Surgery Lectures - Gastric and Duodenal Ulcer PDF

LECTURE NR. 1 Gastric and duodenal ulcer Elements of anatomy and physiology 3011 The stomach is the most dilated part of the digestive tube, having a capacity of 1000– 1500 ml in the adult. It is situated between the end of the oesophagus and the duodenum – the beginning of the small intestine. It lies in the epigastric, umbilical, and left hypochondrial regions of the abdomen, and occupies a recess bounded by the upper abdominal viscera, the anterior abdominal wall and the diaphragm. Macroscopic anatomy The stomach has : two openings, two curvatures, two surfaces and two omenta. 1. Openings  Gastro-oesophageal junction The oesophagus communicates with the stomach via the cardiac ori.ce, which is situated on the left of the midline at the level of T10. The intra-abdominal oesophagus (antrum cardiacum) is short and conical. After passingthrough the diaphragm it curves sharply to theleft, and becomes continuous with the cardiac orifice of the stomach. The right margin of the oesophagus is continuous with the lesser curvature of the stomach, while the left margin joins the greater curvature at an acute angle (incisura cardiaca).  Gastroduodenal junction 9 The pylorus forms the gastric outlet and communicates with the duodenum. It lies to the right of the midline at the level of the upper border of L1 and may be identified on the surface of the stomach by a circular groove (duodeno-pyloric constriction) covering the front of the organ. 2. Curvatures  Lesser curvature (Curvatura Ventriculi Minor) This extends from the cardiac to the pyloric orifices, thus forming the right or posterior border of the stomach. It is a continuation of the right border of the oesophagus and lies in front of the right crus of the diaphragm. It crosses the body of L1 and ends at the pylorus. A welldemarcated notch, the incisura angularis, is seen distally although its position varies with the state of distension of the stomach. Attached to the lesser curvature are the two layers of the hepatogastric ligament (lesser omentum). Between these two layers are the left gastric artery and the right gastric branch of the hepatic artery. 1  Greater curvature (Curvatura Ventriculi Major) This is directed mainly forward, and is four to five times longer than the lesser curvature. It starts from the incisura cardiaca and arches backward, upward, and to the left; the highestpoint of the convexity is on a level with the sixth left costal cartilage. It then descends downwards and forwards, with a slight convexity to the left as low as the cartilage of the ninth rib,before turning to the right, to end at the pylorus. Directly opposite the incisura angularis of the lesser curvature, the greater curvature presents a dilatation, which is the left extremity of the pyloric part; this dilatation is limited on the right by a slight groove, the sulcus intermedius, which is about 2.5 cm, from the duodenopyloric constriction. The portion between the sulcus intermedius and the duodenopyloric is termed the pyloric antrum.with the duodenum. It lies to the right of the midline at the level of the upper border of L1 and may be identified on the surface of the stomach by a circular groove (duodeno-pyloric constriction). The left part of the curvature gives attachment to the gastrosplenic (lineal) ligament, while to its anterior portion are attached the two layers of the greater omentum, separated from each other by the right and left gastroepiploic vessels. 3. Surfaces  Anterosuperior surface This surface is covered by peritoneum and lies in contact with the diaphragm, which separates it from the base of the left lung, the pericardium, the seventh–ninth ribs, and the intercostal spaces of the left side. The right half lies in relation to the left and quadrate lobes of the liver together with the anterior abdominal wall. The transverse colon may lie on the front part of thissurface when the stomach is collapsed.  Posteroinferior surface This surface is covered by peritoneum, except over a small area close to the cardiac ori.ce; this area is limited by the lines of attachment of the gastrophrenic ligament, and lies in apposition with the diaphragm, and frequently with the upper portion of the left suprarenal gland. Other relations are to the upper part of the front of the left kidney, the anterior surface of the pancreas, the left colic flexure, and the upper layer of the transverse mesocolon. The transverse mesocolon separates the stomach from the duodenojejunal flexure and small intestine. Thus the abdominal cavity is divided into supra and infra-colic compartments. The anterior boundary of the lesser sac (omental bursa) is formed by this surface. This potential space can be accessed via an opening on the free border of the lesser omentum, which contains the common hepatic artery, the common bile duct and the portal vein (the foramen of Winslow). Parts of the stomach The stomach is divided into a pyloric part and body by a plane passing through the incisura angularis on the lesser curvature and the left limit of the opposed dilatation on the greater curvature. The body is further subdivided into the fundus and cardia by a plane passing horizontally through the cardiac orifice. Distally a plane passing from the sulcus intermedius at right angles to the long axis of this portion further subdivides the pyloric portion. To the right of this plane lies the pyloric antrum. At operations, a slight groove may be seen in the serosal surface at the gastroduodenal junction. A small, super.cial subserosal vein, lying within this groove and vertically across the front of the gut may be evident. This is the prepyloric vein of Mayo) and drains into the right gastric vein. At operation, palpation of this area reveals the pyloric ring between the thick walls of the pyloric region and the thin walls of the duodenum. 2 4. Omenta  Lesser omentum This extends from the inferior and posterior surfaces of the liver to the stomach and proximal 3.0 cm of the duodenum. The free border of the lesser omentum between the porta hepatis and the duodenum contains the hepatic artery, the portal vein, the common bile duct, lymph glands, lymph vessels and nerves. Behind this free edge is the opening into the lesser sac or epiploic foramen (of Winslow). The remainder of the lesser omentum, extending from the left end of the porta hepatis to the lesser curvature, contains the right and left gastric arteries and the accompanying veins, as well as lymph glands, lymph vessels and branches of the anterior and posterior vagus nerves.  Greater omentum This is formed along the greater curvature of the stomach by the union of the peritoneal coats of the anterior and posterior gastric surfaces. On its left it shortens into the gastrosplenic omentum, containing the short gastric branches of the splenic artery between its two layers. On the right it is continued for 3.0 cm along the lower border of the.rst part of the duodenum. From its origin the greater omentum hangs down in front of the intestines as a loose apron, extending as far as the transverse colon, where its two layers separate to enclose that part of the colon. The upper part of the greater omentum contains the greater part of the right and left gastroepiploic arteries and their accompanying veins, lymph vessels, lymph glands, nerve filaments, fat and areolar tissue. Blood Supply 1. Arterial Supply The coeliac artery, the artery of the foregut, supplies the stomach by its three branches. It arises from the front of the aorta between the crura of the diaphragm and is a short wide trunk, surrounded by the coeliac lymph nodes and flanked by the coeliac ganglia of the sympathetic system. The main branches are the left gastric artery, the hepatic artery and the splenic artery.  The left gastric artery This runs to the left, gives off an ascending oesophageal branch, and supplies the upper part of the stomach. However, it may arise directly from the aorta (5–6.7%), and may provide one or both of the inferior phrenic arteries or a common trunk for the two. The left gastric artery turns downwards between the layers of the lesser omentum and runs to the right along the lesser curvature. Having divided into two parallel branches, these divide further supplying the anterior and posterior gastric walls. These vessels anastomose freely with arteries from the greater curvature. Around the incisura angularis, the two main branches then anastomose with the two branches of the right gastric artery. The hepatic artery may arise directly from the left gastric.  The hepatic artery This is the second branch of the coeliac trunk and passes downwards as far as the first part of the duodenum. At the opening into right border of the lesser sac it turns forwards (epiploic foramen) and curves upwards between the two layers of the lesser omentum towards the porta hepatis, to supply the liver. The gastroduodenal and right gastric arteries are given off as it turns into the lesser omentum. The right gastric artery passes to the left between the two layers of the lesser omentum, and runs along the lesser curvature of the stomach before dividing into two branches that anastomose with the branches of the left gastric artery. It also gives off branches to the anterior and posterior gastric walls, anastomosing with branches 3 from the right gastroepiploic artery. The gastroduodenal artery descends behind the first part of the duodenum, which it supplies by multiple small branches. The terminal divisions are the superior pancreaticoduodenal artery, supplying the second part of the duodenum and head of the pancreas, and the right gastroepiploic artery. The right gastroepiploic artery passes along the greater curvature of the stomach between the layers of the greater omentum and gives off branches to the anterior and posterior gastric walls before anastomosing with the left gastroepiploic artery.  The splenic artery This passes to the left along the upper border of the pancreas, behind the peritoneum and the stomach, to supply the spleen. Division into the terminal branches close to the spleen is called a magistral splenic (~1–2 cm from the hilum), but earlier division is called a distributing splenic. During its course it gives off branches to the pancreas; just before entering the splenic hilum it gives off the short gastric arteries supplying the gastric fornix, and the left gastroepiploic artery. The latter passes downwards and to the right along the greater curvature of the stomach, between the two layers of the greater omentum, to anastomose with the right gastroepiploic artery at the mid-portion of the greater curvature. It gives off branches to the anterior and posterior gastric walls, which anastomose with branches of the gastric arteries along the lesser curvature. 2. The Venous Drainage The gastric veins are similar in position to that of the arteries along the lesser and greater curvatures. These veins drain either directly or indirectly into the portal system.  Left gastric vein This runs to the left along the lesser curvature, receiving the oesophageal veins below the oesophageal hiatus in the diaphragm. It usually drains directly into the portal vein at the superior border of the pancreas.  Right gastric vein This runs along the lesser curvature to the right towards the pylorus. Posterior to the first part of the duodenum it joins the portal vein. It also receives the prepyloric vein which receives the veins from the first 2 cm of the duodenum.  Left gastroepiploic vein This passes to the left along the greater curvature and with the short gastric veins drains into the splenic vein or its tributaries. The splenic vein is joined with tributaries from the pancreas as well as the inferior mesenteric vein; these ultimately form the portal vein with the superior mesenteric vein.  