25. 1 Acute pancreatitis

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Содержание Julian britton, kenneth i. bickerstaff, and adrian savage Investigation of the biliary tract

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• Acute biliary pancreatitis. Treatment tactics, 134.96kb.
• The problem of acute pain and its substantial relief is common for every medical field., 344.88kb.

In the treatment of Raynaud's syndrome, patients with painful digital ulceration are occasionally encountered. This almost always implies widespread palmar and digital arterial obstruction, since ischemic ulceration does not result from vasospasm. In one study a healing rate of 85% was achieved in a group of 100 such patients after scrubbing of the ulcer with soap and water, antibiotics as selected by culture, and conservative dйbridement. These results are equal to the healing rate achieved after thoracic sympathectomy and once again emphasize the critical lack of data supporting thoracic sympathectomy for either vasospasm or ischemia.

Periarterial digital sympathectomy has been suggested as an improved method of sympathectomy. Proof that this procedure produces results superior to randomized nonoperative therapy is conspicuously lacking. Direct microvascular bypass of occluded segments of palmar and digital arteries has been reported in recent years with occasional relief of symptoms. These have been carefully selected cases, primarily traumatic in etiology, in patients with normal vessels elsewhere. There appears little likelihood that these techniques are of benefit in patients with generalized small-vessel disease. Arteriovenous reversal at the wrist has been advocated as a method of providing retrograde arterial perfusion to ischemic hands for limb salvage. 22 The usefulness of this procedure in patients with Raynaud's syndrome remains to be proved.

OVERVIEW

Raynaud's syndrome is the symptomatic expression of episodic digital vasospasm that has multiple causes and can be seen in association with many seemingly unrelated disorders. Most patients exhibit variable degrees of both vasospasm and palmar-digital arterial occlusions, although most cluster toward one end of the spectrum. Abnormal hemorrheologic parameters have been an inconsistent finding.

An objective evaluation of both medical and surgical treatments is hampered by a lack of controlled trials, poor definition of patient groups for the purpose of comparing results, variable follow-up, and a total unavailability of generally applied and accepted objective tests of digital blood flow and digital artery closure characteristics. Conservative treatment consisting of cold and tobacco avoidance is adequate for the majority of patients with mild to moderate symptoms. About 10% of patients with Raynaud's syndrome have sufficiently severe and frequent or prolonged episodes to require drug therapy. Generally favorable anecdotal results have been achieved in about half of these patients after a variety of pharmacologic treatments. The one current preference is the use of extended-release nifedipine 30 mg. at bedtime. Conservative therapy is recommended, even in the difficult group of patients with severe pain or persistent digital ischemia with localized gangrene. Constant and meticulous attention to the fundamental principles of conservative therapy, including cessation of tobacco use and gentle cleansing and dйbridement of ulcers, leads to gratifying results in most patients.

Whereas upper-extremity sympathectomy undoubtedly causes dramatic improvement in occasional patients, the result in any single patient is unpredictable and usually disappointing. Sympathectomy appears to have its best long-term results in those mildly symptomatic patients who need it least. Similarly, digital artery sympathectomy or hand artery microvascular repair is not frequently used, and lumbar sympathectomy should be considered in the few patients who present with primary lower extremity Raynaud's syndrome and whose symptoms cannot be controlled by conservative measures and medical therapy.

23.1 Benign diseases of the biliary tract


JULIAN BRITTON, KENNETH I. BICKERSTAFF, AND ADRIAN SAVAGE


INTRODUCTION

Benign diseases of the biliary tract are one of the most common surgical problems in the world. Gallstones affect millions of people in the West, while oriental cholangitis is common in the East. Surgery plays an important part in treatment: over half a million cholecystectomies are performed each year in the United States of America. New percutaneous techniques avoid the need for a conventional abdominal incision; they are playing an increasing role in treatment but a thorough understanding of the basic anatomy, physiology, and pathology of the biliary tract is required. Footnote 5


ANATOMY

Development

The liver and the biliary tract are derived from the foregut. The liver first appears in the 3-week embryo as a hollow endodermal bud from the distal foregut. This bud, the hepatic diverticulum, consists of rapidly proliferating cells that penetrate into the ventral mesogastrium. These cells eventually develop into the liver; the connection between the hepatic diverticulum and the foregut is preserved to form the bile duct. A ventral outgrowth of the bile duct gives rise to the gallbladder and the cystic duct. As the intestine rotates the entrance from the bile duct into the duodenum moves to a posterior position and the common bile duct comes to lie behind the duodenum and pancreas.


Within the developing liver the bile ducts are distributed in a segmental fashion. Bile is secreted by the liver cells into bile canaliculi. The canaliculi drain into ductules and on into larger segmental bile ducts which are tributaries of either the left or the right hepatic ducts. The left hepatic duct drains segments II, III, and IV; segments V, VI, VII, and VIII drain into the right hepatic duct. The caudate lobe (segment I) lies astride the inferior vena cava posteriorly and drains into both the right and the left hepatic ducts. This segmental anatomy of the liver and its ducts is important in liver and biliary tract surgery (Fig. 1) 1224 and is discussed in more detail in Section 22.1.


Extrahepatic bile ducts

The right and left hepatic ducts join to form the common hepatic duct at the hilum of the liver. The confluence usually lies outside the liver itself and in front of the right portal vein. The left hepatic duct has a relatively long extrahepatic course on the posterior aspect of the quadrate lobe (segment IV) where it is accessible to the surgeon, whereas the right hepatic duct enters liver tissue almost immediately. In fact this normal arrangement only occurs in 60 per cent of individuals. There are a large number of anatomical variants. The most common (20 per cent) is for one of the main tributaries of the right duct, usually the right anterior duct, to enter the common hepatic duct directly (Fig. 2) 1225. In 12 per cent of individuals there is a triple confluence formed by the right posterior, right anterior, and left hepatic ducts. One important variation is the presence of an anomalous subvesical duct, the duct of Luschka, which runs in the gallbladder fossa. It is found in 12 to 50 per cent of individuals, drains a variable portion of the right liver and is potentially vulnerable during a cholecystectomy.


