Rectal/perianal mass and colorectal cancer

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22 Rectal/perianal mass and colorectal cancer

Colorectal cancer is the third most common cause of cancer mortality in most developed countries. Screening and early endoscopic intervention form the crux of management strategy.

Rectal or Perianal Mass

There are three ways a patient with a perianal or rectal mass may present:

The causes of a lump in the rectum are listed in Box 22.1.

History

Establish when the lump was first recognised and whether it has changed over time. An intermittent nature suggests that the lump relates to prolapse of a lesion from the rectum (e.g. haemorrhoids or rectal prolapse). Determine if the lump could be manually reduced when the lump is external to the anus. Haemorrhoids are a classic example of a potentially reducible lump, but the differential diagnosis includes rectal prolapse and hypertrophied anal papilla. An acute time course favours conditions such as thrombosed internal or external haemorrhoids. Tenderness suggests an infective process such as an ischiorectal abscess (Chapter 12).

If a rectal lump is found, ask about painful straining or feeling of incomplete rectal evacuation. The sense of faecal urgency associated with these symptoms is referred to as tenesmus; these complaints may occur with any irritating lesion of the rectum.

Another key symptom is rectal bleeding. Never ignore rectal bleeding and never assume it has a benign cause; bleeding should raise the suspicion of colorectal cancer. Ask about a family history of gastrointestinal disease and, in particular, colon cancer or polyps. Less commonly, a solitary rectal ulcer secondary to prolapse of the rectum can cause bleeding and tenesmus. The passage of mucus may occur with benign or malignant tumours as well as ulceration. Systemic symptoms such as weight loss (e.g. with malignancy) or fever (e.g. with an abscess) may also help point towards the correct diagnosis. A history of menstrual bleeding associated with a tender lump may suggest a perineal endometrial deposit that rarely occurs.

Physical examination

Inspection

Careful inspection is crucial (see Chapter 12) but, importantly, one must expect to find an abnormality. Place the patient in the left lateral position with the buttocks well over the edge of the couch. Part the buttocks, looking for perianal skin tags, which may be associated with pruritus due to suboptimal hygiene. These are usually haemorrhoidal remnants, but they can occasionally be an indicator of a systemic process such as Crohn’s disease (Chapter 15). A perianal haematoma may be visible, which is usually small (under 1 cm). Rectal prolapse can occur at any age; suspect this if the anus is patulous or gaping. Ask the patient to strain; perineal descent may be seen and sometimes rectal prolapse (circumferential folds of red mucosa) may be demonstrated.

Palpation

To begin digital rectal examination, warn the patient, then apply gentle but firm pressure to the anal verge with the flat of the well lubricated right index fingertip. The initial contraction of the sphincter will relax after several moments and allow the finger in. The examination will be uncomfortable for the patient; if it is painful, desist. Note the resting muscle tone of the sphincter, and ask the patient to squeeze down on the examining finger to evaluate active tone. Note the anorectal ring where the external anal sphincter spreads out to become pelvic floor and the narrow anal canal (3 cm long) gives way to the spacious rectum. Palpate the coccyx between finger and thumb. This will lead you onto the pelvic floor; feel one side, then the other. Pronation and supination of the forearm may not give sufficient ‘degrees of freedom’ to the pulp of the index finger; change your angle of approach by squatting or sitting beside the examination couch to better feel the smooth mobility of normal mucosa over the midline groove of the prostate (in males).

Expect to feel a mass. If you feel a mass, determine its size, shape (e.g. polypoid, plaque or ulcer), consistency (soft, firm or hard; it may indent like faeces), surface texture (smooth or granular) and mobility. Tenderness of the lesion suggests an inflammatory process. Decide whether the lesion is mobile or fixed to surrounding structures, such as the prostate, pelvic floor or sacrum. Tethering implies that the pathological process has extended beyond the limits of the muscularis propria to involve the adjacent structure or organ. Fixation may occur as a result of fibrosis, but usually indicates malignant infiltration.

Ask yourself: ‘Will I be able to describe this mass in my notes or referral letter?’ An example is: ‘On the left lateral wall of the rectum about 2 cm from the anorectal ring is a hard, fixed mass, 3 cm in diameter that does not indent’.

