SURGICAL JAUNDICE (Obstructive Jaundice).pptx

Surgical jaundice

1. SURGICAL JAUNDICE (Obstructive Jaundice) Presenter : Dr Rizwan Khan RKDF Medical College, Bhopal

2. Anatomy

3. Porta hepatis R elation of structures at the porta hepatis from before backwards are: „ Hepatic ducts in the front „ Branches of hepatic artery „ Branches of portal vein.

4. Blood supply G allbladder is supplied by the cystic artery which is usually a branch of right hepatic artery. Bile duct is supplied by two vertical arteries arising from the hepatic artery running along the bile duct at 3 and 9 o’clock position and giving of circumferential arteries anteriorly and posteriorly .

5. Lymphatic supply L ymphatics of gallbladder drain into the cystic lymph node of Lund. Efferent from the cystic lymph nodes drains into the pericholedochal lymph nodes and lymph nodes at the porta hepatis and supeorior and posterior pancreatico dudenal lymph nodos . These lymphatic then passes into the celiac lymph nodes

6. GENERAL OUTLINE

7. Definition It is the jaundice that develops due to biliary obstruction, partial or complete or intermittent. It causes conjugated hyperbilirubinaemia . Normal serum bilirubin level is 0.2-0.8 mg%. Scleral icterus is visible when serum bilirubin level exceeds 2.5 mg%.

8. Bilirubin metabolism and enterohepatic circulation Aged red cells get lysed in the reticuloendothelial cells and breakdown into haem and globin . Bilirubin is combined with albumin and transported to liver. In the liver bilirubin get separated from albumin and conjugated to bilirubin glucuronide by glucuronyl transferase .

9. This conjugated bilirubin glucuronide is water soluble and can be excreted in kidney (So in obstructive and hepatic jaundice bile pigment - bilirubin is seen in the urine). This conjugated bilirubin is excreted through biliary canaliculi reaching intestine. In the intestine, it is converted into stercobilinogen and urobilinogen by intestinal bacteria

10. 70% of this is absorbed in the colon and brought back to liver as enterohepatic circulation . Unabsorbed stercobilinogen colours faeces brown. Circulating urobilinogen is taken up by kidneys for excretion .

11. Normal urinary urobilinogen is 100-200 mg/day . It is absent in obstructive jaundice. Normal faecal stercobilinogen is 300 mg/day . It is also absent in obstructive jaundice.

12. Pathophysiology in obstructive jaundice Obstructive jaundice, often called as surgical jaundice occurs due to intrahepatic or extrahepatic biliary outflow obstruction . It leads into cholestasis which means conjugated hyperbilirubinaemia ; probably due to impaired bile flow and impaired bile formation. Bile acid secretion into the gut is impaired causing defective absorption of fat and fat-soluble vitamins like vitamin K;

13. this , in turn causes poor synthesis of prothrombin and conversion of prothrombin to thrombin causing widened PT and PT INR . Factors II, VII, IX, and X are vitamin K-dependent clotting factors. PT indicates the extrinsic pathway of coagulation ; whereas partial thromboplastin time represents the intrinsic pathway . Bile acid stasis causes hepatocytes injury .

14. Fat malabsorption causes steatorrhoea and also deficiencies of vitamins A (visual problem, thick skin), D ( osteomalacia ), E (peripheral neuropathy, cerebellar ataxia, posterior column dysfunction), K (bleeding tendencies). Persistent cholestasis may be associated with deposits of cholesterol in the skin ( cutaneous xanthomatosis ), occasionally in bones and peripheral nerves.

15. Bilirubinostasis (bile plugs) cause hepatocytes degeneration , small duct and ductular obstruction , pericholangitis , oedema, bile leak, liver infarction and biliary cirrhosis . Obstruction may be due to benign conditions like biliary tree stones (most common cause) or strictures or sclerosing cholangitis ; or due to malignant conditions like carcinoma of pancreas or cholangiocarcinoma .

16. Extrahepatic obstruction may be L uminal ( stones , infestations [ ascariasis , clonorchis sinensis and schistosomiasis ) or M ucosal/wall ( growth, stricture [post-inflammatory, postsurgical or post-RT ], , primary sclerosing cholangitis ) or E xternal compression ( pancreatitis, pancreatic tumour, compression by nodal mass ).

