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Acute and Chronic Gallbladder and Acute and Chronic Gallbladder and

Acute and Chronic Gallbladder and - PowerPoint Presentation

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Acute and Chronic Gallbladder and - PPT Presentation

Biliary Tract Disease Omer Basar MD To be continued QUESTIONS MuseeRodin1 jpg Gallbladder C arcinoma Risk factors Gallstone gt 3cm Adenomatous GB polyps gt 1 cm ID: 1012063

bile biliary patients duct biliary bile duct patients stones ercp pancreatitis pain obstruction cholecystectomy acute liver jaundice stone endoscopic

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1. Acute and Chronic Gallbladder and Biliary Tract Disease Omer Basar, MD

2. To be continued….

3. QUESTIONSMusée_Rodin_1.jpg

4. Gallbladder CarcinomaRisk factors:Gallstone > 3cmAdenomatous GB polyps > 1 cmPorcelain GBChronic S. Typhi carrier stateXanthogranulomatous cholecystitisAnomalous pancreaticobiliary junctionPatients with PSC

5. Biliary ColicIntermittent obstruction of the cystic duct, NO inflammation of the gallbladder

6. Moderately severeEpigastric and RUQ painSudden onset, growing in intensity over 15 minutes, remaining constant for 1-3 minutes (comes and goes but constant pain, not colicky)and resolves slowly in up to 3 hoursRadiates to inter-scapular regionNausea commonUsually after heavy mealA positive reaction to analgesics

7. Normal PENormal LabsUS is usually diagnosticAfter initial attack 10-30% have NO further SxRemainder are at high risk of developing Sx Gas, Bloating FlatulenceDyspepsia}are NOT related to stones

8. How is a patient with biliary colic treated? Biliary colic should be treated with nonsteroidal anti-inflammatory drugs (e.g. diclofenac, indomethacin) In addition, spasmolytics (e.g. butylscopolamine) for severe symptoms, opioids (e.g. buprenorphine) may be indicated

9. Impacted stone in the bile duct, inflammation of GB mucosa, ischemia 2/2 dilation of GB, secondary bacterial infection in 50%Acute Cholecystitis

10. Severe localized pain in RUQ, back and right shoulderNausea with some emesis is commonPain lasting >3-6hr favors Acute Cholecystitis over biliary colic

11. Febrile but usually, <102F unless complicated by gangrene/perforation(+) Murphy singWBC 12-15K, normal LFTs, normal T BiliUS, HIDA scan50% resolve spontaneously in 7-10 days If left untreated 10% complicated by perforation / peritonitis

12. Are antibiotics indicated in acute cholecystitis? Antibiotics in mild acute cholecystitis are NOT recommended at all times Unless: cholangitis, bacteriemia/sepsis, abscess perforation

13. Intermittent obstruction of CBDCholedocholithiasis

14. Often asymptomaticif symptomatic it is indistinguishable from colicJaundice + pain favor stonePainless jaundice + palpable GB favor malignancyIf Tbili > 4 suspect stone, if > 10 suspect malignant obstruction ERCP or PTC

15. ASGE strategy to assign risk of CBD stone in patients with symptomatic cholelithiasisPredictors:Very strongCBD stone on imagingClinical ascending cholangitisBilirubin > 4mg/dlStrongDilated CBD (>6mm) on US with (GB in situ, no surgery)Bilirubin level 1.8 - 4 mg/dlModerateAbnormal liver biochemical test other than bilirubinAge >55 yClinical gallstone pancreatitisany very strong predictor--------Highboth strong predictor-------------HighNo predictors present-------------Low

16. CholangitisImpacted stone in CBD causing: Stasis + bacterial super infection  Early bacteremia

17. Charcot’s triad (pain + fever + jaundice) If bacteremia confusion/deliriumFever (95%), RUQ tenderness (90%), Jaundice (80%), Peritoneal sings (15%), Confusion (15%)

18. Leukocytosis (80%), T Bili > 2 mg/dl (80%), ALP elevatedERCP, PTCHigh mortality if unrecognized!!!!

19. What is the recommended treatment for bile duct stones? Endoscopic sphincterotomy and stone extractionAlternatives:Intraoperative ERCP or Laparoscopic bile duct exploration in combination withCholecystectomy

20. In the case of altered anatomy (e.g. previous Roux-en-Y anastomosis, bariatric surgery):Percutaneous or balloon endoscopy-assistedIn the case of failed endoscopic therapy:cholecystectomy combined with bile duct exploration or intraoperative ERCP

21. Are there effective strategies to prevent recurrent bile duct stones? There is NO general recommendation for the pharmacological prevention

22. Which patients with acute biliary pancreatitis should undergo ERCP? Biliary pancreatitis with suspected coexistent acute cholangitis: antibiotics should be initiatedERCP, within 24 hrERCP is probably indicated in patients with biliary pancreatitis and obstructed bile duct