Right gastroepiploic vein This runs to the right as far as the head of the pancreas. Usually it joins the superior mesenteric vein and thus drains into the portal vein. However, considerable variations may occur and the right gastroepiploic may enter the portal vein directly, or it may join the splenic vein. There is no gastroduodenal vein. 3. Lymphatic Drainage The lymphatics of the stomach can be divided into three systems:  Intramural This consists of three networks; submucosal, intermuscular and subserosal.  Intermediary This consists of numerous small channels between the subserosal network and the extramural collecting systems. 4  Extramural This consists of four major zones of lymphatic drainage, corresponding to the arterial supply of the stomach. Ultimately all zones drain into the coeliac nodes around the coeliac arterial trunk on the anterior aspect of the aorta. The lymphatic drainage of the stomach can be divided into four zones :  Zone 1 This comprises the upper twothirds of the lesser curvature and a large part of the body of the stomach. These drain into the left gastric nodes lying along the left gastric artery. These nodes are joined by lymphatics coming down from the lower part of the oesophagus, and their efferents proceed to the coeliac nodes.  Zone 2 This is from the distal part of the lesser curvature, including the lesser curvature of the pyloric region, to the suprapyloric nodes along the right gastric artery. Efferent channels from the suprapyloric nodes drain to the hepatic and ultimately to the coeliac and aortic nodes.  Zone 3 This zone includes the pyloric part of the stomach as well as the right half of the greater curvature. The lymphatics from these areas drain into the right gastroepiploic nodes in the gastrocolic ligament, lying along the right gastroepiploic vessels, and into the pyloric nodes on the anterior surface of the head of the pancreas. The direction of lymph flow is from above downwards, towards the pylorus and the nodes between the head of the pancreas and second part of the duodenum. From these groups, collectively called the subpyloric glands (which also drain the.rst part of the duodenum), efferent vessels pass along the gastroduodenal artery to the hepatic nodes along the hepatic artery, and thence to the coeliac nodes.  Zone 4 This comprises the left half of the greater curvature and the gastric fornix. The lymph vessels from here pass to the left gastroepiploic nodes, lying along the left gastroepiploic artery. These drain to the pancreatico-lienal nodes along the splenic artery, before terminating in the coeliac nodes. 4. Nerves The autonomic nervous system consists of two components, cholinergic – mostly parasympathetic, and adrenergic – mostly sympathetic nerves. However, a third component of the autonomic system, which is neither cholinergic nor adrenergic, has been recognised within the gastrointestinal tract – the peptidergic system.  Parasympathetic Nerve Supply The anterior and posterior vagal trunks and their branches form the parasympathetic nerve supply to the stomach. Afferent fibres are also present in the vagi. 1. Anterior vagus This is derived mainly from the left vagus nerve but also includes.bres from the right vagus and also some sympathetic fibres from the splanchnic nerves. It enters the abdominal cavity through the oesophageal hiatus in the diaphragm. It is usually single but may be divided into multiple trunks. Having given off several fine branches to the lower end of the oesophagus and cardiac part of the stomach, the anterior trunk breaks up into its main branches. Latarjet divided the nerves of the anterior vagus into two distinct functional divisions. The first division, consisting of the direct branches, supplies the fornix and body, i.e. the 5 “reservoir” part of the stomach. The second division, through the hepatic branches, supplies the pylorus and first part of the duodenum, i.e. the “sphincteric” part of the stomach. 2. Posterior vagus This is mainly formed by.bres from the right vagus nerve and enters the abdomen posterior to the oesophagus. After entering the abdomen it divides into two main branches: the coeliac and the posterior gastric. It then continues along the lesser curvature innervating the posterior gastric wall although only extending to the incisura angularis. The lowest branch is sometimes referred to as “the posterior nerve of Latarjet”. These nerves do not innervate the pylorus and prepyloric region.  Sympathetic Nerve Supply This is derived almost entirely derived from the coeliac plexus. The gastric branches of the coeliac plexus accompany the vessels supplying the stomach – the left gastric, hepatic and phrenic arteries.  Peptidergic System Peptidergic cells are derived embryologically from neuroectoderm and are referred to as APUD cells because they synthesize monoamines through a process of amine precursor uptake and decarboxylation (APUD). They are also referred to as neuroendocrine cells. A large number of biologically active peptides have been detected in these APUD cells within the gut. These peptides include gastrin, vasoactive intestinal peptide (VIP), somatostatin, enkephalin, neurotensin and substance P. Microscopic anatomy The wall of the stomach and the proximal 3.0 cm of the duodenum are composed of four coats. From without inwards these are the serous, muscular, submucous and mucous coats. The mucous coat is separated from theluminal contents by a layer of gastric mucus.  Serous Coat (Adventitia) This is formed by the peritoneum, which is a thin layer of loose connective tissue covered with mesothelium. It is attached to the muscular coat, except at the greater and lesser curvatures, where it is continuous with the greater and lesser omentum respectively.  Muscularis externa The muscularis externa is composed of smooth, unstriped or involuntary fibres and is made up of three layers: an external longitudinal, middle circular, and an inner oblique layer.  Submucous coat This is a layer of loose areolar tissue with some elastic.bres that lies between the muscularis mucosae and the muscularis externa. It is rich in mast cells, macrophages, lymphocytes, eosinophilic leucocytes and plasma cells.Within this layer the vessels and nerves divide before entering the mucous membrane. It contains arteries, veins, lymphatics and Meissner’s nerve plexuses.  Mucosa This consists of three components: the muscularis mucosae, the lamina propria, and the epithelial lining. 6 Mucosal zones The mucous membrane of the entire stomach is lined by glands that open into the gastric pits. The gastric mucosa can be divided into three zones, based on the predominant cell types within the glands :  Cardiac zone - These glands secrete mucus  Pyloric zone - These glands secrete mucus. They also produce endocrine, paracrine or neurocrine regulatory peptides by virtue of the APUD cells contained in their glands.  Oxyntic zone - These glands produce nearly all the enzymes and hydrochloric acid secreted in the stomach as well as producing mucus. 3 The secretory epithelial cells and their roles Four major types of secretory epithelial cells cover the surface of the stomach and extend down into gastric pits and glands :  Mucous cells - secrete alkaline mucus that protexts the epithelium against shear stress and acid  Parietal cells - secrete hydrochloric acid  Chief cells - secrete pepsin, a proteolytic enzyme  G cells – secrete the hormone gastrin Physiology Gastric secretions  Mucus secretion The cells of the gastric glands secrete about 2500 ml of gastric juice daily. This contains a variety of substances and gastric enzymes, whose role is to kill ingested bacteria, aid protein digestion, stimulate the flow of bilary and pancreatic juices and provide the necessary pH for pepsin to begin protein degradation. The most abundant epithelial cells are mucussecreting columnar cells, which cover the entire luminal surface and extend down into the glands as “mucous neck cells”. These cells secrete bicarbonate-rich mucus that coats and lubricates the gastric surface, and serves an important role in protecting the epithelium from acid and other chemical insults. It is made up of glycoprotein subunits bound by disulphide bonds and forms a water-insoluble gel that is impermeable to H+ ions. Production is stimulated by luminal acid and vagal activity, and is increased by prostaglandins. Therefore aspirin non-steroidal anti-in.ammatory drugs (NSAIDs) increase the damage to the stomach by inhibiting prostaglandin formation as well as by crystallising out in the gastric cells. Bicarbonate is also secreted from parietal cells. Gastric cells also can turn over rapidly inresponse to injury, as there is a rich mucosal blood flow providing oxygen, bicarbonate and nutrients and removing acid. Blood flow is normally increased simultaneously with acid secretion and is reduced by aspirin and alcohol.  Pepsinogen secretion The chief cells secrete pepsinogens, contained in zymogen granules. These are the precursors of the pepsins (proteases) in gastric juice. Once secreted, pepsinogen I is activated by the presence of gastric acid into the active protease pepsin. This is an endopeptidase that is 7 largely responsible for the initiation of protein digestion into smaller peptides and polypeptides. It acts at pH 1.5–2.5 and above pH 5.4 is inactivated. It is released mainly by vagal stimulation but also by histamine gastrin secretion, alcohol, cortisol, caffeine and acetazolamide. Pepsinogen release may also occur during periods of hypoglycaemia and prolonged increased intracranial pressure.  Hormone secretion The principal hormone secreted from the gastric epithelium is gastrin, a peptide that is important in control of acid secretion and gastric motility. Intrinsic factor, a glycoprotein secreted by parietal cells, is necessary for intestinal absorption of vitamin B12. It acts by combining with the vitamin B12 and is necessary for its attachment to receptors in the terminal ileum. Lack of intrinsic factor due to reduction in parietal cell mass following gastric surgery, or the production of antibodies to the cells, called pernicious anaemia, leads to megaloblastic anaemia. Secretion of intrinsic factor occurs following vagal, gastrin or histamine stimulation of the parietal cells. The Formation and Secretion of Gastric Acid Stimulation of the parietal cells results in acid secretion. These cells contain multiple tubulovesicular structures within their cytoplasm that on stimulation move to the mucosal membrane and fuse with it, producing a microvillous appearance that increases the surface area. This results in the presence of the H+-K+ ATPase that transports the H+ onto the luminal surface. This secretion is isotonic with other.uids and its pH is 4 mg/dL), alkaline phosphatase, the transaminases, and amylase may be present. Severe jaundice is suggestive of common bile duct stones or obstruction of the bile ducts by severe pericholecystic inflammation secondary to impaction of a stone in the infundibulum of the gallbladder that mechanically obstructs the bile duct, known as Mirizzi's syndrome. Diagnosis Ultrasound is the most useful radiographic test for diagnosing acute cholecystitis, with sensitivity and specificity of 85% and 95%, respectively. It is sensitive for identifying the presence of gallstones. Ultrasound also shows the presence of thickening of the gallbladder wall (>4 mm), pericholecystic fluid, gallbladder distention, impacted stone, and a sonographic Murphy's sign (focal tenderness directly over the gallbladder). Symptoms attributable to biliary tract pathology are usually the result of obstruction, infection, or both. Obstruction can be extramural (e.g., pancreatic cancer), intramural (cholangiocarcinoma), or intraluminal (choledocholithiasis). Similar to infections in other parts of the body, biliary infections are usually due to three factors: a susceptible host, sufficient inoculum, and stasis. The most common symptoms related to biliary tract disease are abdominal pain, jaundice, fever, and nausea and vomiting. 