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wholemeal bread and bran) is often recommended,
although in some patients with very sensitive colons
and significant symptoms of pain, a lower fibre diet
can often be helpful.
Colovesical fistula is treated by resection of the
affected segment of the colon after disconnection
from the bladder wall; a primary colorectal anastomosis is fashioned and the defect in the bladder
repaired (although sometimes the bladder hole is so
small that it will heal itself after a urinary catheter is
left in place for a few days).
Angiodysplasia
This term is applied to one or multiple small (<5mm)
mucosal or submucosal vascular malformations, usually a dilated vein or sheaf of veins. Because they
occur most commonly in the elderly, they are considered to be degenerative vascular anomalies. The caecum and ascending colon are the sites most usually
involved, although they may be found anywhere in
the small or large bowel.
Clinical features
They are usually asymptomatic, and were unknown
before the advent of mesenteric angiography and
colonoscopy. Their only clinical manifestation is
bleeding, which may take the form of continuous
chronic intestinal blood loss, presenting with anaemia, or recurrent acute dark or bright red rectal
bleeding, which may occasionally be severe and
threatening. Recurrent bleeding is common.
lifeThey account for as much as 5% of such emergency
cases.
Special investigations
• Colonoscopy is the investigation of choice,
although it is often difficult to visualize the
acutely. The lesions appear as bright red 0.5–1cm
diameter submucosal lesions with small, dilated
vessels visible on close inspection. They are not
visible on CT colonography.
• Mesenteric angiogram. Actively bleeding angiod-
ysplasias may be detected on angiography as
contrast medium leaks into the bowel lumen.
caecum
Treatment
Blood transfusion is necessary if bleeding is severe.
Colonoscopic electrocoagulation or argon plasma
coagulation may be curative. Resection, usually a
right hemicolectomy, is rarely required.
Colitis
Colitis, inflammation of the colon, presents with diarrhoea and often lower abdominal pain, with blood
and mucus per rectum. The most common causes of
colitis are:
1
Inflammatory bowel disease, including both ulcer-
ative colitis and Crohn’s colitis.
Antibiotic- associated colitis, for example pseu-
2
domembranous colitis due to Clostridium difficile
(see Chapter5).
3
Infective colitis, for example Campylobacter and
amoebic colitis.
Ischaemic colitis, due to mesenteric ischaemia,
4
occurring spontaneously (a poorly understood
condition, as often the main supplying vasculature is patent on subsequent investigation), or following ligation of the inferior mesenteric artery in
aortic surgery or its exclusion following placement
of a covered aortic stent.
Ulcerative colitis
Ulcerative colitis is an inflammatory disease of the
large bowel that involves the rectum and extends for a
variable distance proximally in the colon. Women are
more often affected than men, and it is found in any
age from infancy to the elderly, but the maximum
incidence is between the ages of 15 and 30with a
second peak between 50 and 70.
Aetiology
The aetiology of ulcerative colitis is unknown,
although it appears to combine genetic factors, environmental stimuli and altered immune responses; it
is one of the few diseases in which smoking appears
to be protective.
1
Genetic:
a First- degree relative affected in 10% of patients.
b Monozygotic twins have a 10% concordance.
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c Ashkenazi Jews have a five- fold higher risk
than other groups.
Association with human leucocyte antigen
d
(HLA)-
DRB1*0103.
Environmental:
2
a
Incidence is higher in developed countries.
b
Smoking is protective (half the incidence of
smokers).
non-
c
Appendicectomy before the age of 20 appears
protective.
Previous episode of enteric infection (e.g.
d
Salmonella, Campylobacter) doubles the risk
of later ulcerative colitis.
3
Immune response:
a Epithelial barrier impaired.
b Dendritic cell numbers reduced.
c Exaggerated T- cell (Th2) response.
Pathology
The rectum and sigmoid colon are principally
affected, but the whole colon may be involved.
