Surgery Paper Chase - Tripod



Surgery Paper Chase

11/12/02 3-4PM

Colon Cancer

Dr. Armstrong

I. Case: A 45 year old woman presents to your office with rectal bleeding. Flexible sigmoidoscopy reveals an adenomatous polyp in the rectosigmoid. An abbreviated family history reveals that her mother died of colon cancer

II. Next step: the patient has polyp, know its either sessile or pedunculated, know the size, it could have been a biopsy, from finding of the polyp, one of them is to remove the entire polyp and do colonscopy, because you have to rule out if there are other lesions, the presence of polyp is a risk factor for cancer colon, that doesn’t rule out the possibility of cancer in the right side, and its mandatory to do colonscopy and remove the entire polyp, can do biopsy and its adenomatous, but next to it could have been a cancer

III. History of patient: important to know when the family member had cancer, if it was under 50 or not, there was just one polyp its HNPCC, not FAP

IV. Colon cancer risk factor is: age

V. All syndromes responsible for 5-10% of colon cancers, but the majority of colon cancers arise de novo without family history, without polyps, without UC, and the factor is the age, over 60 years of age, any patient under 50 is very important, and in these syndromes, the history of the family history under 50 is important, if died 85 then its not important

VI. Patient has rectal bleeding, should know if its bright red blood, or if its dark blood, if you sees right red blood, its comin gfrom the rectum, usually you don’t see bright red blood from the cecum, the quantity, if you see lots of blood, in young bleeding its meckel’s, in old its diverticular or angiodysplasia, in patient with bleeding from the rectum, the relation of blood with feces must know, if have normal formed stools, or diarrhea, the origin of the lesion could be distal if the stool was already formed, then on the way out through the rectum it gets painted with streak of blood, if its mixed with feces, source of bleeding could be proximal

VII. CEA only done after positive diagnosis of the colon cancer, don’t need it if just have adenomatous polyp, use it for follow up, it tells you about recurrence

VIII. Blood diarrhea, is different, what do yo mean by rectal bleeding, is it formed with blood on the outside or is it bloody diarrhea, este paciente, la proxima quedaria, hacer una colonscopia, vamos hablar de la historia familiar, que mas haria

IX. Risk factors cancer colon: high fat, low fiber, UC, history familiar, age (most important after 65-70), in people under 50 its family history, UC and crohn’s disease (don’t forget of crohn’s disease)

X. This patient, if had a metastasis, it would go to the liver

XI. Case: Colonscopy reveals 4 other adenomatous polyps cattered throughout the colon and a cnacer in the ascending colon. Further family history reveals that her mother was diagnosed with colon cancer at age 67, a maternal aunt had endometrial cancer at age 45, and her maternal grandfather had rectal cancer diagnosed at age 54

XII. We are talking about 3 generations, and at least there was one person under age 50, so we can say the impress HNPCC, or lynch syndrome (at least 3 generations, someone under 50 years old, associated with endometrial or ovary, not cervix, gastric and pancreatic cancer, renal carcinomas, and another important thing, the tendency of these cancers associated with lynch, increased risk of cancer being on the right side of the colon

XIII. Polyps risks

A. Villous adenoma: 30-40% risk of cancer in that lesion at time of diagnosis

B. Adenomatous tubular cancer: less risk of cancer at time of diagnosis

C. Multiple adenomatous 100’s: 100% risk of developing cancer

D. Inflammatory polyp: no risk for cancer

E. Hamartoma: peutz jehgers, juvenile

F. Adenomatous polyp comes from mucous (tubular mas abajo, villous arriba), hamartomas combine tisusses from different primary layers and the incidence they said that the incidence of cancer in peutz jeghers was zero, but not anymore, now they are saying that there is somewhat increased in incidence in peutz jeghers

XIV. Multiple adenomas polyposis: begin from below, capture entire colon, sigmoidscopy can diagnose it, so screening is sigmoidoscopy, but to diagnose lynch syndrome have to diagnose with colonscope, may have one lesion on left side and a few others on right side, father who has it gives each child a 50% chance to get it, no reason why this patient should have rectal procedure before age of 10, its from 10-20 years old when should do it, the children should get genetic mapping to see who will get the defect

