Gallbladder

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Gallbladder (1) Shape  Pear-shaped. (2) Length  7.5 to 12.5 cm. (3) Capacity  About 50 ml, but capable of considerable distension. (4) Anatomical subdivisions  A fundus, a body & a neck which terminates in narrow infundibulum. (5) Muscle fibres of gallbladder wall  Arranged in.a crisscross manner, being esp. well developed in neck. (6) Mucus memb.  Contains indentations of mucosa, that sinks into muscle coat, called crypts of Luschka. Duct System (1) Cystic duct (a) Length  About 2.5 cm. (b). Connects Infundibulum of gallbladder to common hepatic duct to form bile duct. (c) Contains  Spiral valve of Heister. (2) Common hepatic duct (a) Length Less than 2.5 cm. (b) Formed by Union of right & left hepatic ducts. (3) Bile duct (a) Length  About 7.5 cm. (b) Formed by  Union of cystic & common hepatic ducts. (c) Parts  Four (i) Supraduodenal portion  About 2.5 cm long runs in free edge of lesser omentum. (ii) Retroduodenal portion, (iii) Infraduodenal portion  Lies in a groove, but at times in a tunnel on posterior surface of pancreas (iv) Intraduodenal portion Passes obliquely thru the wall of 2nd part of duodenum where it is surrounded by sphincter of Oddi. It terminates by opening on summit of papilla of Vater. Arterial Supply Of Gallbladder (1) Cystic artery, a branch of right hepatic artery, which is usually given off behind the common hepatic duct. (2) Accessory cystic artery, from gastroduodenal artery (occasional). Variations (1) Right hepatic artery &/or cystic artery cross in front of common hepatic duct & cystic duct. (2) Hepatic artery takes a tortuous course in front of origin, of cystic duct, or right hepatic artery is tortuous & cystic artery is short. (Tortuosity is known as 'caterpillar turn' or “Moynihan's hump”.) Lymphatics (1) Subserosal & submucosal lymphatics drain into cystic lymph node of Lund,


which lit in the fork created by junction of cystic & common hepatic ducts  Nodes at hilum of liver Celiac lymph nodes. (2) Subserosal lymphatics also connect with subcapsular lymphatics of liver. INVESTIGATION OF THE BILIARY TRACT Ultrasonography It is noninvasive & is now the gold standard imaging technique for the investigation of gallstone, & is also the prime investigation for jaundice; (1) It demonstrates biliary calculi, size of gallbladder, thickness of gallbladder wall, presence of inflammation around the gallbladder, size of common bile duct &, occasionally, the presence of stones within the biliary tree. (2) It also show a carcinoma of the pancreas occluding the common bile duct. Plain Radiograph It shows radio-opaque gallstones in 10% of patients, calcification of the gall bladder (porcelain gall bladder), & limey bile. Oral Cholecystography (Graham-Cole Test). Though discarded, it is still used to show diverticulae & polyps, & to assess gallbladder function. Intravenous Cholangiography Biligram (meglumine ioglycamate) is given intravenously, which is rapidly secreted by the liver into the biliary tree. Subsequent radiography clearly defines the ducts & the adder delineating the presence of stone disease. Radioisotope Scanning Techietium-99m labeled derivatives of imino-diacetic acid A, PIPIDA) arc excreted in the bile & are used to visualize biliary tree. Computerized Tomography (CT) only value is in staging of carcinoma of the gallbladder or ducts, to define its extent, the presence of lymphadcno-y &. the presence of metastases. Magnetic Resonance Cholangiopancreatography Now becoming the standard technique for investigation of biliary tree; a clear outline of the biliary tree can demonstrated with the detection of bile-duct stones. Endoscopic Retrograde Cholangiopancreatography (ERCP) Ampulla of Vater is cannulated with the aid of a fibre-optic endoscope, & the bile ducts are visualized after injecting water-soluble contrast. Bile can be sent for cytological & microbiological examination, & brushing: taken from strictures for cytological studies. Therapeutic procedures can be performed eg, removal of stones & stenting of strictures.


