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Seminar on gi malig.pptx

COLORECTAL CARCINOMA AND ITS MANAGEMENT.....

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Seminar on gi malig.pptx

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  2. 2. GASTRO INTESTINAL MALIGNANCIES {ANAL CANAL CARCINOMA AND ITS MANAGEMENT} PRESENTED BY - DR ABHISHEK JOHARI {J.R.2 GENERAL SURGERY} MODERATOR – DR SMITA CHAUHAN SINGH {DNB GENERAL SURGERY}
  3. 3. What this presentation covers INTRODUCTION  EPIDEMIOLOGY  ETIOLOGY  RISK FACTORS  CARCINOGENESIS  MORPHOLOGY/PATHOLOGY  CLINICAL FEATURES  CLASSIFICATION  SCREENING  DIAGNOSIS  STAGING  TREATMENT  FOLLOW UP  RECENT ADVANCES
  4. 4. ** Colorectal cancer (CRC) starts in the colon or rectum **3rd most common form of cancer **2nd leading cause of cancer deaths in US **Mortality has declined over the past 20 years with better screening, diagnosis and treatments **Screening for/removing polyps early is the best way to prevent and cure CRC
  5. 5. Colorectal CancerColorectal Cancer Sporadic (average risk) (65-85%) Family History (10-30%) Hereditary nonpolyposis colorectal cancer (HNPCC) (5%) Familial adenomatous polyposis (FAP) (1%) Rare syndromes (<0.1%)
  6. 6. Adenocarcinoma 98% of all cancers in large intestine  arise in adenomatous polyps, generally curable by resection
  7. 7. Epidemiology peak incidence: 60 to 70 years of age < 20% cases before age of 50 adenomas – presumed precursor lesions for most tumors males affected ≈ 20% more often than females
  8. 8. Epidemiology worldwide distribution highest incidence rates in United States, Canada, Australia, New Zealand, Denmark, Sweden, and other developed countries
  9. 9. Etiology genetic influences: ulcerative colitis or polyposis syndrome hereditary nonpolyposis colorectal cancer syndrome (HNPCC, Lynch syndrome) germ-line mutations of→ DNA mismatch repair genes
  10. 10. Etiology environmental influences: dietary practices  low fiber  high carbohydrates  high fat content  decreased intake of (vitamins A, C, and E)
  11. 11. Colorectal Cancer Risk FactorsColorectal Cancer Risk Factors Age  90% in 50 yrs and older Gender  male predominance, Race/Ethnicity  African Americans in U.S.,  Alaska Natives, some American Indian tribes, Ashkenazi Jews Increased risk with: Personal history of inflammatory bowel disease, adenomatous polyps, colon cancer,etc **Lifetime risk for CRC increases for members in which index case is young {<50 yrs}and relative is first degree.
  12. 12. Risk Factors - PolypsRisk Factors - Polyps Different types • Hyperplastic Minimal cancer potential • Adenomatous Approximately 90% of colon and rectal cancers arise from adenomas
  13. 13. Normal to Adenoma to Carcinoma Human colon carcinogenesis progresses by the dysplasia/adenoma to carcinoma pathway
  14. 14. Genetic Model of Colorectal CancerGenetic Model of Colorectal Cancer Normal Epithelium Adenoma Late Adenoma Late Cancer Early Cancer Dwell Time: Many decades 2-5 years 2-5 years Mutation APC K-ras p53 Bat-26 (HNPCC) Bat-26 (Sporadic) Optimum phase for early detection
  15. 15. Carcinogenesis chromosome instability pathway
  16. 16. Carcinogenesis mismatch repair (microsatellite instability) pathway
  17. 17. Morphology begin as in situ lesions tumors in the proximal colon: polypoid, exophytic masses that extend along one wall of the cecum and ascending colon
  18. 18. Morphology in the distal colon: annular, encircling lesions that produce “napkin-ring” constrictions of the bowel and narrowing of the lumen both forms of neoplasm eventually penetrate the bowel wall and may appear as firm masses on the serosal surface
  19. 19. Clinical Features asymptomatic for years symptoms develop insidiously cecal and right colonic cancers: fatigue weakness iron deficiency anemia left-sided lesions: occult bleeding changes in bowel habit crampy left lower quadrant discomfort anemia in females may arise from gynecologic causes, but it is a clinical maxim that iron deficiency anemia in an older man means gastrointestinal cancer until proved otherwise
  20. 20. SYMPTOMS RECTAL BLEEDING LOWER RECT. TENESMUS ALT. OF BOWEL HABITS UPPER.
