Large Bowel Tumours for Residents-1.pptx

large bowel tumors general surgery presentation

1. Large Bowel Tumours For Residents JCB Dakubo

2. OUTLINE BASIC SCIENCE Anatomy Physiology Epidemiology Classification Pathology Pathogenesis Staging MANAGEMENT Diagnosis Screening Surgical Rx and its principles Radiotherapy Chemotherapy Follow-up

3. PART ONE BASIC SCIENCE

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5. Embryonic origin of segments of the intestine and derived arterial supply 7/23/2019 5

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7. Venous drainage of Rectum bowel 7/23/2019 7

8. Venous drainage of Rectum bowel 7/23/2019 8

9. Lymphatic drainage of the rectum 7/23/2019 9

10. Lymphatic drainage of the Rectum bowel 7/23/2019 10

11. Sympathetic supply of the intestine 7/23/2019 11

12. Visceral pain is transmitted along the sympathetics, since the viscera has no specialized pain fiblres. This is useful clinically in helping us predict the diseased organ The stomach and duodenum are innervated by sympathetic fibres from T8 and T9 (foregut) The jejunum, ileum up to proximal 2/3 of transverse colon are innervated from T10 (midgut) Distal 1/3 of transverse colon to rectum are innervated from T11, T12 (hindgut) 7/23/2019 12

13. So pain from foregut structures is experienced in the epigastrium Pain from the Mid-gut is experienced in the central abdomen (peri-umbilical region) Pain from hind-gut structures is experienced in the hypogastrium 7/23/2019 13

14. Projection of visceral pain on the abdomen 7/23/2019 14

15. Nerve supply of the Rectum bowel 7/23/2019 15

16. Nerve supply of the Rectum bowel 7/23/2019 16

17. Fascia Planes of the pelvis 7/23/2019 17

18. Physiology of the Large bowel Right Colon It is the ‘fermentation Chamber’ of the gut Consortia of bacteria break down Soluble Non- Statch polysaccharides into short chain fatty acids (acetic acid, propoinic acid and butyric acid) Indigestible fats and proteins are also similarly broken down into indoles and other substances The content of the right colon is therefore still liquid Completion of digestive enzyme denaturation occurs here 7/23/2019 18

19. Left Colon . It is the ‘desiccation chamber’ of the colon Maximal absorption of water and electrolytes take place here to produce solid faeces . Temporary storage of faeces takes place here in the sigmoid and then moved into the rectum by mass movement of the bowel Rectum It is mainly for storing faeces and its evacuation. It initiates the defaecation reflex, The recto-Anal Inhibitory reflex and anal continence 7/23/2019 19

20. Types of movements in the colon Peristalsis Segmental movements Mass movements 7/23/2019 20

21. Epidemiology About 1.2 million new cases of large bowel malignancies are diagnosed and about 600,000 people succumb to this condition annually worldwide Adenocarcinomas of the large bowel develop from adenomas which are either the conventional adenomas or Serrated adenomas

22.   Age adjusted incidence rate per 100,000 population Countries ≥ 50.0 N. America, UK, Europe, Scandinavia, Russia, Australia 26.0 Turkey, Italy, Greece, Brazil, Argentina, Chile 15.0 China, South Africa, Mexico 7.4 India, North Africa, Ethiopia, Kenya, Uganda, Middle East <4.6 Sub-Saharan African Countries 7/23/2019 22

23. Badoe 1956-1965 Badoe 1970-1975 Naaeder et al 1987-1991 Dakubo et al 1997-2007 M 23 35 66 197 F 18 25 68 167 TOTAL 41 60 137 359 Approximate annual new cases N o of cases per 100,000 pop./yr 4.1 1 10 1.3 26.8 1.8 32.6 1.2 Population of Accra during study period 388,396 715,177 1,431.099 2,905,726 Published studies on colorectal cancer in Accra since 1956 to date and the population of Accra during the study periods . 7/23/2019 23