Occasionally you may feel a mass through the rectal wall; these arise most commonly in the sigmoid colon (e.g. a diverticular mass). Alternatively, there may be a hard, relatively immobile mass anterior to the rectum near the tip of the finger on deep palpation associated with a tumour that has spread from a primary elsewhere (such as in the stomach); this is termed a Blumer’s shelf. Other masses that might be felt include a tampon or a pessary lying in the vagina, or lateral lumps from enlarged lymph nodes infiltrated with tumour from a primary rectal carcinoma.

As a general rule, benign processes are soft, whereas malignant processes are hard. Fixed, irregular lesions with friable mucosa are more often malignant. Blood on the examining finger is an important sign of friable mucosa.

Sigmoidoscopy and proctoscopy

A sigmoidoscope or proctoscope may allow you to see the lesion that you have felt, exclude other impalpable lesions (e.g. multiple rectal polyps, or areas of ulceration that might be suggestive of inflammatory bowel disease) and take a biopsy of the lesion for histological examination.

The examination is most commonly performed with the patient in the left lateral decubitus position. In some centres, particularly those equipped with specialised tables, the examination is performed with the patient in the jack-knife position resting on the knees. Usually, adequate clinical information can be achieved without rectal preparation. When the rectum is totally loaded, it can be cleared by inserting an enema; full mechanical bowel preparation is not needed for this examination. Most patients will be anxious about proctoscopy or sigmoidoscopy. They need not see the instrument (Figs 22.1 and 22.2). The examiner needs to reassure the patient, pointing out that the diameter of the instrument is less than the diameter of a large stool and that the examination will be discontinued if there is excessive discomfort.

With the patient in position, lift the uppermost buttock upwards and gently insert the lubricated instrument with the obturator in place in the line of the anal canal. Note that the line of the anal canal is toward the patient’s umbilicus for the first 3–4 cm, then angles posteriorly. Once the instrument has been inserted into the lower rectum, remove the obturator. The sigmoidoscope can usually be passed with deft insufflation (reassure the patient that you are putting air in and tell them not to be embarrassed) and minor deviations to the level of the rectosigmoid junction at about 15 cm from the anal verge. At the rectosigmoid junction there is usually acute angulation, which can make progression into the sigmoid colon more difficult. In older patients who are likely to have diverticulosis, it is always best to stop at this point if there is any degree of difficulty. It is important to realise that the rectum is covered with peritoneum to a greater extent anteriorly than laterally or posteriorly. The limit of peritonealisation anteriorly is usually about 7–10 cm from the anal verge so you need to be more careful with the depth of biopsy above the level of the peritoneal reflection to minimise the risk of rectal perforation. Biopsy may be best left to the specialist.

If further examination is required (e.g. colon cancer is confirmed), full colonoscopy should be performed at a later stage (see below).

Tumours of the Colon and Rectum

History

A colorectal tumour can present with any symptom referable to the gastrointestinal tract; such symptoms include a recent change in bowel habit (constipation or diarrhoea), abdominal pain, bleeding (occult or major) or, rarely, an abdominal catastrophe (perforation or bowel obstruction). Other symptoms include weight loss, lethargy and those of disseminated metastatic disease (e.g. bone pain, jaundice, pathological fracture and, uncommonly, thrombophlebitis migrans, skin nodules or acanthosis nigricans).

The classic right-sided colon cancer is soft, protuberant and located where the lumen is large and the contents semisolid; anaemia is therefore more likely than obstruction. The classic left-sided colon cancer is annular, stenosing and located where the lumen is narrow and contents are firm; consequently, obstruction is more likely (Fig 22.3). Cancers may form a fistula into the bladder or elsewhere. Advanced cancers may be asymptomatic, while a very early caecal cancer may occasionally present with appendicitis, having obstructed the appendiceal opening.

History taking should include any family history of colon polyps, and colorectal or breast cancer, and past history of screening or surgery for bowel cancer. Weight loss, recent change of bowel habit, rectal bleeding, abdominal pain and tenesmus are all indications for further investigation.

Rarely, infective endocarditis caused by Streptococcus bovis or Clostridium septicus is the first manifestation of colon cancer.

Investigation

Diagnosis is made on the basis of history, physical examination and special investigation (Table 22.1).

