The normal pressure into the biliary tree fluctuates between 5 and 10 cm H2O. Anything interfering with bile's normal flow causes pressure elevation. The intraluminal pressure can reach up to 30 cm H2O in complete obstruction; the bile excretion from the hepatic cell is interrupted when the pressure exceeds 10–15 cm H2O [4].

Cholestasis favors microbe growing and proliferation within the bile, which otherwise, in normal condition, is sterile by bacteria. The cholangitis is ascending from duodenum microbial flora. As pressure is increased into the biliary tree, the barrier from the strong conjunction between the hepatic cell and bile microduct is impaired resulting in increased permeability and bile backflow within hepatic sinusoids; hence, this backflow within the blood allows the entrance of microbes and their degradation products into systemic circulation. Cholangitis mainly happens in acute obstruction. The increased biliary pressure pushes the bacterial infection into the biliary canaliculi, hepatic veins, and perihepatic lymphatics causing bacteremia [5]. The onset of acute cholangitis involves both increased bacteria into the biliary tree and elevated intraductal pressure. Thus a translocation of bacteria and endotoxin into the vascular system occurs (cholangio-venous reflux). The increased intraductal pressure in acute cholangitis tends to make the ductules more permeable to the transloca…

The raised pressure in the biliary tree can restrict gradually the production of bile by the hepatic cell. However, the risk of biliary lithogenesis is low, because of the observed higher reduction in secretion of cholesterol and phospholipids than those of bile salts. The latter, as known, ensures the cholesterol solubility into the bile. Sequentially, when the obstruction is repaired and the intraluminal pressure is normalized, then inversely, the restoration of cholesterol and phospholipids secretion is faster than those of bile salts which favors lithogenesis; thus, increasing the risk of cholesterol crystal segmentation and micro gallstones formation. The latter has resulted in early stent obstruction, which was inserted for bile duct drainage and decompression in the management of obstructive jaundice [7], [10].

Cholestasis affects hepatic blood flow which explains the worsened liver dysfunction. Apart from the secretory capacity, obstructive jaundice influences significantly the metabolic and synthetic capacity of the liver. The substances normally excreted by the liver, in obstruction, a backflow into the systemic circulation causing major toxicity. The increased bile salts inhibit hepatic cytochrome P450 and reduction of oxidative or aerobic metabolism, which increase the oxidative stress and hepatic apoptosis. The inhibited hepatic cytochrome P450 and its dependent, microsomal mixed function oxidase (MF…

The blockage of bile salts into the intestinal tract induces the proliferation of the normal microbial flora, dysfunction of the intestinal mucosal barrier, bacterial translocation, and ultimately increases endotoxin absorption [7].

The intestinal barrier failure including immunological, biological and mechanical disruption leads to increased intestinal permeability, [19] which plays a pivotal role in the development of septic and renal complications. The mechanism of intestinal barrier dysfunction and hyper-permeability has been attributed to the decreased intestinal epithelial cell proliferation and altered expression of tight junction proteins [20]. It has been found that the gut regulatory peptides bombesin and neurotensin can prevent this alteration and reduce endotoxemia [21]. The modulation of gut barrier function by probiotics has been proposed [22].