7 A. Abdominal pain Gallstones and inflammation of the gallbladder are the most frequent causes of abdominal pain from biliary tract disease. Acute obstruction of the gallbladder by calculi results in biliary colic, a common misnomer because the pain is not colicky in the epigastrium or right upper quadrant. Biliary colic is a constant pain that builds in intensity, and can radiate to the back, interscapular region, or right shoulder. The pain is described as a bandlike tightness of the upper abdomen that may be associated with nausea and vomiting. This is due to a normal gallbladder contracting against a luminal obstruction, such as a gallstone impacted in the neck of the gallbladder, the cystic duct, or the common bile duct. The pain is most commonly triggered by fatty foods, but it can also be initiated by other types of food or even occur spontaneously. An association with meals is present in only 50% of patients, and in these patients, the pain often develops more than 1 hour after eating. The pain of biliary colic is distinct from that associated with acute cholecystitis. Although biliary colic can also be localized to the right upper quadrant, the pain of acute cholecystitis is exacerbated by touch, is somatic in nature, and is often associated with fever and leukocytosis. Irritation of the visceral and parietal peritoneum due to transmural inflammation from cholecystitis results in a positive Murphy's sign. This physical exam finding (in a patient abruptly arresting his or her inspiratory effort because of pain as the examiner palpates under the right costal margin) is indicative of acute cholecystitis B. Jaundice When the serum concentration of bilirubin exceeds about 2.5 mg/dL, a yellowish discoloration of the sclera becomes evident (scleral icterus). Jaundice represents a similar discoloration of the skin, with serum bilirubin levels in excess of 5 mg/dL. The changes in color represent deposition of bile pigments in the affected tissues. The presence of conjugated bilirubin in the urine is one of the first changes noted by patients. Disorders resulting in jaundice can be divided into those causing “medical” jaundice, such as increased production, decreased hepatocyte transport or conjugation, or impaired excretion of bilirubin, and those causing “surgical” jaundice through impaired delivery of bilirubin into the intestine. Common causes of increased bilirubin production include the hemolytic anemias and acquired causes of hemolysis, including sepsis, burns, transfusion reactions, and medications. Impaired excretion of bilirubin leads to intrahepatic cholestasis and conjugated hyperbilirubinemia and can be due to conditions like viral or alcoholic hepatitis, cirrhosis, and drug-induced cholestasis. C. Fever Significant elevations in body temperature (≥38.0°C) represent a systemic manifestation of an initially localized inflammatory process. Bacterial contamination of the biliary system is a common feature of acute cholecystitis or choledocholithiasis with obstruction, and can be expected following percutaneous or endoscopic cholangiography. The combination of right upper quadrant abdominal pain, jaundice, and fever, known as Charcot's triad, signifies an active infection of the biliary system termed acute cholangitis. The addition of an altered mental status and hypotension to the above findings represents severe cholangitis and is termed pentad of Reynolds. 8 Paraclinical diagnosis 1. Laboratory tests Biliary colic, in the absence of gallbladder wall pathology or common bile duct obstruction, does not produce abnormal laboratory test values. On the other hand, obstructive choledocholithiasis is commonly associated with both liver dysfunction and acute cellular injury with resultant elevations in liver function tests. Hepatocellular injury results in increased levels of unconjugated or indirect reacting bilirubin due to an increase in bilirubin production or a decrease in hepatocyte uptake with conjugation. Conjugated or direct hyperbilirubinemia is due to defects in bilirubin excretion (intrahepatic cholestasis) or extrahepatic biliary obstruction. In addition to hyperbilirubinemia, an increased alkaline phosphatase level is virtually pathognomonic of bile duct obstruction. In patients with a high clinical suspicion of cholecystitis, but with associated elevations of bilirubin, alkaline phosphatase, and aminotransferase, cholangitis should be suspected. Serum transaminase (aspartate and alanine) levels can also be mildly elevated in biliary system disease, either because of direct injury of the liver adjacent to an inflamed gallbladder or from the effect of biliary sepsis on hepatocellular membrane integrity. Leukocytosis, composed primarily of neutrophils, is often present with acute cholecystitis or cholangitis, but is a nonspecific finding that does not distinguish them from other infectious or inflammatory causes. 2. Plain Radiographs Although frequently obtained during the initial evaluation of abdominal pain, plain radiographs of the abdomen in patients with complaints localized to the right upper quadrant are rarely helpful. Only about 15% of gallstones contain enough calcium to render them radiopaque and therefore visible on plain abdominal films. Plain films are important to exclude other potential diagnoses, such as perforated ulcer with free intraperitoneal air, bowel obstruction with dilated loops of bowel, or right lower lobe pneumonia on chest x-ray, that may mimic biliary tract disease. 3. Ultrasonography Ultrasound of the abdomen is an extremely useful and accurate method for identifying gallstones and pathologic changes in the gallbladder consistent with acute cholecystitis. Abdominal ultrasound, if performed by an experienced operator, should be part of the routine evaluation of patients suspected of having gallstone disease, given the high specificity (>98%) and sensitivity (>95%) of this test for the diagnosis of cholelithiasis. In addition to identifying gallstones, ultrasound can also detail signs of cholecystitis such as thickening of the gallbladder wall, pericholecystic fluid, and impacted stone in the neck of the gallbladder. It is often the initial screening test for patients with suspected extrahepatic biliary obstruction. Dilation of the extrahepatic (>10 mm) or intrahepatic (>4 mm) bile ducts suggests biliary obstruction. Intraoperative ultrasound is now used frequently to further evaluate intrahepatic lesions, assess resectability, and determine involvement of vascular structures. 9 4. Oral Cholecystography Once considered the diagnostic test of choice for gallstones, oral cholecystography has been replaced by ultrasonography. It identifies filling defects in a visualized, opacified gallbladder after oral administration of a radiopaque compound that passes into the gallbladder. Oral cholecystography is of no value in patients with vomiting, biliary obstruction, jaundice, or hepatic failure. 5. Computed Tomography Although abdominal CT scanning is probably the most informative single radiographic tool for examining intra-abdominal pathology, its overall value for the diagnosis of biliary tract disease pales in comparison to ultrasonography. The disadvantage is largely because gallstones and bile appear nearly isodense on CT; that is, it is difficult to distinguish gallstones from bile, unless the stones are heavily calcified. CT identifies gallstones within the biliary tree and gallbladder with a sensitivity of only about 55% to 65%. Conversely, CT is more accurate at identifying the site and cause of extrahepatic biliary obstruction. Abdominal CT is a powerful tool for evaluating biliary tract disease when the differential diagnosis includes a question of hepatobiliary or pancreatic neoplasm, liver abscess, or hepatic parenchymal disease (e.g., biliary cirrhosis, organ atrophy). Use of CT cholangiogram provides improved definition of the biliary tract comparable to magnetic resonance cholangiography. Angiograms have now essentially been replaced by triple-phase liver CT angiogram. 6. Cholangiography Cholangiography functionally involves the installation of contrast directly into the biliary tree and is the most accurate and sensitive method available to anatomically delineate the intrahepatic and extrahepatic biliary tree. It is most useful when the precise location or cause of biliary pathology needs to be ascertained. MRC is noninvasive and provides excellent anatomic detail. No contrast is administered because bile/water density is phase- contrasted. CT cholangiography requires the administration of intravenous (IV) contrast that is excreted in the biliary system. Neither of these is considered invasive. Both endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC) are invasive procedures with a 2% to 5% risk of complications but offer the opportunity for a therapeutic intervention. ERCP is most useful in imaging patients with hepatobiliary malignancies and choledocholithiasis. It illustrates distal common bile duct or ampullary obstruction, can provide tissue samples for pathologic diagnosis, and can palliate patients with complete biliary obstruction using prosthetic stents. However, it gives no information regarding tumor size, local invasion, or distant spread, and is of limited use in staging. Transhepatic cholangiography is the preferred technique in patients with proximal biliary obstruction or in patients in whom ERCP is not technically possible. Percutaneous transhepatic cholangiography can be followed by placement of transhepatic catheters, which can decompress the biliary system, function as anatomical landmarks during surgical reconstruction, or provide access for nonoperative dilation of strictures. 10 7. Scintigraphy Biliary scintigraphy is useful to visualize the biliary tree, assess liver and gallbladder function, and diagnose several common disorders including cholecystitis. Although it is an excellent test to decide whether the common bile and cystic ducts are patent, biliary scintigraphy does not identify gallstones or give any detailed anatomic information. Nonvisualization of the gallbladder at 2 hours after injection is reliable evidence of cystic duct obstruction. Biliary scintigraphy followed by CCK administration is helpful for documenting biliary dyskinesia when gallbladder contraction accompanies biliary tract pain in patients without evidence of stones (CCK hepatobiliary 2,6-dimethyl-iminodiacetic acid [HIDA]). These agents are iminodiacetic acid (IDA)-based compounds and are processed in the liver and excreted (H originally stood for hydroxy, but today stands for hepatobiliary because other IDA derivatives, such as proisopropyl-IDA [PIPIDA], are more commonly used, but are still referred to as HIDA scans). 8. Laparoscopy Advancement in laparoscopic skill has coincided with the increased use of laparoscopy for diagnosis and treatment of biliary tract disorders. It is most effective when used in conjunction with laparoscopic ultrasound in the staging and operative management of biliary malignancies. Intraoperative ultrasound is now used frequently to further evaluate intrahepatic lesions, assess resectability, and determine involvement of vascular structures. Although the need for laparoscopy may have diminished as a result of advancements in radiologic techniques like CT, laparoscopy still best identifies micrometastases much beyond the discrimination of the CT scan; in addition, biopsy of micrometastases can be undertaken with the laparoscope. 