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Dear students, This is only for your revision and NOT A FULL TEXT.
Polyps The term ‘polyp’ is a clinical description of any elevated tumour. It covers a variety of histologically different tumours Colorectal Adenocarcinoma Adenomatous Polyp to Cancer Sequence l Multiple polyps particularly ifvillous or tubulovillous high risk l Risk increases with polyp size l Once size reaches 2cm there is ahigh risk of invasive malignancy l Adenomatous polyp develops (note protective effect of aspirin and NSAID) l Polyp may be flat or polypoid l May be detected and treated atthis stage colonoscopically(dye spray/polypectomy) l Polyp may be tubular adenoma(lowrisk) or villous/tubulovillous higher risk l Single polyps particularly iftubular low risk Hereditary Non Polyposis Colon Cancer l Multiple colonic polyps l Dominant inheritance l Usually a strong family history ofcolon cancer l Require ongoing screening l Genetic counseling l Amsterdam criteria Treatment of Polyp Disease l Endoscopic polypectomy l Trans anal endoscopic resection l Trans anal endoscopic microsurgery l Histological examination ofexcision margins/polyp stalk l Consider risk/benefits ofsegmental resection if tumour present Familial Adenomatous Polyp Syndromes l Familial adenomatous polyposis(FAP) l Direct inheritance or pointmutation l Entire colon carpeted with polyps l Inevitable malignancy by late teenageyears l Require prophylactic surgery l Associated polyp disease elsewhere l Retinal changes and abdominaldesmoids Familial adenomatous polyposis ( FAP) l general neoplastic disorder ofthe intestine. l The main risk is large bowelcancer, l It is inherited as a Mendeliandominant and the gene responsible (APC gene) has now been identified on theshort arm of chromosome 5 (Bodmer). l Males and females are equallyaffected. l sporadically without anyprevious sign or history, l preexisting adenomatosis. l FAP can be associated -desmoidtumours and osteomas. Epidermoid cysts can also occur (Gardner’s syndrome); l desmoid tumours in the abdomeninvade locally to involve the intestinal mesentery l Clinical features. l age of 15 – 30 years l Symptomatic patients. l affected family l loose stools, l lower abdominal pain, l weight loss, l diarrhoea and the passage ofblood and mucus. l a double-contrast barium enema.If in doubt l colonoscopy -- biopsies l Asymptomatic patients. l affected families - screening. l Pigmented spots in the retina(CHIRPES) and deoxyribonucleic acid (DNA) tests for the FAP gene should makescreening mote reliable in the future. l If the diagnosis is made duringadolescence, operation is deferred usually to the age of 17 or 18. Screening policy 1. All members of the family - examined at the age of10—12 years, repeated every 1—2 years. l 2. Most - get polyps - at 20 - operation. l 3. If -no polyps at 20, continue with 5-yearly examination until age 50; if thereare still no polyps there is probably no inherited gene. l Carcinomatous change mayexceptionally occur before the age of 20. l Examination of blood relatives,including cousins, nephews and nieces, is essential and a family tree should beconstructed and a register of affected families maintained. Treatment l Colectomy with ileorectalanastomosis has in the past been the usual operation because it avoids anileostomy in a young patient. l The rectum is subsequently cleared of polypsby snaring or fulguration. l The patients are examined byflexible sigmoidoscopy at 6-monthly intervals thereafter. -develops carcinomain the rectal stump.. l The alternative -operation -restorative proctocolectomy with an ileoanal anastomosis. -higher complicationrate than ileorectal anastomosis. Colorectal Adenocarcinoma -THE LARGE INTESTINE l Strongly related to age 85% ofcases over 60 l Rare below the age of 40 l Until age 40 male to female ratio1:1 l Over age 40 male to female ratio1.5:1 l Worldwide approx one million newcases a year l 9% of all annual cancer diagnosisworldwide l Rates vary across world l Highest rates in developed world l Appears to be associated with a change to a western diet, observed in migrant populations Distribution of colorectal Adenocarcinoma l Appendix 1% l Caecum 13% l Ascending colon 5% l Transverse colon 8% l Descending colon2% l Sigmoid colon 18% l Rectum 29% l Anus 2% Epidemiology l Age l Lower risk in populations eatinghigh fibre low fat diets l However difficult to exactlyanalyse the relationship l Inverse relationship betweenintake of vegetables and colorectal adenocarcinoma l Weaker inverse relationship tofruit l Metaanalysis suggests a significant intake in risk associated with the ingestion ofred and processed meat l Possible relationship withincreased fat consumption History l Depends on site within colon l If right sided often present withFe deficiency anaemia l If left sided altered to freshblood in stool l Change in bowel habit l Increased frequency of defaecation l Change from normal l Diarrhoea l Tenesmus l Rectal Leakage l Lesion protruding from anus l Constipation is less often asymptom of colorectal carcinoma than diarrhoea l Symptoms from secondary disease Diagnostic Investigations l Double contrast ba enema l Flexible sigmoidoscopy l Colonoscopy (Beware missing rightsided pathology) l CT colonography l MRI colonography l Faecal occult bloods (false+ve/-ve) Colorectal Adenocarcinoma Staging Investigations l CT scan of thorax, abdomen andpelvis l For rectal adenocarcinoma MRI scan of pelvis l CEA (is the patient a secretor) Dukes l Dukes original description A BC l A tumour confined to the mucosa l B tumour invading into themuscularis l C tumour invading lymph nodesor metastatic disease l Subsequent modifications eg Dand C1/C2 l DUKES STAGE D has been addedmore recently to show that metastases l Stage B may be dividedaccording to whether the tumour has just penetrated the outer surface of thebowel wall (B1) or the surrounding tissues are involved (B2), and stage C according to whether the apical nodesare involved (C2) or not (C1).