23. in the absence of cholangitis or obstructed bile duct an early ERCP is NOT indicated in patients with biliary pancreatitis In patients with suspected biliary pancreatitis without cholangitis, EUS or MRCP may prevent potential ERCP and prevent its risks

24. When should cholecystectomy be performed in patients with gallbladder stones after ERCP of bile duct stones? In patients with simultaneous gallbladder and bile duct stones, Early laparoscopic cholecystectomy should be performed within 72 h after ERCP for CBD stone if no pancreatitis

25. What is the best time to perform cholecystectomy after acute biliary pancreatitis? Cholecystectomy during the same hospital admission is the preferred option in patients with mild acute biliary pancreatitis

26. How are symptomatic bile duct stones treated in pregnancy? During pregnancy symptomatic bile duct stones should be treated by endoscopic sphincterotomy and stone extraction The use of x-rays is not contraindicated provided care is taken to minimize radiation exposure

27. What is the preferred diagnostic method for intrahepatic bile duct stones? If intrahepatic bile duct stones:abdominal ultrasound MRCP

28. Should asymptomatic intrahepatic bile duct stones be treated? Asymptomatic intrahepatic bile duct stones do NOT always have to be treated. The treatment decision should be made individually for each patient and interdisciplinarily for symptomatic intrahepatic bile duct stones

29.

30. Acalculous Disorders of the Biliary Tract

31. SODBiliary type pain +/- abnormal liver tests or recurrent pancreatitis. Histology shows muscular hypertrophy, inflammation and fibrosis in 60% of patientsClassical patient: Female, 4th-5th decade, recurrent pain after cholecystectomy

32. Diagnoses: Diagnosis of exclusion of other GI diseaseManometry showing basal sphinchter pressure >40 mmHg HIDA scan can be used as screening test (delayed CBD drain of radiotracer)

33. Milwaukee classification is outdated and should no longer be usedEPISOD trail and Rome IV consensus meeting criteriaEPISOD showed no benefit of ERCP+sphincterotomy in patient with post-cholecystectomy pain these patients have functional biliary pain (no more Type 3 SOD)

34. Type 1 SOD biliary pain, LFTs>2X, CBD>12mm, (esp during pain) now considered to have organic sphincter stenosis NOT functional  ERCP+sphincterotomyType 2 SOD now termed suspected functional biliary sphincter disorder (FBSD) or suspected biliary SOD, 50% of patients benefit from ERCP+sphincterotomy

35. Suspected functional biliary sphincter disorder (FBSD) or suspected biliary SOD are at high risk of Post-ERCP Pancreatitis (2-35X compared to normal population)They benefit from:pancreatic stenting, rectal indomethacin,Peri-procedural LR infusions

36. Post-cholecystectomy syndrome Persistence of biliary colic or RUQ pain with a variety of gastrointestinal symptoms similar to those in patients with cholecystitis prior to cholecystectomy Can represent either a continuation of symptoms caused by gallbladder pathology or the development of new symptoms

37. Symptoms include:fatty food intolerance nausea, vomiting, heartburn flatulence indigestion diarrhea jaundice intermittent episodes of abdominal pain

38. EtiologyExtrabiliary disordersreflux esophagitis, esophageal motility disorderspeptic ulcer disease, IBS, Pancreatitis and its complicationsPancreatic tumors Hepatitis Mesenteric ischemia DiverticulitisBiliary etiologies Bile salt-induced diarrhea, Retained calculi, Bile leak, Biliary strictures, Cystic duct remnant, SOD Type 1 and Type 2Extra-intestinal causes psychiatric and neurologic disorders, intercostal neuritis, wound neuroma, coronary artery disease unexplained pain syndromes

39. PSCDiffuse intra+/-extrahepatic BD inflammation and fibrosisLeads to biliary cirrhosis with PHTN. 70% men with average age 40 at diagnosis. Of PSC cases 70-80% are associated with IBD. Conversely, 5% of IBD cases develop PSC. Median survival ~12 years. ANCA may be positive‘Beads on a string appearance’ on ERCP/MRCP‘onion-skin’ fibrosis on liver bx

40. UDCA helps normalize LFTS but no effect on histology/outcomeERCP is used for dominant stricture both for treatment and r/o cholangiocarcinoma (PSC+elevated Ca-19.9) After diagnosis of PSC Annual colonoscopy Prophylactic cholecystectomy

41. Cholestasis

42. Differential diagnosis of intra-and-extra hepatic cholestasis in adults. NASH and ASHBenign infiltrative disorders amyloidosis, sarcoidosisDILI cholestatic formGenetic diseaseBenign intarhepatic cholestatis 1-3, PFIC 1-3, cholestasis of pregnancy, erythropoetic porphyriaInfiltration by malignant diseaseNodular regenerative hyperplasiaPara-neoplastic Hodgkin’s disease, RTCCSepsisTPNVascular disease Budd-Chiari, sinusoidal obstruction syndrome, congestive hepatopathy)Viral hepatitis cholestatic formPBCPSCIgG4-associated cholangitisSecondary sclerosing cholangitis, cholangiolithiasis, ischemia (schock, polytrauma), telengiectasia, vasculitis,infectious disease (HIV and other immunodeficiency)Cystic fibrosisDILI (drug induced cholangiopathy)Ductal plate malformations: Caroli syndrome, congenital liver fibrosisGVHDIdiopathic ductopeniaLangerhans cell histiocytosisHepatocellular cholestasis:Extra-hepatic cholestasis:

43.

