Several risk components have been identified by McPhee, Papadakis and Tierney (2007) revolving in the condition of hepatic portal interruptions and increased vein pressure in the esophageal area. These include (a) age, (b) severity of liver disease and (c) alcohol abuse (McPhee, Papadakis and Tierney, 2007 p. 509). According to Sox, Blatt and Higgins et al. (2007), the documented incidence of esophageal bleeding among patients accounts to approximately thirty percent (p. 291). Varices commonly occur on patients with advanced liver cirrhosis.
In fact, esophageal varices develop in approximately 65% of patients with severe cirrhosis (Porth, 2005 p. 936). From recent epidemiological reports of 2002, 42% of untreated patients of esophageal varices die within six weeks of bleeding conditions, while approximately 66% die due to the various complications brought by the esophageal bleeding (e. g. infection, nutritional deficit, etc. ) (Sox, Blatt and Higgins et al. , 2007 p. 291). b. Pathophysiology of the Health Alteration
Anatomically, the most significant channels are those linking the portal and coronary veins that facilitate the reversal of blood flow and formation of thin-walled varicosities in esophageal submucosal layer (Porth, 2005 p. 936). If unusual high pressure (above 12 mm Hg: portal hypertension exists) occurs in these varicosities, these vessels start to enlarge and distend resulting in esophageal varices (McPhee, Papadakis and Tierney, 2007 p. 509). Another cause of esophageal varices is the blocking of the portal vein used in blood draining.
If the primary veins –inferior vena cava and portal hepatic channel – are blocked or constricted, the blood immediately finds alternative route to drain venous returns. Consequently, the returning blood utilizes the venous channels present in the esophageal area causing increase in pressure, which eventually leads to varices (Irwin and Rippe, 2005 p. 70-71). According to Sox, Blatt and Higgins et al. (2007), esophageal varices are commonly subject to mechanical trauma, irritation due to digestive acids and enzymes, and bleeding due to vascular ruptures (p. 291).