TNM l T1 Tumour confined to mucosa l T2 Tumour invading into submucosa l T3 Tumour invading through serosaor into pericolic fat l T4 direct extension to anotherorgan Staging l No-No lymph nodes l N1-Lymph nodes up to three in theprimary drainage groups l N2 Lymph nodes more than three l M0-No metastatic disease l M1 Metastatic disease l Note that with either stagingsystem there is importance in being aware of tumour differentiation(good/moderate/poor) l Mucin secretion status, mucinsecreting colorectal tumourshave a poorer prognosis . Presence or absenceof lymphovascular invasion will effect prognosis l Note final characteristic oftumour and its complete staging will not be apparent until examination of theresected specimen TREATMENT FOR COLORECTAL CANCER l SURGERY Removal of all or part of the organ, together withregional lymph nodes, i.e. Colectomy, Hemicolectomy, Sigmoid colectomy,Anterior resection or Abdominoperineal resection of rectum In all of these cases an anastomosis and/or colostomy (temporary or permanent)will be required.
For localised disease a local excision of the tumour may be sufficient. The excisionmay be endoscopic for more distaltumours. l RADIOTHERAPY Thenormal colon is too sensitive to radiation damage to allow radical radiotherapyto be given. Smaller doses ofradiation may be given preoperatively to make an inoperable tumour operable, orpostoperatively to increase survival.
l CHEMOTHERAPY5-Fluorouracil (5FU) is the drug most commonly given, either to improve survivalafter surgery, or palliatively.5FU is often given in combination withFolinicacid (FA – Calcium leucovorin)or Levamisole. l Unless advanced secondary diseaseor major co-morbidity segmental resection, usually with primary anastomosis l Wide excision with removal of allmacroscopically diseased tissue, including resection of other involved organsif appropriate
Bowel Preparation l If full bowel preparation rememberrisks of significant elctrolyte inbalance and dehdration particularly in theelderly l Right sided resection needs noprep l Left sided resection can be donewith no prep or enema only unless need for on table colonoscopy l AP needs no prep Surgical Treatment of Colonic Adenocarcinoma l Segmental resection to includelymph node drainage unless resection purely palliative l Consider post operative adjuvantchemotherapy dependant upon combination of pre-operative staging, operativefindings and histological staging Obstruction- Colorectal Adenocarcinoma l Consider stent l Hartmanns procedure l Defunctioning proximal colostomyor ileostomy l On table lavage and primaryanastomosis l Subtotal colectomy Treatment of Rectal Adenocarcinoma l Depends upon staging and heightfrom anal verge l Critical investigation is accurateMRI scan of pelvis which assesses circumferential resection margin (Mercury) l If margin not threatened andtumour characteristics favorable then surgery, nature dependant upon site l If margin threatened then considerneoadjuvant therapies l Short course radiotherapy(Swedish) over 1/52 followed immediately by surgery l Long course chemoradiotherapy over6/52 period with repeat MRI at 2-3/12 followed by surgery l Long course treatment may requirepretreatment colostomy Surgery for Rectal Adenocarcinoma l If low rectal eg palpable bystandard surgical finger then generally AP resection with permanent stoma l If above this level then anteriorresection. If low anterior resection,difficult procedure or pre-op radiotherapy then will probably requiredefunctioning stoma (usually loop ileostomy)
Laparoscopic Colorectal Surgery l Several trials indicate equivalentoncological outcome(Classic) l Higher initial costs may becompensated by shorter hospital stay and earlier return to work l Better cosmetic outcome l Marked learning curve 50-100 cases Post Surgical Effects l Increased frequency of defaecationand looseness of stool l Faecal incontinence particularlyin elderly patient with poor sphincter function and low resection and orradiotherapy l Disturbance of urinary functionparticularly post AP or low anterior resection l Impotence in patients post lowanterior resection or AP resection particularly if pre operative radiotherapy l Stoma formation Complications of Surgery l Chest, wound and urinary tractinfections l Deep venous thrombosis(D V T)leading to pulmonary embolus l Anastomotic leak (Approx 5%). Usually requires reoperation and stomaformation l CAUTION Any deterioration inpatients condition over first week postoperatively including apparentcardiovascular events should be considered to be due to leak until otherwiseproven Complications of Surgery (AP) l Failure of healing of perinealcomponent of AP wound, particularly post radiotherapy l May be avoided by prophylacticTRAM flap l Urinary dysfunction particularlycommon in this group of patients l Late formation of a perineal orstomal hernia Long Term Outcome l Dukes A 90% five year survival l Dukes B 60% five year survival l Dukes C 30% five year survival l Dukes C is however very variablebecause of presence of some patients with distal metastatic disease Treatment of Liver Secondaries In Colorectal Adenocarcinoma l Hepatic surgery has an excellentsafety profile with very low morbidity and mortality l In appropriate cases with noevidence of other intra abdominal disease and generally no other secondarydisease should be offered liver resection l Liver resection may be veryextensive and require more than one procedure to allow hepatic recovery l Further resections for recurrentliver secondaries may be appropriate l Chemotherapy, standard regimes andpossible role for new biological agents acting on angiogenesis l Radiofrequency ablation l Laser ablation l Cryotherapy Long Term Follow up of Colorectal Adenocarcinoma l Follow up may be for holisticreasons if no further intervention would be appropriate l Follow up generally aimed atdetecting treatable recurrence particularly in the liver and detecting furtherpolyp disease Long Term Follow up of Colorectal Adenocarcinoma l Protocol driven l 3/12 CEA and 6/12 CT scan forfirst two years l Then 6/12 CEA and annual CT scanfor three years l Full colonoscopy within 6/12 ofresection if not achieved preoperatively l Colonoscopy three yearly until age80yrs
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