Table 22.1 Preoperative assessment of patients with colorectal carcinoma

Investigation Comment
Blood count, electrolytes, creatinine and liver function tests Results probably will be normal; useful base-line assessment if major surgery planned
Carcinoembryonic antigen (CEA)

Chest x-ray Useful—not necessary if patient is healthy or if CT chest is contemplated together with the CT abdomen/pelvis Colonoscopy with biopsy of tumour Essential unless patient presents acutely with bowel obstruction/perforation Abdominopelvic CT Essential especially if a laparoscopic colectomy is being considered Transrectal ultrasonography (TRUS) Essential for staging of rectal cancer which determines the course of management

Note: Intravenous pyelogram, abdominal ultrasound and MRI may be indicated in special circumstances.

Preoperative investigations should include a full blood count, electrolyte tests and liver function tests. Baseline carcinoembryonic antigen can be sought to aid follow-up, although the benefit of this is controversial (Ch 17). A chest x‑ray examination may detect metastatic disease. If advanced disease is suspected, computed tomography (CT) scanning of the abdomen may be useful; surgery may still be needed for palliation.

Colorectal cancer

Aetiology

Colorectal tumours can arise from any of the tissue elements found in the large bowel. The most common neoplasms develop from the mucosa (the columnar glandular lining of the large bowel) as premalignant adenomatous polyps, which can develop into adenocarcinoma. Endocrine, lymphatic, smooth muscle and fatty tissue neoplasms are rare.

Inherited factors are indicated in 30% of colorectal cancers. Many of the inherited factors are still unidentified; they are either genetic (information is transmitted on the basis of gene sequence) or epigenetic (information is transmitted through gene expression without alteration in the DNA sequence). Both processes are not mutually exclusive. Epigenetic processes important in normal development and differentiation may be misdirected to cancer, via altered methylation (e.g. DNA hypermethylation), post-translational modification of histones, or chromatin remodelling, which leads to inactivation of tumour suppressor genes, activation of oncogenes or altered imprinting patterns. Recent evidence indicates that such events may be modified by diet and drugs.

There are many identified genes involved in colorectal cancer, including the adenomatous polyposis coli gene (APC) on chromosome 5, the ras oncogenes (K-ras) on chromosome 12, the tumour suppressor gene (p53) on chromosome 17 and the deleted colorectal cancer gene (DCC) on chromosome 18. Downstream mechanisms of colorectal carcinogenesis include defects in Wnt signalling, DNA mismatch repair (MMR) and apoptosis.

Most sporadic colorectal cancers (70%) are caused by mutational inactivation of APC. These tumours are characterised by chromosomal instability with changes to large segments of chromosomes. On the other hand, defective DNA MMR characterised by microsatellite instability (MSI) is responsible for a smaller subset (15–25%) of colorectal cancers. In HNPCC, the majority are due to germline mutaions in the MMR genes on chromosome 2 or 3, MLH1, MSH2, MSH6, PMS1 and PMS2 among others, whereas sporadic MSI tumours are associated with epigenetic silencing of the MLH1 promotor through hypermethylation. Patients with tumours caused by defective DNA MMR might not benefit from 5-fluorouracil (5-FU)-based chemotherapy.

Genetic tests for mutations in the APC and other genes have been developed. Genetic understanding will have implications for screening, surveillance and therapy in the near future.

Sporadic colon cancer in a first-degree relative above the age of 55 years is associated with twice the risk of developing colorectal cancer compared with the rest of the population. If there is one first-degree relative diagnosed before the age of 55 or two first/second degree relatives on the same side of the family diagnosed at any age involved, the risk is increased up to sixfold.

Inflammatory bowel disease (particularly longstanding ulcerative colitis of more than 8 years) leads to an increased incidence of colon cancer (Ch 14).

Familial adenomatous polyposis: classic and attenuated

FAP is caused by an inherited autosomal-dominant gene located on chromosome 5q. Polyps usually appear in the second decade of life. Patients usually have no symptoms until colon cancer develops. More than 95% of patients will have polyps on sigmoidoscopy by the age of 30 years, so the condition can usually be diagnosed by sigmoidoscopy in adults. The number of polyps in a colectomy specimen of a patient with FAP averages approximately 1000. Colorectal cancer inevitably occurs in patients with FAP by the age of 50 years, approximately 10–15 years after the first onset of polyps. Where a mutation in APC is identified in the proband, predictive testing can be done on other family members to identify individuals at risk. Those found negative for the family-specific APC mutation do not require screening beyond that offered to individuals with average risk.

The presence on sigmoidoscopy of more than 100 polyps that are adenomas histologically establishes the diagnosis (Fig 22.4). Such patients should be referred to a centre of expertise because it can be difficult to detect cancer early in these cases.