24. Distribution of cancers in the colon and rectum 7/23/2019 24

25. In Sub-Saharan Africa about 50% of cancers of the large bowel are located in the rectum Of these about 80% of them are within reach of the examining finger Emphases on the importance of Per Rectal Examination

26. Risk factors for developing large bowel tumours 1. Age; Age alone is a risk factor for the development of colon and rectal cancers. The peak is in the sixth decade of life when enough gene mutations have accumulated to cause cancer

27. 2. Environmental factors a. Imbalance in the energy equation; high energy intake against low energy expenditure (obesity) b. intake of refined diets, red or processed meat, fat. c. Alcohol abuse d. Smoking e. Low intake of vegetables, fruits, folate , fish etc d. Consumption of milk and calcium is protective 7/23/2019 28

28. 3. Luminal - Long transit time - Low amounts of short chain fatty acids (butyrate derived from bacterial fermentation of soluble non-starch polysaccharides if the main colonocyte fuel). High concentrations of it slows the progression of adenomas into large ones and also transition to malignancy. - High colonic Ph - High concentration of secondary and tertiary bile salts 7/23/2019 29

29. Classification of large bowel tumours Benign (polyp) Malignant

30. POLYPS A polyp is any projection mass from the wall of a luminal structure which leads to elevation of the mucosa Two main types of polyps are Neoplastic polyps Non-neoplastic polyps ( Pseudopolyps / hyperplastic polyps) 7/23/2019 31

31. Some neoplastic polyps are premalignant while others are not. Polyps that are not premalignant include: The hamartomas , the junenile polyps, Peutz-Jegher’s Polyps Lieomyomas Lipomas Neurofibroma 7/23/2019 32

32. Polyps that originate from the epithelium are referred to as Adenomas. Cancers of the large bowel develop from these adenomas 7/23/2019 33

33. 7/23/2019 34 Category Type of Adenoma Qualification of dysplasia Conventional Adenomas Tubular Adenoma Tubulovillous Adenoma Villous Adenoma ±High-grade dyspasia /invasive adenocarcinoma Serrated Adenomas Sessile Serrated Adenoma/polyp Traditional Serrated Adenoma Mixed Serrated polyps; unidentified ± dysplasia (low/high-grade) ± high-grade dysplasia With or without dysplasia Hyperplastic Polyp Microvesicular type (MVHP) Goblet cell-rich type (GCHP) No dysplasia No dysplasia A Simplified 2010 WHO Classification of Adenomas that cause cancer of the large bowel

34. Adenomatous polyps Features of increased risk of malignant transformation Size; diameter more than 1cm Sessile/Flat adenomas Morphological type; Villous, Tubulo -villous, Tubular High grade dysplasia Bleeding tendencies

35. Flat Polyps Typically measure 2cm in size and elevated less than 2.5cm above the surrounding normal mucosa. Those larger than 2cn are termed ‘lateral spreading’ lesions. They are associated with a malignancy rate of 5-23%; for lesions that measure from 1.6-2.0cm the malignancy rate is 10.4% while whilst those larger than 2.0cm in diameter the malignancy rate rises to 22.1%.. Besides polyp size the other feature of these polyps that is associated with increased risk of malignancy is the presence of central depression.  They are mostly located in the right colon and are easy to miss at colonoscopy, barium enema and virtual colonoscopy studies. 7/23/2019 36

36. SERRATED POLYPS/ADENOMAS Serrated adenomas are characterized by saw-tooth appearance on histology. They are rare polyps usually of the proximal colon and have diameter greater than 1cm. They have high incidence of microsatellite instability (MSI-H), are associated with varied degrees of dysplasia and are premalignant. They are sub-classified into Sessile serrated adenoma/polyp, traditional serrated adenoma, hyperplastic polyps and mixed serrated polyps unclassified. 7/23/2019 37