Initially, there is oedema of the mucosa, with contact
bleeding and petechial haemorrhage, proceeding to
ulceration; the ulcers are shallow and irregular.
Oedematous islands of mucosa between the ulcers
may form pseudopolyps. The wall of the colon is
oedematous and fibrotic and, therefore, may become
rigid with loss of its normal haustrations. The changes
are confluent, with no unaffected ‘skip lesions’ as
found in Crohn’s disease. The inflamed colon does
not generally become adherent to its neighbouring
abdominal viscera, as the inflammatory process
intrain ulcerative colitis is not transmural (unlike in
Crohn’s disease).
Microscopically, the principal locus of the disease
is mucosal; small abscesses form within the mucosal
crypts (‘crypt abscesses’). These abscesses break
down into ulcers whose base is lined with granulation
tissue. The walls of the colon are infiltrated with neutrophils; there is oedema and submucosal fibrosis. In
the chronic, burntand atrophic, the bowel wall may be thinned.
out disease, the mucosa is smooth
Clinical features
Manifestations of ulcerative colitis may be fulminant,
intermittent or chronic. The most common scenario is
of diarrhoea, with urgency, frequency, blood and
mucus. There may be accompanying cramp- like
abdominal pains. Examination often reveals nothing
but there may be mild tenderness in the LIF, and blood
on the glove of the examining finger after rectal examination. The rectal mucosa may feel oedematous.
In severe attacks, there is fever, tachycardia, severe
bleeding and risk of perforation. Anorexia and loss of
weight occur in the acute episodes.
Special investigations
Investigations aim to make the diagnosis, differentiate it from Crohn’s colitis, exclude complications and
assess the proximal extent.
Sigmoidoscopy reveals oedema of the mucosa with
•
contact bleeding in the early mild cases, proceeding to granularity of the mucosa and then frank
ulceration with pus and blood in the bowel lumen.
Biopsy will provide histological confirmation of
the diagnosis.
Colonoscopy enables the whole of the large
•
bowel to be inspected, the proximal extent of
disease to be noted and biopsy material to be
obtained. A full colonoscopy should not be performed in the acute phase due to increased risk
of perforation.
•
CT scan demonstrates typically left- sided mural
thickening, which is symmetrical and continuous
(compared with Crohn’s disease which is asymmetrical with segmental involvement, although
pancolitis can occur). Local perforations or
abscesses may be identified, as may extracolonic
manifestations, such as sacroiliitis and evidence
of primary sclerosing cholangitis. The extent of
colonic inflammation can also be assessed acutely
by CT scan.
Barium enema is very uncommonly used now.
•
The classic picture of a smooth, narrow drainpipe
colon due to oedema and fibrosis with loss of
haustration is rarely seen nowadays.
• Examination of the stools reveals pus and blood
visible to the naked eye or under the microscope;
stool culture should be performed to exclude
infections, including Clostridium difficile.
Differential diagnosis
Ulcerative colitis may be difficult to differentiate from
other causes of diarrhoea (see earlier in this chapter),
especially the dysenteries and carcinoma, or Crohn’s
colitis (Table 27.2). Differentiation from colonic
Crohn’s disease may be particularly difficult, even
when the resected colon is examined by an expert
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Table27.2 Crohn’s colitis and ulcerative colitis
Crohn’s colitis Ulcerative colitis
Clinical features Perianal disease common, e.g. anal fissure
Pathology
Macroscopic differences Any part of colon may be involved (skip
Microscopic differences Granulomas present. No granulomas.
* Ten per cent of cases cannot be assigned clearly to one or other disease and are labelled as ‘IBD- Unclassified’.
and anal fistula.
Gross bleeding uncommon. Often profuse haemorrhage.
Small bowel may also be affected. Small bowel not affected (although so-
lesions).
Transmural involvement. Mucosal involvement only.
Fistulates into adjacent viscera. No fistulas.
Pseudopolyps less common. Pseudopolyps of regenerating mucosa.