17. lntrahepatic cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane. Causes include hepatocellular disease (e.g. viral hepatitis, hepatitis/ cholestasis ( thiazides , chlorpromazine), biliary cirrhosis . In hepatocellular disease, interference in the 3 major steps of bilirubin metabolism- uptake, conjugation and excretion usually occur.

18. The lack of bilirubin in the intestinal tract is responsible for the pale stools in biliary obstruction . The cause of itching ( pruritus ) associated with biliary obstruction is related to the accumulation of bile acids in the skin.

19. Severe biliary obstruction causes cell damage usually in 1 month and, if unrelieved, may lead to secondary biliary cirrhosis. Acute cholangitis is another complication associated with obstruction of the biliary tract and is the most commonly seen in stricture, most often at the level of the CBD.

20. Bile flow obstruction  stasis  colonization and multiplication of bacteria  concomitant increased intraductal pressure  reflux of biliary contents  bacteremia , septicaemia  septic shock.

21. Effects of Obstructive Jaundice In liver. Enlarged green bile stained liver ( hydrohepatosis ) shows dilated intrahepatic biliary radicles . Once intraductal CBD pressure increases bile secretion from liver is reduced causing formation of 'white bile ' in CBD. Biliary cirrhosis may develop later. In the biliary tree: Recurrent inflammation- cholangitis , fibrosis can occur.

22. In bowel: Absence of bile from bowel impairs digestion , reduces fat absorption making faeces bulky and fatty . Vitamin K absorption is reduced causing fall in prothrombin level raising PT-INR . Retention of bile salts and bile pigments in blood and body fluids occurs. Altered coagulation profile; hepatorenal syndrome and renal failure ; sepsis .

23. Classification of Causes of Obstructive Jaundice 1. Congenital : Biliary atresia , choledochal cyst. 2. Inflammatory : Ascending cholangitis , sclerosing cholangitis . 3. Obstructive : CBD stones, biliary stricture, parasitic infestation. 4. Neoplastic : Carcinoma of head or periampullary region of pancreas, cholangiocarcinomas , Klatskin tumour. 5. Extrinsic compression of CBD by lymph nodes or tumours.

24. Clinical features Severe jaundice. Pruritus , more on the back and forearms. Fever , may or may not be present. Loss of weight . Loss of appetite . Pain in right hypochondrium , Palpable gallbladder . Hydrohepatotic palpable, smooth, soft, non-tender liver.

25. Courvoisier's law may suggest inflammatory/ neoplastic cause. Charcot's triad/ Reynold's pentad as presentation in cholangitis . Steatorrhoea (more fatty stool) due to improper absorption of fat soluble vitamins.

26. Courvoisier’s law If in a jaundice patient, the gallbladder is palpable, then it is not due to choledocholithiasis as the gallbladder would have been " brosed by previous cholecystitis . Exceptions „ Double impaction of stone—one at common bile duct and another at cystic duct „ Primary CBD stone „ Distended gallbladder due to large stone load.

27. Clinical assessment of jaundice Jaundice is defined as yellowish discoloration of skin, eyes and mucous membrane due to excessive bilirubin in blood. Jaundice is looked for in upper bulbar sclera, soft palate, undersurface of tongue, palms, soles and general body skin. Clinical jaundice is seen when the bilirubin level is more than 2 mg %.

28. Investigations for Obstructive Jaundice Serum bilirubin : Normal value is less than 1.0 mg% . Both direct and indirect bilirubin are assessed. Direct is increased in obstructive jaundice, i.e. conjugated hyperbilirubinaemia . van den Bergh's test is done. Serum albumin, globulin and A:G ratio . Normal S. albumin is more than 3.5 gm%.

29. Prothrombin time : Normal value is 12-16 seconds . It is significant if it is more than 4 from the control or more than one and half times the control. It is corrected by injection vitamin K, 1 0 mg IM OD for 5 days or by FFP-5-10 units . Serum alkaline phosphatase , SGPT, SGOT, 5' nucleotidase .

30. TLC may be raised with neutrophilia in inflammatory conditions. Serum ALP and GGT are relevant enzymes in biliary obstruction; especially ALP/GCT ratio is more relevant in differentiating between obstructive jaundice and hepatitis. Ultrasound abdomen . ERCP to visualise the site of obstruction, brush biopsy, bile sample for analysis.