37. Hyperplastic polyps . Small polyps typically located in the distal colon and rectum (90% in the rectosigmoid). About three-qaurters of these polyps measure less than 0.5cm, and less than a quarter are larger than 1.5cm. They are subdivided based on their mucin characteristics into: 1. Microvesicular hyperplastic polyps (Goblet cell-poor hyperplastic polyps) and 2. Mucin poor hyperplastic polyps (Goblet cell-rich hyperplastic polyps) 7/23/2019 38

38. Traditional Serrated adenoma. They have a viliform configuration and appear protuberant or pedunculated rather than sessile with a uniform population of dysplastic epithelial cells that have elongated nuclei and eosinophilic cytoplasm. They measure less than 1.5cm in diameter. About 80% of these lesions are located in the left colon, mostly in the rectosigmoid.   7/23/2019 39

39. Mixed Serrated polyps. They contain components of both sessile serrated and traditional serrated polyps. 7/23/2019 40

40. THE POLYPOSIS SYNDROMES   These are syndromes some of which are still not well characterized. The polyps in these syndromes are premalignant lesions and include: 7/23/2019 41

41. Familial Adenomatous Polyposis syndrome (FAP). It is an inherited adenoma syndrome which is autosomal dominant with more than 95% penetrance. It accounts for <1% of colorectal cancer and arises as a result of APC germline mutation located on chromosome 5. Variants of this condition are Gardner’s syndrome, Turcot’s syndrome and Oldfield’s syndrome 7/23/2019 42

42. Gardner’s syndrome . The APC gene is mutated. In addition to the colorectal polyposis the patients have either of multiple sebaceous and dermoid cysts, desmoids tumours or osteomas of the skull and mandible. 7/23/2019 43

43. Turcot’s syndrome . It is a description of familial adenomatous polyposis coli in association with malignant tumours of the central nervous system. It arises as a result of APC gene mutation. The polyposis of the colon and rectum is associated with medulloblastoma, anaplastic astrocytomas and ependymomas, and glioblastoma. 7/23/2019 44

44. Oldfields Syndrome . There is APC gene mutation and shows phenotylically as colorectal polyposis, and carcinomas elsewhere in addition to multiple sebaceous cysts. 7/23/2019 45

45. 2. Juvenile polyposis syndrome . It is a rare disease and the polyps involve the large bowel but could be in conjunction with polyps in other part of the gastrointestinal tract. It has increased risk of colorectal, stomach and small bowel cancer. The diagnosis is considered when ≥ 3 juvenile polyps are found in the colon, juvenile polyps in stomach or small bowel, juvenile polyps with a positive family history of juvenile polyposis syndrome. 7/23/2019 46

46. Juvenile polyposis of the stomach in a 16yr old girl 7/23/2019 47

47. 3. Hyperplastic / Serrated polyposis syndrome. It is characterized by numerous hyperplastic polyps distributed throughout the large bowel. They are diagnosed clinically based on: At least 5 histologically diagnosed hyperplastic polyps proximal to the sigmoid colon, of which 2 are of diameters greater than 1cm; OR Any number of hyperplastic polyps that occur proximal to the sigmoid colon in an individual who has a first-degree relative with hyperplastic polyposis syndrome; OR More than 30 hyperplastic polyps of any size that are distributed throughtout the colon. 7/23/2019 48

48. 4. Peutz-Jeghers Polyposis Syndrome. Very rare disease, it is invariably familial with few sporadic cases reported. It is an autosomal dominant trait The polyps are frequently in the upper small bowel, but the stomach and the large bowel are not spared. It is a premalignant condition for cancers of the colorectum, breast, stomach, small bowel and pancreas. 7/23/2019 49

49. 5. Cowden’s syndrome. It is a very rare disease. It is a PTEN gene mutation. Polyps are found in all sections of the bowel including the oesuphagus and these are in association with fibrocystic disease of the breast, non-toxic goitre , breast and thyroid cancers 7/23/2019 50