Thickened bowel wall. No thickening of bowel wall.
Malignant change risk increases with
length of time from diagnosis and extent of
disease- surveillance required.
pathologist. Indeed, about 10% of cases have to be
labelled as ‘inflammatory bowel disease unclassified’
(IBD-
U). Colitis due to cytomegalovirus (CMV)
should also be considered, especially in those who
are immunosuppressed.
*
Perianal disease rare, apart from anal
fissure.
called ‘backwash ileitis’ may be seen).
Disease extends proximally from rectum.
Malignant change risk increases with
length of time from diagnosis and extent of
disease– surveillance required.
Malignant change
Patients with ulcerative colitis who have had chronic
pancolitis (affecting the whole large bowel), particularly
if the first attack was in childhood, have a higher risk of
developing carcinoma of the colon than those without
inflammatory bowel disease. Statistics indicate that
Complications
Local
• Toxic dilation, in which the colon dilates in a ful-
minant colitis, leading to perforation.
• Haemorrhage (acute, or chronic with progressive
anaemia).
• Stricture.
• Malignant change (see later in this chapter).
General
• Weight loss and anaemia.
• Arthritis (including ankylosing spondylitis) and
uveitis.
5–12% of patients with colitis of 20 years’ duration will
develop malignant change. Patients should, therefore,
be offered surveillance colonoscopy in order to detect
and treat the dysplasia that heralds malignant change.
Even in the absence of a pancolitis, patients with
ulcerative colitis and Crohn’s colitis are at greater risk
of developing carcinoma of the large bowel than a
normal individual. Moreover, the tumours occurring
in patients with IBD are more likely to affect a younger
age group, be poorly differentiated and be multiple
compared with those arising in a sporadic nature.
Often, the condition is diagnosed late, as both the
patient and doctor may attribute the symptoms
(bleeding, diarrhoea and pus) to the colitis.
• Dermatological manifestations: pyoderma gangrenosum, erythema nodosum, other skin rashes
and ulceration of the legs.
• Primary sclerosing cholangitis is associated
with ulcerative colitis, as it is with Crohn’s
disease.
Treatment
Initially this is medical in the uncomplicated case, but
surgery is required when medical treatment fails or
when complications arise.
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Medical treatment
Corticosteroids given systemically, by rectal infusion
or in combination, will often produce remission in an
acute attack. Salicylates such as mesalazine are used
to maintain a remission. In more severe cases, antibodies to tumour necrosis factor alpha, such as infliximab or adalimumab, or immunosuppressants
such as azathioprine, ciclosporin or tacrolimus may
be required. Increasing evidence now supports use of
second and third line immunosuppressants/biologics, such as ustekinumab (a monoclonal antibody to
the p40 subunit of interleukins 12 and 23) and vedolizumab (a monoclonal antibody to the α4β7expressed on gutvery important that decisions to escalate medical biologic therapy are made in a joint inflammatory bowel
disease clinic setting that involves the patient, a gastroenterologist and a colorectal surgeon.
homing T- helper lymphocytes). It is
integrin
Surgery
The indications for surgery are the following.
•
Fulminant disease not responding to medical
treatment (defined as the passage of more than six
bloody motions per day, with fever, tachycardia
and hypoalbuminaemia).
• Chronic disease not responding to medical
treatment.
Malignancy or dysplasia that is not endoscopically
•
resectable.
•
Complications of colitis already listed.
The initial procedure comprises removal of the colon
(subtotal colectomy) with preservation of the rectal
stump and formation of an end ileostomy. Subsequently,
further surgery can be considered, once the patient has
recovered from the acute episode. Options include:
a
Removal of the rectum and anus with a permanent
ileostomy.
b Removal of the rectum with restoration of intesti-
nal continuity with an interposed pouch of ileum
(ileoanal pouch, or Parks’ pouch
c Formation of an ileorectal anastomosis in a small
number of eligible patients, although this must be
accompanied with an agreed plan for ongoing rectal
surveillance for the presence of neoplasia and topical treatment to reduce inflammation in the rectum.