31. PTC to decompress, assess proximal dilated obstructed biliary system if ERCP fails; dine polythene catheter can be kept in situ to have biliary drainage; PTC- stenting across the obstruction can be done under image (C-arm) guidance. MRCP - Noninvasive diagnostic tool. It shows 96% sensitivity ; 99% specificity. CT scan in case of tumours to assess operability.

32. Tumour markers : CA 19/9 is useful for carcinoma pancreas ( more than 70 units/L ). Endoscopic US (EUS): It is done through endoscope. It is more accurate in assessing pancreatic mass, staging of the disease, to identify involvement of portal venous system, CBD stones.

33. It is also useful in EUS-guided FNAC, celiac axis neurolysis , EUS-guided immunotherapy. lntraductal US (/DUS): It is very useful in assessing tumour stage, tumour margin in bile duct cancer. It is also used in assessing pancreatic duct to differentiate pancreatic cancer and chronic pancreatitis.

34. CT/MR angiogram or venogram to assess vascularity and portal venous system in malignancy. Urine tests : Fouchet's test for bile pigments, Hay's test for bile salts and test for urobilinogen in urine. Fouchet's test : 1 0 ml of urine+ 5 ml of BaCl2+ pinch of MgSO4 causes formation of BaSO4 which is filtered over a filter paper and few drops of Fouchet's reagent is added.

35. Green or blue colour signifies presence of bile pigments in the urine. Hay's test for bile salt: Sprinkle sulphur to 2 ml of urine. In presence of bile salts sulphur sinks to the bottom. Ehrlich's test : 5 ml of freshly voided urine + 1 ml of Ehrlich reagent (p- dimethyl amino benzaldehyde ) and wait for 5 minutes. Formation of red colour signifies presence of urobilinogen in urine.

36. Normally it is present in traces; in obstructive jaundice , it is absent; and in haemolytic jaundice, it is in excess.

37. Preoperative preparation of patient with obstructive jaundice Proper diagnosis and assessment Injection vitamin K IM 10 mg for 5 days Fresh Frozen plasma -often requires 6 bottles or more Adequate hydration is most important 5/10% dextrose. Blood transfusion in case of anaemia Oral neomycin , lactulose Mannitol 100-200 ml BD IV to prevent hepatorenal syndrome

38. Repeated monitoring by doing prothrombin time, electrolytes. Antibiotics like third generation cephalosporins . Calcium supplements as calcium chloride IV. Preoperative decompression is indicated if bilirubin is> 12 mg%, sepsis, hepatorenal syndrome, severe malnutrition or cardiopulmonary disease.

39. Correction of coagulopathy , prevention of renal failure, infection, hepatic encephalopathy and electrolyte imbalance (correction of hypoglycaemia and dilutional hyponatraemia due to water retention; avoiding isotonic saline infusion).

40. Treatment of Obstructive Jaundice CBD stones -ERCP stone removal, choledocholithotomy , transduodenal sphincteroplasty , choledochojejunostomy or choledochoduodenostomy . Carcinoma periampullary or head of pancreas -Whipple's operation or triple bypass or ERCP stenting . Biliary stricture - stenting , choledochojejunostomy , Rouxen -Y hepaticojejunostomy .

41. Biliary atresia -Kasai's operation or liver transplantation. Choledochal cyst -excision, hepaticojejunostomy , mucosal resection.

42. Postoperative Management Monitoring with prothrombin time, bilirubin , albumin, creatinine , electrolyte estimation . FFP or blood transfusion . Antibiotics . Observation for septicaemia, haemorrhage, pneumonia, pleural effusion, bile leak . Care of t ube and drains . T-tube cholangiogram in 10-14 days. TPN, CVP line, nasogastric tube, urinary catheter .

43. PERIAMPULLARY CARCINOMA

44. It includes a group of malignant tumors arising at or near the ampulla : „ Adenocarcinoma from head of pancreas adjacent to the ampulla (within 2 cm. Ampullary tumor . „ Distal bile duct carcinoma „ Duodenal carcinoma adjacent to the ampulla .

45. Etiological factors for development of carcinoma pancreas Smoking Alcohol Diet: Diet high in protein and fats. Chronic pancreatitis Diabetes Genetic: BRCA2 gene.

46. Clinical features Painless progressive jaundice Epigastric pain: Dull aching epigastric pain, radiating to the back,worse at night and in supine position with some relief in leaning forwrad . Nonspecific symptoms: Malaise, weight loss, nausea and vomiting. „ Diarrhea or steatorrhea . „ New onset diabetes mellitus.

