Diseases of the BILIARY SYSTEM 6th year..pptx

Diseas of billiary

1. Diseases of the BILIARY system Dr / Rashed ALEEZI Consultant HBP surgeon

2. Biliary Tract Extrahepatic biliary tract Gallbladder Cystic duct Common hepatic duct Common bile duct Intrahepatic biliary tract

3. Biliary Tree ; aNATOMY Bile is secreted by hepatocytes into bile canuliculi which drain into interlobular bile ducts. Progressively larger ducts formed. Left and right hepatic ducts emerge from porta and merge to form common hepatic duct (4cm) Joined on the right by the cystic duct from the GB to form the common bile duct (8-10cm long, 5-6mm diameter) Runs in free edge of lesser omentum , passes posterior to D1 and head of pancreas Comes in contact with pancreatic duct on the left side of D2 Usually unite in the duodenal wall to form hepatopancreatic ampulla (of Vater ) Ampulla opens into descending part of duodenum at summit of major duodenal papilla, 8-10cam from pylorus

4. Biliary Duct – blood supply Arterial supply Proximally: cystic artery Middle: right hepatic artery Distally: posterior superior pancreaticduodenal a. Venous drainage Proximally: drainage directly into liver Distally: posterior superior pancreaticduodenal v. Lymph drainage Cystic LN, node of omental foramen, hepatic LN’s

5. Gallbladder and cystic duct Pear shaped sac lies to the right of the quadrate lobe in GB fossa on the visceral surface of liver Concentrates and stores bile secreted by the liver Cholecystokinin produced by intestinal mucosa during digestion, passes to GB and causes it to contract and release bile Fundus , body and neck Mucosal membrane arranged into spiral folds (valves of Heister ) at GB neck and cystic duct

6. Gallbladder and cystic duct Anterosuperiorly GB fossa of liver Fundus projects from inferior border of liver, located at tip of 9 th costal cartilage in MCL where lateral edge of rectus abdominis meets costal margin Posteroinferiorly Neck: lesser omentum . Omental ( epiploic ) foramen lies immediately to the left. Body: D1 Fundus : transverse colon

7. Gallbladder and cystic duct G.B Function : Store and concentrate bile. Secrete glycoprotein and hydrogen ion. Contraction stimulated by CCK and vagus nerve and inhibited by sympathetic stimulation, VIP, and somatostatin Sphincter of oddi : Regulates bile flow, prevents back flow, and diverts bile into G.B. Basal resting pressure of 13 mm Hg above duodenal pressure. CCK causes relaxation

8. Anomalies: The classic description applies only in one third of the patients G.B: abnormal portions, intrahepatic , rudimentary, or duplicated. Bile ducts: duct of Luschka , accessory right hepatic duct.

9. Anomalies: Arteries : i n 50 % of population Right hepatic artery from SMA (20%) 2 right hepatic arteries (5%) Cystic artery can arise from left hepatic, common hepatic, gastroduodenal , or SMA(10%).

10. LIVER TESTS Transaminases Alanine amino transferase (ALT) Aspartate amino transfersase (AST) Special considerations: 1. AST is also present in other tissues (muscle, brain, kidney, intestine). ALT is more specific for liver. 2. Even very mild liver abnormalities can cause slightly elevated AST/ALT - for example, mild fatty liver. Serum Bilirubin (Bile Acids)Rationale : Liver is virtually the only mechanism for excretion Cholestasis from any cause results in “ back-up ” of these compounds in blood Interpretation: Cholestasis : extrahepatic or intrahepatic Disadvantages: Does not distinguish hepatocellular disease, in which hepatocytes don ’ t make bile, from bile duct obstruction

11. Tests of Cholestasis /Reduced Bile Flow Enzymes released as a Accumulation in liver/blood consequence of decreased of substances normally bile flow excreted in bile Alkaline phosphatase Bilirubin or 5 ’ - nucleotidase Bile salts Leucine aminopeptidase g- glutamyl transpeptidase

