INFECTIONS
Intestinal amoebiasisAmoebiasis is an infestation with Entamoeba histolytica. This parasitehas a worldwide distribution and is transmitted mainly in contaminated drinking water.
Pathology
The ulcers, which have been described as bottlenecked because of their considerably undermined edges, have a yellow necrotic floor, from which blood and pus exude. In 75%, they are confined to the lower sigmoid and upper rectum.
Biopsy
Endoscopic biopsies or fresh hot stools are examined carefully to look for the presence of amoebae. It is important to emphasise, however, that the presence of the parasite does not indicate that it is pathogenic (Fig. 65.32).
Clinical features
Dysentery is the principal manifestation of the disease, but it may come in various other guises. Appendicitis or amoebic caecal mass In tropical countries where amoebiasis is endemic, this is a constantly recurring problem. To operate on a patient with amoebic dysentery without precautions may prove fatal. The bowel is friable, and satisfactory closure of the appendix stump becomes difficult or impossible, especially in cases where a palpable mass is present. When there is an amoebic mass, there tends to be tenderness on deep palpation over the caecum and the sigmoid.
Perforation
The most common sites are the caecum and rectosigmoid; usually, perforation occurs into a confined space where adhesions have formed previously, and a pericolic abscess results, which eventually needs draining. When there is sudden faecal flooding into the general peritoneal cavity, drainage of the region of the perforation, gastrointestinal aspiration, intravenous fluid, antibiotics and a full course of emetine are sometimes successful. Severe rectal haemorrhage as a result of separation of the slough is liable to occur.Granuloma
Progressive amoebic invasion of the wall of the rectum or colon, with secondary inflammation, can produce a granulomatous mass indistinguishable from a carcinoma.Ulcerative colitis
A search for amoebae should always be made in the stools of patients believed to have UC.Other
Other presentations include the following:
Fibrous stricture may follow the healing of extensive amoebic ulcers.
Intestinal obstruction is a common complication of amoebiasis, and the obstruction is the result of adhesions associated with pericolitis and large granuloma.
Paracolic abscess, ischiorectal abscess and fistula occur from perforation by amoebae of the intestinal wall followed by secondary infection.
Treatment
High-dose intravenous steroids in this situation can be catastrophic. Metronidazole (Flagyl) is the first-line drug, 800 mg three times daily for 710 days. Diloxanide furoate is best for chronic infections associated with the passage of cysts in stools. Intestinal antibiotics improve the results of the chronic stages, probably by coping with superadded infection.
Typhoid and paratyphoid
( TyphoidParalytic ileus is the most common complication of typhoid. Intestinal haemorrhage may be the leading symptom. Other surgical complications of typhoid and parathyroid include:
haemorrhage;
perforation;
cholecystitis;
phlebitis;
genitourinary inflammation;
arthritis;
osteomyelitis.
Typhoid ulcer
Perforation of a typhoid ulcer usually occurs during the third week and is occasionally the first sign of the disease. The ulcer is parallel to the long axis of the gut and is usually situated in thelower ileum.
( Paratyphoid B
Perforation of the large intestine sometimes occurs in paratyphoid B infection; vigorous intravenous antibiotic therapy is given. Occasionally, surgery may be required to defunction the colon. In cases where severely diseased bowel is present, a colectomy may be necessary, as for UC.
Tuberculosis of the intestine
Tuberculosis can affect any part of the gastrointestinal tract from the mouth to the anus. The sites affected most often are the ileum, proximal colon and peritoneum. There are two principal types.
( Ulcerative tuberculosis
Ulcerative tuberculosis is secondary to pulmonary tuberculosis and arises as a result of swallowing tubercle bacilli. There are multiple ulcers in the terminal ileum, lying transversely, and the overlying serosa is thickened, reddened and covered in tubercles.
Clinical features
Diarrhoea and weight loss are the predominant symptoms, and the patient will usually be receiving treatment for pulmonary tuberculosis.
Radiology
A barium meal and follow-through or small bowel enema will show the absence of filling of the lower ileum, caecum and most of the ascending colon as a result of narrowing and hypermotility of the ulcerated segment (Fig. 65.33).
Treatment
A course of chemotherapy is given. Healing often occurs provided the pulmonary tuberculosis is adequately treated. An operation is only required in the rare event of a perforation or intestinal obstruction.
( Hyperplastic tuberculosis
This usually occurs in the ileocaecal region, although solitary and multiple lesions in the lower ileum are sometimes seen. This is caused by the ingestion of Mycobacterium tuberculosis by patients with a high resistance to the organism. The infection establishes itself in lymphoid follicles, and the resulting chronic inflammation causes thickening of the intestinal wall and narrowing of the lumen. There is early involvement of the regional lymph nodes, which may caseate. Unlike CD, with which it shares many similarities, abscess and fistula formation is rare.Clinical features
Attacks of abdominal pain with intermittent diarrhoea are the usual symptoms. The ileum above the partial obstruction is distended, and the stasis and consequent infection lead to steatorrhoea, anaemia and loss of weight. Sometimes, the presenting picture is of a mass in the right iliac fossa in a patent with vague ill health. The differential diagnosis is that of an appendix mass, carcinoma of the caecum, CD, tuberculosis or actinomycosis of the caecum.Radiology
A barium follow-through or small bowel enema will show a long narrow filling defect in the terminal ileum.
Treatment
When the diagnosis is certain and the patient has not yet developed obstructive symptoms, treatment with chemotherapy is advised and may cure the condition. Where obstruction is present, operative treatment is required and ileocaecal resection is best.