Percutaneous Transhepatic Cholangiography (PTC) 1) Under fluoroscopic control. the Chiba or Okuda needle is advanced into the,liver thru & 8th intercostal space in the mid-axillary line to a point about 2 cm short of the right margin of the vertebral column. The stilette is then removed & while injecting contrast e.g. meglumine iothalamate) the needle is slowly withdrawn until contrast is seen entering a bile radical. 2) It enables placement of a catheter into the bile ducts to provide external biliary drainage or the insertion of indwelling stents. Catheter can be left in situ, for later choledochoscopy in order to diagnose strictures, take biopsies & remove stones. Peroperative Cholangiography During cholecystectomy a catheter is placed in the cystic duct & contrast injected into the biliary tree. Subsequent imaging will defines the anatomy & confirms the presence or absence of stones. Operative Biliary Endoscopy (Choledochoscopy) At operation a flexible Fibre-optic endoscope is passed down the cystic duct into CBD, enabling stone identification & removal under direct vision. CONGENITAL ANOMALIES

BILIARY ATRESIA Etiology Unknown; may be the result of an inflammatory process possibly viral in origin. Types (1) Correctable lesion Variable lengths of biliary tree are occluded, but a patent portion of extrahepatic duct communicates with intrahepatic ducts. (2) Non-correctable lesion No such communication exists. Clinical Features Symptoms (1) Initially bile-stained meconium, & later pale stools. (2) Dark urine. (3) Steatorrhea, which gives rise to biliary rickets. (4) Severe pruritus. Signs (1) Jaundice, present at birth or appear by the end of 1st week, & deepens progressively. (2) Clubbing. (3) Skin xanthomas.


Diagnostic Investigations (1) Liver function tests Point towards obstructive jaundice e.g., a high alkaline phosphatase with low transaminase levels. . (2) Radioisotope scanning Reveal nonvisualization of biliary tree & failure of isotope to reach intestine. (3) Cholangiography at laparotomy Confirm the diagnosis. Treatment (1) In correctable lesion A Roux en Y jejunal loop is anastomosed to patent portion of extrahepatic biliary tree communicating with intrahepatic ducts. (2) In non-correctable lesion Hepatic portojejunostorriy Fibrous tissue, where hepatic ducts should leave the liver at porta hepatis, is dissected free & divided flush with liver capsule. To this areas a loop of jejunum is anastomosed. CHOLEDOCHAL CYST It is due to a specific weakness in a part, or whole of wall of common bile duct. Commonest type is a fusiform dilatation of CBD. Clinical features Usually appear at the age of 6 months.but may be delayed for upto 20 years: (1) Attacks of jaundice of obstructive type (2) Upper abdominal pain (3) Pyrexia (4) A swelling in upper abdomen Diagnostic investigations (1) Intravenous cholangiography (2) Ultrasound Treatment Cyst should be excised, & a choledochojejunostomy performed. OTHER ANOMALIES (1) Absence of gallbladder (2) Phrygian cap (3) Floating gallbladder Organ hangs on a mesentery, which makes it liable to undergo torsion. (4) Double gallbladder Gallbladder is twinned, one of which may be intrahepatic. (5) Absence of cystic duct (6) Low insertion of cystic duct Cystic duct opens into common duct near ampulla.


(7) Accessory cholecystohepatic duct It may open into gallbladder, & cause leakage after cholecystectomy. CHOLELIATHASIS (GALLSTONES) CLASSIFICATION (1)Cholestrol Stones It consists almost entirely of cholesterol and are often solitary large and smooth. (2)Mixed stones (a) Cholestrol is the major component (b) Other components include Ca bilirubinate,Ca phosphate,Ca carbonate,Ca palmitate,& proteins. (c) Usually they are multiple & often faceted. (3) Pigment stones (a) Composed almost entirely of Ca bilirubinate. (b) They are mostly small, black. & multiple. (c) Some are hard & coral-like, while others are soft like concretions of sludge. ETIOLOGY Predisposing Factors 1)Fat 2)Fertile 3)Flatulent 4)Female 5)Forty Exciting Factors For cholesterol & mixed stones (J) Metabolic Supersaturated or lithogenic bile  Bile has an excess of cholesterol relative to bile salts & phospholipids, thus allowing cholesterol crystals to form. (a) Conditions increasing bile cholesterol (i) Aging (ii) Women, esp. those taking contraceptive pills (iii) Obesity (iv) Clofibrate (b) Conditions decreasing bile salts in bile (i) Estrogen (ii) Ileal disease (iii) Resection or bypass of ileum (iv) Cholestyramine therapy (2) Infection Often bile from patients with gallstones is sterile, but organisms have been isolated from gallstones; the radiolucent centre may represent mucus plugs derived from bacteria (Moynihan 's aphorism).


