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Surgical anatomy and physiology The gall bladder is pear-shaped, 7.5-12 cm long, with a normal capacity of about 50 ml, but capable of considerable distension in certain pathological conditions. The anatomical divisions are a fundus, a body and a neck that terminates in a narrow infundibulum. The muscle fibres in the wall of the gall bladder are arranged in a criss-cross manner, being particularly well developed in its neck. The mucous membrane contains indentations of the mucosa that sink into the muscle coat; these are the crypts of Luschka. The cystic duct is about 3 cm in length but variable. Its lumen is usually 1-3 mm in diameter. The mucosa of the cystic duct is arranged in spiral folds known as the valves of Heister. Its wall is surrounded by a sphincteric structure called the sphincter of Lutkins. While the cystic duct joins the common hepatic duct in its supraduodenal segment in 80 per cent of cases, it may extend down into the retroduodenal or even retropancreatic part of the bile duct before joining. Occasionally the cystic duct may join the right hepatic duct or even a right hepatic sectorial duct. The common hepatic duct is usually less than 2,5 cm long and is formed by the union of the right and left hepatic ducts. The common bile duct is about 7,5 cm long and formed by the junction of the cystic and common hepatic ducts. It is divided into four parts:

the supraduodenal portion, about 2,5 cm long, running in the free the retroduodenal portion; the infraduodenal portion lies in a groove, but at times in the intraduodenal portion passes obliquely through the wall of the

edge of the lesser omentum;

a tunnel, on the posterior surface of the pancreas;

second part of the duodenum where it is surrounded by the sphincter of Oddi. It terminates by opening on the summit of the papilla of Vater. The arterial supply of the gall bladder is critical. It is proposed that arterial damage during cholecystectomy may cause ischaemia and result in postoperativeKnowledge is the highest power Nothing to stand before it. Pandi 1

bile-duct stricture. The cystic artery, a branch of the right hepatic artery, is usually given off behind the common hepatic duct. Occasionally, an accessory cystic artery arises from the gastroduodenal artery. Surgical physiology Bile, as it leaves the liver, is composed of 97 per cent water, 1-2 per cent bile salts, and 1 per cent pigments, cholesterol and fatty acids. The liver excretes bile at a rate estimated to be approximately 40 ml/hour. The rate of bile secretion is controlled by cholecystokinin which is released from the duodenal mucosa. With feeding there is increased production of bile. Functions of the gall bladder The gall bladder is a reservoir for bile. During fasting resistance to flow through the sphincter is high, and bile excreted by the liver is diverted to the gall bladder. After feeding the resistance to flow through the sphincter of Oddi is reduced, the gall bladder contracts and the bile enters the duodenum. These motor responses of the biliary tract are in part effected by the hormone cholecystokinin. The second main function of the gall bladder is concentration of bile by active absorption of water, sodium chloride and bicarbonate by the mucous membrane of the gall bladder. The hepatic bile which enters the gall bladder becomes concentrated 5-10 times, with a corresponding increase in the proportion of bile salts, bile pigments, cholesterol and calcium. The third function of the gall bladder is the secretion of mucus approximately 20 ml is produced per day. With total obstruction of the cystic duct in a healthy gall bladder, a mucocele develops on account of this function of the mucosa of the gall bladder. Incidence of gallstones A 'fat, fertile, flatulent, female of fifty' is the classical sufferer from symptomatic gallstones. Useful as this clinical memorandum is, it should be tempered with the knowledge that cholelithiasis occurs in both sexes from childhood to the centenarian. In men the disease tends to occur in the older age groups at which point the incidence is equal to that of women. Stones are rarer inKnowledge is the highest power Nothing to stand before it. Pandi 2