12. LIVER TESTS Albumin Rationale Liver is the sole source Interpretation of Decreased Level Decreased liver production Increased renal/GI loss ( nephrotic syndrome; protein losing enteropathy in inflammatory bowel disease Protein malnutrition Disadvantages Prolonged half-life No unique interpretation Prothrombin Time Rationale Liver is sole source of vitamin K-dependent clotting factors, including those critical for PT Factor VII has very short half-life (hours) Interpretation of Increased PT Hepatocyte protein synthesis impaired Vitamin K deficiency/Coumadin therapy Disseminated intravascular coagulopathy Advantages Rapidly reflects changes in liver function

13. Patterns of Abnormal Liver Tests Hepatocellular Cholestasis Major: AST/ALT Alkaline Phosphatase Minor: Bilirubin Bilirubin PT/albumin AST/ALT PT ( Vit K deficiency)

14. 14 ■ Ultrasound ■ Plain radiograph ■ Magnetic resonance cholangiopancreatography : ■ Multidetector row computerised tomography scan ■ Radioisotope scanning ■ Endoscopic retrograde cholangiopancreatography ■ Percutaneous transhepatic cholangiography : anatomy and biliary strictures ■ Endoscopic ultrasound ■ Peroperative cholangiography GALLBLADDER AND BILIARY TREE - IMAGING TECHNIQUES

15. Plain Films

16. Ultrasound Ultrasound is 95% sensitive for stones, 80% specific for cholecystitis . It is 98% sensitive and specific for simple stones. Wall thickening (2-4mm) false positives! Distension Pericholecystic fluid, sonographic Murphy’s. Dilated CBD(7-8mm).

17. CT Scan

18. HIDA scan HIDA scan does not detect gallstones HIDA scan identifies an obstructed gallbladder ( eg , gallstone impacted in the neck of the gallbladder). HIDA scan is the most sensitive and specific test for acute cholecystitis . A poorly contracting gallbladder ( biliary dyskinesia ) might cause the patient's symptoms, and HIDA scan makes the diagnosis. Acute acalculous cholecystitis is diagnosed most accurately with HIDA scan.

19. MRCP Magnetic resonance cholangiography (MRCP) images obtained from the newest diagnostic equipment are comparable in quality to those obtained with Endoscopic Retrograde Cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography . Ductal or intravenous injection of contrast medium is not necessary and the patient is not exposed to irradiation.

20. ERCP ERCP is diagnostic and therapeutic. Provides radiographic and endoscopic visualization of biliary tree. Do when CBD dilated and elevated LFTs. Complications include bleeding, perforation, pancreatitis, cholangitis .

21. Percutaneous transhepatic cholangiography Percutaneous transhepatic cholangiography : anatomy and biliary strictures: It is only undertaken once a bleeding tendency has been excluded and the patient’s prothrombin time is normal. Antibiotics should be given prior to the procedure. Bile can be sent for cytology. In addition, PTC enables the placement of a catheter into the bile ducts to provide external biliary drainage or the insertion of indwelling stents.. Transhepatic cholangiogram showing a stricture of thecommon hepatic duct

22. Biliary Disease Gallbladder Disorders - Cholelithiasis - Cholesterolosis - Cholecystitis Extrahepatic Bile Duct Disorders - Choledocholithiasis - Cholangitis - Biliary Atresia - Choledochal cysts Tumors

23. Choledochal Cysts Present most often before 10 yrs of age Jaundice, abdominal pain, abdominal mass Delayed diagnosis can lead to complications: Pancreatitis Spontaneous perforation Cholelithiasis Cholangitis Secondary biliary cirrhosis Portal hypertension Carcinoma

24. Biliary Atresia Type I – Disease limited to common bile duct Type II – Disease limited to hepatic bile ducts Type III – Obstruction of ducts above porta hepatis

25. Cholelithiasis (Gallstones) Gallstone disease, or cholelithiasis , is one of the most common surgical problems worldwide. Gallstones are abnormal, inorganic masses formed in the gallbladder and, less commonly, in the common bile or hepatic ducts. Women are more likely to develop gallstones than men, with a ratio of 2:1. Gallstones develop insidiously, and they may remain asymptomatic for decades. Migration of a a gallstone into the opening of the cystic duct may block the outflow of bile during gallbladder contraction. The resulting increase in gallbladder wall tension produces a characteristic type of pain ( biliary colic ). Cystic duct obstruction, if it persists for more than a few hours, may lead to acute gallbladder inflammation ( acute cholecystitis ).