50. 6. MUTYH-Associated Polyposis (MAP). An autosomal recessive lesion with clinical features similar to Familial Adenomatous Polyposis Coli. The mutation is in the MYH gene which is a repair gene for APC. It is associated with duodenal polyposis. 7/23/2019 51

51. Classification: Cancer Histological types of cancers of the large bowel: Adenocarcinoma (95% of the cancers). Well, Moderately-well diffrerentiated , mucinous , anaplastic , signet-ring cell Neuroendocrine tumours Squamous cell carcinoma Lymphoma Gastrointestinal stromal tumours (GIST) Etc 7/23/2019 52

52. Classification of adenocarcinoma Sporadic cancers Colitis associated cancers (these are cancers developing in the large bowels of patient with ulcerative colitis, Crohns disease and the Irritable Bowel Disease In colitis associated CRC there is a generalised field change, genetically, and so multiple tumours can develop at the same time or soon after each other The risk of developing a cancer is related directly to the extent of bowel affected and the duration of the disease

53. Sporadic Colorectal Cancers are further divided into; Hereditary cancers Non-Hereditary cancers Familial cancers Hereditary cancers are those associated with; FAP HNPCC In Sporadic cancers the field change is usually focal and can be single or multiple 7/23/2019 54

54. Hereditary and Nonhereditary cancers Non-hereditary cancers; account for about 94-96% of all colorectal cancers Individuals have no family history or inherited predisposition to colorectal cancer Usually affects individuals above the age of 50 years 7/23/2019 55

55. Hereditary Colorectal cancers , Runs in families with varied degrees of penetrance Accounts for 4-6% Two major types a) FAP: Ave. age of onset 40yrs, Extracolonic tumours , Periampullary duodenal tumour [4-6% pts], Desmoid tumours [10-20% pts], osteomas b) HNPCC, The Lynch syndrome: Ave. age of onset 44yrs, Penetrance is 70-85%, extracolonic tumours are endometrail , proximal ureteric , Gastric, Biliary , Small intestine, CNS 7/23/2019 56

56. C) Familial Cancers. Some cases of colorectal cancers are diagnosed in people with family history of colon cancer but they do not qualify to be put in any of the two types of hereditary cancer above Lynch I. The affected family develop cancers of the colon and rectum only Lynch II. The family develop cancers of the colon and of other organs: uterus, stomach, ureter, biliary tree, etc 7/23/2019 57

57. PATHOGENESIS AND SPREAD OF CRC These cancers develop through a prototypic stepwise accumulation of gene mutations and epigenetic changes that are handed done from one generation of cells to the other through cell division . At least four accumulated gene mutations are required for the cancer to develop The initial morphological change noticeable is the adenoma which after 5- 20 years develops into a carcinoma

58. Molecular Mechanisms that cause aberrant genes leading to crc . Chromosomal Instability ( cin ) Microsatellite Instability (MSI) c pG island methylator phenotype ( cimp ) 7/23/2019 59

59. A typical series of gene mutations that precede a CRC development FAP los/ mut , 5p Norrmal epithelium DNA hypermethylation Hyperproliferative epithelium K- ras mutation 12q Early adenoma DCC loss at 18q Intermediate adenoma P 53 loss at 17p Late adenoma Other alterations Carcinom a Metastasis 7/23/2019 60

60. Morphological events following the genetic changes 7/23/2019 61

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62. Morphology of Colorectal Cancer Fungating, cauliflower, Proliferative (typically found in the caecum and ascending colon) Annular, scirrhous, string stricture, infiltrative, tubular (typically found in the descending colon) Ulcerative (typically found in the rectum and rectosigmoid) 7/23/2019 63

63. Spread of colon and rectal cancers Within the bowel wall (longitudinal, circumferential and radial) Through the bowel wall and then out into adjacent structures Lymphatic (Upwards, lateral to internal iliac nodes, downwards and into inguinal lymph nodes Blood Transperitoneal 7/23/2019 64