Africa and in southern India, but not in north India. Causal factors in gallstone formation The aetiology of gallstones is probably multifactorial. Factors implicated are: (1) metabolic; (2) infective; and (3) bile stasis. Cholesterol and mixed stones Metabolic Cholesterol, insoluble in water, is held in solution by a detergent action of bile salts and phospholipids with which it forms micelles. Bile containing cholesterol stones has an excess of cholesterol relative to bile salts and phospholipids, thus allowing cholesterol crystals to form. Such bile is termed 'supersaturated , or 'lithogenic'. Bile cholesterol increases with age and is raised in women, particularly those taking the contraceptive pill, in obesity and by clofibrate - a drug used in the treatment of certain hyperlipoproteinaemias. The concentration of bile salts in bile is reduced by oestrogens, and also by factors which interrupt the intrahepatic circulation of bile salts (e.g. ileal disease, resection or bypass and cholestyramine therapy). These conditions are all associated with an increased incidence of stones, but there are still some people with cholesterol supersaturation who remain free of stones, suggesting that there are other factors of importance. Infection. The role of infection in causing stones is unclear. Often bile from patients with gallstones is sterile, but organisms have been cultured from the centres of gallstones: the radiolucent centre of many gallstones may represent mucus plugs originally formed around bacteria (Moynihan's aphorism: 'A gallstone is a tombstone erected to the memory of the organism within it , ). Helicobacter pylori antigens have been isolated within gall bladders containing stones. Bile stasis Gall bladder contractility is reduced by oestrogens, in pregnancy and after truncal vagotomy, situations in which the incidence of gallstones is increased. Patients on long-term parenteral nutrition have a high incidence of stones. Lack of good oral intake precludes the release of cholecystokinin, the hormonal stimulantKnowledge is the highest power Nothing to stand before it. Pandi 3

of gall-bladder contraction released from the duodenal mucosa. Pigment stones are seen in patients with haemolysis in which bilirubin production is increased. Examples are hereditary spherocytosis, sickle cell anaemia, thalassaemia, malaria and mechanical destruction of red cells by prosthetic heart valves. Pigment stones are found in the ducts of patients with benign and malignant bile duct strictures. Pigment stones in Oriental countries are associated with infestations of the biliary tree by Clonorchis sinensis and Ascaris lumbricoides. Escherichia coli is often found in the bile of these patients. This bacterium produces the enzyme -glucuronidase which converts the bilirubin into its unconjugated insoluble form. These stones are often present throughout the biliary tree including the intrahepatic ducts. The effects and complications of gallstones Stones are found throughout the biliary tract and their complications relate to obstruction of the cystic duct, of the intrahepatic radicals or of the ampulla of Vater. Obstructive complications may be aggravated by the presence of infection leading to cholangitis and abscess formation. Nevertheless, gallstones can be asymptomatic; it is estimated that between 85 and 90 per cent of patients who have gallstones remain asymptomatic. In the UK the prevalence of gallstones at the time of death is estimated to be 17 per cent and possibly increasing. Thus, the mere presence of gallstones is not an indication for a surgical approach. For this reason symptoms must be analysed with care. A typical patient may fulfil Saint's triad having gallstones, diverticulosis of the colon and a hiatus hernia, yet with symptoms that cannot be directly contributed to any of these. When considering management of a patient with gastrointestinal symptoms it is important to take a specific history and consider whether or not the pain from which the patient suffers is typical or not of biliary tract disease. Effects and complications of gallstones In the gall bladder: Silent stones; Chronic cholecystitis; Acute In the bile ducts: Obstructive jaundice; Cholangitis; AcuteKnowledge is the highest power Nothing to stand before it. Pandi 4

cholecystitis; Gangrene; Perforation; Empyema; Mucocele; Carcinoma

pancreatitis In the intestine: Acute intestinal obstruction ('gallstone ileus') Acute cholecystitis Pathology About one-fifth of patients first present with acute cholecystitis; in about one-third there is clinical or pathological evidence of previous chronic cholecystitis. It is usually due to persistent impaction of a stone in the neck of the gallbladder. The result is initially a chemical inflammation of the gallbladder wall perhaps due to the mucosal toxin lysolecithin, produced by the action of phospholipase on biliary lecithin. This is soon followed by bacterial infection. Because the cystic duct is occluded the inflammatory process is particularly aggressive and the gallbladder becomes acutely distended, with accompanying lymphatic and venous obstruction. The serosa may be covered by a fibrinous exudate and subserosal haemorrhage gives the appearance of patchy gangrene. The gallbladder wall itself is grossly thickened and oedematous and the underlying mucosa may show hyperaemia or patchy necrosis. Histologically, three grades of inflammation are recognized: acute cholecystitis, acute suppurative cholecystitis, and acute gangrenous cholecystitis. Rarely an abscess or empyema develops within the gallbladder, while perforation of an ischaemic area leads to a pericholecystic abscess, bile peritonitis, or a cholecystoente