26. Types of Gallstones Mixed (80%) Pure cholesterol (10%) Pigmented (10%) Black stones (contain Ca bilirubinate , a/w cirrhosis and hemolysis ) Brown stones ( a/w biliary tract infection)

27. pathophisyology Bile is made and secreted by hepatocytes ; stored in GB Wall of GB innervated with sympathetic& parasympathetic nerves from celiac plexus Composition of bile: Bilirubin (by-product of haem degradation) Cholesterol (kept soluble by bile salts and lecithin) Bile salts/acids ( cholic acid/ chenodeoxycholic acid): mostly reabsorbed in terminal ileum( entero -hepatic circulation). Lecithin (increases solubility of cholesterol) Inorganic salts (sodium bicarbonate to keep bile alkaline to neutralise gastric acid in duodenum) Water (makes up 97% of bile

28. Pathophisyology ; cont…. Gallstone formation occurs because certain substances in bile are present in concentrations that approach the limits of their solubility. Under normal conditions , a delicate balance occurs among the levels of bile acids, cholesterol, and phospholipids. When bile isconcentrated in the gallbladder, it can become supersaturated with these substances, which then precipitate from solution as microscopic crystals. The crystals are trapped in gallbladder mucus, producing gallbladder sludge. Over time, the crystals grow, aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and/or stones produces the complications of gallstone disease.

29. Pathophisyology ; cont…. The 2 main substances involved in gallstone formation are cholesterol and calcium bilirubinate . Cholesterol gallstones More than 80% of gallstones contain cholesterol as their major component. Liver cells secrete cholesterol into bile along with phospholipid (lecithin) in the form of small spherical membranous bubbles, termed unilamellar vesicles. Liver cells also secrete bile salts, which are powerful detergents required for digestion and absorption of dietary fats. Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. This happens mainly in the gallbladder, where bile is concentrated by reabsorption of electrolytes and water.

30. Pathophisyology ; cont…. Compared with vesicles (which can hold up to 1 molecule of cholesterol for every molecule of lecithin), mixed micelles have a lower carrying capacity for cholesterol (about 1 molecule of cholesterol for every 3 molecules of lecithin). If bile contains a relatively high proportion of cholesterol to begin with, then as bile is concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol-carrying capacity of the micelles and residual vesicles is exceeded. At this point, bile is supersaturated with cholesterol, and cholesterol monohydrate crystals may form. Thus, the main factors that determine whether cholesterol gallstones will form are (1) the amount of cholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentration and extent of stasis of bile in the gallbladder.

31. Pathophisyology ; cont…. Calcium, bilirubin , and pigment gallstones Bilirubin , a yellow pigment derived from the breakdown of heme , is actively secreted into bile by liver cells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water soluble and stable, but a small proportion consists of unconjugated bilirubin . Unconjugated bilirubin , like fatty acids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calcium enters bile passively along with other electrolytes. In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may be present in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize from solution and eventually form stones. Over time, various oxidations cause the bilirubin precipitates to take on a jet-black color, and stones formed in this manner are termed black pigment gallstones. Black pigment stones represent 10-20% of gallstones in the United States

32. Pathophisyology ; cont…. Bile is normally sterile, but in some unusual circumstances ( eg , above a biliary stricture), it may become colonized with bacteria. The bacteria hydrolyze conjugated bilirubin , and the resulting increase in unconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals. Bacteria also hydrolyze lecithin to release fatty acids, which also may bind calcium and precipitate from solution. The resulting concretions have a claylike consistency and are termed brown pigment stones. Unlike cholesterol or black pigment gallstones, which form almost exclusively in the gallbladder, brown pigment gallstones often form de novo in the bile ducts. Prerequisites for formation of brown pigment gallstones include intraductal stasis and chronic colonization of bile with bacteria. this combination is most often encountered in patients with  postsurgical biliary strictures  or  choledochal cysts .

