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Benign Tumours
Polyp
A polyp is a circumscribed lesion which projects above the surrounding mucous membrane. It may or may not have a stalk. In the colon, the polyp can be hamartomatous or neoplastic (adenomatous polyp).
Hamartomatous Polyp
These are disorders of growth and consist of an abnormal mixture of those tissues normally found in the organ concerned. The two hamartomas encountered are the Peutz-Jeghers and the juvenile polyps.
Peutz-Jeghers polyps They occur as part of the Peutz-Jeghers syndrome, which consists of pig-mented spots in the. mucous membrane of the oral cavity and skin together with multiple hamartomatous polyps of the gastrointestinal tract. The common sites are the jejunum and ileum although they can also occur in the stomach and colon. There is very little risk of malignant change.
Adenomatous Polyp
It has been defined as a sharply demarcated circumscribed elevation of dysplastic epithelium, which is usually small but may at times be large and may or may not have a pedicle.
The dysplasia may be mild, moderate or severe and different grades can be seen in one adenoma. The sigmold and the descending colon are the commonest sites.
The vast majority of colonic carcinomas arise in pre-existing colonic adenomas.
In order to make a diagnosis of malignancy in a colonic polyp, the malignant epithelial cells should be seen traversing the muscularis mucosa into the stalk. Adenomatous polyps of larger size have the highest malignant potential. The chances of malignancy also increase with increasing grades of dysplasia.
Because the lesions have a malignant potential they should be removed. Fibre-endoscopic removal facility is now available in an increasing number of centres. It is important that the polyp is removed whole and the extent of any invasion of the stalk is accurately assessed.
If malignant change is diagnosed in a colonic polyp, no further treatment is usually carried out if excision of the polyp is complete and the contained carcinoma is moderately or well differentiated. If the carcinoma is poorly differentiated, further resection is carried out regardless of whether the excision was complete or incomplete. Further excision is also carried out if the base of the stalk is involved by the tumour.
Familial Poly posts Coll
This is an inherited autosomal dominant disease in which multiple polyps arise in the colon in early adult life. Presenting symptoms consist of mucus and bloody diarrhoea. The polyps tend to be more common in the distal colon and are seen at different stages of development, from very small to large.
If untreated, 10 per cent of the patients will develop cancer within five years and 20 per cent within 20 years of onset. Surveillance of the siblings should start at about 14 years of age.
Complete colectomy is advisable. A stump of rectum can remain and the terminal ileum is anastomosed to it. The rectum is followed up and polyps coagulated before they become malignant.
Gardner's Syndrome
In this syndrome, familial polyposis coll is associated with extraintestinal manifestations which include osteoma skull, desmoid tumours of the abdominal wall and mesentery, Upomas, flbromas, etc. These patients have the same risk of developing colonic cancers as with polyposis coll alone.
Turcot's Syndrome
This rare syndrome has an autosomal recessive inheritance. Colonic polyposis is associated with central nervous system malignancy.
Carcinoma Colon and Rectum
Incidence and mortality rates of colorectal cancer vary widely throughout the world. The highest incidence is seen in developed countries of north America, northern and western Europe, and New Zealand. Intermediate rates are described in The Small and Large Intestines
eastern and southern Europe while lower rates are found in Asia, Africa and most countries of Latin America.
In the developed countries, nearly 70 per cent of the tumours of the large bowel are situated in the colon while 30 per cent are in the rectum and at the rectosigmoid junction. In India, rectal cancer is much more common than cancer of the colon.
Aetiology
The aetlological postulates for the carcinoma of. large bowel are the following.
1. Diet
a. Dietary fibre hypothesis A large intake of dietary fibre reduces the intestinal transit time, and the carcinogens have less time in contact with the bowel wall and bacteria have less time in which to produce carcinogens.
b. Animal fat hypothesis Carcinoma colon is common in -:he high income group. It is suggested that increased dietary fat leads to an increased concentration of bile acids in the faeces. Anaerobic bacteria produce carcinogens from bile acids in the colon.
c. Vegetable hypothesis There is evidence that colorectal cancer is less common in those that eat cabbage, brussel sprouts and other similar vegetables. These vegetables contain indoles which help enzymes in degrading noxious environmental chemicals.