(3) Bile stasis Gallbladder contractility is reduced by; (a) Estrogens (b) Pregnancy (c) Truncal vagotomy (d) Long-term parenteral nutrition For pigment stones (1) Hemolytic disorders, in which bilirubin production is increased, e.g. in (a) Hereditary spherocytosis (b) Sickle-cell anemia (c) Thalassemia. (d) Malaria (e) Mechanical destruction of RBCs by prosthetic heart valves Benign & malignant strictures of biliary ducts. Cirrhosis (4) Infestation of biliary tree by Ascaris lumbricoides & Clonorchis sinensis. (5) E coli infection -» This bacterium produces (5- glucuronidase which converts bilirubin into its unconjugated, insoluble form. COMPLICATIONS (CLINICAL EFFECTS) OF CHOLELITHIASIS (A) In the gallbladder (1) Silent stones (2) Chronic cholecystitis (3) Acute cholecystitis (a) Gangrene, (b) Perforation (c) Empyema (4) Mucocele (5) Carcinoma of gallbladder (B) In the bile ducts (1) Obstructive jaundice (2) Cholangitis (3) Acute pancreatitis (C) In the Intestine Acute intestinal obstruction (gallstone ileus) CHOLECYSTITIS Chronic & acute calculous cholecystitis are. part of the same spectrum of disease & are caused by inflammation within the gallbladder secondary to obstruction of the. cystic duct by stones. CLINICAL FEATURES Symptoms (1) Pain (a) Site  Right hypochondrium. (b) Radiation Back & shoulder. (c) Onset


(i) Chronic attack begin after eating, but not so closely related as peptic ulcer. It begins gradually 15-30 min. after meal & last for 30-90 min. (ii) Acute attack begin suddenly, or Superimposed on pain of chronic cholecystitis (d) Duration (i) Chronic attack lasts for less than' 12 hours, & is characterized by episodes of pain, (ii) Acute attack lasts for more than' 12 hours. (e) Severity  Varying; mild discomfort to excruciating. (f) Precipitated by Fatty foo<f(chronic)i & movement & breathing (acute). (g) Relieved by  Nothing, except analgesic drugs, (h) Associated factors  Nausea & vomiting; in acute attack fever with rigors may be present. (2) Flatulent dyspepsia It is a feeling of fullness after food associated with belching & heartburn. It is brought on by a large'or a fatty meal. Signs (1) General signs Present in acute cholecystitis; (a) Patient is distressed, & lies quietly, breathing shal-lowly. (b) Tachycardia 90-100 beats/min. (c) Pyrexia 100-102 °F, & there may be rigors. (2) Local signs (a) Tenderness in right hypochondrium, just below the tip of 9th rib where edge of rectus abdominis muscle crosses the costal margin (gallbladder point). (b) Rigidity in right hypochondrium (acute). (c) Murphy's sign May be positive.This is elicited by asking the patient to breathe in whilst gently pressing the gallbladder point with your thumb pointing towards feet. Patient will experience pain & catch her breath just before the zenith of inspiration. (d) A mass, consisting of inflamed gallbladder with adherent omentum attached, may be felt (acute). (e) Boas's sign may be-present There is an area of hyperesthesia between 9th & 11 th ribs posteriorly on right side (acute). DIAGNOSTIC INVESTIGATIONS (1) Ultrasonography Show the presence of stones (acoustic shadow) in an inflamed gallbladder with edema around the gallbladder ,-v wall; also demonstrates biliary calculi & dilatation of biliary tree. (2) Plain x-ray abdomen Show radio-opaque gallstones (3) Oral cholecystography (QCG) Presence of gallstones can be detected (filling defects). (4) CTscan Useful for patients in whom U/S is difficult eg, obese or those with excessive bowel gas.