XV. FAP and gardner’s syndrome: gardner was not a surgeon, he said that originally there was multiple adenomatous polyposis, tumors of the face osteomas quijasdo, frontal bones, and sebaceous cysts, then they were adding, and now there are 12 things included, look it up in the book, two risks: polyps of the duodenum and these patients develop adenomatous polyps in duodenum, with malignant potential to devlop cancer of duodenum, have operated the colon, think don’t have risk for colon cancer, but eventually may die from cancer of duodenum, the other thing important to remember, is that they develop desmoid tumors, not dermoid, which are soft tissue tumors, locally invasive, not cancers because don’t metastasise, grow inside mesentery of small bowel, obstruct superior mesenteric artery and vein, and cause ischemia and gangrene of the bowel, and end up with short bowel, FAP and gardner’s syndrome are the same with multiple ccysts, but gardner’s has other manifestations

XVI. FAP

A. Hundred of adenomas

B. Risk of colorectal cancer 100%

C. Extracolonic features

D. Autosomal dominant inheritance

E. APC gene mutation, truncated proteins pedigree mutation

F. In vitro synthesized protein assay

G. Screening: flexible sigmoidoscopy q1-2 y starting in puberty, genetic testing

H. Treatment: total proctocolectomy or total abdominal colectomy and ileorectal anastomosis with rectal surveillance: if you do proctocolectomy remove entire rectum, give colostomy, no risk of colon cancer now, but its been shown that this lesion is a lesion of the mucosa, so why not use the same ooperation used for the UC, remove abdominal colon, remove the mucosa of the rectum, perofmr ileal pouch and anastomsis it down there, do abdominal colectomy, rectal mucostectomy, ileoanal pouch anastomosis, then do proctoscope examination for rectal surveillance, but if you leave the rectum in you have to make sure that ehy have to follow up, patient must understand risk of cancer, and come for proctoscope every 6 months for the rest of their life

XVII. HNPCC

A. Early oset colorectal cancer: mean age 45

B. Tumors predominante in right colon

C. Develop before age of 50

D. Increased synchorous and metachronous colorectal neoplasms: synchronous can have two cancers, on left and on right, metachronous is have one cancer at one year, then another cancer another year

E. Increased incidence of extracolonic neoplasms

F. Increased incidence of extracolonic neoplasms: Neodmetrial, small bowel, gastric, renal pelvis, and ureter, ovarian, and skin, in familky history ask about other cancers, in famil, or in herself, and if female, ask about ovary, hard to understand why skin is involved because its not adenomatous tissue

G. Amsterdam criteria: at least 3 relatives with colorectal cancer, one affectered person is a first degree relative of the other two, at least two successive generations affected, one affect eperson diagnosed prior to age 50

H. Mismatch repair gene germline mutation

I. Microsatellite sinstability/replication error phenotype

J. Screening: coonscopy q1-3y starting age 21

K. Treatment: colon cancer: total abd colectomy plus ileorectal anastomosis

L. Rectal cancer: total proctocolectomy

M. Prophylactic colectomy controversial, if have multiple poylposis, should do the FAP should do it, if lynch and only 5 polyps and do biopsy and they are benign, you shouldn’t do a colectomy at the time, but if they have cancer, obviously have to do it

XVIII. Juvenile polyps

A. Hamartomas, the risk of juvenile poyps to develop it is 0, but th eproblem is that they grow big and bleed, they are major cause of bleeding painless in children, if it was painful bleeding then its fissure, the feces rubs against it and see blood on the surface of feces, lose circulation and amputated by themselves, when child strains polyp comes out, and then it goes back in, you check and it’s a hamartoma, you remove with snare, don’t worry about it

B. Peutz jegher’s: pigmentation is found in the mucosa of the lips, tongue, mouth inside, in the thumb, extraGI manifestation, and it could be in the small or large bowel, and lately its become found that it could be cancer

C. Cronkhite Canada syndrome: this is polyposis that is associated with lesions de ectoderm, alopecia and problems with nails, very rare, but if you have patient with this you have to think about possibility

D. Turcot syndrome: CNS tumors

E. Submucosa polyps: lymphomas, lympoid polyps, the form of polyp is pushing into th elumen, not because hypertrophy of mucous, but because submucousa is pushing it out