3
).
Most patients requiring urgent surgery for ulcerative colitis are either on corticosteroids or have recently
received them. In these patients, surgical procedures
must, therefore, be covered by an increased dosage of
corticosteroids to compensate for presumed suppression of endogenous glucocorticoids, which can then
be tailed off gradually in the postoperative period.
Crohn’s colitis
Crohn’s disease,4 although most commonly found in
the terminal ileum (see Chapter 25), may occur anywhere in the gastrointestinal tract from the mouth to the
anus. It may be confined to the large bowel or there may
be involvement of both the small and large intestine.
Clinical features
Colonic Crohn’s disease closely mimics ulcerative colitis in its clinical manifestations. Unlike ulcerative colitis, the affected segment of colon may become adherent
to adjacent structures with abscess formation and fistulation. Perianal involvement with abscesses, anal
fissure(s) and multiple anal fistulas is also common and
indeed may be the first manifestation of the disease.
Treatment
This is similar to that of Crohn’s disease of the small
intestine (see Chapter25). Resection of involved large
bowel may require segmental colectomy if there is
limited disease involvement or total excision with a
permanent ileostomy for extensive disease. Restorative
proctocolectomy and ileoanal (Parks’) pouch formation is only performed in very few cases of Crohn’s
disease affecting only the large bowel because of the
immediate risks of sepsis and fistulation, and the
chance of recurrence within the small bowel.
Tumours
Classication
Benign
• Adenomatous polyp.
• Papilloma.
3
Sir Alan Parks (1920–1982), Colorectal Surgeon, St Mark’s
Hospital, London, UK.
4
Burrill Bernard Crohn (1884–1983), Gastroenterologist,
Mount Sinai Hospital, NewYork, USA.
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• Lipoma.
Neurofibroma.
•
•
Haemangioma.
Malignant
1 Primary:
a
Carcinoma.
Lymphoma.
b
c
Neuroendocrine tumour (see Chapter25).
2
Secondary: invasion from adjacent tumours, for
example stomach, bladder, uterus and ovary.
Carcinoma
Carcinomas affecting the large bowel are common.
They are the third most common cause of death from
malignant disease in the UK, next in frequency to
cancers of the lung and prostate in men, and lung and
breast in women.
Colonic carcinoma may occur at any age. Women
are affected slightly more often than men (although,
interestingly, the incidence of rectal cancer is roughly
equal in the two sexes). The sigmoid is the most common part of the colon affected, although the rectum
accounts for oneper cent of tumours of the large bowel are multiple
(synchronous).
third of all large bowel cancers. Five
Predisposing factors
Increasing age, pre- existing adenomatous polyps,
ulcerative and Crohn’s colitis and a number of inherited colorectal cancer syndromes are risk factors for
the development of carcinoma of the large bowel.
Inherited syndromes such as familial adenomatous
polyposis (FAP) and hereditary non- polyposis colon
cancer (HNPCC) account for a small proportion of
colorectal cancers, and potential carriers should be
offered screening (see later in this chapter). Family history alone is sufficient to increase the risk, and it has
been estimated that one firstcolon cancer aged over 45 years increases one’s lifetime risk from 1in 50 to 1in 17; if the relative was diagnosed before 45, the lifetime risk increases to 1in 10.
degree relative having
Familial adenomatous polyposis
This is a rare disease, but it is important because it
invariably proceeds to colorectal carcinoma unless
treated and accounts for 0.5% of all colon cancers. It
has an autosomal dominant inheritance, and is associated with mutation in the FAP gene; 25% of cases are
spontaneous mutations. The polyps first appear in
adolescence; symptoms of bleeding and diarrhoea
commence about the age of 21 years and malignant
change occurs between 20 and 40 years of age.