47. Normal dimension of pancreatic duct In the head region—5 mm In the body—3 mm In the tail—2 mm.

48. „Rarely patient may present with S/S of acute pancreatitis . Migratory thrombophlebitis (Trousseau sign ).

49. Resectable tumor Tumor localized to the pancreas „ No evidence of SMV or portal vein involvement „ Preserved fat plane between the tumor and the SMA and celiac trunk branches „ No evidence of distant metastasis.

50. Borderline resectable disease Unilateral or bilateral SMV-PV impingment . „ Less than 180 degree tumor abutment on SMA. „ Abutment or encasement of hepatic artery, if reconstructible . „ Short segment occlusion of SMV, if reconstructible .

51. Signs of inoperability Ascites „ Peritoneal metastasis „ Multiple liver metastasis „ Extensive lymph node metastasis „ Invasion of growth to IVC „ Invasion of growth to superior mesenteric vessels, portal vein or celiac axis.

52. Structures will remove in Whipple’s Whole of duodenum up to 10 cm of proximal jejunum „ Head and neck of pancreas including uncinate process „ Distal 40–50% of stomach „ Lower end of common bile duct (CBD) „ Gallbladder „ Pericholedochal , periduodenal and peripancreatic lymph nodes.

53. Maintain continuity following resection for Whipple’s operation Pancreaticojejunostomy (end to side) Hepaticodochojejunostomy (end-to-side) 10–15 cm beyond the pancreaticojejunostomy Beyond 10–15 cm of hepaticodochojejunostomy gastrojejunostomy

54. Steps of Whipple operation Anesthesia Position of the patient Antiseptic cleaning and draping Incision Exploration of abdomen Assessment for resectability Exposure of the duodenum and the head of the pancreas Kocherisation of duodenum

55. Exposure of the pancreas Exposure and dissection of superior mesenteric vessels Dissection of hepatoduodenal ligament and portal structures Cholecystectomy and division of bile duct Division of gastrohepatic omentum and lymph nodes Distal gastrectomy

56. Division of the neck of the pancreas Division of the jejunum Division of uncinate process Removal of specimen Reconstruction Pancreaticojejunal anastomosis Hepaticodochojejunostomy Gastrojejunal anastomosis Closure of transverse mesocolon rent

57. Feeding jejunostomy Placement of drain Closure of abdomen

58. Adjuvant therapy Radiotherapy. „ Cytotoxic chemotherapy: Combination chemotherapy with: 5 Fluorouracil + Cyclophosphamide + Methotrexate or vincristine 5 Fluorouracil + Mitomycin Gemcitabine

59. Choledocholithiasis

60. Primary bile duct stones S tones that form in bile duct itself. The bacterial enzyme hydrolyzes bilirubin diglucuronide into free bilirubin which then precipitates and form a complex with cholesterol . Principal composition of the pigment stone is calcium bilirubinate . Pigment stones are either brown or black.

61. Brown stones are associated with infection in the biliary tree. Black stones are associated with chronic hemolytic diseases.

62. Secondary bile duct stones S tones that form in gallbladder and then migrate into the bile duct.

63. Retained or residual bile duct stones Stones in the bile duct detected within two years following cholecystectomy . Stones missed during cholecystectomy with or without bile duct exploration. S tones have the characteristics of secondary bile duct stones.

64. Recurrent bile duct stones Stones which form within the bile duct 2 years after initial operation. It has the characteristics of primary bile duct stones.

65. Clinical features „ Charcot's triad „ Obstructive jaundice: Itching, clay colored stool „ Associated pancreatitis may cause pain in the back „ Abdominal tenderness may be present in right upper quadrant during an attack of cholangitis „

66. Charcot’s triad „Intermittent pain Intermittent jaundice. „ Intermittent fever. It is triad of symptoms suggest cholangitis .

67. Reynold’s pentad „ Charcoat’s triad (Intermittent pain, intermittent jaundice, intermittent fever). „ Along with mental status changes and evidence of shock (hypotension). ! It is is found in severe cholangitis with septicemia .

68. Treatment E ndoscopic sphincterotomy and bile duct stone extraction by a Dormia basket catheter introduced through the endoscope followed by laparoscopic cholecystectomy . In absence of such facilities conventional open cholecystectomy with bile duct exploration is the standard operation.