9. FDG-PET Scanning Fluorodeoxyglucose positron emission tomography (FDG-PET) is a whole-body technique that allows detection of unsuspected metastases that may lead to major changes in the surgical management of these patients. PET imaging with the fluorinated glucose analogue, FDG, can be used to exploit the metabolic differences between benign and malignant cells for imaging purposes. Therefore, FDG-PET imaging has become well established for differentiation of benign from malignant lesions, staging malignant lesions, detection of malignancy recurrence, and monitoring therapy for various malignancies. Recent studies have shown that FDG-PET is accurate in predicting the presence of nodular cholangiocarcinoma (mass >1 cm) and gallbladder carcinoma (sensitivity, 78%). FDG-PET is not useful for detection of carcinomatosis, and inflammatory changes related to biliary stents may cause interpretation difficulties. 11 IV. Laparoscopic cholecystectomy Indications for Cholecystectomy  Urgent: Acute cholecystitis Emphysematous cholecystitis Empyema of the gallbladder Perforation of the gallbladder Previous choledocholithiasis with endoscopic duct clearance  Elective Biliary dyskinesia Chronic cholecystitis Symptomatic cholelithiasis Contraindications to laparoscopic cholecystectomy include:  coagulopathy,  severe chronic obstructive pulmonary disease,  end-stage liver disease, and  congestive heart failure. Patients undergoing laparoscopic cholecystectomy should be prepared and draped in a similar fashion to open cholecystectomy. The patient is supine on the operating table with the surgeon standing on the patient's left. The pneumoperitoneum is created with carbon dioxide gas, either with an open technique or by closed-needle technique. With the open technique, a small incision is made either above or below the umbilicus into the peritoneal cavity. A special blunt-tipped cannula (Hasson) with a gas-tight sleeve is inserted into the peritoneal cavity and anchored to the fascia. This technique is often used following previous abdominal surgery and should avoid infrequent but life-threatening trocar injuries. In the closed technique, a special hollow insufflation needle (Veress) with a retractable cutting sheath is inserted into the peritoneal cavity through a periumbilical incision and used for insufflation. There is no difference in inadvertent bowel or tissue injury between the two techniques. The laparoscope with the attached video camera is then inserted into the umbilical port and the abdomen inspected. The additional ports are inserted under direct vision. The medial 5-mm cannula is used to grasp the gallbladder infundibulum and retract it laterally with the pull toward the right pelvis, to expose the triangle of Calot; it is important to widely expose the triangle of Calot with this direction of retraction to fully enable identification of possible aberrant biliary anatomy. This maneuver may require taking down the adhesions between the omentum or duodenum and the gallbladder. Most of the dissection can be performed using a dissector, hook, or scissors. The junction of the gallbladder and cystic duct is identified and dissection continued until the cystic artery and duct is clearly seen entering the gallbladder. A helpful anatomic landmark is the cystic lymph node. Careful extended dissection of the base of the gallbladder off the liver bed is essential to define the duct and artery. The outdated infundibular technique of cystic duct dissection and identification does not fully expose the triangle of Calot and leads to misidentification and is a setup for bile duct injury. Partial 12 dissection of the base of the gallbladder off the liver bed before dividing either the artery or cystic duct enables identification of all the anatomy and minimizes risk for bile duct injury. The next step is ligation of the cystic artery. The artery is usually encountered running parallel to and behind the cystic duct. Clips are placed proximally and distally on the artery, which is then divided. If indicated, an intraoperative cholangiogram may now be performed by placing a hemoclip proximally on the cystic duct, incising the anterior surface of the duct, and passing a cholangiogram catheter into the cystic duct. Once the cholangiogram is completed, two clips are placed distally on the cystic duct, which is then divided. A large cystic duct may require placement of a pretied loop ligature or a standard suture tied laparoscopically for secure closure. Finally, the gallbladder is dissected out of the gallbladder fossa with electrocautery. Just before removing the gallbladder from the liver, the operative field is carefully searched for hemostasis. The gallbladder is then dissected off the liver and removed through the umbilical port. If the gallbladder is acutely inflamed, gangrenous, or entered during the dissection, a plastic specimen retrieval bag should be used for removal from the abdominal cavity. Any bile or blood that has accumulated should be irrigated and sucked away, and if stones were spilled, they should be retrieved. Any concern about bile accumulation or leak should prompt placement of a closed-suction drain through one of the 5- mm ports and left underneath the right lobe of the liver close to the gallbladder fossa. 13 LECTURE 9 Complications of biliary lithiasis Acute lithiasic cholecystitis Pathophysiology Acute cholecystitis is related to gallstones in 90% to 95% of cases. Obstruction of the cystic duct leading to biliary colic is the initial event in acute cholecystitis. If the cystic duct remains obstructed, the gallbladder distends, and the gallbladder wall then becomes inflamed and edematous. Initially, acute cholecystitis is an inflammatory process with a thickened and reddish wall with subserosal hemorrhage. The mucosa may show hyperemia and patchy areas of necrosis. In the most common scenario, the gallstone dislodges, and the inflammation will gradually resolve. In the most severe cases, this process can lead to ischemia and necrosis of the gallbladder wall (5%-10%). Acute gangrenous cholecystitis results in formation of an abscess or empyema within the gallbladder. When gas-forming organisms are part of the secondary bacterial infection, gas may be seen in the gallbladder lumen and in the wall of the gallbladder on imaging resulting in emphysematous cholecystitis. Clinical Presentation Right upper quadrant pain, similar in severity to but much longer in duration than pain from previous episodes of biliary colic, is the most common symptom of acute cholecystitis. Other common symptoms include:  fever,  nausea, and  vomiting. On physical exam, right upper quadrant tenderness and guarding are usually present inferior to the right costal margin, distinguishing the episode from simple biliary colic. When inflammation spreads to the peritoneum, patients develop more diffuse tenderness, guarding and rigidity. A mass, the gallbladder and adherent omentum, is occasionally palpable, and Murphy's sign, inspiratory arrest with deep palpation in the right upper quadrant, may also be present. A mild leukocytosis is usually present (12,000-14,000 cells/mm3). In addition, mild elevations in serum bilirubin (>4 mg/dL), alkaline phosphatase, the transaminases, and amylase may be present. Severe jaundice is suggestive of common bile duct stones or obstruction of the bile ducts by severe pericholecystic inflammation secondary to impaction of a stone in the infundibulum of the gallbladder that mechanically obstructs the bile duct, known as Mirizzi's syndrome. 1 Diagnosis Ultrasound is the most useful radiographic test for diagnosing acute cholecystitis, with sensitivity and specificity of 85% and 95%, respectively. It is sensitive for identifying the presence of gallstones. Ultrasound also shows the presence of:  thickening of the gallbladder wall (>4 mm),  pericholecystic fluid, gallbladder distention,  impacted stone, and  a sonographic Murphy's sign (focal tenderness directly over the gallbladder). Biliary radionuclide scanning is used less frequently today but may be helpful in atypical cases. No filling of the gallbladder with the radiotracer ( 99mTc-HIDA) after 4 hours indicates an obstructed cystic duct with a sensitivity and specificity for acute cholecystitis of 95%. A normal HIDA scan excludes acute cholecystitis. CT scan, although performed frequently in patients with abdominal pain, may identify some of the findings mentioned previously, similar to ultrasonography, but is less sensitive than ultrasonography for acute cholecystitis. The differential diagnosis:  Perforated or penetrating peptic ulcer  Myocardial infarction  Pancreatitis  Hiatal hernia  Right lower lobe pneumonia  Appendicitis  Hepatitis  Herpes zoster Management After the diagnosis of acute cholecystitis is made, IV fluids, antibiotics, and analgesia should be initiated. Antibiotics should cover gram-negative aerobes as well as anaerobes. More than half of patients with acute cholecystitis have positive cultures from the gallbladder bile. An antibiotic appropriate for the common biliary tract pathogens isolated from the bile in patients with acute cholecystitis should be selected. Parenteral analgesia should also be administered. Unfortunately, narcotics increase biliary pressure, whereas nonsteroidal analgesics, which inhibit prostaglandin synthesis, reduce gallbladder mucin production and therefore relieve pressure and pain. 2 Complications of acute cholecystitis Acute cholecystitis may progress to:  empyema of the gallbladder,  emphysematous cholecystitis, or  perforation of the gallbladder despite antibiotic therapy. In each case, emergency cholecystectomy is warranted, if the patient can withstand an anesthetic. 1. Empyema occurs with bacterial proliferation in an obstructed gallbladder and results in a pus-filled organ. Patients with empyema of the gallbladder may be toxic with more marked fever and leukocytosis. Laparoscopic cholecystectomy may be attempted, but the conversion rate is high. 2. Emphysematous cholecystitis develops more commonly in men and patients with diabetes mellitus. Severe right upper quadrant pain and generalized sepsis are frequently present. Abdominal films or CT scans may demonstrate air within the gallbladder wall or lumen. Prompt antibiotic therapy to cover the common biliary pathogens (E. coli, Enterococcus, Klebsiella, and so forth) as well as Clostridium species and emergency cholecystectomy are appropriate treatments. 3. Perforation of the gallbladder occurs in up to 10% of cases of acute cholecystitis. Perforation is a sequelae of ischemia and gangrene of the gallbladder wall and occurs most commonly in the gallbladder fundus.  The perforation is most frequently (50% of cases) contained within the subhepatic space by the omentum, duodenum, liver, and hepatic flexure of the colon, and a localized abscess forms.  Less commonly, the gallbladder perforates into and adjacent viscus (duodenum or colon) resulting in a cholecystoenteric fistula. Rarely, the gallbladder perforates freely into the peritoneal cavity leading to generalized peritonitis. With gallbladder perforation, the abdominal tenderness, fever, and white blood cell count are more pronounced or higher than in uncomplicated acute cholecystitis. Localized right upper quadrant pain and tenderness, which becomes diffuse and generalized, should raise the suspicion of free gallbladder perforation. Intravenous fluids, antibiotics, and emergency cholecystectomy are the treatment of choice in patients with gallbladder perforation. In most patients, cholecystectomy can be performed and is the best treatment of complicated acute cholecystitis. Occasionally, the inflammatory process obscures the structures in the triangle of Calot precluding safe dissection or ligation of the cystic duct. In these patients partial cholecystectomy, cauterization of the remaining gallbladder mucosa, and drainage avoids injury to the common bile duct. 3 In patients considered too unstable to undergo laparotomy because of concurrent medical comorbidities, percutaneous transhepatic cholecystostomy can drain the gallbladder. Success rates approaching 90% have been reported with percutaneous cholecystostomy in managing critically ill patients thought to have acute cholecystitis. However, this procedure leaves in the gallbladder, which may be partially gangrenous and a source of ongoing sepsis. Interval laparoscopic cholecystectomy should then be performed after a delay of 3 to 4 months to allow the patient to recover and the acute inflammation to resolve. Cholecystectomy is the definitive treatment for patients with acute cholecystitis. There are two approaches to the timing of surgery:  Immediate surgery; that is, within 72 hours of the onset of symptoms;  Delayed surgery; that is, after recovery from the acute attack with intravenous fluids and antibiotics. Surgery should be performed approximately 6 weeks after the acute inflammation has resolved. Most surgeons now advocate early surgical intervention in the treatment of acute cholecystitis. This is due to the improved safety of current techniques, the effectiveness of perioperative antibiotics, and the high risk (at least 50%) of recurrent acute cholecystitis if surgery is delayed.  