(5) Percutaneous transhepatic cholangiography (PTC), or peroperative cholangiography To detect associated duct stones. TREATMENT Treatment Of Acute Cholecystitis (1) Conservative treatment followed by cholecystectomy (a) Nasogastric aspiration. (b) Intravenous fluids. (c) Analgesics. (d) Antibiotics  A broad-spectrum antibiotic effective against G-vc aerobes is most appropriate, eg. cephazolin, (cefamezin), ccfuroxime (zinacef). or gentamicin. (e) When the inflammation is subsiding usually by 3rd day, nasogastric tube is removed, & fluids followed by fat-free diet are given. (f) Cholecystectomy may either be performed on the next available, list, or the patient is sent home to return 6 weeks later (when the inflammation has completely resolved). (2) Routine early operation Good results are obtained, if operation is undertaken within 48 hours of onset of attack. Treatment Of Cholelithiasis & Chronic Cholecystitis Non-SurgicalTreatment (1) For pain (a) Analgesics may. be given. Severe pain require opiates, which is given alongwith hyoscine butylbro-mide (to counteract spasm of sphincter of Oddi). (b) Patient should be put on low-fat diet until cholecystectomy. (2) Medical dissolution of gallstones Gallstones can be dissolved as long- as they are radio-lucent & gallbladder is functioning. Drugs (a) Bile acids. (b) Chenodeoxycholic acid  15 mg/kg/day for 6 months. However, it may causes diarrhea. (c) Ursodeoxycholic acid (Urosofalk)  10 mg/kg/day for 6 months. (3) Local dissolution of gallstones Methyl ter-butyl ether (MTBE) is a powerful organic solvent which dissolves cholesterol gallstones within hours; (a) It is administered locally via a pigtail or other self-retaining catheter introduced percutaneously into the GB under radiological control. (b) When dissolution is achieved, the GB liquid contents are aspirated & the catheter removed. (4) Lithotripsy (a) Extracorporeal shock waves/produced by spark-gap (Dornier system), piezoceramic (Wolf system) or electromagnetic (Siemens system) generators are


focused by a concave reflector & targeted under ultrasound guidance to the stones, thereby inducing fragmentation; the debris pass into bile duct beyond. It is suitable for patients with 1 -3 stones in a functioning gallbladder, (b) Alternatively, a rotary mechanical lithotripter (Kinsey-Nash) can be inserted percutaneously under radiological control into GB. which fragments the calculi. SurgicalTreatment Preparation for operation (1) Prophylactic antibiotics e.g. 2nd-generation cephalosporin. (2) Premedications. (3) Provision is made for peroperative cholangiography. Operative choices (1) Open cholecystectomy (a) Incision  Right paramedian, or right subcostal incision (Kocher's incision). (b) Examine  All abdominal organs, including gallbladder. (c) Isolate the gallbladder area with packs. (d) Aspirate the gallbladder if it greatly distended, thru fundus via trocar & cannula attached to a suction apparatus. (e) Grasp the neck of gallbladder with sponge-holding forceps. (f) Display the junction of cystic, common hepatic & bile ducts via dissection, & identify cystic artery & its relation to common hepatic duct, (g) Cholangiography is performed, to confirm the anatomy of biliary tree, & to check for stones in main ducts, (h) Ligate the cystic duct, & then divide it. (i) Dissect the gallbladder from its bed, from below & upwards, dividing the peritoneum on gallbladder, (j) Secure hemostasis, & close the abdominal wall, (k) Drainage is not-mandatory; if used, it should be a 3 mm closed suction,drain. With severe inflammation in Calot's triangle (a) Open the gallbladder, extract all stones & bile, & excise as much of wall of gallbladder as possible. Cystic duct opening is closed by catgut suture from within. (b) An alternative is cholecystostomy. (2) Laparoscopic cholecystectomy (a) Patient is placed in the supine position with the table tilted 20° reversed Trendelenburg. (b) Pneumoperitoneum is created & four ports are placed in the abdomen, usually at the umbilicus & the epigastrium (10-mm ports), with two 5-mm ports laterally. (c) Calot's triangle is laid widely open by dividing the peritoneum on the posterior & on the anterior aspect. (d) Cystic duct is carefully defined as is the cystic artery; both are clipped & divided. (e) Gallbladder is then removed from the gall bladder bed & once free removed via the umbilical or epigastric port. (3) Minicholecyslectomy (4) Cholecystostomy (a) 2 stay sutures arc inserted on either side of fundus of gallbladder.