2. Colorectal cancers are known to arise from preexisting polyps.
3. The association between colorectal cancer and familial polyposis coll, ulcerative colitis and Crohn's disease has been discussed elsewhere.
4. Heredity may make cells susceptible to cancer by the presence of oncogenes. Another class of cancer genes, tumour suppressor genes) inhibit tumour growth and oncogenesis occurs when these genes are lost. Mutational activtion of oncogenes (e.g. ras gene) or loss of tumour suppressor genes is initiated by carcinogenic agents. Promoters, such as bile acids, may stimulate growth of a benign neoplasm, and perhaps other promoters cause malignant change to occur.
5. Patients with a previous ureterosigmoidostomy have an increased incidence of colorectal cancer, possibly as a result of the formation of N-nitroso compounds.
Half of all colorectal cancers occur in the rectum and rectosigmoid area. 25 per cent occur in the sigmoid, the remaining 25 per cent are equally distributed between the caecum, ascending, transverse and descending colon. Between 2-5 per cent of patients have more than one colorectal cancer (synchronous tumours). Patients who have had one colorectal cancer resected have a 3-5 per cent chance of developing another subsequent colorectal tumour (metachronous tumour). This
justifies investigation of the entire colon in any patient presenting with a colorectal tumour.
Colorectal cancers tend to be ulcerating or infiltrating; less commonly they arc polypoid in type. The polypoid form tends not to be as invasive as the ulcerating/infiltrating type and has a better prognosis. The ulcer shows the typical raised everted irregular edges and necrotic centre of a malignant ulcer. When it grows around the circumference of the colon it forms an annular constricting cancer liable to cause intestinal obstruction. This is more common in left-sided cancers. Occasionally, much mucin production gives the colloid appearance.
Histologically, the vast majority of colorectal cancers are adenocarcinomas. They may be well-differentiated, moderately well-differentiated or poorly differentiated.
Spread
Direct spread takes place thr.ough the colonic wall, especially at points where blood vessels enter. Longitudinal spread is not a marked feature and distal intramural spread of more than 1 cm beyond" the gross margins of the tumour is unusual. The peritoneum provides a tough defence but once penetrated, peritoneal dissemlnation may occur. The lymphatic spread is usually embolic, by a steady progression from paracolic nodes to the para-aortic nodes. Venous invasion is seen once the tumour has penetrated through the entire intestinal wall.
A characteristic feature of colorectal cancer Is the occasional development of implantation metastasis. Malignant cells shed from a tumour can implant at a distant site. Implantation may be responsible for some suture line recurrences.
The lymph nodes draining the colon (Fig. 45.3) are grouped as follows.
1. The epicolic lymph nodes, situated In the immediate vicinity of the bowel wall.
2. The paracolic lymph nodes, lying in relationship to the leash of blood vessels proceeding to the colonic walls.
3. The intermediate lymph nodes, arranged along the UeocoUc, right colic, midcolic, left colic and the sigmoid arteries. In the last instance the paracolic lymph nodes are often absent.
4. The main lymph nodes, aggregated around superior and inferior mesenteric vessels where they take origin from the abdominal aorta.
Stoging
Originally, Dukes described three stages.
A. Tumour spread as far as, but not through the
muscularis propria. B. Tumour spread through the bowel wall into
perirectal (pericolic) tissue. C. Those with lymph node involvement.
45.22; Dukes original classification of colorectal cancer and 11s later modification, (a) Tumour spread as tar as, but not through the muscularls proprla. (b) Tumour spread through the bowel wall Into the perirectal (perlcolic) tissues, and (c) Those with lymph node Involvement. Astler Coller modification: A inframucosal lesion 6., Tumour Into, but not beyond the muscularls proprla By Spread through the wall into peritoneal tissue C, lymph nodes involved but tumour confined to bowel wall C, lymph nodes Involved and tumour through bowel wall
Later he subdivided the C stage into the following.
C) Only local nodes involved.
•Cn Mesenteric nodes involved at the level of the llgation of the vascular pedicle.
Duke's classification was further modified by Astler and CoUer
A Intramucosal only. B« Tumour into, but not beyond the muscularls
propria.