If symptoms began within 72 hours of the time of presentation, laparoscopic cholecystectomy is performed.  If symptoms began more than 72 hours before the time of presentation and the patient is responding to medical management (i.e., a nasogastric tube, intravenous fluids, nothing by mouth, and antibiotics), then surgery is delayed for 4-6 weeks.  Deterioration or failure to improve on medical management is an indication for surgery. 4 Cholecystectomy: Indications and Technique Indications for Cholecystectomy  Urgent: Acute cholecystitis Emphysematous cholecystitis Empyema of the gallbladder Perforation of the gallbladder Previous choledocholithiasis with endoscopic duct clearance  Elective Biliary dyskinesia Chronic cholecystitis Symptomatic cholelithiasis Contraindications to laparoscopic cholecystectomy include:  coagulopathy,  severe chronic obstructive pulmonary disease,  end-stage liver disease, and  congestive heart failure. Patients undergoing laparoscopic cholecystectomy should be prepared and draped in a similar fashion to open cholecystectomy. The patient is supine on the operating table with the surgeon standing on the patient's left. Laparoscopic surgery requires a space for visualization and instrument manipulation, and this space is usually created by establishing a pneumoperitoneum with carbon dioxide. The pneumoperitoneum is created with carbon dioxide gas, either with an open technique or by closed-needle technique With the open technique, a small incision is made either above or below the umbilicus into the peritoneal cavity. A special blunt-tipped cannula (Hasson) with a gas-tight sleeve is inserted into the peritoneal cavity and anchored to the fascia. This technique is often used following previous abdominal surgery and should avoid infrequent but life-threatening trocar injuries. In the closed technique, a special hollow insufflation needle (Veress) with a retractable cutting sheath is inserted into the peritoneal cavity through a periumbilical incision and used for insufflation. There is no difference in inadvertent bowel or tissue injury between the two techniques. Once an adequate pneumoperitoneum has been established, an 11-mm trocar is inserted through the supraumbilical incision. The laparoscope with attached video camera is then inserted through the umbilical port, and an examination of the peritoneal cavity is performed. Both forward viewing (0-degree) and angled (30-degree) laparoscopes are available. With either the open or closed techniques, additional trocars are inserted under direct vision. Most surgeons use a second 11-mm trocar–placed subxiphoid and two additional 5-mm trocars positioned subcostally in the right upper quadrant in the midclavicular and anterior axillary lines. Also available are 5-mm cameras and 3-mm instruments. 5 Trocar placement for laparoscopic cholecystectomy. The laparoscope is placed through a 10-mm port just above the umbilicus. Additional ports are placed in the epigastrium and subcostally in the mid-clavicular and near the anterior axillary lines. The two smaller ports are used for grasping the gallbladder and placing it in the ideal position for an antegrade cholecystectomy.  The lateral port is used to retract the gallbladder cephalad elevating the inferior edge of the liver and exposing the gallbladder and cystic duct.  The medial 5-mm cannula is used to grasp the gallbladder infundibulum and retract it laterally to further expose the triangle of Calot. This maneuver may require bluntly taking down any adhesions between the omentum or duodenum and the gallbladder. The junction of the gallbladder and cystic duct is identified by stripping the peritoneum off the gallbladder neck and removing any tissue surrounding the gallbladder neck and proximal cystic duct. This dissection is continued until the triangle of Calot is cleared of all fatty and lymphatic tissue and the gallbladder infundibulum is elevated off the liver bed. At this point two structures (cystic artery and cystic duct) should be seen entering the gallbladder. Most of the dissection can be performed using a dissector, hook, or scissors. The junction of the gallbladder and cystic duct is identified and dissection continued until the cystic artery and duct is clearly seen entering the gallbladder. A helpful anatomic landmark is the cystic lymph node. Careful extended dissection of the base of the gallbladder off the liver bed is essential to define the duct and artery. The outdated infundibular technique of cystic duct dissection and identification does not fully expose the triangle of Calot and leads to misidentification and is a setup for bile duct injury. Partial dissection of the base of the 6 gallbladder off the liver bed before dividing either the artery or cystic duct enables identification of all the anatomy and minimizes risk for bile duct injury. The next step is ligation of the cystic artery. The artery is usually encountered running parallel to and behind the cystic duct. Clips are placed proximally and distally on the artery, which is then divided. If indicated, an intraoperative cholangiogram may now be performed by placing a hemoclip proximally on the cystic duct, incising the anterior surface of the duct, and passing a cholangiogram catheter into the cystic duct. Once the cholangiogram is completed, two clips are placed distally on the cystic duct, which is then divided. A large cystic duct may require placement of a pretied loop ligature or a standard suture tied laparoscopically for secure closure. Finally, the gallbladder is dissected out of the gallbladder fossa with electrocautery. Just before removing the gallbladder from the liver, the operative field is carefully searched for hemostasis. The gallbladder is then dissected off the liver and removed through the umbilical port. If the gallbladder is acutely inflamed, gangrenous, or entered during the dissection, a plastic specimen retrieval bag should be used for removal from the abdominal cavity. Any bile or blood that has accumulated should be irrigated and sucked away, and if stones were spilled, they should be retrieved. Any concern about bile accumulation or leak should prompt placement of a closed-suction drain through one of the 5- mm ports and left underneath the right lobe of the liver close to the gallbladder fossa. 1. The gallbladder is retracted cephalad using the grasper on the gallbladder fundus and laterally at the infundibulum. The peritoneum overlying the gallbladder infundibulum and neck and the cystic duct is divided bluntly, exposing the cystic duct. 7 2. View obtained after dissection within the triangle of Calot demonstrating the cystic duct and cystic artery clearly entering the gallbladder. At this point it is safe to ligate and divide the cystic duct. 3. Once the gallbladder cystic duct junction has been clearly identified, clips are placed proximally and distally on the cystic duct, and the duct is sharply divided. 8 3. A, After the cystic artery is divided, the gallbladder is dissected out of the liver bed using cautery. B, The liver bed is then irrigated and inspected. C, The gallbladder is removed through the supraumbilical incision. 9 LECTURE 10 Mechanical jaundice Definition Jaundice (hyperbilirubinaemia) is a syndrome of varied aetiology that is recognized clinically when serum bilirubin exceeds 40 mol/L. Jaundice - yellowing of the skin and sclera from accumulation of the pigment bilirubin in the blood and tissues. The bilirubin level has to exceed 35-40 mol/L before jaundice is clinically apparent Etiopathogeny and physiopathology The excess bilirubin may be either conjugated or unconjugated and may result from: excess bilirubin production; impaired uptake by the hepatocyte; failure of conjugation; impaired secretion of conjugated bilirubin into the bile canaliculi; impairment of bile flow subsequent to secretion by hepatocytes (cholestatic or obstructive jaundice). The cholestatic defect may be congenital but much more commonly is acquired as a result of: haemolysis; liver disease (acute or chronic); adverse drug reaction; biliary tract obstruction (intrahepatic or extrahepatic). In clinical practice, hepatocellular and cholestatic jaundice comprise the majority of cases. Hepatocellular jaundice is due to parenchymatous liver disease, which may be:  acute (viral hepatitis, liver cell necrosis, acute alcoholic hepatitis, etc.) or  chronic (various types of cirrhosis - primary biliary, etc.). The principal defect is the failure of secretion of conjugated bilirubin into the bile canaliculi. Serum transaminases are grossly elevated, especially in acute disease. In patients with alcohol-related liver disease, -glutamyltransferase ( -GT) is elevated. Acute hepatitis due to viral infection or drugs may also cause a cholestatic picture, in which case alkaline phosphatase and 5'-nucleotidase are elevated. The hyperbilirubinaemia is predominantly of the conjugated variety, with the presence of bilirubin in the urine. Cholestatic jaundice is the result of impaired bile flow to the duodenum subsequent to the secretion of conjugated bilirubin into the bile canaliculi. The block may be intrahepatic (drugs, hepatitis, obstruction of the intrahepatic biliary tree) or extrahepatic. The latter is known as large bile duct obstruction and constitutes the most important surgical subgroup of cholestatic jaundice as it is always the result of organic disease, e.g. ductal calculi, pancreaticobiliary cancer. 1 The biochemical features of cholestasis include the following: Conjugated hyperbilirubinaemia. Elevation of alkaline phosphatase, 5'-nucleotidase and -GT. The enzyme 5'-nucleotidase is the most reliable since its level is not influenced by bone disease and the enzyme is not induced by alcohol. Minimal or no elevation of serum transaminases. Presence of bilirubin in the urine: conjugated bilirubin is water soluble and is therefore filtered in the glomerulus. Elevation of serum cholesterol and bile acid, although these are not routinely measured in patients with cholestatic jaundice. These biochemical markers of cholestasis do not distinguish between intrahepatic and extrahepatic obstruction. In haemolytic jaundice, the unconjugated hyperbilirubinaemia results from haemolysis. Bilirubin is not present in the urine because the unconjugated pigment is insoluble in water and is carried in the plasma bound to albumin. The excess bilirubin production is accompanied by increased secretion of the conjugated pigment in the bile and therefore increased production of urobilinogen by bacterial decomposition in the distal small intestine. The urine therefore contains an excess amount of urobilinogen and urobilin. Classification  Prehepatic (haemolytic) jaundice Haemolytic/congenital hyperbilirubinaemias Excess production of unconjugated bilirubin (from red blood cells) exhausts the capacity of the liver to conjugate the extra load, e.g. haemolytic anaemias (hereditary spherocytosis, sickle cell disease, hypersplenism, thalassaemia)  Hepatic (hepatocellular) jaundice 1. Hepatic unconjugated hyperbilirubinaemia  Failure of transport of unconjugated bilirubin into the cell,e.g. Gilbert's syndrome  Failure of bilirubin-glucuronide glucurdnosyltransferase test activity, e.g. Crigler- Najjar syndrome 2. Hepatic conjugated hyperbilirubinaemia Hepatocellular injury results in failure of excretion of bilirubin into the biliary system. Causes include: (a) Infections: viral hepatitis (b) Poisons: carbon tetrachloride, aftatoxin (c) Drugs: paracetamol, halothane  Posthepatic (obstructive) jaundice Posthepatic conjugated hyperbilirubinaemia Anything that blocks the release of conjugated bilirubin from the hepatocyte or prevents its delivery to the duodenum. These are the most common causes of jaundice that present to a surgical service, e.g. gallstones blocking common bile duct, periampullary carcinomas, portal lymphadenopathy, sclerosing cholangitis. 