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GALLBLADDER CANCER.pptx
- 1. GALLBLADDER CANCER DR SUJANPANDEY SURGERY RESIDENT
- 2. ANATOMY OF GALLBLADDER •Length = 7 to 10 cm • Capacity = 30-50 ml • Divided into Fundus Body Infundibulum neck
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- 4. INTRODUCTION EPIDEMIOLOGY: Most commonbiliary malignancy. Occurs in 6th -7th decade Two to three times more common in women than in men. Highest incidence in india ,pakistan ,north america ,native americans and immigrants from latin america. Only 15-17% are resectable. 5 year overall survival is <5%(median survival rate 6 months.
- 5. ETIOLOGY 3% ofgallstones with cholecystitis will develop carcinoma of gallbladder. 90% of carcinoma of gallbladder is associated with gallstones. Risk of developing carcinoma in gallstone disease is 7–10 times more than general population. Relative risk is less if stone size is less than 2 cm it is 10 or more in number and if stone size is more than 3 cm. Choledochal cyst, anomalous pancreaticobiliary duct junction (20%), cholesteroses of gallbladder, gallbladder polyp more than 10 mm in size or more than 3 in number or adenomatous polyp, PSC.
- 6. Chronic typhoidcarriers, carcinogens, inflammatory bowel disease, hepatitis B and hepatitis C virus infection. Porcelain gallbladder is more prone for malignant transformation (10-25%) and 90% of them are inoperable tumours. Nitrosamines. Infection :H pylori , salmonella Polypoid lesions (GB polyp), xanthogranulomatous cholecystitis.
- 7. PATHOLOGY • SITE OFORIGIN: Fundus (60%) Body (20%) Neck (10%)
- 8. • Morphological Typesof Carcinoma Gallbladder Polypoid/papillary- • Better prognosis. • Cauliflower appearance • Fil lumen with only minimal invasion of wall • Lower incidence of node metastasis Nodular- • Mass forming • Show early invasion through wall into liver or neighbouring organ ,but easier to control surgically because of sharply defined borders. Infiltrative: • most common form • Cause thickening and induration of gallbladder wall • spread in subserosal plane . • Margin not well defined Combined (nodular-infiltrative).
- 9. Histological types Adenocarcinomas (80-90%) Squamous/adenosuamous(2-4%) Neuroendocrine carcinoma(3%) Sarcoma (0.2 -1.6%) Unspecified (1.1%) melanoma (<1%).
- 10. Spread of CarcinomaGallbladder: • GB located under liver adjacent to segment Ivb and V . • Wall considerably thinner than other hollow organs . • Lacks submucosal layer. • Has thin wall , a narrow lamina propria , only single muscle layer. • Serosa along liver edge is more densely adherent to liver (cystic plate).
- 11. Modes of spread •Direct spread to liver (segment IV and V), bile duct, duodenum, colon and kidney. • Lymphatic—lymph node of Lund, periportal nodes, peripancreatic and periduodenal nodes. • Intraperitoneal • Intraductal • Blood spread—to liver(m/c), lungs and bones. • Perineural spread is also known to occur.
- 12. STAGING • NEVIN STAGINGSYSTEM • JAPANESE BILIARY SURGICAL SOCIETY • AJCC / TNM STAGING SYSTEM 8TH EDITION
- 13. NEVIN STAGING • StageI – Intramural • Stage II – Spread to muscularis propria • Stage III – Spread to serosa • Stage IV – Spread to cystic lymph node of Lund • Stage V – Direct spread to adjacent organs/metastases.
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- 16. Features of Carcinomaof Gallbladder: • Pain in right hypochondrium, mass in right upper abdomen which is hard and nontender. • Jaundice is common. • Significant weight loss in short duration, anorexia • Acute presentation of cholecystitis. • Palpable nodular liver secondaries, ascites. • It is common in places where there is more prevalence of gallstone disease. • It is common in females.
- 17. • Incidentally confirmedas carcinoma gallbladder histologically after cholecystectomy for chronic cholecystitis. • Palpable mass is clearly an omnious finding and predicts a high rate of irresectability and advance disease. • Jaundice is representative of locally advance disease. • Sign of advance disease (wt loss, jaundice ,anorexia ,palpaple mass) • Three clinical presentations – 1. Clinically obvious type with pain, obstructive jaundice, mass. 2. Early GB cancer mimics GB stone disease. 3. Atypical as unusual features.