Bg Spread through the wall into peritoneal tissue. C, Lymph nodes involved but tumour confined
to bowel wall. Cg Lymph nodes involved and tumour through
bowel wall.
Astler and CoUer stage A Is not an invasive carcinoma. g) and C stages are also different from Duke's own modification of stage C into C, and Cn. "
Prognostic Factors 1. Htstological grading Poorly differentiated tumours have a worse prognosis than do moderately or well-differentiated tumours.
2. Depth of tumour invasion The survival rate decreases and the locoregonal failure increases when the lesion extends completely through the bowel wall.
3. Lymph node status The presence of Involved lymph nodes significantly worsens the prognosis. This is particularly so if more than four nodes are involved or if the node at the site of vascular ligation is involved.
4. Venous (nuasion Venous invasion is associated with a higher incidence of hepatic metastases.
5. Intestinal obstruction The increased peristalsis in intestinal obstruction may cause rapid lymph flow which might enhance lymphatic embolisatlon.
6. Carcinoembryonic antigen Very high CEA values in colorectal carcinoma may indicate disseminated disease.
CEA has an Important role in the postoperative follow-up for tumour recurrence in patients who have undergone surgery for colorectal cancer. Elevated levels can predict recurrence before the disease is clinically apparent.
Clinical Features
Carcinoma of the colon usually occurs in patients over 50 years of age but may occur earlier In adult life. Men are more frequently affected than women (3:2) although carcinoma of the right colon Is encountered more often in women.
The presenting clinical features vary widely in the different group of patients according to the type of lesion.
1. In the nonstenosing lesions, frequent attacks of dysentery and diarrhoea are common.
2. In the stenosing lesions, chronic obstruction characterised by alternate constipation and diarrhoea often occurs. The constipation is progressive. The diarrhoea is due to excessive use of purgatives to overcome the constipation;
or irritation by the accumulated hard faeces to excessive mucus secretion.
3. In a left colonic lesion, the patient may at times present with acute obstruction because (i) stenosing lesions are commoner on the left side, (11) the left colon has a narrower lumen than the right, and (ill) the contents of the left colon are more solid.
4. If the ileocaecal valve remains closed during intestinal obstruction, the caecum distends massively and perforation may eventually occur. It may give rise either to peritonitis or to a localised pericollc abscess. If this should burst Into another organ such as the bladder, a malignant fistula results.
5. Colicky pain is common in stenosing lesions. In advanced cancer, pain may be very severe.
6. Malignancy at particular locations has certain characteristic features.
Pelvic colon Colicky pain and tenesmus Transverse Reflex symptoms (acidity, colon heartburn, nausea and vomiting) Caecum and Lump that fails to resolve, ascending progressive anaemia, the colon proliferative growth may become an apex of intussusception. 7. Clinical features can be due to metastatic spread, e.g. liver enlargement and ascites.
Investigations
Stool examination Presence of blood and mucus in the stool raises the suspicion.
SIgmoldoscopy and colonoscopy Radiography may not always visualise an early growth in the sigmold and pelvirectal area. Sigmoidoscopy helps to diagnose majority of these lesions. The flexible colonoscope is being increasingly used as an alternative to sigmoidoscopy. Colonoscopy can survey the entire colon and both polyp and carcinoma of the colon can be diagnosed at an early stage. There is some debate as to whether a colonoscopy or barium enema should be the initial investigation if rectal examination and sigmoidoscopy are normal. Colonoscopy is more accurate in detecting the neoplasm and more comfortable for the patient, and many feel that this should be the first Investigation. A compromise may be the use of flexible sigmoi-doscopy and double contrast barium enema. Once the lesion has been seen, it should be biopsied.
Barium enema This shows a constant irregular filling defect (Fig. 45.23 and 45.24) but an early growth may be missed. For the right colon, a barium meal examination gives a better picture but it is inadvisable if there is any evidence of chronic obstruction since an acute obstruction may be precipitated by the meal.
Contrast enema This Is useful for early cases. The barium emulsion is partly evacuated and air is injected per rectum into the colon and further films taken. The wall of the colon thus becomes delineated, and even early cases with minor irregularity of the mucosa may be diagnosed.