Affected individuals usually have congenital hypertrophy of the retinal pigment epithelium (CHRPE)
which is a useful, nonVariants such as Gardner’s syndrome
colonic polyps are associated with desmoid tumours
and osteomas of the mandible and skull.
Treatment generally comprises a total colectomy
with excision of the rectum, ideally before the age of 25.
Options are to have a permanent ileostomy, or to consider restoration of intestinal continuity with an ileoanal
(Parks’) pouch. If the polyps are not profuse in the
rectum, it is possible to resect the colon while leaving
behind the rectum to which an ileorectal anastomosis
is performed, and then carry out regular surveillance
of the rectal stump via flexible sigmoidoscopy.
invasive screening test.
5
exist in which
Hereditary non- polyposis colon
cancer (HNPCC)
HNPCC accounts for less than 5% of colorectal cancers, and is also dominantly inherited. It results from
mutations in a family of genes affecting DNA mismatch repair, which leads to genomic instability; 60%
of cases are due to a mutation in the MSH2 gene and
30% in the MLH1 gene. Other implicated genes are
MSH6, PMS2, PMS1 and MLH3. Tumours tend to
occur in the right colon, and arise before the age of 50.
Occurrence of colon cancer in at least three family
members spanning two generations, with one before
the age of 45, strongly suggests this syndrome. It is
also associated with tumours of the ovary, uterus, kidney, ureter, small bowel, stomach and skin.
Pathology
Macroscopically, the tumours can be classified into
the following groups:
•
Ulcerating.
•
Papillomatous.
Annular.
•
•
Stricturing.
Microscopically, these are all adenocarcinomas.
5
Eldon John Gardner (1909–1989), Geneticist, later
Professor of Zoology, Utah State University, Logan, Utah.
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Spread
• Local: encircling the wall of the bowel and invading the layers of the colon, eventually involving
adjacent viscera (small intestine, stomach, duodenum, ureter, bladder, uterus, abdominal wall,
etc.).
• Lymphatic: to the regional lymph nodes, eventually spreading via the thoracic duct, and may
involve supraclavicular nodes in late cases.
•
Bloodstream: to the liver via the portal vein, and
also to the lungs.
Nerves: perineural invasion is the process of neo-
•
plastic invasion of nerves.
Transcoelomic: producing deposits of malignant
•
nodules throughout the peritoneal cavity.
Staging
Historically, colorectal cancer was staged according
to the classification of Dukes,
the extent of transmural extension and lymph node
spread (see Chapter28), although the TNM staging
system (see Chapter7) is more commonly used nowadays. This leads to stages of disease from one to four
according to how far the tumour has spread through
the bowel wall (stages 1 and 2), to the draining lymph
nodes (stage 3) or if there is metastatic (distant)
spread (stage 4).
6
and depended upon
2 Intestinal obstruction due to a stricturing tumour,
more commonly found in the left (sigmoid or
descending) colon (see Chapter30).
3
Perforation of the tumour, either into the general
peritoneal cavity or locally with the formation of a
pericolic abscess, or occasionally by fistulation
into adjacent viscera, for example a gastrocolic fistula or colovesical fistula.
The effects ofsecondary deposits
(metastases)
The patient may present with jaundice, hepatomegaly
or abdominal distension due to ascites.
The general effects ofmalignant
disease
Presenting features may be anaemia, anorexia or loss
of weight.
Tumours of the left side of the colon, where the
contained stool is solid, are typically stricturing
tumours, so obstructive features predominate. In
contrast, tumours of the right side tend to be proliferative and here the stools are semifore, obstructive symptoms are relatively uncommon
and the patient with a carcinoma of the caecum or
ascending colon often presents with anaemia and
loss of weight.
liquid, and, there-
Clinical features
The manifestations of carcinoma of the colon can be
divided, as with any tumour, into those produced by
the tumour itself, those arising from the presence of
secondaries (metastases), and the general effects of
the tumour.