Attenuated FAP is a less severe form of the condition, manifest with 10 or more but 100 or less colonic polyps (on average 30) and a later onset of colorectal cancer.

Surgical management is the only acceptable approach unless there are other contraindications.

Medical management may be a useful adjunct in some cases. Non-steroidal anti-inflammatory drugs have been shown to lead to partial regression of polyps but complete regression does not occur.

A variant of FAP known as Gardener’s syndrome consists of all the features of FAP plus a number of extracolonic manifestations that may include desmoid tumours (non-metastasising fibrous tumours, commonly found in the abdominal wall in surgical wounds), osteomas (which can affect the long bones, skull and mandible), lipomas, fibromas, dental abnormalities (e.g. extra teeth) and, rarely, neoplasms of the biliary tree, liver, adrenal or thyroid.

Both the classical and variant types of FAP can cause upper gastrointestinal tract polyposis. Proximal small bowel adenomas are observed in over 50% of cases, classically involving the duodenal papillae, which have malignant potential. For this reason, 1–3-yearly screening with upper endoscopy (including side-viewing endoscopy) is recommended from the age of 25–30; subsequent management is determined by staging for duodenal adenomatosis (based on number, size, histology and degree of dysplasia of polyps).

Polyps and the polyp-cancer sequence

Dysplastic proliferation of the mucosa leads to a heaping-up of the regular parallel ‘tubular’ glands and their cells, causing a polyp (adenoma). As long as the dysplastic cells are confined to their normal position above the muscularis mucosa, the adenomatous polyp is not malignant; this is because lymphatics rarely cross the muscularis mucosa.

Adenomatous colorectal polyps may be found in up to 40% of the population in Western countries by the age of 60 years, but only a minority develop into cancer. The pathologist recognises malignant change in a polyp when dysplastic cells cross the muscularis mucosa. Malignant spread then occurs both by direct extension along the bowel as well as through the muscle layers of the bowel wall to serosa and adjacent organs. Lymph nodes can be involved and distant spread may be lymph or blood-borne.

The neoplastic lesion is ‘superficial’ if it is an adenomatous polyp with absence of invasion in the lamina propria, or if it is an early carcinoma with invasion of the lamina propria but the depth of penetration was limited to the submucosa in the colon. Superficiality relates to the potential for complete cure after endoscopic mucosal resection.

Adenomas grow in different microscopic architectural patterns reflecting the extent of their de-differentiation from the parent glandular structure:

Laterally spreading tumours refer to flat lesions over 10 mm in diameter.

Malignant risk in a polyp depend-on the size, microscopic architecture and site of the polyp (Table 22.2). The risks are greater with increase in size, villous architecture, and rectal site.

Table 22.2 Risk of invasive carcinoma in colorectal adenomas

Parameter   Proportion of polyps with carcinoma (%)
Size (mm) ≤ 5 0
  6–15 2
  16–25 20
  26–36 40
  ≥ 37 > 60
Architecture Tubular 4
  Tubulovillous/villous 30
Site Right colon 6
  Left colon 8
  Rectum 23

Modified from Nusko G, Mansmann U, Altendorf HA, et al. Risk of invasive carcinoma in colorectal adenomas assessed by size and site. Int J Colorectal Dis 1997; 12:267–271

The malignant risk of a polyp may be identified by its endoscopic appearance. Advances in endoscopic technology with zoom, narrow band imaging and high-definition white-light imaging have allowed further morphological assessment of the polyp using the Kudo pit pattern (Fig 22.6) and the Paris classification (Fig 22.7) in defining those polyps likely to have submucosal invasion. Together with differentiation into granular (polyps with nodules on the surface) and non-granular (polyps with a smooth surface) subtypes, the endoscopist is able to determine whether or not a polyp would be suitable for endoscopic mucosal resection (Table 22.3).

image

Figure 22.6 Kudo pit pattern.

From Kudo S, Hirota S, Nakajima T, et al. Colorectal tumours and pit pattern. J Clin Pathol 1994; 47:880–885.

image

Figure 22.7 Paris grading.

From Paris Workshop Participants. The Paris endoscopic classification of superficial neoplastic lesions: esophagus, stomach, and colon. Gastrointest Endosc 2003; 58(suppl 6):S3–S43, with permission.