64. Staging of colon and rectal cancer Staging systems in use are the TNM, Astler Coller Modification of the Duke’s staging system and now the Modified Astler Coller (MAC) system 7/23/2019 65

65. Dukes’ Classification ( Astler-Coller modification) Carcinoma in situ (may be referred to as high grade dysplasia) – Intramucosal carcinoma that does not penetrate the muscularis mucosae. Stage A – tumors invade through the muscularis mucosae into the submucosa but do not reach the muscularis propria . Stage B1 – tumors invade into the muscularis propria . Stage B2 – tumors completely penetrate the smooth muscle layer into the serosa. 7/23/2019 66

66. Stage C – tumors encompass any degree of invasion but are defined by regional lymph node involvement. 3. Stage C1 – tumors invade the muscularis propria with pericolic or perirectal lymph nodes involved. 4. Stage C2 – tumors completely penetrate the smooth muscle layer into the serosa with lymph nodes at the highest point of ligature involved. 5. Stage D – lesions with distant metastases. 7/23/2019 67

67. The Modified Astler Coller System (MAC) Stage A . The tumour is confined to the mucosa Stage B 1 . The tumour extends to but does not penetrate the muscularis propria Stage B 2. The tumour penetrates the muscularis propria into the serosa or adventitia but lymph nodes are not invaded Stage B 3. Tumour directly invades or is adherent to other organs and there are no lymph node deposits Stage C1. The tumour is limited to the bowel wall with less than 4 lymph nodes invaded by tumour Stage C 2. The tumour is limited to the bowel wall with 4-6 lymph nodes invaded by tumour Stage C3. The tumour is limited to the bowel wall with 7 or more lymph nodes invaded by tumour Stage D. Presence of distant metastasis, local condition unimportant 7/23/2019 68

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69. PART TWO MANAGEMENT

70. SCREENING

71. Screening = employing simple and cheap tools which are widely available and accessible, minimally invasive and less discomforting, highly sensitive and with a high negative predictive value to detect conditions that lead to deadly diseases or the disease itself in its early stages (preclinical stage) in the general population Screening is therefore employed in asymptomatic people who are at risk of a particular disease

72. Purpose/aims of screening = to reduce the incidence of the disease and to reduce death rates in people affected with the disease In colorectal cancer: Primary prevention = to detect polyps which when treated will prevent cancer from developing Secondary prevention = detect cancer in early stage (Stage A) which when treated will prevent death from occuring

73. Cost effectiveness of screening Screening has to be cost effective. So it has to be directed at the population at risk. Mass screening in populations are also used when the incidence or prevalence of the disease is high When these two c onditions are not met screening will most likely not be cost effective

74. Opportunistic screening: In transiting economies opportunistic screening is used. In these populations colorectal cancer incidence has not reached epidemiological proportions to warrant population screening hence people who present with symptoms referable to the large bowel, even if the diagnosis is obvious, still, the whole of the large bowel examined. Thus an opportunity is taken of the patient’s complaint to screen him/her

75. Screening methods for colorectal tumours Guaiac occult blood test Haemoccult test (Immunochemical test) Faecal DNA test Sigmoidoscopy Colonoscopy Faecal porphyrin quantification: - HaemoQuant , currently used in clinical research

76. The guaiac test It is the most widely used. It detects iron through an oxidative process that is catalysed by peroxidases and catalases. It detects both haem and non- haem compounds. Some vegetables (cucumber, cauliflower)that contain peroxidase can turn the test falsely positive Vit C and citrus fruits (because of the anti-oxidant properties that can inhibit the colour reaction in the test) can turn the test falsely negative There are therefore some restrictions the patient must go through to help increase the negative predictive value of the test. These are: to abstain from meat and iron containing substances including drugs, citrus fruits, vit C and vegetables for at least three days