Local effects
1 Change in bowel habit is the most common symp-
tom, usually with an increased frequency of looser
stool (diarrhoea), or less frequently constipation.
The diarrhoea may be accompanied by mucus
(produced by the excessive secretion of mucus
from the tumour) or bleeding, which may be
bright, dark or occult, depending on the proximity
of the tumour to the anus.
6
Cuthbert Esquire Dukes (1890–1977), Pathologist, St Mark’s
Hospital, London, UK.
Examination
This should seek evidence of the following.
1 The presence of a mass palpable either per abdo-
men or per rectum.
Clinical evidence of intestinal obstruction.
2
3 Evidence of spread (hepatomegaly, ascites, jaun-
dice or supraclavicular lymphadenopathy).
4 Clinical evidence of anaemia or loss of weight sug-
gesting malignant disease.
Special investigations
• Occult blood in the stool is frequently present and
should be tested for. This is now typically via a faecal immunochemical test (FIT).
• Rigid or flexible sigmoidoscopy in the outpatient
setting will reveal tumours in the rectosigmoid
region and allow positive evidence by biopsy to be
obtained. Even if the tumour is not reached
directly, the presence of blood or mucus coming
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down from above is strongly suspicious of malignant disease, and warrants further investigation.
Colonoscopy, enables the entire colon to be
•
inspected and a biopsy to be obtained. This is the
gold standard investigation.
•
CT colonography (‘virtual colonoscopy’) has
replaced barium enema as the investigation of
choice if colonoscopy is not available or appropriate. It will usually reveal the tumour and associated stricture or filling defect (‘appledeformity), and can also detect associated liver
metastases. It is important to remember that a
negative CT scan does not definitely exclude the
presence of a small tumour, particularly in the
presence of extensive diverticulosis.
•
Staging CT scan of the chest, abdomen and pelvis
should be performed once the diagnosis has been
confirmed, in order to assess the local extent of
disease and whether there is any sign of metastatic
disease.
core’
Differential diagnosis
Diseases producing local symptoms
• Diverticular disease.
• Inflammatory bowel disease.
•
Infective colitis and other causes of diarrhoea and
constipation (see earlier in this chapter).
Treatment
Surgery
The principle of operative treatment is wide resection
of the tumour together with its regional lymphatics
and blood supply. In elective surgery, resection with
restoration of intestinal continuity with a primary
anastomosis can generally be achieved, with the risks
of infection reduced with preoperative bowel preparation and oral antibiotics taken the day before. In
cases of malignant large bowel obstruction, in which
bowel preparation is contraindicated, the primary
goal is to relieve obstruction. It may be possible to
achieve primary resection with restoration of continuity at the same time, with or without a defunctioning stoma. The surgical alternatives are resection with
a proximal end stoma (Hartmann’s procedure, if the
sigmoid colon is resected), or an initial defunctioning
proximal stoma alone. If there is available expertise,
an endoscopically placed colonic stent can be considered initially in order to relieve the obstruction, with a
view to a planned, elective surgical resection several
weeks later.
Adjuvant therapy
Adjuvant chemotherapy with 5- fluorouracil (5- FU),
in combination with folinic acid and oxaliplatin
(FOLFOX) or with capecitabine and oxaliplatin
(CAPOX), may reduce the risk of recurrent disease;
for metastatic disease, oral therapy with capecitabine
is the preferred choice. Biological therapy with monoclonal antibody therapy such as cetuximab and
panitumumab (both against the epidermal growth
factor receptor) or pembrolizumab (binds to the programmed cell death receptor 1, potentiating Tanti- tumour responses) may be considered as second
line therapy for metastatic disease.
cell
Follow- up
• Cross- sectional CT imaging is performed to detect
local recurrence and the appearance of liver, lung
and other metastases; metastatic spread to the
liver in the absence of other disease may be treated
by resection of the affected liver segment(s).