69. Problems with ERCP stone extraction „Procedure may not be possible „ Stones larger than 1. 5 cm is not suitable for extraction endoscopically unless there is facility for contact lithotripsy. „ Risk of post procedure cholangitis , pancreatitis, bleeding or rarely duodenal perforation remains.

70. Mechanical flushing If the retained stone is small (< 1cm ). Bile duct is irrigated with a heparinized saline (250 mL of normal saline mixed with 25,000 IU of heparin) by passing the fluid through the T-tube tract for consecutive 5 days. An injection of hyoscine may relax the ampulla of vater and may facilitate the expulsion of small stones.

71. Contact dissolution If the stone is a pure cholesterol one, contact dissolution by infusing monooctanoin or methyl terbutyl ether via the T-tube tract.

72. Burhene technique „Patient is discharged home with the T-tube in situ, and a waiting period of 4–6 weeks allows the T-tube tract to get matured. „ „ A Dormia basket catheter is introduced through the T-tube tract into the bile duct and the stones may be removed. „

73. Extracorporeal shock wave lithotripsy Retained or recurrent bile duct stone may be fragmented by using extracorporeal shock wave lithotripsy.

74. Pott’s scissor is better to cut and extend the incision in the common bile duct after making incision using no 15 blade.

75. Bakes dilator no. 3 F

76. Dormia basket

77. Desjardin’s choledocholithotomy forceps

78. Fogarty catheter

79. Carcinoma gallbladder

80. Risk factors Gallstone disease. Choledochal cyst. Anomalous pancreaticobiliary duct junction. Gall bladder polyp >1 cm. Adenomyomatosis of gallbladder. Chronic typhoid carriers Carcinogenes , e.g. nitrosamines.

81. Clinical features Symptoms and signs suggestive of acute cholecystitis . Symptoms and signs of chronic biliary tract disease—right upper quadrant pain, jaundice. General symptoms and signs suggestive of a malignant disease—anorexia, weight loss, generalized weakness. Symptoms and signs suggestive of disease outside the biliary tract—gastric outlet obstr -

82. uction and gastrointestinal bleeding . Symptoms and signs suggestive of advanced malignant disease—palpable gallbladder mass, hard nodular liver and ascites . „ Carcinoma of gallbladder is suspected in a patient who has long standing history of gallstone disease in which a recent change in symptomatology and pain has occurred.

83. TNM staging Primary tumor (T ) „ Tx - Primary tumor cannot be assessed. „ T0- No evidence of primary tumor . „ Tis - Carcinoma in situ. „ T1- Tumor invades lamina propria or muscular layer. T1a- Tumor invades lamina propria . T1b- Tumor invades muscularis propria . „

84. T2-Tumor invades perimuscular connective tissue. No extension beyond serosa or into the liver . T3-Tumor invades beyond the serosa . Tumor invades into the liver. Tumor invades into one adjacent organ—stomach, duodenum, colon, pancreas, omentum or extrahepatic bile duct .

85. T4-Tumor invades portal vein or hepatic artery and two or more extrahepatic organ or structure. Regional lymph nodes (N) : „ Nx :- Regional lymph nodes cannot be assessed. „ N0- No regional lymph node metastasis. „ N1- Metastasis to nodes along the cystic duct, common bile duct, hepatic artery or

86. or portal vein. N2- Metastasis to periaortic , pericaval , superior mesenteric arteryand or/celiac artery lymph nodes. Distant metastasi (M): „ M0- No distant metastasis. „ M1-distant metastasis present.

87. Structures to remove in radical cholecystectomy Cholecystectomy with a 2 cm wedge of liver tissue at the gallbladder bed to ensure a tumor free margin. Some advocates resection of segments V and IVb . „ Lymph node dissection removing pericholedochal , periportal , hepatoduodenal , nodes along the hepatic artery, portal vein, lymph nodes behind 2nd part of duodenum, peripancreatic nodes around the head of

88. pancreas and lymph nodes around the celiac plexus.

89. Non resectable Patient factors : 1 . Age: Elderly patient tolerate radical surgery poorly 2 . Poor general condition 3 . Comorbid condition 4 . Sepsis. Tumor factors : Distant metastasis: Intraperitoneal or extraabdominal

90. 2. Extensive metastasis in both lobes of the liver 3 . Invasion of growth into the portal vascular structures 4 . Invasion of growth into the duodenum, pancreas or colon.