Figure 65.33 Ileocaecal tuberculosis; absent ascending colon and caecum with dilatation of terminal ileum (courtesy of Dr V.K. Kapoor, Delhi, India).
Actinomycosis of the ileocaecal region
Abdominal actinomycosis is rare. Unlike intestinal tuberculosis, narrowing of the lumen of the intestine does not occur and mesenteric nodes do not become involved. However, a local abscess spreads to the retroperitoneal tissues and the adjacent abdominal wall, becoming the seat of multiple indurated discharging sinuses. The liver may become involved via the portal vein.Clinical features
The usual history is that appendicectomy has been carried out for an appendicitis. Some 3 weeks after surgery, a mass is palpable in the right iliac fossa and, soon afterwards, the wound begins to discharge. At first, the discharge is thin and watery, but later it becomes thicker and malodorous. Other sinuses may form and a secondary faecal fistula may develop. Pus should be sent for bacteriological examination, which will reveal the characteristic sulphur granules.
Treatment
Penicillin or cotrimoxazole treatment should be prolonged and in high dosage.
TUMOURS OF THE SMALL INTESTINE
Compared with the large intestine, the small intestine is rarely the seat of a neoplasm, and these become progressively less common from the duodenum to the terminal ileum.Benign
Adenomas, submucous lipomas and gastrointestinal stromal tumours (GISTs) occur from time to time, and sometimes reveal themselves by causing an intussusception. The second most common complication is intestinal bleeding from an adenoma, in which event the diagnosis is frequently long delayed because the tumour is overlooked at barium radiology, endoscopy and even surgery.
PeutzJeghers syndrome
This is an autosomal dominant disease. The gene STK11 on chromosome 19 has been found in a proportion of patients with this condition. This consists of:
intestinal hamartomatosis is a polyposis affecting the whole of the small bowel and colon, where it is a cause of haemorrhage and often intussusception;
melanosis of the oral mucous membrane and the lips.
The melanosis takes the form of melanin spots sometimes present on the digits and the perianal skin, but pigmentation of the lips is the sine qua non (Fig. 65.34).
Long-term follow-up of patients with PeutzJeghers syndrome has shown reduced survival secondary to complications of recurrent bowel cancer and the development of a wide range of cancers. These include colorectal, gastric, breast, cervical, ovarian, pancreatic and testicular cancer. It is therefore important to keep these patients under surveillance. This can be done by endoscopy or contrast examinations every 3 years to detect early gastrointestinal cancers. It is also important to make sure that female patients attend cervical and breast screening programmes.
Histology
The polyps can be likened to trees. The trunk and branches are smooth muscle fibres and the foliage is virtually normal mucosa.
Treatment
As malignant change rarely occurs, resection is only necessary for serious bleeding or intussusception. Large single polyps can be removed by enterotomy, or short lengths of heavily involved intestine can be resected. The incidence of further lesions developing problems in the future can be reduced by thorough intraoperative examination at the time of the first laparotomy. Using on-table enteroscopy, polyps suitable for removal can be identified. Those lesions within reach can be snared by colonoscopy.
Figure 65.34 Melanin spots on the lips of a patient afflicted with PeutzJeghers syndrome (courtesy of Major P.C.M. Manta, Indian Medical Service).
Malignant
LymphomaThere are three main types, as follows:
Western-type lymphoma. These are annular ulcerating lesions, which are sometimes multiple. They are now thought to be non-Hodgkins B-cell lymphoma in origin. They may present with obstruction and bleeding, perforation, anorexia and weight loss.
Primary lymphoma associated with coeliac disease. There is an increased incidence of lymphoma in patients with coeliac disease; this is now regarded as a T-cell lymphoma. Worsening of the patients diarrhoea, with pyrexia of unknown origin together with local obstructive symptoms, are the usual features.
Mediterranean lymphoma. This is found mostly in North Africa and the Middle East and is associated with -chain disease. Unless there are particular surgical complications these conditions are usually treated with chemotherapy.
Carcinoma
Like small bowel tumours, these can present with obstruction, bleeding or diarrhoea. Complete resection offers the only hope of cure (Fig. 65.35).Carcinoid tumour
These tumours occur throughout the gastrointestinal tract, most commonly in the appendix, ileum and rectum in decreasing order of frequency. They arise from neuroendocrine cells at the base of intestinal crypts. The primary is usually small but, when they metastasise, the liver is usually involved, with numerous secondaries, which are larger and more yellow than the primary; when this has occurred, the carcinoid syndrome will become evident. The tumours can produce a number of vasoactive peptides, most commonly 5-hydroxytryptamine (serotonin), which may be present as 5-hydroxyindoleacetic acid (5-HIAA) in the urine during attacks.
The clinical syndrome itself consists of reddish-blue cyanosis, flushing attacks, diarrhoea, borborygmi, asthmatic attacks and, eventually, sometimes pulmonary and tricuspid stenosis. Classically, the flushing attacks are induced by alcohol.
Treatment
Most patients with gastrointestinal carcinoids do not have carcinoid syndrome. Surgical resection is usually sufficient. In the cases found incidentally at appendicectomy, nothing further is required. In patients with metastatic disease, multiple enucleations of hepatic metastases or even partial hepatectomy can be carried out. The treatment has been transformed by the use of octreotide (a somatostatin analogue), which reduces both flushing and diarrhoea, and octreotide cover is usually used in patients with a carcinoid syndrome who have surgery to prevent a carcinoid crisis. Carcinoid tumours generally grow more slowly than most metastatic malignancies; the patients may live with the syndrome of metastatic disease for many years.