• Surveillance colonoscopy is undertaken at intervals to detect new tumours and local recurrence;
having had one colorectal cancer is a risk factor for
further ones.
• Carcinoembryonic antigen (CEA) blood test at
intervals can highlight possible recurrence if the
levels start to rise again after treatment.
The patient withincurable disease
Even if secondary spread is present and incurable,
appropriate palliation is key. This may still be
achieved by resection of the primary tumour, even if
the primary is asymptomatic. If this is not possible or
appropriate, the tumour may be stented to relieve
obstruction. Where stenting is not possible, a palliative bypass or stoma may be considered. Systemic
cancer therapy, in particular chemotherapy, may
antihelp to alleviate symptoms. It is important to involve
the palliative care team early in this process in order
to provide a holistic and patientdecision- making and symptom relief.
centred approach to
Prognosis
Stage 1 tumours (through the inner bowel lining of
the bowel or into the muscle wall) are usually curable,
with 91% 5- year survival. Five- year survival with stage
2 tumours (spread through to the outer muscle wall of
the bowel), in which the disease is still confined to the
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bowel wall, is around 84%, and the presence of lymph
node metastases in stage 3 disease gives a 65% 5survival. Metastatic disease (stage 4) has an overall
10% 5-
year survival.
year
Colonic surgery (see Figure27.2)
The different colonic resections are based on the blood
supply to the colon coming from the superior mesenteric artery (midgut components, i.e. caecum, ascending colon and twothe inferior mesenteric artery (hindgut components,
i.e. distal transverse colon, descending colon, sigmoid
and rectum) together with a free vascular anastomosis
between the principal arteries via the marginal artery
(of Drummond
in the case of lymph node positive disease, at least in
part dependent upon the adequacy of resection (adequately clearing the affected draining lymph nodes),
surgery for cancer involves en bloc resection of the adja-
cent mesentery where lymphatic drainage occurs. This
allows the best possible histopathological staging of the
tumour, with adjuvant chemotherapy considered when
tumour cells are present in the removed, draining
lymph nodes or blood vessels. In practice, this means
resecting as far down the principal artery as is possible
and safe, since the lymphatic drainage runs alongside
the arterial inflow. In non- cancer operations, more
conservative surgical techniques may be employed.
thirds of the transverse colon) and
7
). Since survival from colonic cancer is,
Colostomy
When the bowel is brought to the surface and opened,
it is termed a ‘stoma’ (from the Greek meaning
mouth); in the case of the colon, such an opening is
termed a ‘colostomy’. Stomas may be permanent, for
example when the distal bowel has been removed, or
temporary, when there is a possibility of restoring
continuity with more surgery at a future date.
7
Sir David Drummond (1852–1932), Professor of Medicine,
University of Durham, Durham, UK. He demonstrated the
artery by tying o the right, middle, left colic and sigmoid
arteries in cadavers and injecting contrast into the ileocolic
artery and showing it owed around to the rectum.
Indications forcolostomy
formation
The common indications for colostomy formation are:
•
To divert faeces to allow healing of a more distal
anastomosis or fistula.
To decompress a dilated colon, as a prelude to
•
resection of the obstructing lesion.
Following removal of the distal colon and rectum
•
in a patient who is either not fit enough to tolerate
the effects of an anastomotic leak or whose anorectal function would lead to poor control/incontinence if bowel restoration is performed.
•
Intractable faecal incontinence.
The ability of the patient to manage the colostomy
needs to be borne in mind; in a patient with poor dexterity, such as following a stroke or secondary to severe
Parkinson’s disease, or with poor eyesight, creation of a
stoma may be undesirable, even on a temporary basis.
Types ofcolostomy
Loop colostomy
The colon is brought to the surface and the antimesenteric border opened. A temporary rod or similar device
may be used to stop the opened bowel loop from falling
back inside, particularly if there is a thick abdominal
wall. A loop colostomy is used temporarily to divert faeces and is more simple to reverse; more commonly, a
loop ileostomy is preferred because of the better blood
supply to the bowel facilitating subsequent closure.