91. Chemotherapy 5-Fluorouracil M itomycin Cisplatin

92. Cholangiocarcinoma

93. Etiological factors „Stone disease: bile duct stones. „ Bacterial induced endogenous carcinogenes in the bile. Sclerosing cholangitis and ulcerative colitis. „ Choledochal cyst Parasitic infestation of bile duct : Clonorchis sinensis .

94. Types of cholangiocarcinoma Depending on the sites of involvement of the biliary tree : Intrahepatic . Extrahepatic −Proximal : Arises either from right or left hepatic ducts or the confluence or the proximal common hepatic duct ( Klatskin’s tumor ) −Middle : Involves the common hepatic duct and the proximal common bile duct −Distal : From distal common bile duct and the periampullary region.

95. − Distal: From distal common bile duct and the periampullary region . Depending on the gross appearance Scirrhous type: causes diffuse thickening of wall of the bile duct. Nodular variety. Papillary variety: Mainly involves the distal bile duct and the periampullary region.

96. Friable vascular growth may fillll the bile duct lumen and bleeds easily leading to hemobilia . H istological types „ Majority are adenocarcinoma . „ Rare types may include squamous cell carcinoma, adenosquamous cell carcinoma, lymphoma, carcinoid , melanoma and very rarely APUDOMAS.

97. Bismuth colrette classification of klatskin tumors

98. Clinical features „Obstructive jaundice. Dull upper abdominal pain „ Anorexia , weight loss „ May present with acute cholangitis „ Gallbladder may be palpable in distal bile duct lesion.

99. Treatment Advanced disease: Palliative treatment for relief of jaundice either by surgical bilioenteric bypass or endoscopic stenting or percutaneous transhepatic biliary drainage (PTBD ). Inoperable hilar lesion: Surgical bilioenteric bypass ( Anastomosis of a Roux-en-Y loop of jejunum to segment III duct)

100. Middle cholangiocarcinoma : excision extending from below the confluence of the hepatic duct down upto the duodenum along with pericholedochal lymph nodes . Distal or periampullary cholangiocarcinoma : Whipple pancreaticoduodenectomy . Klatskin’s tumor : E xcision of the tumor with both right and left hepatic duct anastomosis with a Roux en Y loop of jejunum.

101. Adjuvant therapy Radiotherapy. Chemotherapy C ombination chemotherapy with 5-fluorouracil + mitomycin Doxorubicin

102. Choledochal Cyst

103. Theories First theory : Babbit hypothesis. There is anomalous pancreaticobiliary duct junction. there is reflux of pancreatic juice into the bile duct. It causes increase in pressure in the bile duct and also there is enzymatic destruction of bile duct wall leading to ductal weakening and dilatation . Second theory : Abnormal canalization of bile duct during embryogenesis with distal obstruction. The distal obstruction causes

104. increased proximal pressure leading to ductal dilatation. „ Third theory : Pathogenesis of choledochal cyst involves abnormalities of autonomic innervation of the extrahepatic biliary tree. There is reduction of postganglionic neurons in the narrow distal portion of the cyst in comparison to the dilated part of the cyst.

105. Clinical features Classic triad of choledochal cyst: „ Jaundice „ Right upper quadrant mass and „ Right upper quadrant abdominal pain. Other symptoms are: Nausea, pruritis and weight loss. „ Adults may present with: features of acute pancreatitis or acute cholangitis . „ May rarely present with acute rupture of the cyst with S/S of acute biliary peritonitis.

106. Todani classification „ TypeI : Dilatation of extrahepatic biliary tree— Ia -Cystic, Ib -Focal, Ic-Fusiform . „ Type II: Saccular diverticulum of extrahepatic bile duct. „ Type III: Dilatation of intraduodenal part of bile duct— Choledochocoele . „ Type IVa : Dilatation of both intrahepatic and extrahepatic biliary tree . „ Type IVb : Multiple extrahepatic cysts.

107. „ Type IVb : Multiple extrahepatic cysts.

108. Treatment T otal excision of the choledochal cyst and hepaticodochojejunostomy with a Roux-en-Y limb of jejunum . Type III choledochal cyst ( Choledochocele ) is treated either by transduodenal sphincteroplasty or sphincterotomy . Type V ( Caroli’sdisease ) „ Confined to one lobe or segment— lobectomy or segmental resection „ Di#use disease involving both lobe —liver transplantation.

109. Diffuse disease involving both lobe —liver transplantation.