The main bile duct runs from the confluence of the hepatic ducts to the papilla of Vater (Fig. 3) 1226. It is normally 10 to 12 cm in length and about 6 mm in diameter in anatomical specimens. In life, the upper limit of normal diameter on ultrasound is 7 mm. On direct cholangiography, when the duct is deliberately distended, it is up to 12 mm. The entrance of the cystic duct divides the bile duct into the common hepatic duct above the entrance and the common bile duct below. The supraduodenal portion of the bile duct lies in the free edge of the lesser omentum, anterior to the portal vein and to the right of the hepatic artery. The right hepatic artery normally crosses the common hepatic duct posteriorly, but occasionally it lies in front of the duct. Inferiorly the bile duct curves laterally away from the portal vein and passes behind the first part of the duodenum. It then runs across the posterior part of the head of the pancreas, either in a groove or in a tunnel within the gland. As the bile duct traverses obliquely through the wall of the duodenum it is joined by the main pancreatic duct of Wirsung. The exact arrangement of this junction is variable. Normally both ducts unite to form a common channel of variable length and enter the bowel through the papilla of Vater on the posteromedial wall of the second part of the duodenum. In about 10 per cent of individuals there is no common channel and each duct enters separately. There are very few muscle fibres in the wall of the bile duct, but the proximal bile and pancreatic ducts and the common channel are surrounded by circular and longitudinal smooth muscle. This muscle complex is known as the sphincter of Oddi and the muscle fibres are structurally, embryologically, and functionally distinct from the musculature of the duodenum (Fig. 4) 1227.


Gallbladder and cystic duct

The gallbladder is a pear-shaped reservoir 5 to 12 cm in length and situated on the under surface of the liver along the junction between the right and the left liver. It is covered by peritoneum and separated from liver by the connective tissue of the cystic plate. Anatomically, the gallbladder is divided into the fundus, the body, and the neck. The fundus is the widest part of the gland and usually reaches to the free anterior edge of the liver. The neck leads to the cystic duct, and when distended by a stone has the appearance of a diverticulum known as Hartmann's pouch. This pouch occasionally lies very close to the common hepatic duct.


The gallbladder may lie more or less embedded within the liver, or it may be suspended on a mesentery formed from two layers of the peritoneum. The latter variation predisposes to torsion of the gallbladder. Other rare anomalies include agenesis of the gallbladder, in which the ventral pouch off the bile duct fails to form, and duplication or lobulation of the organ where the pouch itself divides to a variable extent.


The cystic duct runs from the neck of the gallbladder to the bile duct and is variable in length. The wall of the cystic duct contains muscle fibres which form the sphincter of Lutkens, while the mucosa is arranged in the spiral valves of Heister. The triangle bounded by the common hepatic duct medially, the cystic duct inferiorly, and the inferior surface of the liver superiorly is known as Calot's triangle. The fact that the cystic artery runs within the triangle makes this an important area of dissection during cholecystectomy. The cystic duct joins the supraduodenal portion of the bile duct either at an acute angle or after running parallel to the bile duct for a short distance. In 5 per cent of people the cystic duct spirals behind the common hepatic duct and enters the bile duct low down within the pancreas. Occasionally the cystic duct actually runs within the wall of the bile duct for a variable distance, and rarely it joins the right hepatic duct. These variations are important since the bile duct can easily be damaged if the precise anatomy is not recognized at operation.


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.


INVESTIGATION OF THE BILIARY TRACT

Plain radiography

A plain abdominal radiograph may show radio-opaque gallstones (Fig. 7) 1230 or air in the biliary tree (Fig. 8) 1231. This is a useful investigation in patients who present acutely and is an essential preliminary to any contrast study of the biliary tract. Calcification in the right upper quadrant is not proof of biliary tract disease and neither does the presence of gallstones mean that they are the cause of the patients symptoms.


Two unusual appearances are diagnostic of biliary disease. Gas in the lumen or in the wall of the gallbladder is diagnostic of emphysematous cholecystitis, while the appearance of air in the biliary tree and distal small bowel obstruction suggests gallstone ileus. Another cause of biliary air is a biliary–enteric fistula, either created surgically (Fig. 8) 1231 or as a result of a stone ulcerating from the gallbladder into the bowel, usually the duodenum and very occasionally the colon.


Ultrasound

An ultrasound scan is the initial investigation in any patient suspected of biliary tract disease (see Section 6.5 27). It is non-invasive, painless, and can be easily performed on patients who are unwell. Adjacent organs can be examined simultaneously. Ultrasonography may provide unsatisfactory results in patients with obesity, ascites, and gaseous distension, and are dependent on the skill and experience of the operator.


Stones within the gallbladder can be detected with a sensitivity and specificity of over 90 per cent. They appear as reflective foci which cast an acoustic shadow (Fig. 9) 1232 and which move with changes in posture; they may form a layer in the gallbladder. The presence of local tenderness and the thickness of the gallbladder wall allow acute and chronic cholecystitis to be distinguished. A layer of oedema may also appear as a sonolucent zone between the gallbladder and the liver in patients with acute cholecystitis. Polyps within the lumen can be identified but ultrasound cannot, at present, assess gallbladder function accurately.