Gastrointestinal stromal tumours
These tumours can be either benign or malignant. Increased size is associated with malignant potential. GIST is a type of sarcoma that develops from connective tissue cells. It is found most commonly in the stomach but can be found in other sites of the gut. It occurs most commonly in the 50- to 70-year age group. Although its cause is unknown, patients with neurofibromatosis have an increased risk of developing these types of tumour.Symptoms
Patients may be asymptomatic. Other symptoms include lethargy, pain, nausea, haematemesis or melaena.
Treatment
Surgery is the most effective way of removing GISTs as they are radioresistant. Glivec (imatinib) is a tyrosine kinase inhibitor that has been shown to be effective in advanced cases.
Figure 65.35 Small bowel adenocarcinoma.
TUMOURS OF THE LARGE INTESTINEBenign
The term polyp is a clinical description of any elevated tumour. It covers a variety of histologically different tumours shown in Table 65.3.
Polyps can occur singly, synchronously in small numbers or as part of a polyposis syndrome. In familial adenomatous polyposis (FAP), more than 100 adenomas are present. It is important to be sure of the histological diagnosis because adenomas have significant malignant potential.
Table 65.3 Classification of polyps of the large intestine
ClassVarietiesInflammatoryInflammatory polypsMetaplasticMetaplastic or hyperplastic polypsHarmartomatousPeutzJeghers polypJuvenile polyp
NeoplasticAdenoma
Tubular
Tubulovillous
VillousAdenocarcinomaCarcinoid tumour
Adenomatous polyps
Adenomatous polyps vary from a tubular adenoma (Fig. 65.36), rather like a raspberry on a stalk, to the villous adenoma, a flat spreading lesion. Solitary adenomas are usually found during the investigation of colonic bleeding or sometimes fortuitously. Villous tumours more usually give symptoms of diarrhoea, mucus discharge and occasionally hypokalaemia. The risk of malignancy developing in an adenoma increases with increasing size of tumour; for example, in 1-cm-diameter tubular adenomas there is a 10% risk of cancer, whereas with villous adenomas over 2 cm in diameter, there may be a 15% chance of carcinoma. Adenomas larger than 5 mm in diameter are usually treated because of their malignant potential. Colonoscopic snare polypectomy or diathermy obliteration with hot biopsy forceps can be used. Huge villous adenomas of the rectum can be difficult to remove even with techniques per anus, and occasionally proctectomy is required; the anal sphincter can usually be preserved.
Familial adenomatous polyposis
FAP is clinically defined by the presence of more than 100 colorectal adenomas. Over 80% of cases come from patients with a positive family history. However, 20% arise as a result of new mutations in the adenomatous polyposis coli gene (APC). This has been identified on the short arm of chromosome 5 (Bodmer). It is less common than hereditary non-polyposis colorectal cancer (HNPCC) and accounts for less than 1% of colorectal cancer. Although the large bowel is mainly affected, polyps can occur in the stomach, duodenum and small intestine. The main risk is large bowel cancer, but duodenal and ampullary tumours have been reported. It is inherited as a Mendelian dominant condition. The risk of colorectal cancer is 100% in patients with FAP. Males and females are equally affected. It can also occur sporadically without any previous sign or history, presumably by new mutations. There is often, in these cases, a history of large bowel cancer occurring in young adulthood or middle age, suggesting pre-existing adenomatosis.FAP can be associated with benign mesodermal tumours such as desmoid tumours and osteomas. Epidermoid cysts can also occur (Gardners syndrome); desmoid tumours in the abdomen invade locally to involve the intestinal mesentery and, although non-metastasising, they can become unresectable (Summary box 65.8).
Summary box 65.8FAP
Autosomal dominant inherited disease due to mutation of the APC gene
More than 100 colonic adenomas are diagnostic
Surgery is the only means of preventing colonic cancer
Polyps and malignant tumours can develop in the duodenum and small bowel
Clinical features
Polyps are usually visible on sigmoidoscopy by the age of 15 years and will almost always be visible by the age of 30 years. Carcinoma of the large bowel occurs 1020 years after the onset of the polyposis. One or more cancers will already be present in two-thirds of those patients presenting with symptoms.
Symptomatic patients
These are either patients in whom a new mutation has occurred or those from an affected family who have not been screened. They may have loose stools, lower abdominal pain, weight loss, diarrhoea and the passage of blood and mucus. Polyps are seen on sigmoidoscopy, and the number and distribution of polyps, and usually cancers if they are symptomatic, are shown on a doublecontrast barium enema. If in doubt, colonoscopy is performed with biopsies to establish the number and histological type of polyps. If over 100 adenomas (Fig. 65.37) are present, the diagnosis can be made confidently, but it is important not to confuse this with non-neoplastic forms of polyposis.
Asymptomatic patients
Direct genetic testing will reveal mutations in 80% of cases. In the presence of an identified mutation in a family with FAP, any resulting negative tests for this can be interpreted to mean that these individuals do not carry the mutation. They can therefore be withdrawn from surveillance programmes and warned that they are at normal population risk of developing colorectal cancer. In those families where a mutation cannot be identified, then surveillance is recommended annually.
The site of the mutation within the gene has important effects on the phenotype. Truncations of the carboxy end of the APC protein have a smaller effect on tumour suppressor function. This results in the attenuated FAP variant.
If there are no adenomas by the age of 30 years, FAP is unlikely. If the diagnosis is made during adolescence, operation is usually deferred to the age of 17 or 18 years or when symptoms or multiple polyps develop.
Screening policy
At-risk family members are offered genetic testing in their early teens.
At-risk members of the family should be examined at the age of 1012 years, repeated every year.
Most of those who are going to get polyps will have them at 20 years, and these require operation.