Carclnoembryonic antigen CEA is not specifically associated with large bowel cancer; high levels are also found in the sera of patients with other gastrointestlnal malignancies. It is, however, helpful in detecting recurrence after curative surgical resection.
Screening
Carcinoma of the large bowel has a median doubling time of 130 days, suggesting that at least 5 years and often 10-15 years of silent growth takes place before symptoms appear. It was hoped that the earlier detection by screening will Improve this situation. Screening can be divided Into selective screening of high-risk groups and general screening of the population. The high risk groups include patients with a long history of ulceratlve colitis, a past history of polyps or colon cancer, and perhaps those with a strong family history. This group should have a regular barium enema and/or colonoscopy every 1 or 2 years.
As far as the general population screening is concerned, opinion is divided on the best course of action. The American cancer society recommendations are as follows.
1. Annual digital rectal examination beginning at the age of 40.
2. Guaiac slide test for faecal occult blood annually after the age of 50
3. Flexible sigmoldoscopy every 3-5 years beginning
at the age of 50.
It is possible that carcinomas may be detected at an earlier stage but perhaps the cost may not justify the benefit for the few positive cases identified. Moreover, we do not know whether survival will be Improved.
Complications
1. Obstruction Carcinomas of the left colon are more likely to cause obstruction than those of the right.
2. Perforation This may occur either through the lesion itself or through the caecum as a result of closed loop obstruction. Faecal peritonitis may' result.
3. Fistula formation A sigmold lesion may perforate into the urinary bladder. Pneumaturia and frequent urinary tract infections result. Differentiation with veslcocollc fistula due to divertlcular disease may be difficult.
Treatment
Treatment will vary according to whether intestinal obstruction is present or not.
1. No intestinal obstruction After preoperative preparation of the bowel, the abdomen is opened. If the growth is operable, a wide surgical excision of the lesion and its regional lymph drainage is done.
If the growth is Inoperable, either a short circuit or colostomy is done.
2. With intestinal obstruction The first aim is to relieve the obstruction by a proximal colostomy and if the growth is operable, resection with anastomosis is done at a second sitting.
Preoperative preparation A general physical examination is performed. Haemoglobin, blood urea and electrolyte determinations are undertaken routinely. Chest X-ray and intravenous pyelography are ordered. Anaemia is corrected and the blood Is grouped and cross matched for the day of surgery.
The chief source of sepsis in colonic surgery Is from the endogenous bacteria within the bowel lumen. It is advisable to eliminate the faecal load and reduce the number of bacteria as much as possible prior to operation. The various ways of achieving this are the following.
1. The patient takes only liquids by mouth for 3 days preoperatlvely and is admitted two days before surgery. A laxative is given the night before surgery. In addition to this, oral cum systemic antibiotic prophylaxis Is exhibited.
2. Alternatively, whole gut lavage (contraindicated in obstructing lesions or severe Inflammatory bowel disease) is advisable, which involves tngestion (or instillation through a nasogastric tube) of large quantities of fluid; the absorptive capacity of the small bowel is overwhelmed and the colon is cleared of faecal matter. A solution containing polyethylene glycol (PEG) minimises the risk of fluid overload and excessive dehydration.
3. In patients who have obstructive symptoms, on-table bowel irrigation may be safer and more effective.
4. Prophylactic antibiotics are advocated in addition to mechanical cleaning. Systemic antibiotics or oral nonabsorbale antibiotics may be used for direct attack on the bacteria of the large bowel. The use of oral antibiotics remains controversial. Systemic antibiotics, however, are important.
5. Three doses of perioperative regimen of intravenous cephradine (500 mg) and metronidazole (500 mg) without mechanical irrigation have also been found fairly satisfactory.
Operation The abdomen is opened through a short paramedian incision which is extended if the growth is removable. The liver is palpated for secondary deposits, the peritoneum is inspected and palpated for neoplastic implantations, draining nodes are palpated and the fixity of the- neoplasm Is ascertained.
Radical surgery is the ideal. The contraindications to radical surgery are (i) growth extensively fixed to the posterior abdominal wall, (11) nodes fixed to the posterior abdominal wall or big vessels, and (ill) liver metastases (Liver metastasis is not necessarily a contraindication to resection as the best palliative treatment for carcinoma of the colon is removal of the primary tumour).