(b) Fundus is opened & stones are removed from interior by Desjardin's forceps, aided by a finger milking up a stone or stones from Hartmann's pouch. (c) A large Foley catheter is placed in gallbladder & balloon inflated. (d) Opening in gallbladder is closed about the tube. (e) Catheter is brought to surface thru a separate stab incision If) Abdominal incision is closed & catheter is connected to a sterile bag. (g) 7-10 days later, cholangiography is performed via catheter & if no obstruction exists, catheter is removed. (5) Percutaneous cholecystolithotnmy CHOLEDOCHOLITHIASIS (STONES IN THE CBD) ETIOLOGY (1) Originate in gallbladder, & pass down the cystic duct. (2) Form.in the ducts itself, called primary duct stones. It may be secondary to: (a) Infestation of biliary tree by Ascaris lumbricoides or Clonurchis sinensis. (b) Conditions causing prolonged biliary obstruction. CLINICAL FEATURES Symptoms (1) Patient may be asymptomatic. (2) Charcot's triad Indicate acute cholangitis: (a) Pain  Similar to pain of cholecystitis. (b) Jaundice  Intermittent or persistent. & obstructive in type (dark urine, pale stools. & pruritus). (c) Fever & rigors. DIFFRENTIAL DIAGNOSIS OF OBSTRUCTIVE JAUNDICE A) Non surgical causes 1)Drugs 2) Alcohol 3)Viral hepatitis 4) Primary bilary cirrhosis B) Surgical causes 1)Choledocholithasis 2) Carcinoma of pancreas 3) Carcinoma of bile duct 4) Stictures of bile duct

Signs (1) Tenderness in epigastrium & right hypochondrium. (2) Gallbladder is impalpable (Courvoisier's law - in obstruction of bile duct due to a stone, distension of the gall bladder seldom occurs: the organ usually is already shrivelled. In obstruction from other causes(CA distension is common). painless enlargement of the gallbladder with jaundice is likely to result from


carcinoma of the head of the pancreas and not from a stone in the common duct, because in the latter the gallbladder is usually scarred from infection and does not distend. Syn: Courvoisier sign. DIAGNOSTIC INVESTIGATIONS (1) Liver function tests Alkaline phosphatase level is greatly increased, while serum aminotransferase level may rise up to 5- folds. (2) Ultrasonography Shows the site of stone in bile ducts, & helps to exclude other surgical causes of jaundice. (3) Endoscopic retrograde cholangiopancreatography (ERCP) Differentiates surgical from medical causes of jaundice. (4) Percutaneous transhepatic cholangiography (PTC) TREATMENT Pre-operativeTreatment (1) Treat liver failure if present-> High intake of glucose to build up store of liver glycogen, (2) Vit K 10 mg (IM or IV) or fresh frozen plasma, to correct clotting derangements. (3) Blood cultures are taken. & broad-spectrum antibiotics are given if there is cholangitis. (4) Renal failure must be prevented, as patients with obstructive jaundice esp. if subjected to operation, are prone to renal failure: (a) Avoid dehydration. (b) Start intravenous fluids (dextrose 5%) 12 hours . before an operation to ensure an urine output of 30 ml/hr. (c) Mannitol. IV, may be given. Minimally InvasiveTechniques (1) Endoscopic papillotomy It is the preferred first technique with a sphincterotomy, removal of the stones using a Dormia basket or the placement of a stent if stone removal is not possible. (2) Percutaneous treatment Percutaneous transhepatic cholangtogram can be performed to provide, drainage & subsequent percutaneous choledochoscopy. Operations (1) Supraduodenal choledochotomy (a) Abdomen is opened by right paramedian, or Kocher's incision. (b) Dissect the biliary tree. (c) If a stone can be felt, manoeuvre it into a position midway between entrance of cystic duct & superior border of duodenum. (d) Stone is steadied between finger & thumb, & duct is opened longitudinally directly on to stone, which is then removed by a malleable scoop or Desjardins' forceps.