33. Pathophisyology ; cont…. Mixed gallstones Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosal inflammation. Lytic enzymes from bacteria and leukocytes hydrolyze bilirubin conjugates and fatty acids. As a result, over time, cholesterol stones may accumulate a substantial proportion of calcium bilirubinate and other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calcium resembling an eggshell that may be visible on plain x-ray films.

34. Gallstones are also associated with certain medical conditions including : 1-Diabetes 2-Liver disease 3-Crohn's disease 4-Blood disorders like sickle-cell anaemia 5-Stomach surgery - gallstones are more common if you have had surgery to remove part of your stomach Gall bladder Stone Risk Factors

35. AGE ; It is uncommon for children to have gallstones. If they do, its more likely that they have congenital anomalies, biliary anomalies, or hemolytic pigment stones. Incidence of GS increases with age 1-3% per year . SEX; More common in women. Etiology may be secondary to variations in estrogen causing increased cholesterol secretion, and progesterone causing bile stasis. Pregnant women more likely to have symptoms. Women with multiple pregnancies at higher risk A major contributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reduces gallbladder contractility, leading to prolonged retention and greater concentration of bile in the gallbladder Oral contraceptives, estrogen replacement tx

36. Gallstone Risk Factors “Female, Fat, Forty, Fertile” Oral contraceptives Obesity Rapid weight loss (gastric bypass pts) Fatty diet DM Prolonged fasting TPN Ileal resection Hemolytic states Cirrhosis Bile duct stasis ( biliary stricture, congenital cysts, pancreatitis, sclerosing cholangitis ) IBD Vagotomy Hyperlipidemia

37. Spectrum of Gallstone Disease 3 clinical stages: asymptomatic, symptomatic, and with complications ( cholecystitis , cholangitis , CBD stones ). Symptoms and complications result from effects occurring within the gallbladder or from stones that escape the gallbladder to lodge in the CBD. Most (60-80%) are asymptomatic A history of epigastric pain with radiation to shoulder may suggest it. A detailed history of pattern and characteristics of symptoms as well as US make the diagnosis.

38. Asymptomatic Gallstones Each year, about 2% of patients with asymptomatic gallstones develop symptoms, usually biliary colic rather than one of the complications of gallstone disease. The present practice of operating only on symptomatic patients, leaving the millions without symptoms alone, seems appropriate. A question is often raised about what to advise the asymptomatic patient found to have gallstones during the course of unrelated studies. INDICATION OF PROFYLACTIC SURGERY Pediatric gallstones Congenital hemolytic anemia Gallstones >2.5cm Porcelain gallbladder Bariatric surgery Incidental gallstones found during intraabdominal surgery Recommended prior to transplantation

39. History Best definition of colic is pain that is severe in epigastrium or RUQ that last 1-5 hrs, often waking patient at night. In classic cases pain is in the RUQ, however visceral pain and GB wall distension may be only in the epigastric area. Once peritoneum irritated, localizes to RUQ. Small stones more symptomatic . Distinguishing uncomplicated biliary colic from acute cholecystitis or other complications is important. Key findings that may be noted include the following: Uncomplicated biliary colic – Pain that is poorly localized and visceral; an essentially benign abdominal examination without rebound or guarding; absence of fever Acute cholecystitis – Well-localized pain in the right upper quadrant, usually with rebound and guarding; positive Murphy sign (nonspecific); frequent presence of fever; absence of peritoneal signs; frequent presence of tachycardia; in severe cases, absent or hypoactive bowel sounds

