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benign biliary diseases.pptx
- 1. BENIGN BILIARY DISEASES PRESENTEDBY: DR. ANJALY MOHAN MODERATED BY: DR. PUNEET K AGARWAL
- 2. CONTENTS • GALL STONES(CHOLELITHIASIS) • EMPYEMA OF GALL BLADDER • ACALCULOUS CHOLELITHIASIS • CHOLECYTOSES • CHOLEDOCHOLITHIASIS • BILE DUCT STRICTURES • BILIARY DYSKINESIA
- 3. CONTENTS • SPHINCTER OFODDI DYSFUNCTION • PRIMARY SCLEROSING CHOLANGITIS • CHOLEDOCHAL CYSTS • PARASITIC INFESTATIONS OF BILIARY TRACT
- 4.
- 5. CHOLELITHIASIS • Most commondisease state of GB and biliary tract • Possible mechanisms: • Increase in solute concentration • Stasis in the GB • Types of gall stones: • Cholesterol stones • Pigment stones: black (hemolysis) and brown (infection)
- 7. • Factors thatpredispose to gallstones formation: • Supersaturation of secreted bile • Concentration of bile in GB • Crystal nucleation • Gallbladder dysmotility (stasis) Natural history: • Most GB stones are asymptomatic • Biliary colic : temporary obstruction of cystic duct, occurs after meal as release of CCK causes GB contraction
- 8. • Prophylactic cholecystectomyis not warranted in patients with asymptomatic cholelithiasis. Indications of prophylactic cholecystectomy: • Patients with hemolytic anemia (sickle cell disease) • Calcified (porcelain) GB • Large (>2.5cm) stones • Common bilio-pancreatic duct channel • Patients undergoing bariatric surgery • Immunocompromised patient before transplant
- 9. Medical management ofgall stones: • Generally unsuccessful and rarely used 1. Oral bile salt therapy 2. Contact dissolution • Cannulation of GB and infusion of organic solvents – 50% recurrence • Extracorporeal shock wave lithotripsy- (single stone upto 2cm size)
- 10.
- 11. • Recurrent attacksof biliary colic – inflammation and scarring of neck of GB and cystic duct – fibrosis • Repeated self limited episodes of inflammation Clinical presentation: • Pain after ingestion of a fatty meal • Located in epigastrium or RUQ • Radiate around the scapula • Lasts a few hours • Bloating, nausea and vomiting
- 12. Diagnosis: • Clinical history+ clinical manifestations • Transabdominal USG: may show • Presence of cholelithiasis • CBD dilatation • GB polyps • Porcelain GB • Evidence of hepatic parenchymal process • Cholesterolosis • GB sludge
- 13. • Treatment: • Electivecholecystectomy in severe/recurrent symptoms • Conservative management in mild cases
- 14.
- 15. Mechanism: • Stone causingblockage of cystic duct – non resolving type leading to inflammation – edema and subserosal haemorrhage – ischemia – necrosis – gangrene • Infection of the stagnant pool of bile – secondary phenomenon • When complicated by gas forming organisms: acute emphysematous cholecystitis
- 16. Presentation: • Fever • RUQpain • Tenderness to palpation & Guarding in RUQ • Positive Murphy’s sign – arrest of inspiration with gentle pressure under right costal margin • Mild elevation of alkaline phosphatases, bilirubin and transaminases level with leucocytosis support the diagnosis
- 17. • Diagnosis: • TransabdominalUSG: may show • Gallstones • Pericholecystic fluid collection • Gallbladder wall thickening • Sonographic Murphy’s sign • HIDA Scan: filling of gallbladder rules out acute cholecystitis • CT Scan: pericholecystic fluid collection, GB wall thickening & emphysematous changes. Though CT is less sensitive than USG
- 18. Treatment: • Most casesare infected with superinfection of the inflamed GB • Patients are started with NBM • Parenteral fluids and antibiotics (broad spectrum) • Parenteral narcotics to control pain • Cholecystectomy - treatment of choice for acute cholecystitis • Early vs delayed cholecystectomy – still debatable • In patients unfit for surgery, cholecystostomy should be considered
- 19.
