Tumours
of the large intestine
Benign
The term ‘polyp’ is a clinical description of any elevated tumour.
It covers a variety of histologically different tumours shown in Table
57.2.
Polyps
can occur either singly, synchronously in small numbers or as part of a
polyposis syndrome. In familial adenomatous polyposis, more than 100 adenomas
are present. It is important to be sure of the histological diagnosis because
adenomas have significant malignant potential.
Adenomatous
polyps
Adenomatous polyps vary from a tubular adenoma (Fig.
57.39), rather like
a raspberry on a stalk, to the villous adenoma, a
Hamartomatous
polyps
Peutz—Jeghers polyps may occur in the colon as either solitary or
multiple lesions. Juvenile polyps may occur as multiple lesions in the colon
often associated with a congenital defect such as a malrotation or Meckels’
diverticulum. They have minimal malignant potential and ate only removed if they
are causing troublesome pain, bleeding or hypoproteinaemia.
Haemangioma
A localised submucous telangiectasis is often the cause of bleeding
which may be profuse. If bleeding is continuing, both angiography and
colonoscopy can help to localise the source. If found by colonoscopy the lesion
can be removed endoscopically, whereas arteriographic detection can be followed
by the use of vasopressin or microspheres to stop the haemorrhage. Often the
only method of detecting it is to operate while the bleeding is in progress. The
distribution of blood within the intestine is noted; scrutiny of the
blood-containing portion of the colon may reveal the lesion but on-table
colonoscopy could be necessary. The tumour is resected once located.
Lipoma
Lipoma is less frequently encountered in the large than in the small
intestine. In the large intestine it is almost always confined to the caecum.
The tumour is submucous and in more than half the cases it is the cause of an
intussusception. On occasion a lipoma at the ileocaecal valve can be confused
with a caecal cancer.
Familial
adenomatous polyposis
Familial adenomatous polyposis (FAP) is a general neoplastic disorder of
the intestine. 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 and the gene responsible (APC gene) has now been identified
on the short arm of chromosome 5 (Bodmer). 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 preexisting
adenomatosis.
FAP
can be associated with benign mesodermal tumours such as desmoid tumours and
osteomas. Epidermoid cysts can also occur (Gardner’s syndrome); desmoid
tumours in the abdomen invade locally to involve the intestinal mesentery and
although nonmetastasising they can become unresectable.
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. Carcinoma of the large bowel
occurs 10—20 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 new proposition 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 ate symptomatic, are shown on a double-contrast barium enema. If in doubt
colonoscopy is performed with biopsies to establish the number and histological
type of polyps. If over 100 adenomas (Fig. 57.40) ate present the diagnosis can
be made confidently but it is important not to confuse this with nonneoplastic
forms of polyposis.
Asymptomatic
patients. Usually members of affected families attend for screening. As yet
there is no reliable means of knowing whether an individual is affected unless
adenomas develop. If there are no adenomas by the age of 30, FAP is unlikely.
Pigmented spots in the retina (CHIRPES) and deoxyribonucleic acid (DNA) tests
for the FAP gene should make screening mote reliable in the future.
If
the diagnosis is made during adolescence, operation is deferred usually to the
age of 17 or 18.
Screening
policy.
1. All members of the family should
be examined at the age of 10—12 years, repeated every 1—2 years.
2. Most of those who are going to
get polyps will have them at 20 and these requite operation.
3. If there are no polyps at 20,
continue with 5-yearly examination until age 50; if there are still no polyps
there is probably no inherited gene. Carcinomatous change may exceptionally
occur before the age of 20. 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. The rectum is subsequently
cleared of polyps by snaring or fulguration. The patients ate examined by
flexible sigmoidoscopy at 6-monthly intervals thereafter. In spite of this, a
proportion of patients develops carcinoma in the rectal stump. The risk of
carcinoma in the St Mark’s series was 10 per cent over a period of 30 years.
The
alternative and now more common operation 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
mote frequently for less severe cases.
Malignant
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. 57.41). Type 4 is the least malignant form. It is likely
that all carcinomas start as a benign adenoma, the so-called
‘adenoma—carcinoma sequence’. The annular variety tends to
give rise to obstructive symptoms whereas the others more commonly will present
with bleeding. Site and distribution of cases of cancer are shown in Fig.
57.42.
Tumours are more common in the left colon and rectum.
The spread of carcinoma of the colon. Generally this is a comparatively
slow growing neoplasm.
Local spread
The tumour is limited
to the bowel for a considerable time; it spreads round the intestinal wall and
usually causes intestinal obstruction before it invades adjacent structures. The
ulcerative type mote 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. The progression of invasion occurs across the submucosa
into the musculatis propia 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 ileo-colic, 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 (30—40 per cent) 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).
Staging
colon cancer. Dukes’ classification was originally described for rectal
tumours (see Chapter 60) 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.
Dukes’
A — confined to bowel wall;
B — through the bowel wall but not involving the free
peritoneal serosal surface;
C —
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:
—
into submucosa;
T2 — into muscularis propria;
—
into pericolic fat but-not breaching serosa;
—
breaches serosa or directly involving another organ.
N — nodal stage:
N0
— no nodes involved;
N1 — 1—2 nodes involved;
N2 — 3 or more nodes.
M — metastases:
—
no metastases;
—
metastases.
Ly — lymphatic invasion:
L0 — no lymphatic vessels involved;
—
lymphatics involved.
V — venous invasion:
V0 — no vessel invasion;
Vi — vessels invaded.