40. History Characteristics of biliary colic include the following : Sporadic and unpredictable episodes Pain that is localized to the epigastrium or right upper quadrant, sometimes radiating to the right scapular tip Pain that begins postprandially , is often described as intense and dull, typically lasts 1-5 hours, increases steadily over 10-20 minutes, and then gradually wanes Pain that is constant; not relieved by emesis, antacids, defecation, flatus, or positional changes; and sometimes accompanied by diaphoresis, nausea, and vomiting Nonspecific symptoms ( eg , indigestion, dyspepsia, belching, or bloating) Patients with the lithogenic state or asymptomatic gallstones have no abnormal findings on physical examination.

41. Clinical features of acute cholecystitis Pain persisting > 6 hours Nausea & vomiting, anorexia Fever +/- chills Hx of similar attacks/documented gallstones Pain becomes more localized to RUQ Murphy’s sign (est. at 97% sensitive for a.c.) Signs of systemic toxicity, dehydration Localized peritoneal toxicity, distention Hypoactive bowel sounds

42. Differential Diagnosis of RUQ pain Gallstone disease (and its related complications) Gastritis/ duodenitis Peptic ulcer disease/perforated peptic ulcer Acute pancreatitis Right lower lobe pneumonia MI If presenting to A&E with RUQ pain all patients should get Blood tests AXR/E-CXR (to exclude perforation/pneumonia) ECG

43. Workup Elevated WBC is expected but not reliable. In retrospective study, only 60% of patients with cholecytitis had a WBC greater than 11,000. A WBC greater than 15,000 may indicate perforation or gangrene. ALT, AST, AP more suggestive of CBD stones Amylase elevation may be GS pancreatitis.

44. Cholecystolithiasis

45. Cholecystitis : Management Conservative R/ ; NPO , IVF, IV antibiotics Non-operative: dissolution therapy ursodeoxycholic acid, chenodeoxycholic acid Operative : Early presentation up to 3days ; cholecystectomy . Late presentation ; conservative R/ , then elective surgery ( after 6 weeks …….) For unstable pts: percutaneous transhepatic cholecystostomy (CT or U/S guided)

46. Laparoscopic Cholecystectomy

47. Laparoscopic Cholecystectomy

48. Gallstone Complications Acute cholecystitis : 10-20% of pts w/ symptomatic gallstones GB gangrene GB perforation GB empyema (pus in the GB) Emphysematous cholecystitis Cholecystoenteric fistula Choledochohlithiasis : 8-15% of pts w/ symptomatic gallstones Cirrhosis Cholangitis Pancreatitis Gallstone ileus

49. Complications of acute cholecystitis Empyema of gallbladder Pus-filled GB due to bacterial proliferation in obstructed GB. Usu. more toxic, high fever Emphysematous cholecystitis More commonly in men and diabetics. Severe RUQ pain, generalized sepsis. Imaging shows air in GB wall or lumen Perforated gallbladder Occurs in 10% of acute chol’y, usually becomes a contained abscess in RUQ Less commonly, perforates into adjacent viscus = cholecystoenteric fistula & the stone can cause SBO ( gallstone ileus )

50. The pathological sequences during a bout of uncomplicated cholecystitis

51. Sequence of pathological processes. Formation of an empyema or mucocele of the gallbladder

52. Sequence of pathological processes leading to perforation of the gallbladder

53. Recap. Stages of Acute Cholecystitis . Gallbladder has a grayish appearance & is edematous. There is an obstruction of the cystic duct and the gallbladder begins to swell. It no longer has the "robin egg blue" appearance of a normal gallbladder. As acute cholecystitis progresses, the gallbladder begins to become necrotic and gets a speckled appearance as the wall begins to die. Gallbladder undergoes gangrenous change and the wall becomes very dark green or black. This is the stage when perforation occurs.