- 20. • CBD Stonesare classified according to point of origin: • Primary: arises de novo in the bile duct, brown stones (bile pigments and cholesterol), more common in Asians and due to infection • Secondary: pass from GB into bile duct • Retained stones: if they are found within 2 year of cholecystectomy
- 21. Clinical presentation: • Clinicallysilent and usually identified on cholangiography, if performed routinely during cholecystectomy • When not silent, symptoms may range from biliary colic to obstructive jaundice • Jaundice with choledocholithiasis is usually painful – acute setting – dilatation of CBD – activation of pain fibres • Charcot’s triad: fever, RUQ pain, jaundice – suggests acute cholangitis – may progress to septic shock • Reynold’s pentad: triad + shock with altered mental status
- 22. Diagnosis: • Altered LFT:neither sensitive nor specific • Leukocytosis: in cases of superinfection • USG abdomen: bile duct stones or dilatation • Patients with jaundice, gallstones and biliary pain, a CBD diameter >8mm : highly suggestive of CBD stones • ERCP: highly sensitive and specific , diagnostic + therapeutic • MRCP: sensitivity (>90%), specificity (100%), non invasive, accurate imaging of the biliary tree
- 23. • Treatment: • ERCP:endoscopic sphincterotomy + stone extraction • Laparoscopic CBD exploration: cholecystectomy + intraoperative cholangiogram + CBD exploration (single setting) • Transcystic approach: via the cystic duct using a cholangioscope • Open CBD exploration: transduodenal sphincteroplasty, choledochoenterostomy (choledochoduodenostomy/-jejunostomy)
- 26. EMPYEMA OF GALLBLADDER • Can be a sequelae of acute cholecystitis or the result of an infected mucocele • GB is distended with pus • Optimal treatment is DRAINAGE (cholecystostomy followed by cholecystectomy)
- 27. ACALCULOUS CHOLECYSTITIS • Inflammationof gall bladder can occur even in the absence of gall stones • In non specific inflammation of GB or in one of the conditions of cholecytoses • Particularly seen in critically ill patients and in patients recovering from shock, burns, trauma • Often missed diagnosis • High mortality
- 28.
- 29. CHOLESTEROSIS • aka “strawberrygallbladder” • Mucosa of the gall bladder appears like a strawberry • Where the yellow specks corresponds to seeds of strawberry (submucous aggregation of cholesterol crystals and esters) • May be associated with cholesterol stones
- 30. CHOLESTEROL POLYPOSIS OFGB • USG may show a non mobile defect with no acoustic shadow • Differential can be an adenomatous polyp • Interval followup is indicated • Surgery indiacted if diagnostic dilemma
- 31. CHOLECYSTITIS GLANDULARIS PROLIFERANS •Polyp of mucus membrane is fleshy and granulomatous • All layers of GB may be thickened • Sometimes there may be an internal septa which separates hyperplastic from normal • Intraparietal mixed calculi may be present • Can be complicatd by intramural/ extramural abscess and fistula formation • Symptomatic patients treated with cholecystectomy
- 33. DIVERTICULOSIS OF GB •usually manifest as black pigment stones impacted in the outpouchings of the lacunae of Luschka • Demonstrated by cholecystography, especially when the gallbladder contracts after a fatty meal • small dots of contrast medium just within and outside the gallbladder • septum may also be present, to be distinguished from the Phrygian cap • The treatment is cholecystectomy
- 35. TYPHOID INFECTION OFGB • Salmonella typhi or typhimurium • Acute cholecystitis can occur • More frequently, chronic cholecystitis occurs • Patients become typhoid carrier secreting bacteria in the bile • Gall stones may be present • Salmonella can be cultured from these stones • Treatment with Ampicillin and cholecystectomy • In penicillin allergy, give flouroquinolones
- 36.
- 42. • ERCP withsphincterotomy, balloon dilation, and stent placement is generally regarded as primary treatment for benign bile duct strictures • Endoscopic and percutaneous therapy can provide long-term success in more than 50% of patients • When this is unsuccessful, surgical management with anastomosis of the biliary tree to a Roux-en-Y jejunal limb has success rates of up to 90%
- 44.
- 45. • may presentwith classic symptoms of calculous biliary disease • but have no ultrasonographic evidence of stones or sludge • dysfunction of the gallbladder creates pain, even in the absence of stones • These patients will have other diagnoses excluded by CT and upper endoscopy and should undergo a CCK-stimulated HIDA scan, in which the radiolabeled iminodiacetic acid will collect in the gallbladder
- 46. • patient isgiven an IV dose of CCK • An ejection fraction less than one third at 20 minutes after CCK administration in patients without stones is considered diagnostic of dyskinesia, • which should be managed with cholecystectomy • In nonresponders, ERCP with sphincterotomy may prove useful
- 47.