77. Haemimmunochemical test (HIT) It uses specific antibodies to detect globins It is more sensitive than gFOBT It does not need dietary restrictions and can be performed on the spot, no need to wait for three days Even with this for it to be reliably positive blood loss of more than 20ml/day is required. Even some cancers bleed less than this <10ml/day

78. Faecal DNA test It extracts human DNA and test for alteration known to cause cancer. Alterations in such genes as APC, RAS, p53, BAT26 (MSI)

79. Risk stratification for the development of CRC Low risk:- person aged less than 50 years and has no other CRC risk Average risk:- Person aged ≥ 50 years and has no other CRC risk Increased risk:- Person of any age with personal or family history of colorectal polyp or cancer, or has inflammatory bowel disease or, has undergone a cholecystectomy High risk:- person with family history of the hereditary colorectal cancer syndromes; FAP and HNPCC

80. Recommended Screening schedules Average risk: 50-75yr olds Either of these three modalities can be used Yearly faecal occult blood test Sigmoidoscopy every 5 years with FOBT in every 3 year Full colonoscopy every 10 years

81. 2. Increased risk (based on personal Hx of Adenoma) Low risk adenoma:- Colonoscopy every 5-10years High risk adenoma:- Colonoscopy every 3 years Incomplete or piecemeal polypectomy :- 2-6 months

82. 2. Increased risk: (based on personal history of CRC):- screen for lynch syndrome. Use the Amsterdam II criteria or The revised Bedestha Criteria and then genetic testing 2. Increased risk: (based on personal history of inflammatory bowel disease) Disease duration of 8-10years:- 1-2 yearly colonoscopy

83. CLINICAL

84. Clinical Presentation Rectal bleeding Change in bowel habits Constipation Diarrhoea Passing mucus PR Unexplained Wt loss Feeling of incomplete emptying of the bowel Pain, Abdominal, anal or pelvic Iron deficiency anaemia Borbogrygmi 11. Tenesmus 12. Feeling of masses; abdominal and rectal 13. Emergency; intestinal obstruction or perforation 14. Fistulae, internal or external 7/23/2019 85

85. CLASSICAL PRESENTATION BY PART OF BOWEL RIGHT COLON Iron deficiency anaemia Diarrhoea Dyspepsia Change in bowel habit RIF Mass LEFT COLON Bleeding PR Borborigmy Change in bowel habits Progressive constipation to obstipation Paradoxical diarrhoea LIF mass

86. Rectum Bright red bleeding PR Change in bowel habits Constipation Passing pencil thin faeces Tenesmus Feeling of incomplete emptying of the bowel Spurious diarrhoea Overflow incontinent diarrhoea in older patients Pelvic or anal pain

87. Clinical/Pathological Diagnosis of Lynch syndrome, Cont Amsterdam Criteria II (1999) There should be at least three relatives with HNPCC-associated cancer (CRC Endometrium, gastric, biliary, Small bowel, proximal Ureteric), of which one should be a first degree relative of the other two At least two successive generations should be affected At least one colorectal cancer should be diagnosed before the age of 50 years FAP should be excluded Tumours should be verified by a pathologist (Has a pooled sensitivity of 78% and a specificity ranging between 46%-68%) 7/23/2019 88

88. Diagnostic Modalities In the diagnosis of colorectal cancer the whole large bowel should be evaluated, the effects of the tumour on adjacent structures should be assessed as well as extent of spread 7/23/2019 89

89. Per rectal examination Colonoscopy is gold standard (other Lower GI endoscpies = proctoscopy , rigid sigmoidoscopy , flexible sigmoidoscpoy ) Barium enema Abdominal ultrasound Endoluminal / transrectal ultrasound IVU for rectal tumours 7/23/2019 90