If there are no polyps at 20 years, continue with 5-yearly examination until age 50 years; if there are still no polyps, there is probably no inherited gene. Carcinomatous change may exceptionally occur before the age of 20 years. Examination of blood relatives, including cousins, nephews and nieces, is essential, and a family tree should be constructed and a register of affected families maintained.
Treatment
Colectomy with ileorectal anastomosis has in the past been the usual operation because it avoids an ileostomy in a young patient and the risks of pelvic dissection to nerve function. The rectum is subsequently cleared of polyps by snaring or fulguration. The patients are examined by flexible sigmoidoscopy at 6-monthly intervals thereafter. In spite of this, a proportion of patients develop carcinoma in the rectal stump. The risk of carcinoma in the St Marks series was 10% over a period of 30 years.
The alternative is a restorative proctocolectomy with an ileoanal anastomosis. This has a higher complication rate than ileorectal anastomosis. It is indicated in patients with serious rectal involvement with polyps, those who are likely to be poor at attending for follow-up and those with an established cancer of the rectum or sigmoid. However, it is now used more frequently for less severe cases. There have been reports of cancers developing after stapled anastomosis when a small remnant of rectal mucosa is left behind.
Postoperative surveillance
Because of the risk of further tumour formation, follow-up is important and takes the form of rectal/pouch surveillance. Gastroscopies are carried out to detect upper gastrointestinal tumours.
Hereditary non-polyposis colorectal cancer (Lynchs syndrome)
This syndrome is characterised by increased risk of colorectal cancer and also cancers of the endometrium, ovary, stomach and small intestines. It is an autosomal dominant condition that is caused by a mutation in one of the DNA mismatch repair genes MLH1, MSH2, MSH6, PMS and PMS2. Most people with this syndrome have mutations in the MLH1 and MSH2 genes.
The lifetime risk of developing colorectal cancer is 80%, and the mean age of diagnosis is 44 years. Most cancers develop in the proximal colon. Females with HNPCC have a 3050% lifetime risk of developing endometrial cancer. The average age of diagnosis is 46 years in this group.
Diagnosis
HNPCC can be diagnosed by genetic testing or Amsterdam criteria II:
three or more family members with a HNPCC-related cancer, one of whom is a first-degree relative of the other two;
two successive affected generations;
one or more of the HNPCC-related cancers diagnosed before the age of 50 years;
exclusion of FAP.
Malignant
EpidemiologyColonic cancer can be diagnosed at operation as involving the large bowel proximal to where the two anti-mesenteric taenia converge (this represents the beginning of the rectum). In the UK, colorectal cancer accounted for 16 000 deaths in 2003 according to Cancer Research UK statistics. It represents a large part of the general surgeons elective and emergency workload. About 22 000 patients are diagnosed with colonic cancer every year. Over the last four decades, the 5-year survival rate has improved from 30% to about 45%.
Genetics
There has been an explosion of information on the molecular genetics of sporadic colorectal cancer. APC mutations occur in two-thirds of colonic adenomas and carcinomas and are thought to present early in the carcinogenesis pathway. K-RAS mutations result in activation of cell signalling pathways. They are more common in larger lesions, thus implying that they are later events in the mutagenesis pathway. Other genes involved include p53.
However, it must be noted that the pathway is not one of a simple stepwise progression of mutations but a complicated array of multiple gene changes, which result in an outcome of cancer. No single mutation is a common theme for all colorectal cancer cases. However, knowledge of certain mutations can be used to assess prognosis and direct adjuvant therapy.
Aetiology
Other factors that have been implicated in the development of cancer have included dietary fibre. The hypothesis is that increased roughage is associated with reduced transit times, and this in turn reduces the exposure of the mucosa to carcinogens. This has been supported by population questionnaire studies. There have also been studies linking increased dietary animal fat, smoking and alcohol to colorectal cancer. There is some evidence that links cholecystectomy, and therefore increased bile acid secretion, to an increased risk of colorectal cancer.
The role of irritable bowel disease (IBD) in colorectal cancer is discussed elsewhere in this chapter.
Adenocarcinoma of the colon
Pathology
Microscopically, the neoplasm is a columnar cell carcinoma originating in the colonic epithelium. Macroscopically, the tumour may take one of four forms (Fig. 65.38). Type 4 is the least malignant form. It is likely that all carcinomas start as a benign adenoma, the so called adenomacarcinoma sequence. This is supported by the observation that the prevalence of adenomas correlates with carcinoma. The distribution of adenoma in the colon also mirrors that of carcinoma. The annular variety tends to give rise to obstructive symptoms, whereas the others will present more commonly with bleeding. The sites and distribution of cases of cancer are shown in Figure 65.39. Tumours are more common in the left colon and rectum.
Figure 65.38 The four common macroscopic varieties of carcinoma of the colon. (1) Annular; (2) tubular; (3) ulcer; (4) cauliflower.
Figure 65.39 Distribution of colorectal cancer by site.
The spread of carcinoma of the colon
Generally this is a comparatively slow-growing neoplasm.
Local spread
The tumour can spread in a longitudinal, transverse or radial direction; it spreads round the intestinal wall and usually causes intestinal obstruction before it invades adjacent structures. The ulcerative type more commonly invades locally, and an internal fistula may result, for example into the bladder. There may also be a local perforation with an abscess or even an external faecal fistula. This type of radial spread to adjacent organs has the largest impact on prognosis. The progression of invasion occurs across the submucosa into the muscularis propria and thence out into the serosa and fat, lymphatics and veins in the mesentery alongside the bowel wall.