R — residual tumour:
R0 — no residual tumour;
—
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 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 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 ate usually of the stenosing
variety. The main symptoms are those of increasing intestinal obstruction.
Pain
is referred to the suprapubic area. Patients will have episodes of colic; a
constant ache may suggest an advanced tumour.
Alteration
of bowel habit. An adult previously having a predictably regular bowel habit
suddenly develops irregularity. There may be increasing difficulty in getting
the bowels to move, requiring laxatives. The episodes of constipation may be
followed by attacks of diarrhoea.
Palpable
lump. The lump that is felt on abdominal, rectal or bimanual palpation is
sometimes not the tumour itself, but impacted faeces above it. When the tumour
is situated in a pendulous pelvic colon, a hard movable swelling may be felt in
the rectovesical pouch on rectal examination.
Distension.
Lower abdominal distension is not uncommon and, as with the pain, is relieved by
passing flatus.
Carcinoma
of the sigmoid
This follows the general pattern of the above, with these differences.
Pain
is usually colicky from the outset.
Tenesmus.
Low tumours may give rise to a feeling of the need for evacuation which may
result in tenesmus accompanied by the passage of mucus and blood, especially
in the early morning.
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; there may be a
palpable tumour present.
• The presence of a mass in the right iliac fossa. Colonoscopy
may be needed to confirm the diagnosis.
• Caecal carcinoma is sometimes discovered unexpectedly at
operation for acute appendicitis or for an appendix abscess failing to resolve.
On rare occasions the appendix is inflamed, or even gangrenous, from the
obstruction to its lumen by the tumour.
• A carcinoma of the caecum can be the apex of an intussusception
presenting with the symptoms of intermittent obstruction.
Metastatic
disease
Patients may present for the first time with liver metastases and an
enlarged liver, ascitis from carcinomatosis peritonei and, more rarely,
rnetastases to the lung, skin, bone and brain.
Methods
of investigation
Sigmoidoscopy. This is part of the routine investigation of patients
passing blood and mucus that is really limited to the rectum.
Flexible
sigmoidoscopy. The 60-cm, fibre-optic, flexible sigmoidoscope is being used
increasingly 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.
Colonoscopy.
This 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 per cent of cases. It tends to be used in patients with bleeding as
their main presenting symptom, those with known polyps and those in whom there
is doubtful radiology. Ideally every case should be proven histologically before
surgery. Full bowel preparation and sedation are necessary.
Radiology.
Double-contrast barium enema is used routinely now. It shows a cancer of the
colon as a constant irregular filling defect (Fig.
57.43). It is the
investigation of choice in patients with predominant change in bowel habit as
their presenting symptom. Ultrasonography is often used as a screening
investigation for liver metastases, 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.
Treatment
Preoperative preparation. Full mechanical bowel preparation before
colonic surgery is essential. The most commonly used method is dietary
restriction to fluids only for 48 hours before surgery; on the day before
operation two sachets of Picolax (sodium picosulphate) are taken to purge the
colon.
When
intestinal obstruction is present, preparation in this way may precipitate
abdominal pain and it may be safer to save preparation to the time of the
operation using an on table lavage technique.
Operations
The test of operability. The abdomen is opened and the tumour assessed
for resectability.
1. 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.
2. The peritoneum, particularly the pelvic peritoneum, is inspected for
signs of small, white, seed-like, neoplastic implantations. Similar changes can
occur in the omentum.
3. 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.
4. 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.
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 rnetastases render the
condition curable nonsurgically. 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 operations.
Carcinoma
of the caecum or ascending colon (Fig. 57.44) is treated when resectable by
right hemicolectomy (Fig. 57.45).
The
abdomen is opened, the peritoneum lateral to the ascending colon is incised and
the incision carried around the hepatic flexure. The right colon is elevated,
with the leaf of peritoneum containing its vessels and lymph nodes, from the
posterior abdominal wall, taking care not to injure the ureter, spermatic vessels in the male or the duodenum. The
peritoneum is separated medially neat the origin of the ileo-colic artery, which
is divided together with the right colic artery when this has a separate origin
from the superior mesenteric. The mesentery of the last 30 cm of ileum, and the
leaf of raised peritoneum attached to the caecum, ascending colon and hepatic
flexure, after ligation of the mesenteric blood vessels, is divided as far as
the proximal third of the transverse colon. When it is cleat that there is an
adequate blood supply at the resection margins, the right colon is resected and
an end-to-end anastomosis fashioned between the ileum and transverse colon.
Carcinoma
of the hepatic flexure. When the hepatic flexure is involved the resection
must be extended correspondingly (Fig. 57.46).
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.
57.46).
Carcinoma
of the pelvic colon. The left half of the colon is mobilised completely
(Fig. 57.47). 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 litigation). Provided that there is no
obstruction primary anastomosis is the rule. Occasionally a
When
a growth is found to be inoperable. In the upper part of the left colon, a
transverse colostomy 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 ileo-colic anastomosis is the best procedure. Over 95 per
cent of colonic carcinomas can, however, be resected.
Adjuvant
therapy
See Chapter 60.
Hepatic
metastases
It is important to biopsy hepatic metastases for histological diagnosis.
Unless they are on the very surface and edge of the liver, they are not usually
resected at the time of colonic surgery. Patients with up to two or three liver
metastases confined to one lobe of the liver may be offered hepatic resection.
Multiple painful hepatic metastases can be palliated by cytotoxic drugs,
cryosurgery or laser therapy (Fig. 57.48).