2 Management of jaundice Lithiasic jaundice Common bile duct lithiasis The main symptom of stones in the CBD is obstructive jaundice. This is often associated with pain, which tends to be upper midline in distribution and aggravated by eating. Some patients are asymptomatic. Most patients present with right upper quadrant pain that radiates to the back and right shoulder, intermittent obstructive jaundice, acholic stools, or bilirubinuria. Intermittent, painful jaundice is usually due to stones and not carcinoma. The dreaded complications are:  cholangitis and  pancreatitis. Investigations  Liver functions tests show direct hyperbilirubinemia and elevated alkaline phosphatase with minimal or no abnormality of hepatocellular function.  The ultrasonogram shows a dilated CBD (>6mm diameter) and sometimes stones within the duct. More definitive evaluation of the CBD is provided by ERCP. ERCP provides the additional advantage of performing sphincterotomy and removing common duct stones. Treatment Choledocholithotomy Common bile duct stones may be removed with:  ERCP,  laparoscopy, or  open surgery. 3 Essentials: Treatment of Choledocolithiasis Treatment of choledocolithiasis 1. ERCP Endoscopic sphincterotomy and removal of common duct stones using forceps, baskets, or balloons has proven safe and effective. It is primarily indicated in the following conditions: 1. Retained stones or stones developing in the CBD after previous cholecystectomy. 2. Severe biliary pancreatitis, where therapeutic ERCP within the first few days of attack has reduced the incidence of mortality to a tenth of what it was. 3. Severe ascending cholangitis, where the patient is extremely ill and the CBD can be decompressed quickly. 4. Planned operation in a patient with stones in both gallbladder and CBD, in which preoperative clearing of the CBD by ERCP allows laparoscopic cholecystectomy and operative cholangiogram to be done without the need to explore the CBD. 2. Laparoscopic CBD Exploration and Choledocholithotomy The experienced laparoscopist can explore the CBD and remove stones through the cystic duct or after choledochotomy at the time of laparoscopic cholecystectomy. Choledochoscopy can also be performed, allowing direct examination of the extrahepatic biliary tract. The safety and success rate of laparoscopic choledocholithotomy is directly 4 related to the experience of the surgeon and must not be attempted by the person who performs laparoscopy infrequently. The procedure is indicated: 1. When, in the course of laparoscopic cholecystectomy, stones are discovered in the CBD, a situation that obtains in 10% to 15% of cases. 2. When preoperative ERCP has failed to cannulate the ampulla in patients known to have CBD stones. 3. Open CBD Exploration The procedure is performed either in conjunction with open cholecystectomy or, in the patient with retained stones, after previous cholecystectomy, especially where ERCP has failed and the laparoscopic approach is either not available or deemed too difficult because of adhesions. The approach is usually through a right subcostal or midline incision. In patients who still have their gallbladder, cholecystectomy is first performed and identification of the CBD (common bile duct) is not difficult. In patients who have had prior cholecystectomy, however, careful dissection of the structures in the subhepatic fossa is required. The CBD is normally to the right of the common hepatic artery and anterior to the portal vein. When a structure that resembles the CBD is identified, it is confirmed by aspiration of bile with a 21-gauge needle on a syringe. The CBD is then dissected and a suitable place for choledochotomy chosen. The best location is just distal to the entrance of the cystic duct but in the supraduodenal part of the structure. Two stay sutures of 3–0 silk are applied to the anterior wall, and the duct is opened between the sutures for about 2 cm. At times, stones are immediately visible and can be removed by irrigation. Some surgeons prefer to perform choledochoscopy early, others later. One simple procedure to follow is to start by irrigating the CBD, both below and above the incision, using a red rubber catheter (#10 or #12). The maneuver may result in removing all or most of the floating stones. Next, a biliary Fogarty catheter is passed distally and, if possible, into the duodenum. The balloon is inflated and pulled snug against the ampulla. The balloon is then deflated slowly as it is pulled up through the sphincter. As soon as the give is felt, the balloon is inflated, pulled up and out of the choledochotomy. If this procedure is unsuccessful after two or three attempts, stone forceps and/or Dormia baskets are used. Several applications of these procedures alternated with liberal saline irrigation may be required. The proximal extrahepatic biliary tract must also be explored both by balloon catheter and stone forceps, if necessary. It is helpful to know before exploration how many stones there are, but even after removing the expected number of stones, completion cholangiogram and/or choledochoscopy is essential.When the CBD has been satisfactorily cleared of stones, the choledochotomy is closed after inserting a T-tube. The closure is accomplished with absorbable 4–0 sutures, ensuring that the T-tube is not kinked inside the duct. The transverse portion of the T-tube often needs to be bivalved or the inferior half excised to facilitate its removal from the duct when the time comes. A closed suction-drain is placed in the right subhepatic fossa. 5 POSTOPERATIVE CARE OF THE T-TUBE The T-tube is allowed to drain freely into a bag. The amount of drainage decreases with time. A T-tube cholangiogram may be obtained safely after postoperative day 7. If no residual stones are seen and dye flows freely into the duodenum, the T-tube is clamped. It is unclamped only if the patient develops pain; otherwise, it is kept clamped until its removal in the office at about 3 weeks, when a well-formed tract has developed. If a retained stone had been identified, it can be removed through this T-tube tract. Unusual Circumstances  IMPACTED STONES In some cases, impacted stones may be located at the distal end and cannot be removed from above. The prudent thing to do in this case is to open the second portion of the duodenum over the ampulla and perform sphincterotomy to remove the stone either from below or by dislodging it upwards. The other alternative is intraoperative or postoperative ERCP.  TOO MANY STONES When stones are too numerous to extract, the prudent procedure is to perform either a choledochoduodenostomy or Roux-en-Y choledochojejunostomy. The choice depends on anatomy, age and condition of the patient. An end-to-side Roux-en-Y choledochojejunostomy is preferred, since it has a lower long-term incidence of stricture or cholangitis. A side-to side Roux-en-Y choledochojejunostomy should not be performed because it is associated with development of the sump syndrome, in which the distal portion of the CBD acts as a collection vestibule for debris and infection.  GIANT STONE IN THE CBD On occasion, a large stone wedged in the CBD cannot be moved up or down. Two techniques may be used in conjunction with one another or with a T-tube to address this problem: 1. Stone fragmentation by extracorporeal short-wave lithotripsy (ESWL) 2. Stone dissolution with chemicals such as monooctanoin has been used successfully to dissolve stones when topically applied. When a T-tube is in place in the management of these giant stones, ESWL can be used to fragment the stones, with subsequent dissolution through octanoic acid infusion into the T- tube or extraction using a Dormia basket through the T-tube tract. Complications Stones that remain after surgery complicate up to 5%-10% of common bile duct explorations. 1. No treatment is necessary for small stones, as they usually pass spontaneously. 6 2. Treatment options for large stones are:  Chemical dissolution by intraductal administration of methyl-tert-butyl ether or mono- octanoin  Mechanical extraction under fluoroscopic guidance 3. Primary or recurrent common bile duct stones can be treated surgically with a biliary- enteric connection to allow stones to pass out of the biliary tree. The two most common methods are choledochoduodenostomy or choledochojejunostomy; transduodenal sphincteroplasty or endoscopic sphincterotomy are also acceptable options. End-to-side or side-to-side Roux-en-Y choledochojejunostomy. 7 LECTURE 11 Mechanical jaundice Neoplastic jaundice Malignant lesion causing obstructive jaundice 1.Carcinoma of gallbladder Majority of tumours are inoperable at the time of diagnosis. Lymphnodes and liver invasion and local spread to duodenum, stomach, and colon is common. 2.Cholangiocarcinoma It is uncommon tumour. It is commoner in males with peak incidence in sixth or seventh decade. High incidence is associated with sclerosing cholangitis, Caroli's disease, choledochal cysts, and ulcerative colitis. The prognosis of distally placed tumour is better than proximally placed tumours. Local and distant metastases are uncommon. Cholangiocarcinoma can be classified according to location as: (1) Intrahepatic tumour (2) Hilar lesions (the most common location) referred to as Klatskin tumour and (3) Distal ductal tumour. Cholangiocarcinoma may occur in between these general locations. Hilar Cholangiocarcinoma – The most common location is either at the confluence of right and left hepatic ducts, or the proximal common hepatic duct, and has been termed Klatskin tumour. Hilar Cholangiocarcinoma are graded according to Bismuth classification: Type 1 lesion involves common hepatic duct only; Type 2 lesion involves right and left hepatic ducts at confluence. First order branches are involved of either (type 3) or both (type 4) of the hepatic ducts. Ultrasound demonstrates dilatation of intrahepatic biliary radicles without any evidence of extrahepatic dilatation. Tumours may be small and difficult to visualize on sonography. Occasionally moderately echogenic tumour may be seen at confluence. Some time no mass seen at confluence except non-union of right and left hepatic biliary radicles. Distal duct Cholangiocarcinoma – The least common location for Cholangiocarcinoma is the distal duct. Ultrasound demonstrates biliary dilatation proximal to an abrupt obstruction. Site of lesion will determine the gallbladder distention. There may be seen intraluminal polypoid lesion within bile duct. 3. Carcinoma of head of pancreas 4. Ampullary tumour 1 I. Carcinoma of the Gallbladder Carcinoma of the GB is the fifth most common malignancy in the gastrointestinal