44. Biliary Strictures

45. CausesPostsurgical damageChronic pancreatitisInfection with liver flukesBiliary cystsPSCIschemiaAutoimmune cholangiopathyHIV cholangitisMalignancy

46. Post-Liver TxCommonly occurs at the ductal anastomosisMultiple intra-extra-hepatic stricture develop after hepatic artery thrombosisTreatment: endoscopic dilation and stenting or re-Tx if underlying severe ischemia is presentRemember: Bile ducts have arterial perfusion, interference with bile ductal blood supply which may occur following bile duct surgery or hepatic artery thrombosis commonly leads to ischemic strictures of the bile duct

47. Pancreatic cancer is the most common cause of malignant biliary obstructionbiliary drainage with metal stent placement for palliation and resectable patients that need neoadjuvant chemo-radiationIf biliary obstruction is prolonged parenchymal damage with fibrosis  secondary biliary cirrhosis (varies with duration and completeness of obstruction)

48. IgG4 CholangiopathyBiliary manifestation of systemic IgG4-related diseaseSerum IgG4 is elevated Intra-extrahepatic stricturesMultifocal IgG4 containing infiltrates in the liver and biliary ductsIgG4-related cholangitis/pancreatitis with distal biliary or pancreatic duct strictures can, if misdiagnosed as malignant, lead to surgical resectionPatient diagnosed with PSC should have their IgG4 levels checked

49. IgG4-related cholangiopathy shares certain radiologic and clinical manifestations with PSC, However:IgG4 responds well to steroids andthere is a lack of association with IBD

50. Fasciola hepaticaAlbendazole or Triclabendazole

51. Neoplastic disorders of the biliary tract

52. Bile Duct CancerRisk factors:Liver flukes (chlonorchis Sinensis)Certain Chemical exposuresAnomalous pancreaticobiliary junctionIntrahepatic biliary stonesPSCProgressive obstructive jaundice, usually painlessBil >12, elevated ALP with mild or no change in transaminases

53. Cholangiocarcinoma60-70% at the bifurcation of hepatic ducts (Klatskin tm)20-30% arise in the distal CBD10% within the liverERCP, EUS, CTOften slowly progressiveAdenocarcinoma of liver is peripheric ColangiCaElevated Ca 19.9 (50%)

54. Klatskin tm Bizmuth Classification

55. Ampullary adenocarcinoma obstructive jaundice often with dilation of the pancreatic and biliary ducts (double-duct sign)may present with bleeding if accompanied by jaundice acholic stool.Relapsing cholangitis is a presentation for ampullary adenocarcinoma, unlike pancreatic or biliary malignancies in which infection is rare.

56. Our database was searched retrospectively for patients with biliary obstruction due to lymphoma between 1999 and 2005. Biliary obstruction secondary to lymphoma was found in 7 (0.6%) of 1123 patients with malignant biliary obstruction. 4 had Hodgkin’s disease and four had non-Hodgkin’s lymphoma. Biliary obstruction occurred as part of the initial or early presentation of lymphoma in two patients. The most common cause of obstruction was compression of the biliary tract by enlarged lymph nodes (six patients)Biliary drainage was performed in all patients including endoscopic stent placement in six patients, nasobiliary drainage in one, and choledochoduodenostomy in one. Hyperbilirubinemia resolved in all but one of the patients with a stent; however, none could be maintained in a stent-free condition. We conclude that lymphoma should be considered in the differential diagnosis of obstructive jaundice, particularly in younger patients. We suggest that biliary drainage by the endoscopic or percutaneous route is necessary for the treatment of these patients. Late benign strictures may develop. Biliary obstruction is a sign of poor prognosis in lymphoma.

57. Carcinoid tumor of the minor duodenal papilla: a rare entity in elderly individuals. Aktaş B, Çoban Ş, Simşek Z, Başar Ö, Arıkök AT, Yüksel O. J Am Geriatr Soc. (A) Endoscopic view of tumor of the minor papilla. (B) Endoscopic ultrasound showing a small mass located in the submucosal layer (arrow). (C) Histological examination of the specimen showing small clusters of subepithelial tumor cells containing nuclei with uniform chromatin (D) Photomicrograph of biopsy specimen stained immunocytochemically for synaptophysin showing positive reaction of tumor cells

58. Thank you and questions?