- 18. DIAGNOSIS • Laboratory examinationgenerally is not helpful except to identify signs of advanced disease, such as: • Anemia • Hypoalbuminemia • Leukocytosis, and • Elevated alkaline phosphate or bilirubin levels. • Carcinoembryonic antigen and carbohydrate antigen 19-9 may be elevated in gallbladder cancer.
- 19. Investigation • Ultrasound abdomen. •CT abdomen to see operability. • US-guided FNAC. • Liver function tests. • MRCP. • Staging Laparoscopy. • CA 19-9 is elevated in 80% of cases.
- 20. USG ABDOMEN • Ultrasonographyis generally the first examination used in the evaluation of right upper quadrant pain. Ultrasonographic findings: Gallbladder cancer include an irregularly shaped lesion in the subhepatic space, heterogeneous mass in the gallbladder lumen, and asymmetrically thickened gallbladder wall . The finding of a polyp larger than 10 mm should raise the suspicion of gallbladder cancer.
- 21. CT abdomen • Forcomplete staging • Evaluation of regional nodes . • Diagnosis of extrahepatic disease • Identify Hepatic artery or portal venous invovement. • More anatomic information than ultrasound .
- 22. CT SCAN Features suggestiveof CA GB : Heterogenous mass replacing gallbladder. Focal or diffuse wall thickening. Heterogenously enhancing discrete intraluminal mass. Discontinous thickening of gallbladder mucosa.
- 23. • MRI/MRCP: • Sensitivitiesof 70-100% for hepatic invasion • 60-75% for lymphnode metastasis. • But does not change the preoperative stage as determined by CT SCAN. • TYPICAL CHOLANGIOGRAPHIC FINDING: long stricture of common hepatic duct.
- 24. Unrestable or incurableCA GB:percutenous biopsy or FNAC for confirmatory tissue diagnosis. PET : • Detects occult peritoneal ,omental and LN metastases. • Sensitivity:57-86% • Specificity:78-94%
- 25. TUMOR MARKER • BESTtumor marker of CA GB carbohydrate antigen 19-9(>20u/ml) 75% sensitivity and specificity . • CEA >4ng/ml is associated with 93% specificity but 50% sensitivity.
- 26. Management modalities available •1)staging laparascopy • 2)laparotomy • 3)interaortocaval lymphnode frozen section • 4)cholecystectomy –simple/radical • 5)multivisceral resection • 6)CBD excision • 7)Major hepatectomy • 8)Adjuvent therapy
- 27. Staging laparoscopy • Preventunnecessary surgical exploration (38-62%) • Can determine oncologicaly unresectable(23%) • Detection rate increases by : laparoscopic ultrasound . inter-aortocaval LN frozen section evaluation.
- 28. Standard Surgical Treatment •Complete resection with negative margins remains the only curative treatment. • T1a with negative cystic duct margin :no further therapy . • T1a with positive cystic duct margin: Resection of cystic duct or CBD to negative margin . • • Radical / extended cholecystectomy: recommended for T1b , T2 and some T3 with localised hepatic invasion and limited regional node involvement.
- 29. RADICAL/EXTENDED CHOLECYSTECTOMY • Cholecystectomy(excision ofwhole GB). • Limited hepatic resection (typically segments IVb and V) • Portal lymphadectomy(cystic duct,pericholedochal ,periportal and posterior pancreaticoduodenal and local interaortocaval lymphnodes,celiac axis node) along with hepatoduodenal ligament .
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- 33. • Frozen sectionbiopsy from cystic duct stump should be done to identify for the existence of microscopic tumour. If present, CBD resection and hepaticojejunostomy is done . Open approach rather than laparoscopic is ideal for carcinoma gallbladder. • Hemihepatectomy with cholecystectomy with nodal clearance. • During laparoscopic cholecystectomy, any suspicious of GB cancer, procedure should be converted into open cholecystectomy.
- 34. • T4 N0:extended cholecystectomy with extended right hepatectomy. • N1 or hilar invasion:Extended cholecystectomy with CBD resection. • N2 or M1 disease :clinical trial (chemoradiation or chemotherapy)
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