54. Abdominal radiograph of acalculous emphysematous cholecystitis demonstrating curvilinear air pattern conforming to the shape of the gallbladder wall CT images of emphysematous cholecystitis - same patient

55. Contrast CT scan showing emphysematous cholecystitis with gallbladder wall disruption (arrow), gas formation (arrowhead), and a biloma Contrast CT scan showing gallstones (arrow) with gallbladder rupture and fluid localized at the gallbladder fossa (arrowhead)

56. Prognosis Uncomplicated cholecystitis as a low mortality. Emphysematous GB mortality is 15% Perforation of GB occurs in 3-15% with up to 60% mortality. Gangrenous GB 25% mortality.

57. Acute a calculous cholecystitis In 5-10% of cases of acute cholecystitis Seen in critically ill pts or prolonged TPN More likely to progress to gangrene, empyema , perforation due to ischemia Caused by gallbladder stasis from lack of enteral stimulation by cholecystokinin Tx : Emergent cholecystectomy usu open If pt is too sick, perc cholecystostomy tube and interval cholecystectomy later on

58. Chronic calculous cholecystitis Recurrent inflammatory process due to recurrent cystic duct obstruction, 90% of the time due to gallstones Overtime, leads to scarring/wall thickening Treatment: laparoscopic cholecystectomy

59. Choledocholithiasis Passage of gallstones into common bile duct occurs in 10-15% of patients with cholelithiasis Majority are cholesterol stones formed in gallbladder Primary calculi arising de novo in ducts are typically pigmented stones in pts with: -Chronic recurrent cholangitis -Congenital anomalies of bile ducts ( Caroli’s disease) -Dilated, sclerosed or strictured ducts

60. Choledocholithiasis May remain asymptomatic May pass spontaneously into duodenum May present as biliary colic or complications - Cholangitis -Obstructive jaundice -Pancreatitis -Secondary biliary cirrhosis PE: may be normal Mild epigastric or RUQ pain Jaundice Completely impacted stones: Severe progressive jaundice Lab Workup  serum bilirubin  alkaline phosphatase  transaminases

61. Choledocholithiasis management Aim to remove the (obstruction and then the gall bladder ) after preparation Preoperative :( monitoring, adequate hydration , IV vitamin K, high glucose intake, antibiotic ) ERCP ( possible complications ) If failed exploration of CBD.

62. Acute Cholangitis Acute cholangitis is a bacterial infection of the biliary ductal system, which varies in severity from mild and self-limited to severe and life threatening. The clinical triad of fever, jaundice, and pain associated with cholangitis was first described in 1877 by Charcot. Etiology The most common causes of biliary obstruction are choledocholithiasis , benign strictures, biliary enteric anastomotic strictures, and cholangiocarcinoma or periampullary cancer. ERC, PTC, and stent placement via either the endoscopic or percutaneous route all are known to cause bacteremia . These procedures are frequently performed in patients with unresectable malignant obstruction

63. Clinical Presentation Severe illness, including jaundice, fever, abdominal pain, mental obtundation , and hypotension ( Reynold’s pentad). Fever is the most common presenting symptom and is often accompanied by chills . Jaundice is a frequent physical finding but may be absent, especially in patients with an indwelling endoprosthesis or biliary stent. Pain is also commonly present but is often mild. Severe pain or marked tenderness should prompt consideration of an alternate diagnosis such as acute cholecystitis . Up to 33% of patients with choledocholithiasis present with toxic cholangitis characterized by septic shock.

64. Management Patients with toxic cholangitis may require intensive care unit monitoring and vasopressors to support blood pressure. Most patients require intravenous fluids and antibiotics. Most patients with cholangitis respond to antibiotic therapy alone with clinical improvement. However, in the 15% of patients who do not respond to antibiotics within 12 to 24 hours or in patients with toxic cholangitis , emergency biliary decompression may be necessary. Biliary decompression may be performed endoscopically or via the percutaneous transhepatic route. In settings where either endoscopic or percutaneous biliary drainage is not possible, common bile duct exploration and placement of a T tube remains a life-saving procedure for seriously ill patients with toxic cholangitis . However, the mortality for patients treated surgically is considerably higher than for patients successfully managed endoscopically .