According to the site of the growth, the radical resection may be (I) right hemicolectomy, (II) left hemlcolectomy, (III) transverse colectomy with its mesocolon, (IV) resection of the sigmoid with its mesocolon.
The large gut has a poor blood supply. Vessels supplying it, viz. lleocolic, right colic, middle colic, left colic and the sigmoids end in the marginal artery which runs along the inner border of the colon and supplies it (Fig. 45.2). In malignancy it Is Imperative that all the nodes draining the corresponding area are resected with the loop of the diseased colon. These nodes are situated along the blood vessels, supplying the colon and some of them (intermediate nodes) are located by the side of the big vessels. Excision of these nodes necessarily involves wider intestinal resection. After resection, it is desirable that an anastomosis is done between two mobile parts of the colon.
Right hemicolectomy means excision of the terminal 6 to 8 inches of the ileum, the caecum, ascending colon, hepatic flexure and the proximal half of the transverse colon. After resection, anastomosis is done between the terminal lleum and the transverse colon.
cinoma caecum, (b) Radical right hemicolectomy tor carcinoma hepatic flexure, and (c) Radical transverse colectomy
The Insets show the restoration of Intestinal continuity. lleocollc after right hemlcholectomy and colocollc after radical transverse colec"omy
Left hemicolectomy removes the distal half of the transverse colon, splenic flexure, descending colon and the fixed upper part of the pelvic colon. Anastomosis is done between the mobile parts of the remaining colon (Fig. 45.26a).
Transverse colectomy with a V-shaped area of mesocolon This is done for carcinoma of the transverse colon. The resection must Include 3 inches of healthy gut on either side of the growth.
After radical pelvic colectomy restorative anastomosis Is done between the remaining upper part of the proximal colon and the rectum (Fig. 45.26b).
Postoperative treatment It includes administration of antibiotics to guard against possible infection of the anastomotic area by Cl welchil. Oral fluids arc allowed only after flatus is passed.
Palliative surgery for nonresectable growths A right colonic growth may be bypassed by Ueotransverse anastomosis (anastomosing distal lleum with transverse colon, side to side). For nonresectable malignancy of the left colon or rectum, palliative colostomy may be on the transverse or the pelvic colon.
Palliative chemotherapy for colorectal cancer has been discussed on page 663.
COLOSTOMY
A colostomy is an artificial opening made into the large bowel In order to divert its contents to the exterior, where they may be collected in a colostomy bag. A colostomy may be permanent or temporary,
Temporary Colostomy
This Is most commonly established to relieve a distal obstruction of the sigmoid colon or rectum by carcinoma. Other indications Include protection of colorectal anastomosis after resection, and to prevent faecal peritonitis from developing after traumatic injury to the rectum or colon.
The colostomy may be on the transverse or pelvic colon. It classically has two stomas. A loop of colon is brought out over a supporting glass rod. The glass rod is removed after a week because by that time, firm adhesions have developed between the serous coat of the colon and the abdominal wall.
As a rule, the colostomy should be opened after 48 hours of exteriorisatlon of the loop. After 48 hours, complete peritoneal sealing occurs. Where there is gross distension and immediate relief is essential, a long rubber tube is passed through an opening made in the proximal 'loop. The tube is secured in position with a purse string suture applied around the opening.
When temporary colostomy needs to be closed, it is usually performed by an intraperitoneal technique as this has been shown to be safer than the extraperitoneal methods, and is accompanied by fewer closure breakdowns. Colostomy closure Is usually performed when the distal lesion for which the temporary colostomy was performed is cured. It is generally done when the stoma is "mature:, i.e. after the colostomy has been established for about two months.
Pelvic Colostomy
For a pelvic colostomy, the incision may be a gridiron incision on the left side, similar to McBumey's incision for the appendix. The Incision should not be very large because Infection in the muscles resulting from leakage of stool, may lead to the development of incislonal hemla.
The opening on the pelvic colon should be done In its uppermost part, otherwise the mobile redun-dant loop of the pelvic colon above the stoma may prolapse through the colostomy during straining. The loop is kept outside the abdomen with the help of a glass rod which is passed through the avascular part of the