  21. 21. Staging Rectal Cancer Modified Dukes staging.. A: Contained within the bowel wall. B: Penetrates the bowel wall. C: Metastasis to Lymph nodes. D:Metastasis to distant organ. TNM Stage I: Confined to the mucosa or contained with bowel wall (T1, T2). Stage II: penetrates the bowel wall (T3, T4). Stage III: Metastasis to lymph nodes (N1, N2). Stage IV: distant spread.
  22. 22. • Patients with a family history, a history of adenomatous polyps, and a history of ulcerative colitis should be considered for colonoscopic surveillance. • Faecal occult blood testing is the only population screening modality that has been shown to reduced colorectal cancer mortality.
  23. 23. Benefits of ScreeningBenefits of Screening Cancer Prevention Removal of pre-cancerous polyps prevent cancer Improved Survival
  24. 24. CRC Screening GuidelinesCRC Screening Guidelines What Else is New?What Else is New? Two new tests recommended: Stool DNA (sDNA) and Computerized tomographic colonography (CTC)-sometimes referred to as virtual colonoscopy.
  25. 25. 2008 CRC Screening GuidelinesGuidelines Beginning at age 50, both men and women at average risk for developingBeginning at age 50, both men and women at average risk for developing colorectal cancer should use one of the screening tests below:colorectal cancer should use one of the screening tests below: Tests That Detect Adenomatous Polyps and CancerTests That Detect Adenomatous Polyps and Cancer Flexible sigmoidoscopy (FSIG) every 5 years*, or Colonoscopy every 10 years, or Double contrast barium enema (DCBE) every 5 years*, or CT colonography (CTC) every 5 years* Tests That Primarily Detect CancerTests That Primarily Detect Cancer Annual guaiac-based fecal occult blood test (gFOBT) with high test sensitivity for cancer*, **, or Annual fecal immunochemical test (FIT) with high test sensitivity for cancer*, **, or Stool DNA test (sDNA), with high sensitivity for cancer*, interval uncertain *Colonoscopy should be done if test results are positive. **For gFOBT or FIT used as screening test, the take-home multiple sample method should be used. gFOBT or FIT done during a digital rectal exam in the doctor’s office is not adequate for screening.
  26. 26. Stool DNA Test (sDNA)Stool DNA Test (sDNA) • Rationale • Fecal occult blood tests detect blood in the stool – which is intermittent and non-specific • Colon cells are shed continuously • Polyps and cancer cells contain abnormal DNA • look for abnormal DNA from cells that are passed .
  27. 27. Stool DNAStool DNA Limitations  Misses some cancers  Sensitivity for adenomas is low  Technology (and test versions) are in transition  Costly  Not clear how to manage positive stool DNA test if colonoscopy is negative
  28. 28. CT ColonographyCT Colonography Rationale  detailed evaluation of the entire colon  high level of sensitivity for cancer and large polyps  Minimally invasive (rectal tube for air insufflation)  No sedation required
  29. 29. CT Colonography (CTC)CT Colonography (CTC) CTC Image Optical Colonoscopy
  30. 30. CT ColonographyCT Colonography 3-D view2-D view PolypPolyp
  31. 31. CTC – Extra-Colonic FindingsCTC – Extra-Colonic Findings Asymptomatic cancers outside of colon and rectum Aortic aneurysms Renal and gall bladder calculi
  32. 32. CT ColonographyCT Colonography Limitations Requires full bowel prep Colonoscopy is required if abnormalities detected, sometimes necessitating a second bowel prep Steep learning curve for radiologists Limited availability
  33. 33. • Colonoscopy is the gold standard investigation. • Barium enema underdiagnose cancer in the sigmoid colon and overdiagnose in the caecum. • Double contrast barium enema should be supplemented by flexible sigmoidoscopy.