65. Gall bladder Stone The majority of cases (approximately 80%)are asymptomatic (silent) gall stones , discovered accidentally by abdominal sonar . Other symptoms are related to site of movement of stone A gall stone may impact in the neck of gall bladder or in the cystic duct giving biliary pain or cholecystitis Biliary pain usually occurs in the epigastrium and right hypochondrium Obstruction of common bile duct leading to pain & jaundice Pancreatitis. Gall stones increase risk of carcinoma of the gall bladder

66. Obstruction of common bile duct leading to pain & jaundice May Complicate to Charcot’s Triad: 1-Pain 2-Jaundice 3-Fever Reynold’s Pentad: 1-Pain 2-Jaundice 3-Fever 4-Altered Mental State 5-Shock Abdominal Ex: 1-Gall Bladder: in 80%Not Distended When gall bladder be distended?? Murphy’s sign +ve 2-Liver:Enlarged?????

67. Gallstone pancreatitis 35% of acute pancreatitis 2ndary to stones Pathophysiology Reflux of bile into pancreatic duct and/or obstruction of ampulla by stone ALT > 150 (3-fold elevation) has 95% PPV for diagnosing gallstone pancreatitis Tx : ABC, resuscitate, NPO/IVF, pain meds Once pancreatitis resolving, ERCP w stone extraction/ sphincterotomy Cholecystectomy before hospital discharge

68. Gallstone ileus Pathogenesis: Gallstone causing small bowel obstruction (usually obstructs in terminal ileum) Gallstone enters small bowel via cholecysto -duodenal fistula ( not via CBD) AXR – dilated small bowel loops May see stone if radio-opaque Treatment NBM Fluid resuscitation + catheter NG tube Analgesia Surgery (will not settle with conservative management) – enterotomy + removal of stone Diagnosis of gallstone ileus usually made at the time of surgery.

69. MALIGNANT BILIARY DISEASE Gallbladder Cancer Cholangiocarcinoma : intrahepatic , hilar tumors distal cholangiocarcinoma ,

70. TUMORS Carcinoma of the Gallbladder : Rare, aggressive and poor prognosis. High risk : porcelain gallbladder (20%), chronic inflammation, stones > 3 cm, symptomatic gallstones, polypoid lesions , choledochal cysts, sclerosing cholangitis , anomalous pancreaticobiliary duct junction, and exposure to carcinogens ( azotoluene , nitrosamines). Lymphatic, venous, and direct invasion. Clinical feature : indistinguishable from cholecystitis and cholelithiasis . US, CT Treatment : Surgery remains the only curative option, however, palliative procedures for patients with unresectable cancer can be performed. 5-year survival rate of all patients with gallbladder cancer is less than 5%

71. Bile Duct Carcinoma Rare tumor and about two third are located at the hepatic duct bifurcation Risk factors : primary sclerosing cholangitis , choledochal cysts, ulcerative colitis, hepatolithiasis , biliary -enteric anastomosis , and biliary tract infections with Clonorchis or in chronic typhoid carriers. 95% are adenocarcinoma Anatomical division : * intrahepatic ; treated like HCC * perihilar ( Klatskin tumors) *proximal *distal

72. Bile Duct Carcinoma Clinical manifestation : painless jaundice , Pruritus , mild right upper quadrant pain, anorexia, fatigue, and weight loss also may be present. About 10% present with cholangitis . LFT, US, CT, PTC, ERCP, MRI Treatment: *surgical resection *surgical bypass for biliary decompression and cholecystectomy for pt with metastasis or unresectable disease. * nonoperative biliary decompression is performed for pt with unresectable disease on diagnostic evaluation. The greatest risk factors for recurrence after resection are the presence of positive margins and lymph node, and surgery is not recommended in recurrence.