(e) Interior of duct is explored upwards & downwards with the scoop for further stones. (f) Drainage of bite duct is carried out by means of a T-tube. Transverse limb is inserted in duct which is closed snugly about the vertical limb. Vertical limb is brought out thru a separate stab wound laterally. Postoperative care (a) Note the character & amount of bile draining from the tube (which is collected in aplastic bag). (b) After 8th day tube may be clamped for increasing periods, & absence of pain & jaundice, & presence of bile in stools indicate satisfactory flow into duodenum. (c) Cholangiography is performed, & if there are no filling defects in a well-outlined duct & contrast enters duodenum freely, then T-tube can be removed. (2) Transduodenal sphincterotomy Duodenum is opened in its 2nd part between stay sutures, & papilla & sphincter are divided at 10 o'clock. (3) Choledochoduodenostomy STRICTURE OF BILE DUCT ETIOLOGY (1) Surgical trauma (postoperative) (2) Stones (3) Primary sclerosing cholangitis (4) Carcinoma of bile duct (5) Carcinoma of head of pancreas Postoperative Stricture It is the result of a preventable error in technique, during the performance of cholecystectomy: (!) Blind plunge application of a hemostat to a bleedingcys-tic or accessory cystic artery, or to right hepatic artery. (2) Should cholecystectomy be performed by dissecting from fundus, loo much traction'applied to freed gallbladder may so tent the bile duct that any forceps intended for cystic duct grasp anguiated main channel. (3) Failure to identify anatomy in Calot's triangle when there is much inflammation. Common hepatic duct is tied instead of cystic duct. (4) Ignorance of anatomical anomalies of bile ducts. (5) Laceration of bile duct while exploration for stones. (6) Injury to bile duct during partial gastrectomy. CLINICAL PRESENTATION OF POSTOPERATIVE STRICTURE (1) Bile duct injuries may be recognized at the time of surgery. (2) Postoperatively by: (a) Profuse & persistent discharge of bile if drainage has been provided. (b) Bilary peritonitis if drainage has not been provided. (c) Deepening obstructive jaundice.


DIAGNOSTIC INVESTIGATIONS (1) Ultrasound (2) Cholangiography via a T-tube if present (3) ERCP (4) Transhepatic cholangiography TREATMENT Pre-operativeTreatment Temporary, external biliary drainage, by passing a cathete, percutaneously into an intrahepatic duct, or by passing a cath eter thru strictures at ERCP & left to drain into duodenum. Operations , (1) Roux en Y choledochojejunostomy (2) Cholecystojejunostomy (3) Choledochoduodenostomy (4) Insertion of a stent CARCINOMA OF GALLBLADDER ETIOLOGY Unknown; however. 90% of patients have cholelithiasis. PATHOLOGY Incidence, (1) Age  70s (2) Female: male ratio  5:1 Types (1) Scirrhous carcinoma (2) Squamous cell carcinoma (3) Mixed squamous-adenocarcinomas Spread (1) By direct invasion of liver & porta hepatis. (2) By lymphatics to hilar lymph nodes. (3) By veins to liver. CLINICAL FETURES Tumor found at cholecystectomy. Acute cholecystitis or a mucocele, when tumor obstructs cystic duct. Obstructive jaundice. A palpable mass in right hypochondrium. TREATMENT (1) On diagnosis at cholecystectomy & if confined to mucosa  Wide excision with resection of adjacent liver & lymph nodes. (2) In other cases, palliation only is possible via chemoradiotherapy. (3) Jaundice may be relieved by a stent.


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