  34. 34. • All patients should have a contrast enhanced computed tomography of the liver and chest to look for metastatic disease. • MRI is the most accurate means of preoperative staging for rectal cancer. • Endoluminal ultrasound is particularly useful in distinguishing benign rectal tumours from early cancer.
  35. 35. Endorectal Ultrasound Accurate evaluation of depth of invasion Good assessment of lymph nodal disease especially if positive Critical for pre-operative and pre-RT staging Important tool in post-operative and post-RT f/u
  36. 36. MRI HIGH RESOLUTION THIN SLICE (<1mm) DEPTH OF EXTRAMURAL SPREAD ACCURATELY IDENTIFIED (AIDS CIRCUMFERENTIAL RESECTION MARGIN)
  37. 37. MRI DETECTS EXTRAMURAL VENOUS INVASION (EMVI)  POOR PROGNOSIS WITHOUT CH/RT IF EMVI PRESENT
  38. 38. • Surgery is the only potentially curative treatment for colorectal cancer. • Anastomotic dehiscence rates should be less that 5% in colonic surgery. • The outcome of rectal cancer surgery is highly dependent on the quality of the surgery, which is based on mesorectal excision. • Anastomotic dehiscence rates after total mesorectal excision tend to be high, and consideration should be
  39. 39. Basic Surgical Approach Level of Tumor Upper rectal Mid rectal Lower rectal Procedure Anterior Resection Low Anterior Resection Local Excision LAR with TME APR
  40. 40. Historical vignettes 1826: Lisfranc 1st report of local excision 1979: Heald introduces TME Total Mesorectal Excision 1984: Buess introduces TEM Transanal Endoscopic Microsurgery
  41. 41. A-B right hemicolectomy A-C extd right hemicolectomy B-C transverse colectomy C-E left hemicolectomy D-E sigmoid colectomy D-F anterior resection D-G (ultra) low anterior resection D-H abdomino-perineal resection A-D subtotal colectomy A-E total colectomy A-H total procto-colectomy A B C D E F G H © CCrISP Australasia 3rd Edition Colorectal Major Resections
  42. 42. Rectal Ca Local excision - Recommended criteria: <10 cm from anal verge Tumour < 4cm and <40% of circumference Favourable T1 stage  Well- moderate differentiation  No lymphovascular or perineural invasion  Non-mucinous tumours No nodal disease
  43. 43. Rectal Ca Local excision – Transanal approaches Transanal excision Full thickness excision with 1cm margin Rectal defect closed transversely Local recurrence high
  44. 44. Rectal Ca Local excision – Transanal approaches Transanal Endoscopic Microsurgery (TEM) Developed for lesions out of reach from transanal approach Can be used for benign lesions above the peritoneal reflection
  45. 45. Rectal Ca Local excision - Ablative procedures Electrocoagulation Used as palliative & curative Rx Disadv: no tissue spec, 1/3 conversion to radical surgery, 20% secondary haemorrhage Poor outcomes Endocavitatory radiation Direct contact radiation 10-12000 cGy Useful in palliative setting In select pts 5yr survival & local control of 76-90%
  46. 46. Radical excision-Total Mesorectal Excision(TME) Introduced by RJ Heald in 1979 Use of sharp dissection under vision to mobilize the rectum rather than the conventional blunt finger dissection Local recurrence: Conventional surgery: 11.7 - 37.4% TME surgery: 1.6 - 17.8% Higher leaks rates reported possibly due to: Devascularisation of distal rectal stump Lower anastamosis Other factors: stomas, drains
  47. 47. Reconstruction of Neorectum  Straight end to end  (Anterior resection syndrome)  Colonic J Pouch  Increases volume of neorectum  Size is critical to functional outcome, recommend 5-8 cm  Sigmoid colon should not be used  lower anastamotic leaks compared to end-to-end anastamosis  Coloplasty  New technique introduced in 1999  Better in narrow pelvis and limited length of colon  Long incision closed transversely