Lymphatic spread
Lymph nodes draining the colon are grouped as follows:
N1: nodes in the immediate vicinity of the bowel wall;
N2: nodes arranged along the ileocolic, right colic, midcolic, left colic and sigmoid arteries;
N3: the apical nodes around the superior and inferior mesenteric vessels where they arise from the abdominal aorta. Involvement of the lymph nodes by the tumour progresses in a gradual manner from those closest to the growth along the course of the lymphatic vessels to those placed centrally.
Bloodstream spread
This accounts for a large proportion (3040%) of late deaths. Metastases are carried to the liver via the portal system, sometimes at an early stage before clinical or operative evidence is detected (occult hepatic metastases).
Transcoelomic spread
Rarely, colorectal cancer can spread by way of cells dislodging from the serosa of the bowel or via the subperitoneal lymphatics to other structures within the peritoneal cavity.
Staging colon cancer
There are several staging systems that are used such as Dukes, tumournodemetastasis (TNM) and Jass. All of them can be used in order to predict prognosis and standardise treatment. Dukes classification was originally described for rectal tumours (see Chapter 68) but has been adopted for histopathological reporting of colon cancer as well. There have been numerous modifications of the original system, leading to some confusion but, in its most basic form, Dukes classification for colon cancer is as follows:confined to the bowel wall;
through the bowel wall but not involving the free peritoneal serosal surface;
lymph nodes involved.
Dukes himself never described a D stage, but this is often used to describe either advanced local disease or metastases to the liver.
TNM classification
The TNM classification is more detailed and accurate but more demanding:
T Tumour stage;
T1 Into submucosa;
T2 Into muscularis propria;
T3 Into pericolic fat but not breaching serosa;
T4 Breaches serosa or directly involving another organ;
N Nodal stage;
N0 No nodes involved;
N1 One or two nodes involved;
N2 Three or more nodes involved;
M Metastases;
M0 No metastases;
M1 Metastases;
Ly Lymphatic invasion;
L0 No lymphatic vessels involved;
L1 Lymphatics involved;
V Venous invasion;
V0 No vessel invasion;
V1 Vessels invaded;
R Residual tumour;
R0 No residual tumour;
R1 Margins involved, residual tumour present.
Clinical features
Carcinoma of the colon usually occurs in patients over 50 years of age, but it is not rare earlier in adult life. Twenty per cent of cases present as an emergency with intestinal obstruction or peritonitis. In any case of colonic bleeding in patients over the age of 40 years, a complete investigation of the colon is required. A careful family history should be taken. Those with first degree relatives who have developed colorectal cancer at the age of 45 years or below are at high risk and may be part of one of the colorectal cancer family syndromes.
Carcinoma of the left side of the colon
Most tumours occur in this location. They are usually of the stenosing variety.
Symptoms
The main symptoms are those of increasing intestinal obstruction. This includes lower abdominal pain, which may be colicky in nature, and abdominal distension. The patient may have a change in bowel habit with alternating diarrhoea and constipation (Summary box 65.9).
Summary box 65.9Symptoms & Signs of colorectal cancer
Right-sided tumours: iron deficiency anaemia, abdominal massLeft-sided tumours: rectal bleeding, alteration in bowel habit, tenesmus, obstruction
Metastatic disease: jaundice, ascites, hepatomegaly; other symptoms and signs from rarer sites of metastasis
There may be considerable overlap between these symptoms
Carcinoma of the sigmoid
In addition to symptoms of intestinal obstruction, a low tumour may give rise to a feeling of the need for evacuation, which may result in tenesmus accompanied by the passage of mucus and blood. Bladder symptoms are not unusual and, in some instances, may herald a colovesical fistula.Carcinoma of the transverse colon
This may be mistaken for a carcinoma of the stomach because of the position of the tumour together with anaemia and lassitude.
Carcinoma of the caecum and ascending colon
This may present with the following:
anaemia, severe and unyielding to treatment;
the presence of a mass in the right iliac fossa; colonoscopy may be needed to confirm the diagnosis;
a carcinoma of the caecum can be the apex of an intussusceptions presenting with the symptoms of intermittent obstruction.
Metastatic disease
Patients may present for the first time with liver metastases and an enlarged liver, ascites from carcinomatosis peritonei and, more rarely, metastases to the lung, skin, bone and brain.
Methods of investigation of colon cancer
Flexible sigmoidoscopy
The 60-cm, fibreoptic, flexible sigmoidoscope is increasingly being used in the out-patient clinic or in special rectal bleeding clinics. The patient is prepared with a disposable enema and sedation is not usually necessary. This is particularly useful in supplementing barium investigations where diagnosis is difficult due to diverticular disease.
Colonoscopy
This is now the investigation of choice if colorectal cancer is suspected provided the patient is fit enough to undergo the bowel preparation. It has the advantage of not only picking up a primary cancer but also having the ability to detect synchronous polyps or even multiple carcinomas, which occur in 5% of cases. Ideally, every case should be proven histologically before surgery. Full bowel preparation and sedation are necessary. However, one must be aware of a small risk of perforation and also the failure to get to the caecum in 10% of cases, even by experienced endoscopists.
Radiology
Double-contrast barium enema is used when colonoscopy is contraindicated. It shows a cancer of the colon as a constant irregular filling defect (Fig. 65.40). False positives occur in 12% of cases and false negatives in 79% of cases.
Ultrasonography is often used as a screening investigation for liver metastases over the size of 1.5 cm, and CT is used in patients with large palpable abdominal masses, to determine local invasion, and is particularly used in the pelvis in the assessment of rectal cancer.
