Cancer gallbladder

Cancer gallbladder

• 1.
  CANCER GALLBLADDER
• 2.
  INCIDENCE • Increases withage • 2-6 times common in women • Common among population in – Western South America – Northern India – North American Indians – Mexican Americans
• 3.
  RISK FACTORS • Gallstones •Porcelain gallbladder • Adenomatous polyps • Chronic infection with S.typhi • Carcinogen exposure(miners exposed to Radon) • Abnormal PancreaticoBiliary Duct Junction(APBDJ)
• 4.
  APBDJ • It ismore common in Asian countries • GB cancers with APBDJ – Tend to occur at an younger age – Lesser degree of female preponderance – Asociated less often with cholelithiasis – High prevalence of K-ras mutations & a late onset of p-53 mutations – High prevalence of premalignant epithelial hyperplasia with a papillary or villous histology.
• 5.
  CANCER & CALCULI •Gallstones are present in 70-90% of patients diagnosed with GB cancer • Only 0.5-3% of patients with cholelithiasis will develop GB cancer • Risk of GB cancer is increased with increasing size & duration of cholelithiasis
• 6.
  PATHOGENESIS • Chronic irritation •Dysplasia-carcinoma in-situ-invasive cancer • p 53 & K-ras(rare) mutations
• 7.
  PATHOLOGY • 80%-adenocarcinoma • Others – Small cell cancer – Squamous cell cancer – Lymphoma sarcoma • Morphologically – Infiltrative – Nodular – Papillary – Combined pattern • Staging systems – Nevin – TNM
• 8.
  CLINICAL PRESENTATION • Earlylesion • Advanced lesion – Asymptomatic – Weight loss – Abdomonal pain – Obstructive jaundice – Anorexia – Duodenal obstruction – Nausea – Palpable mass – Vomiting – Hepatomegaly – ascites
• 9.
  INVESTIGATIONS • Biochemical evidenceof obstructive jaundice • Nonspecific – Anaemia – Leucocytosis – Elevated liver enzymes – Increased ESR – Increased CRP • Tumour markers-CEA/CA 19-9 • USG • CECT • MRI/MRCP • EUS • ERCP/PTC
• 10.
  USG • Mural thickening • Mural calcification • GB mass >1 cm • Loss of normal GB wall-liver interface • Gall stones • Polyps
• 11.
  CECT • Mass protruding into the GB lumen • Mass completely replacing the GB • Focal or diffuse thickening of GB wall • Presence or absence of distant metastasis • Regional lymph node involvement • Local invasion into liver & porta hepatis
• 12.
  STAGE 0 &1A • Carcinoma in situ & T1-cancer that doesnot extend beyond the GB muscularis – Simple cholecystectomy
• 13.
  STAGE 1B • T2lesion- invasion into perimuscular connective tissue of GB – Re-exploration revealed residual disease in 40-76% – Regional lymphnode metastasis in 28-63% • Exploration with en bloc resection of the GB with 2 cm of adjacent liver(non-anatomoic) with regional lymphadenectomy of the hepatoduodenal ligament • En-bloc resection with anatomic resection of liver segments 4b & 5
• 14.
  STAGE II • T3Lesion-locally advanced cancers that perforate the GB serosa or directly involve the liver or adjacent organ • Hepatic resection encompassing segment 4b & 5 or trisegmentectomy with adjacent organs
• 15.
  STAGE III &IV • Unresectable • Median survival with unresectable disease is less than 6 months • If detected intraoperatively – Radio-opaque clips – No data to support debulking cholecystectomy
• 16.
  PROGNOSIS • 5-year survivalrate is 5% • Median survival 12 months(stage IA-III) • Median survival 5.8 months(stage IV)
• 17.
  WHY POOR PROGNOSIS? •Usually diagnosed at a late stage • Aggressive nature • Clinical presentation mimics that of biliary colic/chronic cholecystitis • Incidental diagnosis at surgery • Incidental diagnosis after pathology report
• 18.
  SURVIVAL RATE S.NO STAGE 5 YR.SURVIVAL RATE 1 I 60% 2 II 39% 3 III 15% 4 IV 1% Median survival 12 months(stage IA-III) Median survival 5.8 months(stage IV) NCCN guidelines 2010
• 19.
  EXTENT OF LYMPHADENECTOMY