XIX. Diet: Now not focusing on diet, 50 years ago, this was important factor, now 10-20 years ago they began thinking that its not true, the studies that they did 50 years ago, they did when populations were more stable, where the patients lived in one city for years, and could compared cities, studied Hawaii, mingling of 3 cultures, Polynesians, raza blanca, EEUU and inglaterra, y japonesas que vinieron para trabjaro en campos de pinas, y se mezclaban, americanos blanco tenia cancer colon, japoneas no tenia colon cancer, but when they increased groups, they japonesas aumentaron, y tenia que ver con dieta, los japonesas comieron carne humado que dio cancer de arriba, y no comiocomida occidental, y por eso decidio que high fiber low fat diet caused cancer, but now they don’t pay much attention to it

XX. Clinical case: right sided cancer lesion: the patient will have diarrhea, anemiadull pain, palpable mass, the typical part of this is the patient who has diarrhea, because on right side there are peristaltic waves to and fro that occur outside of time when eat, help with absorption, and these are interrupted, so there won’t be ondas peristalticas que ayuda absorbacion, water, Na and Cl are absorbed, leaving potassium and bicarbonate, so patient won’t have peristaltic waves, also, all of this are mucosa, and you will increase the mucosa layer, and if you have a tumor, and will have a mucous discharge which will contribute bland feces, change in bowel habit, diarrhea is from 2 times a day to once every 2 days, what is important is change in bowel habit, and this patient will have hcnage in bowel habit, and will have anemia, not gross blood, also there’s factors that originate from tumor, and will cause dull pain, not colicky pain, because what comes from the ileo is liquid and can pass, but its obstructive pain, and if patient loses weight can palpate the tumor

XXI. Transverse colon tumor: dilation of proximal side, colicky type pain, because there’s a partial obstruction, each time you try to pass, have resistance, this patient when hear increased persitalsis, here distention on percussion on right side tympanic, distension, and will have decreased in size of the stool, and will have blood possibly

XXII. Right sided lesion: will have finger shaped stool, blood on surface of the stool

XXIII. Classification of TMN of tumors

A. Classified by depth, they begin from mucosa, so therefore must go from mucosa to submucosa to muscularis to serosa, so then it goes to regional nodes, which are associated with terminal arteries, right side, colic artery, left side goes to left colic arter, then it goes to amin branches, SMA and IMA, and then to periaortic nodes, then it will go to metastasis to liver most common, dukes is the most common, but logical is using the TMN classification

B. T1: mucosa

C. T2: submucosa

D. T3: muscularis

E. T4: past musclaris

F. N1: close

G. N2: more far

H. N3: distant

I. If the lesion is on base of this, do staging, stage 1, 2, 3

J. Early stage, where the lesion is on the mucosa, and negative nodes, they have a 90-95% chance of being alive at 5 years

K. Stage 2 where passes the wall, not in the mucosa, but not to serosa, and negative nodes, has 80% 5YS

L. If passes serosa, or to nodes, then has 30-40% 5YS

M. Look for pathological report, don’t think just because have colon cancer, its over, but it can go to just wall, and no nodes, that’a good sign, but if its to nodes or metastasis its bad, if mets to liver, don’t live more than 1 years most likely

N. Isolated mets from cancer colon can resect, if primary lesion and mets to liver, if isolated, if on left side liver, do left hepatic resection, or if one or two lesions on right side, can do wedge resection

XXIV. Treatment

A. Right colectomy: ciego, ascending colon, hepatic flexure, remove ileocolic, artery, right conic, right branch of the midcolic

B. Left colectomy: if in left colon, remove left colic when comes from IMA

C. Anterior resection: if sigmoid cancer, must remove other arteries

XXV. Case: screening for endometrial and ovarian carcinoma are negative, patient undergoes total abd colectomy and ileorectal anastomosis, after genetic counseling and informed consent, the patient aloows her tumor and blood to be sampled and tested for genetic markers of NNPCC. Genetic analysis of her tumor reveals microsatellite instability (replication error phenotype) germline analysis shows hMSH2.

XXVI. Case: annual rigid proctoscopy is scheduled for the patient, don’t need to do sigmoidscopye because don’t have sigmoid, do it annually

XXVII. Family members over 21 are scheduled for colonoscopy

XXVIII. Women in the family are advised about screening for endometrial and ovarian carcinoma

XXIX. Read: gardner’s, lynch, FAP

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