Table 22.3 Risk of malignancy in polyps

Classification SMI (%) M (%)
Granular 7  
Non-granular 14  
Paris grade    
0–Is 7  
0–IIa 3  
0–IIc or IIa+c 46  
Pit pattern    
I–II 0 0
IIIL 0 4
IIIS 4 9
IV 4 18
V 34 35

SMI = submucosal invasion; M = intramucosal cancer.

Adapted from Uraoka T, Saito Y, Matsuda T, et al. Endoscopic indications for endoscopic mucosal resection of laterally spreading tumours in the colorectum. Gut 2006; 55(11):1592-1597; Kudo et al. Pit pattern in colorectal neoplasia: endoscopy magnifying view. Endoscopy 2001; 33(4):367-373.

Other epithelial polyps of the colon include hyperplastic and serrated polyps. Serrated polyps are classified into sessile serrated adenoma and traditional serrated adenoma. Serrated adenomas are characterised by the cytological features of an adenoma and the architectural features of a hyperplastic polyp. As opposed to the adenoma-carcinoma sequence involving the adenomatous polyposis coli gene, the serrated pathway to colorectal cancer involves the v-raf murine sarcoma viral oncogene homolog B1 (BRAF) and K-ras mutations, which account for up to 20% of sporadic colorectal cancers.

The surveillance protocol for serrated polyps has not been fully established, but it has been proposed to follow that used for patients with conventional adenomas.

Hyperplastic polyps are usually considered an incidental finding with no potential for progression to colorectal cancer. However, there is a rare type of hyperplastic polyp syndrome known as hyperplastic polyposis, which has been shown to be associated with hypermethylation of numerous genes. Polyps in this syndrome are large and flat, and hence there is an increased risk of colon cancer. The following definition for hyperplastic polyposis has been proposed:

There is no consensus on these criteria, but these patients are quite distinct because of the frequency, distribution and often large size of the hyperplastic polyps. These polyps may arise in patients with a family history of colorectal cancer, are often large and are found in the right colon. Due to the risk of developing right-sided colorectal cancer, these patients should have a follow-up colonoscopy at a relatively short interval (1–2 years) and have the polyps removed endoscopically.

Stage IV Any T, any N M1 T: primary tumour Tis Carcinoma in situ; intraepithelial (within glandular basement membrane) or invasion of lamina propria (intramucosal) T1 Tumour invades submucosa T2 Tumour invades muscularis propria T3 Tumour invades through the lamina propria into the subserosa or into non-peritonealised pericolic or perirectal tissues T4 Tumour directly invades other organs or structures and/or perforates visceral peritoneum N: regional lymph node NX Regional lymph nodes cannot be assessed N0 No regional nodal metastases N1 Metastasis in 1–3 regional lymph nodes N2 Metastasis in 4 or more regional lymph nodes M: metastasis MX Distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasis

Based on Greene FL, Page DL, Fleming ID, et al. AJCC cancer staging manual. 6th edn. New York: Springer Verlag; 2002, with permission.

Treatment

Polyps are usually excised endoscopically and examined histologically. If cancer is found in the polyp, further surgical resection of that segment of bowel may be indicated. However, a resection may not be necessary if there are:

To ensure adequate margin of excision and accurate staging, lateral spreading tumours should be excised en block via endoscopic mucosal resection or dissection; the specimen should be pinned on a piece of foam for proper orientation during processing.

The Haggitt’s level of invasion (Fig 22.8, Table 22.5) is a useful guide in considering further management for a malignant polyp after endoscopic resection, as it has been validated to determine prognosis in surgical series. Stages 0, 1, 2 and 3 do not require surgery. On the other hand, surgery would be recommended for stage 4. By definition, submucosal invasion in a sessile polyp would require surgery. However, it has been suggested that superficial submucosal invasion (under 300 mm) in such sessile polyps might also be considered low in risk.

image

Figure 22.8 Haggitt’s levels of carcinoma invasion.

From Haggitt RC, Glotzbach RE, Soffer EE, et al. Prognostic factors in colorectal carcinomas arising in adenomas. Gastroenterology 1985; 89:328–336, with permission.

Table 22.5 Haggitt’s levels of carcinoma invasion

Haggitt level Description
0 Intramucosal high grade dysplasia
1 Carcinoma invading the head of the polyp above the junction of the adenoma and the stalk
2 Carcinoma invading the neck of the polyp at the junction between the adenoma and the stalk
3 Carcinoma invading any other part of the polyp
4 Invasion into the submucosa of the bowel wall below the stalk in the pedunculated polyp and in the submucosa of the sessile polyp

Obviously, comorbidity of the patient should be taken into account in the management algorithm.