- 48. • manifested asbiliary tract pain, with normal liver function test results and recurrent pancreatitis • May be caused by a structurally abnormal sphincter or a histologically normal but functionally abnormal one • injury to the sphincter from trauma, due to pancreatitis, gallstone passage, or congenital anomalies – inflammation – fibrosis – elevated sphincter pressure • diagnosis of sphincter of Oddi dysfunction should be suspected in patients with biliary pain and a common duct diameter of more than 12 mm
- 49. • Manometry hasalso been used to make the diagnosis, with sphincter pressure higher than 40 mm Hg predicting good response to therapy • Therapy consists of endoscopic sphincterotomy or transduodenal sphincteroplasty, with approximately equivalent results from the two approaches • In patients with objective evidence of sphincter of Oddi dysfunction, division of the sphincter will improve or resolve the pain in 60% to 80% of patients
- 50.
- 51. • idiopathic, likelyautoimmune process affecting the intrahepatic and extrahepatic biliary trees • associated with other autoimmune diseases, such as ulcerative colitis and Riedel thyroiditis • the disease causes inflammation and scarring in the biliary tree • characterized by progressive chronic cholestasis and advances at an unpredictable rate to biliary cirrhosis and eventually death from liver failure • The microscopic picture is one of inflammation, fibrosis, and cholestasis
- 52. • Clinical Presentation: •fatigue, pruritus, and jaundice • Asymptomatic elevations of alkaline phosphatase levels can also occur and may be associated with evidence of hepatocellular injury and hyperbilirubinemia before clinical manifestations of symptoms • Abnormal liver function tests in a patient observed for inflammatory bowel disease should suggest PSC • Elevation of perinuclear antineutrophil cytoplasmic antibodies can be seen in 80% of patients
- 53. • ERCP isthe preferred route for cholangiography and can demonstrate the characteristic multifocal, diffusely distributed dilations and strictures of the intrahepatic and extrahepatic biliary trees • The sequential stricturing, proximal dilation, and more proximal stricturing create a pattern described as beading or chain of lakes • Other cholangiographic findings include multiple diverticulum-like outpouchings of the bile ducts and multiple short-segment strictures • Liver biopsy tends to show an onion skin concentric periductal fibrosis • With disease progression, periportal fibrosis occurs, progressing to bridging necrosis and eventually biliary cirrhosis
- 56. • Treatment: • Nospecific effective medical therapy exists for PSC • Early in the disease, with mild symptoms, observation is a reasonable approach • Medical therapies are generally targeted to the underlying hepatobiliary disease process; • these include choleretic agents such as ursodeoxycholic acid, immunosuppressive agents, and antifibrogenic agents such as colchicine • However, none of these agents has shown a consistent benefit
- 57. • Surgical optionsinclude biliary reconstructive procedures and liver transplantation • Biliary reconstruction is an option for patients with a dominant stricture at the hepatic bifurcation, for which resection of this region with long-term Silastic stenting can be performed • Orthotopic liver transplantation appears to be the only lifesaving option for patients with progressive hepatic dysfunction from PSC • 5-year survival rates ranging from 75% to 85%
- 58. Immunoglobulin (IgG4) relatedcholangitis • presents with diffuse or segmental narrowing of the intra- or extrahepatic bile ducts • patients often have elevated serum IgG4 levels and concomitant autoimmune pancreatitis, IgG4- related sialadenitis or retroperitoneal fibrosis • Biliary biopsies show lymphoplasmacytic sclerosing cholangitis • Treatment is with systemic steroids
- 59.