  48. 48. Reconstruction of Neorectum Hand sewn sutured anastamosis 1982: Parks and Percy performed the coloanal sutured anastamosis ‘Pulled through’ coloanal anastamosis (Turnbull & Cuthbertson) Stapled anastamosis Circular stapled technique Double staple technique  For low and coloanal anastamosis
  49. 49. Abdominoperineal Resection Described by Sir Ernest Miles 1908 1-2 surgeons TME rectal dissection Anus sutured closed Wide perineal dissection, starting from posterior to lateral then anterior Anterior dissection can proceed cranio-caudal or vice versa Drain the pelvic space Reduced rates of APR  Coloanal anastamosis  Acceptance of smaller margins  Downsizing by chemoradiotherapy
  50. 50. Sacro-coccygectomy with APR
  51. 51. Laparoscopic Resection
  52. 52. Anastomotic leak Inraabdominal abscess, stoma retraction, haemorrhage, Dvt, wound infection,
  53. 53. • stage C colorectal cancer -5-fluorouracil based adjuvant chemotherapy. • Preoperative radiotherapy preferable to postoperative treatment. • Preoperative radiotherapy reduces the risk of local recurrence of rectal cancer,
  54. 54. USE OF CH/RT (NEOADJUVANT/ADJUVANT) PTS WITH POOR HISTOLOGY PTS WITH EXTRA MURAL SPREAD (MRI) PTS WITH INVOLVED NODES (ERUS) PTS WITH EMVI (MRI)
  55. 55. Agent FDA approval status Bevacizumab 2004 (Anti-VEGF Ab) Cetuximab 2004 (Anti-EGFR Ab) Panitumumab 2006 (Anti-EGFR Ab)
  56. 56. The Rational for Neo-adjuvant therapy Early lesions --T1 and T2 -- carry a 10% to 25 % chance of lymph nodal disease. Down staging of T3 tumors aid sphincter savage. Multi-modality approach can cover for metastatic lymph node disease. Radical resection can be very morbid.
  57. 57. Advantages of Neoadjuvant Therapy Sphincter preservation Decreased or delayed local recurrence Increase survival Certainty of treatment Improved symptoms
  58. 58. Disadvantages Treating tumors that don’t need therapy Delaying surgery Increase morbidity sphincter dysfunction sexual dysfunction urinary dysfunction Irradiated bowel
  59. 59. Contra-indications to neo-adjuvant therapy Upper rectal cancers Early T1 lesions Obstruction Known stage IV disease Patient can not tolerate therapy.
  60. 60. • Patients with isolated liver metastases should be considered for liver resection. • Systemic chemotherapy can prolong survival, but is palliative. • Although chemotherapy is still largely based on 5-fluorouracil, newer agents, notably capecitabine and irinotecan, are showing significant promise.
  61. 61. Follow up is carried out for: • Early detection of metastases. • Detection of metachronous polyps or cancers. • Psychological support.
  62. 62. A regimen for follow-up Clinic visits q 6 months CEA q 6 months Rigid Sigmoidoscopy q 6 months Rectal Ultrasound q 6 months Colonoscopy at 1 year CT and PET as clinically indicated.
  63. 63. Rising CEA and Recurrent Disease Rising CEA represents recurrent disease which may be local, distant, or both.
  64. 64. MOLECULAR BIOLOGY  DNA CHIP TECH. – DNA SEQUENCE CHECKED -- APC GENE – FAP -- MISMATCH REPAIR GENES – HNPCC SUCH PTS.(5%) PUT ON A SURVEILLANCE PROG. --PROPHYLACTIC SURGERY
  65. 65. MOLECULAR BIOLOGY DNA SEQUENCE OF MICROSATELLITE INSTABILITY -- GOOD RESPONSE WITH 5 FU CHEMO. P21 MARKER POSITIVE – RADIOSENSITIVE
  66. 66. MOLECULAR BIOLOGY P53 PROTEIN MUTANT EXPRESSED -- RADIORESISTANT KRAS, DCC, AND P53 -- IF +ve – POOR PROGNOSIS MICROSATELLITE INSTABILITY OR LOW Cox2 EXPRESSION & P21 MARKER – IF +ve – GOOD PROGNOSIS
  67. 67. THANK YOU

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