Most colorectal cancer will be amenable to surgical excision. Chemotherapy, radiotherapy and palliative endoscopic stenting have a role in advanced disease.

Surgical treatment aims to remove the tumour with a margin of normal bowel in continuity with draining lymph nodes and blood vessels. Restoration of intestinal continuity is usually possible. In the case of low rectal cancer requiring an abdominoperineal resection, an end colostomy would result. Patients who had laparoscopically assisted colectomy have a similar survival rate to those who had open colectomy at 4 years follow-up. Laparoscopically assisted colectomy also produced better clinical outcomes, such as early recovery, less pain and reduced length of stay. It is believed that there will be reduced incidence of small bowel obstruction and incisional hernia in the long term.

In the case of FAP or dysplastic change in ulcerative colitis, the entire colon is ‘at risk’ and should be resected; the rectum can be preserved in some circumstances, although this is a calculated risk and it must be watched closely.

Traditionally, surgery takes place electively with a fully prepared (clean) bowel. More recently, it was shown that a fully prepared bowel is not needed. In fact, it is beneficial not to prepare the bowel in most colectomies as it avoids dehydration and improves patients’ clinical outcomes. If the operation was performed as an emergency (e.g. for obstruction, bleeding or perforation), the surgeon may elect to form a temporary colostomy.

Small cancers and polyps readily accessible through the anus can sometimes be removed locally. However, local excision of T2 rectal tumour has been shown to have a poor outcome.

At surgery, the surgeon will make a thorough search for spread of the cancer (especially to the liver). It is possible to resect that part of the liver containing metastatic disease, although this is best done at a second operation up to 6 months later. Resection of metastatic disease will be undertaken only if further investigations (angiographic, CT or PET scanning) directed at detecting small metastatic deposits confirm that all metastases can be safely removed.

Rarely, a cancer will be too advanced to remove surgically and palliative stenting, colostomy or medical palliation alone will be the only options.

Chemotherapy

Adjuvant chemotherapy after resection for stage III colon cancer is now the standard of care as it has been shown to improve progress and overall survival. The usual combination is 5-FU infusion (with or without leucovorin) and oxaliplatin (FOLFOX). In the elderly, capecitabine may be used instead of 5-FU to minimise the inconvenience related to infusions.

The benefit of adjuvant chemotherapy in stage II colon cancer remains controversial due to insufficient evidence of benefit. However, it may be considered on an individual basis for patients with adverse features (e.g. T4 tumours, poorly differentiated histology, lymphatic or venous invasion, bowel obstruction or perforation on presentation, and fewer than 10 lymph nodes examined).

In advanced colon cancer, including those with four or fewer resectable metastases, FOLFOX or 5FU, leucovorin and irinotecan (FOLFIRI) in combination with bevacizumab, a recombinant humanised monoclonal antibody to the vascular endothelial growth factor VEGF-A, have been shown to improve survival. The alternate combination with cetuximab, an epidermal growth factor receptor targeted antibody therapy, have also been shown to improve survival in a subset of patients with wild type k-ras.

In rectal cancer (located at 10 cm or less from the anal verge) with advanced stage (T3/T4, N1/N2 as determined from preoperative investigation), survival benefit from chemoradiotherapy of 20–40% has been shown, and preoperative chemoradiotherapy is associated with half the recurrence rate and severe late side effects compared to postoperative treatment. Chemoradiotherapy may also be indicated preoperatively to ‘downgrade’ the tumour.

Colorectal cancer screening

Colorectal cancer screening using faecal occult blood testing has been shown by level I evidence to provide a 15–33% reduction in mortality.

At surveillance colonoscopy, up to 25% of men and 15% of females over the age of 50 years are expected to demonstrate evidence of adenomatous polyps. Such adenoma detection rates have become the benchmark for quality indicators in surveillance programs.

Guidelines frequently change and depend on the risk category, as follows:

category 2—moderately increased risk (family history of sporadic colon cancer):

Colonoscopy every 5 years starting at age 50 years, or at an age 10 years

younger than the age of first diagnosis of colorectal cancer in the family, whichever comes first (the ‘10-year rule’). Sigmoidoscopy plus double-contrast barium enema 5-yearly is an acceptable alternative to colonoscopy if the latter is unavailable, but colonoscopy is considered the ‘gold standard’. CT colonography 5-yearly is an alternative.