90. 7. Whole body spiral CT 8. MRI for pelvic tumours 9. Chest X-Ray 10. Biopsy of tumour for histopathology 11. PET Scan for diagnosing recurrent tumour 11. Serum CEA (Not for diagnosis) 7/23/2019 91

91. Barium Enema 7/23/2019 92

92. Sigmiodoscopy 7/23/2019 94

93. Colonoscopy 7/23/2019 95

94. TREATMENT Four main modalities of treating colon and rectal cancers are employed 1. Surgery (Open or Laparoscopic) 2. Chemotherapy 3. Radiotherapy 4. Target therapy 7/23/2019 96

95. Surgery = Open or Laparoscopic Principles of oncologic resections of the Colon Colon –Right Hemicolectomy - Left Hemicolectomy - Extended Right Hemicolectomy - Transverse colectomy - Sigmoid Colectomy 7/23/2019 97

96. Right Hemicolectomy 7/23/2019 98

97. Transverse colectomy 7/23/2019 99

98. Extended Right Hemicolectomy 7/23/2019 100

99. Left Hemicolectomy 7/23/2019 101

100. Sigmoid Colectomy 7/23/2019 102

101. Treatment Cont’d Principles of oncologic resections of the rectum Rectum 1. Anterior Resection of the rectum 2. Low anterior Resection of the rectum 3. Ultra-Low ARR, no more in vogue 4. Abdominoperineal resection of the rectum and anus. Can be single surgeon or two surgeons = Synchronous combined. 7/23/2019 103

102. Inter- sphincteric resection of the Rectum Local Excision Stenting Each type of the rectal resection includes excision of the mesorectal envelope. Total Mesorectal excision is done for middle third and lower third cancers Principles of rectal resection The bowel incision should be at least 2cm from macroscopic inferior margin of the tumour The Mesorectal excision should be at least 4cm from the macroscopic margin of the tumour

103. Divisions of the rectum for oncologic surgery

104. Anterior Resection of the rectum 7/23/2019 106

105. Low Anterior resection of the rectum 7/23/2019 107

106. Abdomino-Perineal resection of the Rectum (AP Resection) 7/23/2019 108

107. Inter- sphincteric resection of low rectal cancers Medium JPEG

108. Stenting of advanced rectal and colon cancers causing obstruction

109. Hepatic Resection for metastatic tumour Current evidence suggests that localised hepatic tumour should be resected at the same time as the large bowel surgery. However if hepatic resection will not be possible during the large bowel surgery, usually because of the large size and multiplicity of the metastic tumour then hepatic resection is delayed and after surgery appropriate chemothery targeted at the hepatic tumour to shrink it to resectable size is undertaken. A second surgery to resect the liver is then done 7/23/2019 111

110. Treatment Cont’d Chemotherapy 1. For colon cancer the chemotherapy is usually in the adjuvant setting 2. For Rectal cancer the neo-adjuvant Radiotherapy (Short course) or chemoradiation (Long Course) followed by adjuvant chemotherapy gives better outcomes in stage II and above tumours . 7/23/2019 112

111. Treatment Cont’d Chemotherapy agents used; 5Fu Leucovorin Capecitabine Irinotecan Cisplatin ,Oxaliplatin Taxane 7/23/2019 113

112. Treatment Cont’d Target, Biologic, Molecular therapy Bevacizumab, Vascular endothelial growth factor inhibitor Cetuximab = a chimeric monoclonal antibody (mAb) against EGFR Panitumumab = A fully human EGFR mAb 7/23/2019 114

113. Follow-up Serum CEA is checked after therapy. It this is with normal range follow-up checks are performed half yearly. If at any of the checks there is a rise then location of a recurrent tumour should be sort for energetically using good clinical information, abdominal ultrasound, colonoscopy, CT scan, MRI If CEA remain normal then this is combined with yearly colonoscopy and abdominal ultrasound If CEA is raised and source of tumour is difficult to find the best test is PET Scan 7/23/2019 115