portal hypertension. Overall, no variable alone have enough power to assess the presence of esophageal varices without upper endoscopic study(6).

Description