Spiral CT is particularly useful in elderly patients when contrast enemas or colonoscopy are not diagnostic or are contraindicated. In some centres, it is standard investigation above the age of 80 years. With the advent of technology in this field, there has been the introduction of virtual colonoscopy, which is effective in picking up polyps down to size of 6 mm (Fig. 65.41). This may even replace colonoscopy as the standard investigation in the future.
Urograms have a role in left-sided tumours where there is evidence of hydronephrosis on CT or ultrasound.
Figure 65.40 Barium enema showing a carcinoma of the sigmoid colon. It may have an apple core appearance, i.e. a short, irregular stenosis with sharp shoulders at each end.
Treatment
Preoperative preparationRecent literature has suggested that no bowel preparation is safe for right-sided colonic surgery. The most commonly used method is dietary restriction to fluids only for 48 hours before surgery; on the day before the operation, two sachets of Picolax (sodium picosulphate) are taken to purge the colon. In addition, a rectal washout may be necessary. A stoma site is carefully discussed with the stoma care nursing specialist and anti-embolus stockings are fitted; the patient is started on prophylactic subcutaneous heparin, and intravenous prophylactic antibiotics are given at the start of surgery.
When intestinal obstruction is present, preparation in this way may precipitate abdominal pain, and it may be safer to use an ontable lavage technique at the time of the operation (Summary box 65.10).
Summary box 65.10Principles of management of colorectal cancer
Assessment of local and distant tumour spread should be performed both preoperatively and intraoperatively to allow planning of surgerySynchronous tumours occur in about 5% of patients and should be excluded preoperatively
Operations are planned to remove the primary tumour and its draining locoregional lymph nodes
Histological examination of resected tumours contributes to decision making regarding the need for adjuvant therapy
The test of operability
The abdomen is opened and the tumour assessed for resectability.
The liver is palpated for secondary deposits, the presence of which is not necessarily a contraindication to resection because the best palliative treatment for carcinoma of the colon is removal of the tumour.
The peritoneum, particularly the pelvic peritoneum, is inspected for signs of small, white, seed-like, neoplastic implantations. Similar changes can occur in the omentum.
The various groups of lymph nodes that drain the involved segment are palpated. Their enlargement does not necessarily mean that they are invaded by metastases, because the enlargement may be inflammatory.
The neoplasm is examined with a view to mobility and operability. Local fixation, however, does not always imply local invasion because some tumours excite a brisk inflammatory response.
Operations (للإطلاع فقط)
The operations to be described are designed to remove the primary tumour and its draining locoregional lymph nodes, which may be involved by metastases. Lesser resections are indicated, however, should hepatic metastases render the condition incurable surgically. There is some evidence that early division of major blood vessels supplying the involved colon (no-touch technique Turnbull) can slightly improve the number of curative third of the transverse colon. When it is clear that there is an adequate blood supply at the resection margins, the right colon is resected, and an end-to-end anastomosis is fashioned between the ileum and the transverse colon.
Carcinoma of the hepatic flexure
When the hepatic flexure is involved, the resection must be extended correspondingly (Fig. 65.44).
Carcinoma of the transverse colon
When there is no obstruction, excision of the transverse colon and the two flexures together with the transverse mesocolon and the greater omentum, followed by end-to-end anastomosis, can be used. An alternative is an extended right hemicolectomy (Fig. 65.44).
Carcinoma of the splenic flexure or descending colon
The extent of the resection is from right colon to descending colon. Sometimes, removal of the colon up to the ileum, with an ileorectal anastomosis, is preferable.
Carcinoma of the pelvic colon
The left half of the colon is mobilised completely (Fig. 65.45). So that the operation is radical, the inferior mesenteric artery below its left colic branch, together with the related paracolic lymph nodes, must be included in the resection. This entails carrying the dissection as far as the upper third of the rectum. Many surgeons advocate flush ligation of the inferior mesenteric artery on the aorta (high ligation). Provided that there is no obstruction, primary anastomosis is the rule. Occasionally, a protecting upstream stoma may be necessary. The methods of dealing with large bowel obstruction as a result of colon cancer are described in Chapter 66.
Laparoscopic surgery
This has been heralded as the next major advance in colorectal surgery. However, its role needs to be accepted with an element of caution. It is technically demanding with a long learning curve. Patients undergoing such surgery need to be entered into clinical trials. Important technical issues are traction and adequate vision, which are vital, as for open conventional procedures. Hand-assisted methods can be used in particularly difficult cases, but this takes away some of the benefits of the minimal approach. Specimen retrieval is via small incisions. Techniques and technology are rapidly evolving.
When a growth is found to be inoperable
In the upper part of the left colon, an ileostomy is performed. In the pelvic colon, a left iliac fossa colostomy is preferable. With an inoperable growth in the ascending colon, a bypass using an ileocolic anastomosis is the best procedure. A total colectomy needs to be considered for multiple tumours. Over 95% of colonic carcinomas can, however, be resected.Adjuvant therapy
See Chapter 68.
Screening
There is now good evidence from controlled trials that regular bowel screening using faecal occult blood testing of people aged 6069 years can reduce the mortality risk of colorectal cancer by about 15%. Those who test positive for faecal occult blood tests are then offered colonoscopy. These data have prompted the setting up of the National Health Service Bowel Cancer Screening Programme in the UK. Flexible sigmoidoscopy can also be used as the initial screening tool, and early results from a clinical trial look promising.