tract and has a dismal prognosis. The incidence is highest in Israel, Bolivia, Chile, and in native Americans in the sourthwestern United States. The disease occurs most commonly in people over the age of 65 years. The etiology is unknown, but the pattern of distribution among native Indians in both North and South America suggests a strong genetic cause. Gallstones, closely associated with gallbladder cancer, are found in 70% to 90% of patients with cancer. The incidence of GB cancer in cholelithiasis is not high enough to justify prophylactic cholecystectomy in asymptomatic patients. Histologically, the tumor is adenocarcinoma, most often scirrhous. In 15% of patients, the tumor is papillary. The spread is locoregional to the lymphatics. Direct invasion of the liver, duodenum, or stomach occurs frequently. Clinical Picture Most gallbladder cancers are found incidentally at the time of cholecystectomy for gallstones. The tumor may represent a polypoid mass or diffuse thickening of the gallbladder wall or it may have spread extensively to lymph nodes or invaded adjacent organs. If symptoms are present preoperatively, they are indistinguishable from those due to gallstones, although weight loss, anorexia, and jaundice in the absence of choledocholithiasis may be suggestive of the diagnosis. Treatment When the lesion is resectable, cholecystectomy is the treatment of choice, with or without regional lymph node dissection and wedge excision of the liver at the GB fossa. More radical operations have been recommended, but there are no data to justify them. Often the tumor is advanced at the time of surgery and resection is not possible. Occasionally, the presence of cancer is detected postoperatively by the pathologist in the gallbladder specimen. What should be done? No data exist to definitively indicate that reoperation is indicated to perform lymphadenectomy and limited hepatic resection. The approach, however, appears reasonable unless the tumor is only intramucosal, in which case the patient has been adequately treated with cholecystectomy alone. The prognosis is grim, with a 5-year survival rate of less than 15%. II. Extrahepatic Bile Duct Tumor or Cholangiocarcinoma Primary bile duct tumors are usually adenocarcinomas involving the common hepatic or common bile ducts. They may involve the bifurcation of the hepatic duct (hilar); the proximal, middle or distal third; or the ampullary region. These tumors are more common in patients with ulcerative colitis and sclerosing cholangitis. Tumors at the hepatic hilum present a greater surgical challenge and are often unresectable. 2 The classic presentation is progressive, painless jaundice, pruritus, anorexia, and weight loss. Right upper quadrant or deep epigastric discomfort is often present. Hepatomegaly may be present, but the tumor itself is rarely palpable. When the tumor involves the distal common bile duct with a patent cystic duct, an enlarged gallbladder may be palpable (Courvoisier’s sign). Malignant bile duct obstruction may be complicated by cholangitis, but the incidence is not high except following ERCP when prophylactic antibiotic coverage has not been used. Investigations Laboratory findings The serum bilirubin level is generally markedly elevated (>10mg/dl), as is the alkaline phosphatase. Hepatocellular dysfunction, if present, is minimal. Imaging studies Ultrasound, usually performed as the first imaging study, shows dilated intra- and extrahepatic ducts depending on tumor location. Ultrasound examination, however, rarely provides adequate information about the primary pathology.MRC has emerged as the best noninvasive imaging technique On the other hand, ERCP has the advantage of enabling histological diagnosis from biopsy or brushing. Generally, ERCP is most useful for distal bile duct tumors. Preoperative celiac angiography is useful in determining operability by showing whether the portal vein is involved. Types of Bile Duct Tumors  Hilar cholangiocarcinoma or Klatskin tumor In hilar cholangiocarcinoma, also known as Klatskin tumor, the resectability rate is less than 20% Nonetheless, all patients should undergo surgical exploration unless inoperability has been established by imaging studies. At exploration, the tumor is not resectable if any of the following circumstances are found: (1) presence of peritoneal metastasis; (2) invasion of adjacent structures; (3) invasion of portal vein, left and right portal veins, or hepatic arteries; and (4) presence of tumor within secondorder biliary radicles of both hepatic lobes.  Proximal and middle third extrahepatic bile duct When resectable, these tumors are amenable to excision of the hepatic and common ducts and Roux-en-Y hepaticojejunostomy  Distal third bile duct and periampullary lesions The resectability rate for these lesions is greater than 50%, and the surgical treatment of choice is pancreaticoduodenectomy, either of the pylorus-sparing type or the classic Whipple resection. Five-year survival rates of 30% to 49% have been reported for periampullary cholangiocarcinoma. after curative pancreaticoduodenectomy. 3 Treatment Treatment varies by type of tumor, and surgical procedure depends on tumor location. Hilar lesions present the greatest surgical challenge and the worst outcome. Resection for cure Extent of resection depends on the portion of the proximal extrahepatic biliary system involved. The modified Bismuth–Corlett classification of hilar tumors provides a useful anatomic guide for the required resection. Type I and II tumors may be removed without the need to perform hepatic resection. Biliary- enteric anastomosis can be accomplished between either the hepatic duct (Type I) or the right and left hepatic ducts (Type II) and a Roux limb of the jejunum. Type III lesion, if resectable, requires either right (IIIA) or left (IIIB) hepatic lobectomy for cure. Caudate lobe resection may also be required. Unresecable tumors If the tumor cannot be resected, decompression of the biliary tree is required. Several surgical procedures were in use prior to the advent of percutaneous stenting. At the time of surgery, U-tube stenting can be performed. The procedure requires identification of the obstructed left or right hepatic duct system. A silastic tube is placed through the abdominal wall, through the dome of the liver, across the tumor, out of the common bile duct, and through the abdominal wall. The segment of the tube within the bile ducts has multiple perforations. Such tubes tend to be obstructed with sludge but are easily replaceable without operation. Other alternatives, now more commonly used, are placement of stents endoscopically or transhepatically. Endoscopic or transhepatic stenting are equally effective, and selection of one over the other usually depends on the type of expertise available at the institution. Outcome The best 5-year survival rates after curative resection of hilar cholangiocarcinoma have been 30% with an operative mortality of 4%. The 5-year survival after stenting alone is about 5%. Adjuvant therapy Cholangiocarcinoma is resistant to both radio- and chemotherapy. External radiation and local radiation with 192Ir wire have been reported to be of some benefit, and postoperative radiation may reduce recurrence rates. 4 sTreatment of bile duct tumors Treatment of Bile Duct Bismuth–Corlette classification of hilar tumors 5 III. Carcinoma of head of pancreas Adenocarcinoma accounts for 90% of pancreatic malignancy. The tumor is located in the head of the pancreas in two-thirds of cases. Unlike gastric cancer, the incidence of pancreatic cancer has been rising It is twice as common in men as in women. Dietary and occupational factors are believed to be associated with the higher incidence and include smoking; obesity, high-fat and high-protein diet; and exposure to benzidine, betanaphthalene, and ethylene chloride. Mutation of K-ras genes is found in more than 85% of cases. Surgical resection is the only hope for cure, but even then only 5% to 10% of patients survive for 5 years. Clinical Presentation The classical presentation depends on the location of the tumor. Tumors in the head of the pancreas tend to present earlier and are often associated with painless obstructive jaundice. Adenocarcinoma of the body and tail presents late, often with pain and weight loss but without jaundice. Migratory thrombophlebitis (Trousseau’s sign) is seen in 5% to 10%, more commonly with adenocarcinoma of the body and tail. In adenocarcinoma of the head of the pancreas, jaundice is present in more than 90% of patients; weight loss and abdominal pain are seen in more than two-thirds. Typically, abdominal pain radiates to the back in the region of T12–L1. Hepatomegaly is detectable in some 80% of patients, and the gallbladder may be palpable (Courvoisier’s sign). Anorexia, nausea, and vomiting are also common. Diagnosis  Abdominal ultrasonography is usually the first diagnostic test to be obtained. It shows extrahepatic obstruction with dilated common bile duct and gallbladder in more than 75% of patients. A hypoechoic pancreatic mass may or may not be seen.  Abdominal CT is then obtained, and a mass is usually visible if the tumor is larger than 2 cm in diameter. Dilatation of the extrahepatic biliary tree is also seen. CT may show the presence of hepatic metastasis and regional lymphadenopathy. In the past, a direct diagnostic approach with CT guided fine-needle aspiration biopsy was advocated. This procedure, however, is now known to cause peritoneal and abdominal wall tumor spread and is recommended only in patients in whom abdominal exploration is not contemplated.  Magnetic resonance imaging (MRI) provides no advantage over CT, but endoscopic ultrasound may detect lesions less than 2 cm in diameter more reliably than CT.  ERCP is often performed and is indispensable in patients with obstructive jaundice in whom neither tumor nor stone is visualized. It facilitates the performance of needle aspiration biopsy, brush cytology, and pancreatogram when the findings are equivocal. Visualization of the pancreatic duct is possible in over two-thirds of patients. ERCP also allows the placement of a drainage stent to provide relief of obstructive jaundice. 6 Treatment The options depend on several factors, including resectability, the presence of metastasis, and whether or not the tumor can be visualized. Inoperable tumor Pancreatic cancer is inoperable if it is associated with clinical evidence of ascites or distant metastasis. Inoperability may also be indicated with imaging studies that demonstrate the presence of liver or abdominal metastasis and invasion of the portal vein. In these latter circumstances, metastasis and portal vein involvement should be confirmed by laparoscopy. If a patient’s tumor is deemed nonresectable, palliation may be obtained with endoscopic or transhepatic biliary drainage using expandable stents or with operative biliary and gastric bypass performed either laparoscopically or with open abdominal operation. Although endoscopic and surgical bypass are equally effective in the short term, surgical bypass is associated with a lower incidence of recurrent jaundice and cholangitis. Following biliary bypass alone, 15% to 20% of patients develop duodenal obstruction. Another advantage of surgical palliation is that gastric bypass can be done in addition to biliary bypass. Radiation and chemotherapy are relatively ineffective in providing palliation and, in any individual patient, the benefits must be compared with the side effects. Resectable tumor Patients with no demonstrable hepatic metastasis or other evidence of spread are candidates for pancreaticoduodenectomy. Resectability is determined during surgical exploration when the following are demonstrated: 1. The portal and superior veins are not invaded by tumor, and a tunnel can be developed anterior to these vessels and behind the head of the pancreas. 