Anal Canal Cancer

Anal canal cancer is more commonly seen in women, although carcinoma of the anal margin is more common in men (Fig 22.9). Together, these are rare tumours constituting only 3–4% of anorectal malignancies. There is a strong association between anal canal cancer and sexually transmitted diseases, including HIV infection and condyloma acuminata caused by the human papilloma virus.

Anal canal cancer arises at or above the dentate line from transitional zone epithelium, the remnant of the cloacal membrane of early embryonic growth. However, this zone is not fixed in its relationship to other common landmarks. It may extend in the adult for a variable distance over the anal columns into the lower rectum, and it is composed of a variety of epithelia, including stratified squamous non-keratinised, stratified columnar or cuboidal and simple columnar epithelium. This partly explains the confusion that exists in the histological classification of this tumour.

Most tumours of the upper anal canal are poorly differentiated squamous cell carcinomas (SCC), usually showing little keratin production. Other tumours include basaloid carcinoma and malignant melanoma.

Carcinoma of the lower anal canal, below the dentate line is commonly a well differentiated squamous cell carcinoma situated at the anal margin where the modified skin of the pecten becomes continuous with normal hair-bearing skin.

The treatment of anal canal cancer is primarily chemoradiotherapy. Radical surgery is reserved for persistent or recurrent tumour.

Key Points

Further reading

Fuchs C.S., Giovannucci E.L., Colditz G.A., et al. A prospective study of family history and the risk of colorectal cancer. N Engl J Med. 1994;331:1669-1674.

Gastroenterological Society of Australia [GESA]. Early detection, screening and surveillance for bowel cancer: an update for clinicians, 3rd edn. Sydney: Digestive Health Foundation; 2006.

Goldberg R.M., Meropol N.J., Tabernero J. Accomplishments in 2008 in the treatment of advanced metastatic colorectal cancer. Gastroint Cancer Re. 2009;3(suppl 2):S23-S27.

Hyman N.H., Anderson P., Blasyk H. Hyperplastic polyposis and the risk of colorectal cancer. Dis Colon Rectum. 2004;47:2101-2104.

Jass J.R., Burt R., Hamilton S.R., Aaltonen L.A. Hyperplastic polyposis. WHO international classification of tumors. 3rd edn. Berlin: Springer-Verlag; 1989. 135–136

Jasperson K.W., Tuohy T.M., Neklason D.W., et al. Hereditary and familial colon cancer. Gastroenterology. 2010;138:2044-2058.

Kapiteijn E., Marijnen C.A.M., Nagtegaal I.D., et al. Preoperative radiotherapy combined with total mesorectal excision for resectable rectal cancer. N Engl J Med. 2001;345:638-646.

Kudo S., Hirota S., Nakajima T., et al. Colorectal tumours and pit pattern. J Clin Pathol. 1994;47:880-885.

Lynch H.T., de la Chapelle A. Hereditary colorectal cancer. N Engl J Med. 2003;348:919-932.

Mandel J.S., Bond J.H., Church T.R., et al. Reducing mortality from colorectal cancer by screening for fecal occult blood. N Engl J Med. 1993;328:1365-1371.

Mitchell P.J., Haboubi N.Y. The malignant adenoma: when to operate and when to watch. Surg Endosc. 2008;22:1563-1569.

Moser L., Ritz J., Hinkelbein W., et al. Adjuvant and neoadjuvant chemoradiation or radiotherapy in rectal cancer—a review focusing on open questions. Int J Colorectal Dis. 2008;23:227-236.

Nelson H., Sargent D.J., Wieand H.S., et al. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med. 2004;350:2050-2059.

Paris Workshop Participants. The Paris endoscopic classification of superficial neoplastic lesions: esophagus, stomach, and colon. Gastrointest Endosc. 2003;58(Suppl):S3-S43.

Schippinger W., Samonigg H., Schaberi-Moser R., et al. A prospective randomised phase III trial of adjuvant chemotherapy with 5-fluorouracil and leucovorin in patients with stage II colon cancer. Brit J Can. 2009;97:1021-1027.

Tanaka T. Colorectal carcinogenesis: review of human and experimental animal studies. J Carcinogenesis. 2009;8:1-19.