Hepatic metastases
It is important not to biopsy hepatic metastases as this may cause tumour dissemination (Fig. 65.46). Hepatic resection is usually performed as a staged procedure after recovery from colonic resection. Most wait 12 weeks before restaging. By doing this, those with aggressive disease are excluded from further drastic surgery. Reports have shown 30% 5-year survival following hepatectomy for colorectal cancer metastases. Radiological imaging will usually correctly identify colorectal metastases and assess patients suitable for liver resection. At present, the criterion for resection is fewer than three lesions in one lobe of liver. Irresectable symptomatic hepatic metastases may be suitable for other treatments including cytotoxic drugs or ablative treatments.OTHER DISORDERS
Traumatic rupture
The intestine can be ruptured with or without an external wound so called blunt trauma (Fig. 65.47). The most common cause of this is a blow to the abdomen that crushes the bowel against the vertebral column or sacrum; also, a rupture is more likely to occur where part of the gut has been fixed, for example in a hernia, or where a fixed part of the gut joins a mobile part such as the duodenojejunal flexure. Here, the damage may be retroperitoneal and easily overlooked.In small perforations, the mucosa may prolapse through the hole and partly seal it, making the early signs misleading. In addition, there may be a laceration in the mesentery. The patient will then have a combination of intra-abdominal bleeding and release of intestinal contents into the abdominal cavity, giving rise to peritonitis.
Traumatic rupture of the large intestine is much less common. In blast injuries of the abdomen following the detonation of a bomb, the pelvic colon is particularly at risk of rupture. Compressed air rupture can follow the dangerous practical joke of turning on an airline carrying compressed air near the victims anus.
Rupture of the upper rectum can occur during sigmoidoscopy and occasionally during the placement of rectal catheters for barium radiology. Traumatic rupture of the colon can occur during colonoscopy. The most common site is the sigmoid colon, where the formation of a sigmoid loop pushes against the antimesenteric border of the sigmoid colon, stretching it out and eventually perforating it.
Gunshot wounds and impalement injuries to the bowel have more serious consequences because of the introduction of debris from the patients clothing or the missile itself mixing with the bacteria in the patients gut. High-velocity missiles may cause extensive damage to the bowel over a much wider area than just the entry and exit wounds.
Figure 65.47 Traumatic rupture of the small intestine as a result of blunt abdominal trauma.
Treatment
Where rupture is suspected, a plain radiograph in the erect or lateral decubitus position will demonstrate the presence of free air in the peritoneal cavity or indeed in the retroperitoneal tissues. In almost all cases, an abdominal exploration must be performed and, in many instances, simple closure of the perforation is all that is required. In others, for example where the mesentery is lacerated and the bowel is not viable, resection may be necessary.In the case of the large intestine, small, clean tears can be closed primarily; if there is a large tear with damage to the surrounding structures and the adjacent mesentery, resection and exteriorization may be used. Much depends on the amount of intra-abdominal soiling. In the case of retroperitoneal portions of the intestine, for example the duodenum, perforations can involve the front and back walls, and the duodenum in particular has to be carefully mobilised to check that a concealed tear is not overlooked. In all cases, the abdomen is washed out with saline and broad-spectrum intravenous antibiotics are given.
Enterocutaneous or faecal fistula
An external fistula communicating with the caecum sometimes follows an operation for gangrenous appendicitis or the draining of an appendix abscess. A faecal fistula can occur from necrosis of a gangrenous patch of intestine after the relief of a strangulated hernia, or from a leak from an intestinal anastomosis. The opening of an abscess connected with chronic diverticulitis or carcinoma of the colon frequently results in a faecal fistula. Radiation damage is also another cause of fistula formation. The most common cause of enterocutaneous fistula is, however, previous surgery. This happens most often in patients with adhesions following previous operations. Damage to the small intestine occurs inadvertently during dissection of the adhesions and, because of an associated subacute obstruction or abscess, the fistula blows postoperatively. Enterocutaneous fistulae can be divided into:those with a high output, more than 1 litre day1;
those with a low output, less than 1 litre day1.
They can also be described anatomically as simple, with a direct communication between the gut and the skin, or complex, i.e. those with one or more tracts that are tortuous and sometimes associated with an intervening abscess cavity half way along the tract.
The discharge from a fistula connected with the duodenum or jejunum is bile-stained and causes severe excoriation of the skin. When the ileum or caecum is involved, the discharge is fluid faecal matter; when the distal colon is the affected site, it is solid or semisolid faecal matter. The site of leakage and the length of the fistula can be determined by small bowel enema and barium enema, by fistulography and, most importantly, by CT of the abdomen will show up any associated abscesses (Fig. 65.48).
Treatment
This can be very challenging in patients with a high-output fistula. Low-output fistulae can be expected to heal spontaneously, provided there is no distal obstruction. Reasons for failure of spontaneous healing also include:
epithelial continuity between the gut and the skin;
the presence of active disease where, for example, there is CD or carcinoma at the site of the anastomosis or in the tract;
an associated complex abscess.
The abdominal wall must be protected from erosion by the use of appliances. The patient must remain nil by mouth; intravenous nutrition is started and signs of a decrease in fistula output are sought. The higher the fistula in the intestinal tract, the more skin excoriation must be expected, and this is worst in the case of a duodenal fistula. High-output fistulae cause rapid dehydration and hypoproteinaemia. Vigorous fluid replacement and nutritional support are essential. The drainage of an intra-abdominal abscess can be life-saving. This can be achieved by either CT-guided drainage or, occasionally, laparotomy. In patients with a complex
fistula, it may be necessary to bring out a defunctioning stoma upstream of the fistula site, even if this results in a high-output stoma.
Operative treatment
Operative repair should be attempted only after a trial of conservative management. The surgery can on occasion be extremely technically demanding, and an anastomosis should not be fashioned in the presence of continuing intra-abdominal sepsis or when the patient is hypoproteinaemic.STOMAS
ColostomyA colostomy is an artificial opening made in the large bowel to divert faeces and flatus to the exterior, where it can be collected in an external appliance. Depending on the purpose for which the diversion has been necessary, a colostomy may be temporary or permanent (Summary box 65.11).