2. The tumor is not fixed to surrounding organs. 3. The transverse mesocolon is free of invasion. 4. No hepatic metastasis is demonstrated by palpation and intraoperative ultrasound. 5. There is no tumor deposit in lymph nodes that cannot be encompassed in en bloc excision. SURGICAL PROCEDURES Three types of resection are possible:  the classic Whipple pancreaticoduodenectomy  pylorus-preserving pancreaticoduodenectomy, and  total pancreatectomy. Regional pancreatectomy, in which the portal vein is resected and replaced with a vein graft, has not improved survival. Although there is concern about the adequacy of resection when pylorus-preserving pancreaticoduodenectomy is performed, this operation is associated with better nutritional status than the classic Whipple procedure. Postoperative delayed gastric emptying, however, is more common. The macrolide antibiotic erythromycin is useful in improving gastric emptying after pancreaticoduodenectomy. 7 Total pancreatectomy has no survival advantage and is associated with a higher mortality rate and a higher incidence of brittle diabetes than the Whipple procedure. Its use may be indicated, however, in the following clinical situations: 1. The pancreas is so friable that it is unsuitable for anastomosis. 2. Frozen section reveals the presence of tumor at the resection line. 3. Diffuse involvement of the entire pancreas is present. 4. The patient already has insulin-dependent diabetes. The operative mortality rate for pancreaticoduodectomy is now below 5% and in some centers below 2%, but this low mortality rate appears to be achieved only in hospitals where significant numbers of these procedures are performed. Long-Term Outcome The 5-year actuarial survival rate after pancreaticoduodenectomy is 12%. The prognosis is better in small, welldifferentiated and node-negative tumors, and the DNA content of the tumor cells has a significant implication. The 5-year survival rate of patients whose tumor cells are diploid is nearly 40% but less than 10% in those with aneuploid cells. The 5-year survival rate is higher in periampullary tumors (21%–56%) than in tumors of the head of the pancreas. Among periampullary tumors, duodenal tumor has the best prognosis. The overall prognosis of pancreatic cancer is dismal; only 10% of patients are alive 12 months after the diagnosis is made. Algorithm for management of carcinoma of the head of the pancreas. Abbreviations: CT, computed tomography; FNA, fine needle aspiration; ERCP, endoscopic retrograde cholangiopancreatography. 8 LECTURE 12 Hepatic hydatid cyst  Etiology and etiopathogeny - Hydatid disease, or echinococcosis, is a zoonosis that occurs primarily in sheep-grazing areas of the world, but is common worldwide because the dog is a definitive host. Echinococcosis is endemic in Mediterranean countries, the Middle East, the Far East, South America, Australia, New Zealand, and East Africa. Humans contract the disease from dogs, and there is no human-to-human transmission. - The most frequent site of hydatid cysts is the liver (50% to 77% of cases), followed by the lungs (10% to 40% of cases). There are three species of Echinococcus that cause hydatid disease. Echinococcus granulosus is the most common, whereas E. multilocularis and E. oligartus account for a small number of cases. Dogs are the definitive host of E. granulosus, in which the adult tapeworm is attached to the villi of the ileum. Eggs are passed (up to thousands of ova daily) and deposited with the dog's feces. Sheep are the usual intermediate host, but humans are an accidental intermediate host. Humans are an end stage to the parasite. In the human duodenum, the parasitic embryo releases an oncosphere containing hooklets that penetrate the mucosa, allowing access to the bloodstream. In the blood, the oncosphere reaches the liver (most commonly) or lungs, where the parasite develops its larval stage known as the hydatid cyst. Three weeks after infection, a visible hydatid cyst develops and then slowly grows in a spherical manner. A pericyst, a fibrous capsule derived from host tissues, develops around the hydatid cyst. The cyst wall itself has two layers:  an outer gelatinous membrane (ectocyst) and  an inner germinal membrane (endocyst). Brood capsules are small intracystic cellular masses in which future worm heads develop into scoleces. In a definitive host, the scoleces would develop into an adult tapeworm, but in the intermediate host, they can only differentiate into a new hydatid cyst. Freed brood capsules and scoleces are found in the hydatid fluid and form the so-called hydatid sand. Daughter cysts are true replicas of the mother cyst. Hydatid cysts can die with degeneration of the membranes, development of cystic vacuoles, and calcification of the wall. Calcification of a hydatid cyst, however, does not always imply that the cyst is dead. 1  Symptomatology and paraclinic investigations Symptoms - Hydatid cysts are diagnosed in equal numbers of men and women at an average age of about 45 years. - About three fourths of hydatid cysts are located in the right liver and are singular. - The clinical presentation of a hydatid cyst is largely asymptomatic until complications occur. - The most common presenting symptoms are:  abdominal pain,  dyspepsia, and  vomiting. - The most frequent sign is hepatomegaly. - Jaundice and fever are each present in about 8% of patients. Bacterial superinfection of a hydatid cyst can occur and present like a pyogenic abscess. Rupture of the cyst into the biliary tree or bronchial tree, or free rupture into the peritoneal, pleural, or pericardial cavities, can occur. Free ruptures can result in disseminated echinococcosis and a potentially fatal anaphylactic reaction. In cases of diagnostic uncertainty, a battery of serologic tests are available to evaluate antibody response, but all are plagued by low sensitivity and specificity. Complications The complications of hydatic cysts are:  Intrabiliary rupture, which occurs in 5% to 10% of cases.  Intraperitoneal rupture, which is uncommon but may lead to the formation of new cysts in the peritoneal cavity.  Secondary bacterial infection, leading to abscess formation and death of the scolices.  Transdiaphragmatic extension into the pleural cavity. Investigations Useful tests in echinococcal liver cysts include:  laboratory studies,  skin testing, and  radiologic studies. 2 1. Laboratory studies - A blood test will reveal eosinophilia in less than 30% of patients. - The indirect agglutination test is positive in 85% of patients. - The complement fixation test is less sensitive. 2. Skin Test - The Casoni skin test is positive in approximately 90% of cases of hydatid cysts. - A positive Casoni test persists in patients for years after an initial infection. 3. Radiologic Testing  Ultrasound is most commonly used worldwide for the diagnosis of echinococcosis because of its availability, affordability, and accuracy. A number of findings on ultrasound can be diagnostic and depend on the stage of the cyst at the time of the exam. A simple hydatid cyst is well circumscribed with budding signs on the cyst membrane and may contain free-floating hyperechogenic hydatid sand. A rosette appearance is seen when daughter cysts are present. The cyst can be filled with an amorphous mass, which can be diagnostically misleading. Calcifications in the wall of the cyst are highly suggestive of hydatid disease and can be helpful in the diagnosis.  Similar findings are seen on CT or MRI. These cross-sectional imaging studies can also evaluate extrahepatic disease and demonstrate detailed hepatic anatomic relationships to the cyst.  In patients with suspected biliary involvement, ERCP or percutaneous transhepatic cholangiography (PTC) may be necessary.  Treatment Large symptomatic cysts are treated laparoscopically or with open surgery. The steps in operative management include: 1. Isolation of the cyst from the peritoneal cavity to minimize spillage of cyst fluid. 2. Aspiration of the cyst as completely as possible, exercising caution as cyst fluid is often under pressure. 3. Instillation into the cyst cavity of a scolecocidal agent such as hypertonic saline or alcohol. 4. Excision of the hydatid cyst by separating the cyst from the liver along a cleavage plane between the germinal layer and adventitia. 5. Alternatively, the cyst may be removed by liver resection or, when extensive, it may be marsupialized and filled with omentum. 3 - The treatment of hepatic hydatid cysts is primarily surgical. - In general, most cysts are treated, but in elderly patients with small, asymptomatic, densely calcified cysts, conservative management is appropriate. - In preparation for an operation, preoperative steroids have been recommended but are not universally used. The anesthesiologist has epinephrine and steroids available for the potential of an anaphylactic reaction. A number of operations have been used, but in general, the abdomen is completely explored, the liver mobilized, and the cyst exposed. Packing off of the abdomen is important because rupture can result in anaphylaxis and diffuse seeding. Usually, the cyst is then aspirated through a closed-suction system and flushed with a scolicidal agent such as hypertonic saline. The cyst is then unroofed, which can then be followed by a number of possibilities, including:  excision (or pericystectomy),  marsupialization procedures,  leaving the cyst open,  drainage of the cyst,  omentoplasty,  or partial hepatectomy to encompass the cyst. Total pericystectomy or formal partial hepatectomy can also be performed without entering the cyst. Radical (resection) and conservative (drainage and evacuation) surgical approaches appear to be equally effective at controlling disease, although a prospective comparison has never been done. When bile duct communication is diagnosed at operation or preoperatively, it must be meticulously sought out. Simple suture repair is often sufficient, but major biliary repairs, approaches through the common bile duct, or postoperative ERCP may be necessary. Laparoscopic techniques for drainage and unroofing of cysts have been reported in a number of series with encouraging results. - In the past, percutaneous aspiration of hydatid cysts was contraindicated because of the risk for rupture and uncontrolled spillage. - In recent years, however, a number of authors have reported percutaneous aspiration and injection of scolicidal agents with high success rates in highly selected patients. This technique is known as PAIR (puncture, aspiration, injection, and reaspiration) and has become more accepted in some institutions. Two randomized trials, one comparing PAIR to surgery (N=50) and one comparing PAIR to medical therapy, have shown similar success rates. These trials are small and have significant methodologic problems, limiting the ability to draw firm conclusions. Although surgery remains the treatment of choice, further prospective trials are clearly indicated to address this interesting and potentially useful technique. - Chemotherapy for echinococcosis with albendazole or mebendazole is effective at shrinking cysts in many patients with E. granulosus but cyst disappearance occurs in fewer than 50% of patients. - Preoperative treatment may decrease the risk for spillage and is a reasonable and safe practice. - Chemotherapy without definitive resection or drainage is only considered for widely disseminated disease or patients with poor surgical risk. 4 Essentials. Echinococcus Hydatid Cyst 5 LECTURE 13 Acute pancreatitis I. Etiopathogeny and physiopathology It is generally agreed that, no matter what the primary etiology in acute pancreatitis might be, the final common event is activation of pancreatic proenzymes into na

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