Blood supply to the gallbladder and bile ducts

Within the liver the bile ducts are supplied by adjacent arteries. Outside the liver the supply to the bile duct is essentially axial and comes from two arteries that run along either side of the duct, known as the 3 o'clock and 9 o'clock arteries. About 60 per cent of blood flow to the duct arises inferiorly from the retroduodenal and gastroduodenal arteries whilst 38 per cent comes from the hepatic and cystic arteries superiorly (Fig. 5) 1228. The retropancreatic portion of the bile duct is supplied mainly from retroduodenal arteries.

 

The principal blood supply to the gallbladder is derived from the cystic artery; a smaller component arises from vessels passing directly from the liver. The cystic artery runs above and behind the cystic duct and usually arises from the right hepatic artery after the latter has passed behind the bile duct. Variations in this anatomy are common. The cystic artery may arise from the common hepatic artery and pass in front of the bile duct. There may also be two separate cystic arteries supplying the anterior and posterior surfaces of the gallbladder. There are no discrete veins draining the gallbladder and bile duct, although all the arteries are normally accompanied by a small vein or venous plexus. Some veins drain directly from the gallbladder into the liver. Lymphatic drainage is first to the cystic lymph node which is usually seen adjacent to the cystic artery during a cholecystectomy and thence to the retroduodenal lymph nodes. Some lymphatic channels from the fundus drain to lymphatic channels in the liver capsule. Motor and sensory sympathetic nerves from the coeliac plexus reach the gallbladder along the hepatic artery and the parasympathetic motor supply comes from the right and left vagus nerves.

 

PHYSIOLOGY

Bile

The prime function of the biliary tract is to convey bile from the liver where it is formed to the duodenum. Along the way bile is stored and concentrated in the gallbladder until it is required. Bile helps in the digestion of certain foodstuffs and acts as a major excretory pathway.

 

Between 500 ml and 1000 ml of bile are secreted by human hepatocytes every day. The main constituent is water along with bile acids, bile pigments, cholesterol, phospholipids, and all the inorganic ions found in plasma (Table 1) 368. The bile acids are the most important by weight. The precise concentrations of all these molecules are modified subsequently by the epithelium of both the bile ducts and the gallbladder. The pH of bile duct bile is generally above 7, and inorganic ions are normally present in concentrations slightly higher than in plasma with the exception of chloride which is usually lower (Table 2) 369. This is important in clinical practice since patients with a significant bile fistula lose electrolytes rapidly.

 

The bile acids, cholic and chenodeoxycholic acid, are synthesized in the liver from cholesterol and are the major pathway of cholesterol excretion. In the colon they are metabolized by bacteria to deoxycholic and lithocholic acid, respectively; all except lithocholic acid are absorbed back into the portal circulation and are then re-excreted into the bile (Fig. 6) 1229. This enterohepatic circulation of bile salts takes place several times each day. Because of this continuous circulation there is always a pool of bile acids in the body. A small amount is lost from the pool each day in the stools and is made up by hepatic synthesis.

 

The main function of the bile acids in bile is to maintain cholesterol in solution, which they do by forming micelles. Hydrophobic cholesterol is encased in hydrophilic phospholipid and bile salts. Only when the concentration of cholesterol exceeds the capacity of the bile salts and phospholipid to maintain it in micellar solution does bile become lithogenic and liable to form stones. Clinically, increasing the concentration of bile salts in bile artificially makes it possible to render bile unsaturated in cholesterol and so enable dissolution of cholesterol gallstones (see Fig. 24 1247 below). Ingestion of food increases bile flow and this is probably mediated by vagal and hormonal stimuli, although bile salts themselves have a powerful choleretic effect.

 

Bilirubin, the major degradation product of haemoglobin, is conjugated with glucuronide by the hepatocyte and actively secreted into bile. Conjugated bilirubin is converted by the action of bacteria in the bowel into urobilinogen which is reabsorbed into the portal circulation and re-excreted. Some urobilinogen reaches the systemic circulation and is then excreted in the urine where it can be detected. The absence of urobilinogen from the urine implies complete obstruction of bile flow into the bowel.

 

The gallbladder acts as a store for bile in between meals and concentrates the bile by active reabsorption of water and electrolytes. About half the hepatic output of bile is stored in the gallbladder; the other half trickles into the duodenum continuously. Food, and especially fat, in the duodenum releases cholecystokinin, which is the most important stimulus for gallbladder contraction. Contraction of the gallbladder causes the sphincter of Oddi and the second part of the duodenum to relax. The bile duct acts purely as a conduit, for it does not show peristaltic activity. The sphincter of Oddi certainly plays an important part in bile duct function. The muscle of the sphincter is quite separate from duodenal wall muscle both embryologically and functionally, although the action of the two is usually co-ordinated. This co-ordination occasionally breaks down, but whether this is of clinical significance is not known. The role of the autonomic nerves to the gallbladder and the bile duct is also uncertain.

 

Biliary pain

At endoscopic retrograde cholangiopancreatography (ERCP), distension of the bile duct with contrast causes pain and it is probable that a similar effect occurs in normal life. While a rapid increase in intraductal pressure causes pain, slower increases lead to discomfort. Pain from stones in either the bile duct or the gallbladder probably results from acute obstruction to flow. Spasm of the sphincter of Oddi is probably painless, although it may also lead to a rapid rise in intraductal pressure. Pain nerve endings are widely distributed throughout the biliary tract. Most pain fibres return to the central nervous system via the splanchnic nerves, but a significant minority run with the vagus, right phrenic, and intercostal nerves. This wide distribution probably explains some of the clinical variations in the perception of biliary pain.

 

PATHOLOGY

Inflammation

Acute and chronic inflammation of the biliary tract are both common. Inflammation can be caused by chemicals, bacteria, or parasites; the aetiology of primary sclerosing cholangitis is unknown. Following obstruction of the gallbladder by a stone in the cystic duct, bile salts leak into the mucosa and cause inflammation. Bacterial infection soon follows. Bacteria are often present in normal bile, particularly if stones are present or if an anastomosis between the biliary tree and the bowel exists. The most common infecting bacteria are Escherichia coli, Klebsiella, and Streptococcus faecalis. Anaerobic bacteria are present in much smaller numbers. Most significant infections are due to multiple organisms. The frequent occurrence of bacteria in bile, even in the absence of acute inflammation, is the reason why prophylaxis with an appropriate antibiotic before any surgical or radiological procedure on the biliary tract is wise.

 

The Chinese liver fluke, Clonorchis sinensis, Ascaris lumbricoides and, occasionally, a daughter cyst from a ruptured hydatid cyst of the liver are the common parasites which infect the biliary tract, usually in the Middle East and Asia (see Section 41.17 165). Bacterial cholangitis is a common accompaniment, and malignant change in the biliary epithelium may follow chronic infection with Clonorchis sinensis.

 

Obstruction

Obstruction of the main bile duct leads to morphological changes in the liver with marked inflammatory infiltration of the portal tracts. Scarring and fibrosis around the bile ducts results in the eventual development, after weeks or months of obstruction, of secondary biliary cirrhosis. Hepatocyte function deteriorates progressively from the onset of obstruction and is slow to recover once the obstruction is relieved. Similar pathological changes can be seen in the gallbladder wall when chronic inflammation occurs secondary to gallstones. The gallbladder becomes shrunken, fibrotic, and non-functional (see Fig. 25 1248).

 

Neoplasm

Neoplasia of the glandular biliary epithelium is unusual, and benign tumours are almost unknown. Occasionally adenomatous polyps are seen in the gallbladder or the bile duct.

 

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