Summary box 65.11Stomas
May be colostomy or ileostomyMay be temporary or permanent
Temporary or defunctioning stomas are usually fashioned as loop stomas
An ileostomy is spouted; a colostomy is flush
Ileostomy effluent is usually liquid whereas colostomy effluent is usually solid
Ileostomy patients are more likely to develop fluid and electrolyte problems
An ileostomy is usually sited in the right iliac fossa
A temporary colostomy may be transverse and sited in the right upper quadrant
End-colostomy is usually sited in the left iliac fossa
All patients should be counselled by a stoma care nurse before operation
Complications include skin irritation, prolapse, retraction, necrosis, stenosis, parastomal hernia, bleeding and fistulation
Temporary colostomy
A transverse loop colostomy has in the past been most commonly used to defunction an anastomosis after an anterior resection. It is now less commonly employed as it is fraught with complications and is difficult to manage; a loop ileostomy is preferred.
A loop left iliac fossa colostomy is still sometimes used to prevent faecal peritonitis developing following traumatic injury to the rectum, to facilitate the operative treatment of a high fistula-in- ano and incontinence.
A temporary loop colostomy is made, bringing a loop of colon to the surface, where it is held in place by a plastic bridge passed through the mesentery. Once the abdomen has been closed, the colostomy is opened, and the edges of the colonic incision are sutured to the adjacent skin margin (Fig. 65.49). When firm adhesion of the colostomy to the abdominal wall has taken place, the bridge can be removed after 7 days.
Following the surgical cure or healing of the distal lesion for which the temporary stoma was constructed, the colostomy can be closed. It is usual to perform a contrast examination (distal loopogram) to check that there is no distal obstruction or continuing problem at the site of previous surgery. Colostomy closure is most easily and safely accomplished if the stoma is mature, i.e. after the colostomy has been established for 2 months. Closure is usually performed by an intraperitoneal technique, which is associated with fewer closure breakdowns with faecal fistulae.
Double-barrelled colostomy
This colostomy was designed so that it could be closed by crushing the intervening spur using an enterotome or a stapling device. It is rarely used now, but occasionally the colon is divided so that both ends can be brought to the surface separately, ensuring that the distal segment is completely defunctioned.
Permanent colostomy
This is usually formed after excision of the rectum for a carcinoma by the abdominoperineal technique.
It is formed by bringing the distal end (end-colostomy) of the divided colon to the surface in the left iliac fossa, where it is sutured in place, joining the colonic margin to the surrounding skin.
The point at which the colon is brought to the surface must be carefully selected to allow a colostomy bag to be applied without impinging on the bony prominence of the anterosuperior iliac spine. The best site is usually through the lateral edge of the rectus sheath, 6 cm above and medial to the bony prominence (Fig. 65.50).
Closure of the lateral space between the intraperitoneal segment of the sigmoid colon and the peritoneum of the pelvic wall, to prevent internal herniation or strangulation of loops of small bowel through the deficiency, has been practised, but there is no good evidence that it is effective.
Colostomy bags and appliances (Fig. 65.51)
Faeces from a permanent colostomy are collected in disposable adhesive bags. A wide range of such bags is currently available.Many now incorporate a stomahesive backing, which can be left in place for several days. In most hospitals, a stoma care service is available to offer advice to patients, to acquaint them with the latest appliances and to provide the appropriate psychological and practical help.
Complications of colostomies
The following complications can occur to any colostomy but are more common after poor technique or siting of the stoma:prolapse;
retraction;
necrosis of the distal end;
fistula formation;
stenosis of the orifice;
colostomy hernia;
bleeding (usually from granulomas around the margin of the colostomy);
colostomy diarrhoea: this is usually an infective enteritis and will respond to oral metronidazole 200 mg three times daily.
Many of these complications require revision of the colostomy. Sometimes, this can be achieved with an incision immediately around the stoma but, on occasion, reopening the abdomen and freeing up the colostomy may be necessary. Occasionally, transfer to the opposite side of the abdomen may be necessary.
Loop ileostomy
An ileostomy is now often used as an alternative to colostomy, particularly for defunctioning a low rectal anastomosis. The creation of a loop ileostomy from a knuckle of terminal ileum has already been described. The advantages of a loop ileostomy over a loop colostomy are the ease with which the bowel can be brought to the surface and the absence of odour. Care is needed, when the ileostomy is closed, that suture line obstruction does not occur.
Caecostomy
This is rarely used now. In desperately ill patients with advanced obstruction, a caecostomy may be useful. In late cases of obstruction, the caecum may become so distended and ischaemic that rupture of the caecal wall may be anticipated. This can occur spontaneously, giving rise to faecal peritonitis, or at operation, when an incision in the abdominal wall reduces its supportive role and allows the caecum to expand. In such a situation, it should be decompressed by suction as soon as the abdomen is opened. In thin patients, it may then be possible to carry out direct suture of the incised or perforated caecal wall to the abdominal skin of the right iliac fossa, although a resection of this area is really the best treatment. Following on-table lavage, via the appendix stump, the irrigating catheter can be left in place as a tube caecostomy. Caecostomy is only a short-term measure to allow a few days for the condition of the patient to improve. Reoperation should normally follow soon thereafter and a definitive procedure should be carried out.THE END
Printed By:Haider Hashim
7th of December 2011
The small & large intestines Lecture (4, 5 & 6)
Page PAGE 26 of NUMPAGES 26