- 60. • rare, occurringin fewer than 1/100,000 patients • more common in Asian descent • three to eight times more common in women than in men • Considered premalignant and thus requires surgery • Commonly diagnosed in infancy, but many present in adulthood • Pathogenesis relies on the presence of an anomalous pancreaticobiliary junction (APBJ)
- 61. • With APBJ,the pancreatic duct and biliary tree fuse to form a common channel before passage through the duodenal wall • APBJ is seen in up to 90% of patients with choledochal cysts • Pancreatic duct has higher secretory pressures than the biliary tree, exocrine pancreatic secretions reflux up into the bile duct and can inflame and damage the biliary tree, resulting in cystic degeneration
- 63. • Presentation: • classicpresentation of jaundice, right upper quadrant pain, and a palpable mass occurs rarely • Other symptoms include nausea, pruritus, and weight loss • Long standing disease can induce a chronic injury to the liver with cirrhosis • Cholangitis, pancreatitis, hepatic fibrosis, and malignant disease have all been reported at the time of presentation • An unusual presentation is that of acute rupture of the cyst, with subsequent bile peritonitis
- 64. • Most cysticbiliary lesions are originally identified and subsequently diagnosed by imaging • With the current liberal use of CT, the diagnosis of a choledochal cyst is suspected, but it is further classified by MRCP • ERCP is more useful for defining the distal biliary tree and pancreatic duct–bile duct junction • Laboratory studies may identify cholestasis and jaundice • In late stages of disease, secondary hepatic injury and evidence of cirrhosis may be seen
- 65. • incidence ofmalignant disease in patients with biliary cysts ranges from 10% to 30% • Malignant cyst degeneration is common and is thought to relate to chronic mucosal irritation from the refluxed pancreatic enzymes • Surgical management of choledochal cysts consists of resection of the entire cyst and appropriate surgical reconstruction • Type I cysts: complete surgical excision, cholecystectomy, and Roux-en-Y hepaticojejunostomy • Type II cysts should be excised entirely, and in the presence of an APBJ, biliary-enteric diversion by Roux en- Y hepaticojejunostomy is appropriate
- 66. • Type IIIcysts are uncommon and may be approached transduodenally • In the setting of duodenal or biliary obstruction, transduodenal excision or sphincteroplasty can be performed • Type IV cysts affecting only the extrahepatic bile ducts are managed similarly to type I cysts, with excision and hepaticojejunostomy • Those with intrahepatic extension involving only one lobe can be treated with partial hepatectomy and reconstruction • Surgical treatment of Caroli disease ranges from resection if the disease is unilobar to liver transplantation when diffuse disease is detected
- 67. POLYPOID LESIONS OFGALL BLADDER
- 68. Benign masses ofthe gallbladder are common and consist of: • Pseudotumors • Adenomas • Pseudotumors are further divided into cholesterol polyps and adenomyomatosis • Cholesterol polyps appear as pedunculated echogenic lesions of the gallbladder, are usually smaller than 1 cm, and are frequently multiple
- 69. • Adenomyomatosis isseen as a sessile lesion, commonly in the fundus, with characteristic microcysts within the lesion, and is frequently larger than 1 cm • Polyps with size larger than 10 mm is a risk factor for adenocarcinoma, along with growth, presence of gallstones, and age of the patient older than 60 years • Management of all symptomatic polypoid lesions of the gallbladder is laparoscopic cholecystectomy
- 70. • Patients witha polypoid lesion and risk factors for adenocarcinoma or those suspected of having in situ or invasive cancer should undergo open cholecystectomy • because perforation during laparoscopy may spread tumor cells throughout the peritoneal cavity • Asymptomatic lesions smaller than 10 mm with no other risk factors and no ultrasonographic features suggesting malignant disease can be observed with serial ultrasonography
- 71. PARASITIC INFESTATION OFTHE BILIARY TRACT
- 72. BILIARY ASCARIASIS • Theroundworm Ascaris lumbricoides commonly infests the intestines of inhabitants of Asia, Africa and Central America • may enter the biliary tree through the ampulla of Vater and cause biliary pain • Complications include strictures, suppurative cholangitis, liver abscesses and empyema of the gallbladder • antispasmodics can be given to relax the sphincter of Oddi and the worms will return to the small intestine to be dealt with by anti helminthic drugs
- 73. • Operation maybe necessary to remove the worms or deal with complications • Worms can be extracted via the ampulla of Vater by ERCP
- 74. CLONORCHIASIS (ASIATIC CHOLANGIOHEPATIS) • endemicin the Far East • The fluke, up to 25 mm long and 5 mm wide, inhabits the bile ducts, including the intrahepatic ducts • Fibrous thickening of the duct walls occurs • Many cases are asymptomatic • Complications include biliary pain, stones, cholangitis, cirrhosis and bile duct carcinoma
- 75. • Choledochotomy andT-tube drainage and, in some cases, choledochoduodenostomy are required • Because a process of recurrent stone formation is set up, a choledochojejunostomy with a Roux loop fixed to the adjacent abdominal wall is performed in some centres to allow easy subsequent access to the duct system
- 76. Hydatid disease ofbiliary system • A large hydatid cyst may obstruct the hepatic ducts • Sometimes, a cyst will rupture into the biliary tree and its contents cause obstructive jaundice or cholangitis, requiring appropriate surgery
- 77. REFERENCES • LOVE ANDBAILEY, 27TH EDITION • SABISTON TEXTBOOK OF SURGERY, 20TH EDITION • MAINGOT’S ABDOMINAL OPERATIONS, 12TH EDITION • INTERNET
- 78.