End colostomy
An end colostomy is fashioned by dividing the colon
and bringing the proximal end to the surface. It may
be used as a definitive procedure in a patient undergoing total anorectal excision, or following perforated
diverticular disease in which the diseased bowel is
removed and gross faecal contamination makes performing a primary anastomosis to restore continuity
undesirable. In the latter, the distal bowel may be
closed off and left within the abdomen (a Hartmann’s
procedure if the sigmoid colon is removed and rectum closed off) or brought to the surface at a separate
place as a mucus fistula.
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Double- barrelled colostomy
A double- barrelled (Paul–Mikulicz8) colostomy comprises proximal and distal ends of colon brought out
adjacent to each other, like a loop colostomy but with
the intervening colon removed. This type of colostomy
is not commonly used because the distal bowel is usually too short, but it is useful in the treatment of sigmoid
volvulus, in which there is usually sufficient distal colon
to allow a tension-
free double- barrelled colostomy.
Complications ofcolostomy
formation
• Retraction, in which the colon disappears down
the hole out of which it was brought.
•
Stenosis, in which the opening becomes smaller.
This may be due to ischaemia or poor apposition
of colonic mucosa with the skin edge.
•
Parastomal hernia, in which peritoneal contents
herniate through the abdominal wall defect made
to accommodate the stoma.
Prolapse, in which the colon prolapses out of the
•
stoma.
In addition, there may be psychological issues to
address, excess gas production with certain foods,
and leakage with skin excoriation due to ill- fitting
stoma appliances or poorly constructed stomas.
Stoma appliances: principles
Modern- day stoma appliances have made the management of stomas much more straightforward. The
principal components are the collecting pouch, or
bag, into which the faeces collect, and the adhesive
flange, which adheres to the skin and keeps the pouch
in position. The flange is cut to fit the stoma closely,
and any exposed skin is covered with a barrier paste if
needed. Colostomies contrast with ileostomies by the
nature of the effluent. Ileostomy effluent is more liquid and irritant and may cause severe skin excoria-
8
Frank omas Paul (1851–1941), Surgeon, Liverpool
Royal Inrmary, Liverpool. Johann von Mikulicz- Radecki
(1850–1905), Professor of Surgery, successively at Cracow,
Konigsberg and Breslau, Poland.
tion. For this reason, an ileostomy is constructed with
a prominent spout to keep the effluent off the skin, in
contrast to a colostomy, which is constructed flush
with the skin or preferably with a slight spout.
Siting astoma
The optimal position of a stoma should be ascertained
operatively wherever possible. Typically, a
precolostomy is sited on the left, and an ileostomy on the
right. The patient needs to be able to wear the appliance
comfortably, so it should not be placed in an abdominal
crease such that the appliance will not achieve a seal, or
where a belt or waist band of a trouser or skirt usually
sit. The stoma should be fully visible to the patient in its
final position to enable them to empty it as required.
Management ofa colostomy
In the first few weeks after performing a colostomy,
the faecal discharge is often semi- liquid, but this
gradually reverts to normal, solid stools. The colostomy appliances, which are waterproof, allow the
patient to lead a normal life with little risk of leakage
or unpleasant odour.
Although there is obviously no sphincteric control of the colostomy opening, many patients find
that they pass a single stool a day. This can be
helped by preparations such as Fybogel, which produce a bulky, formed stool. Patients may choose to
reduce the amounts of vegetables or fruit eaten,
which may produce diarrhoea and excessive flatus.
Some patients undertake stoma irrigation in order
to have more control over when the stoma produces
its effluent.
Additional resources
Case 67: A symptomless nding on a barium enema
examination
Case 68: Ulcerative colitis
Case 69: A complication of long- standing ulcerative
colitis
Case 70: An elderly woman with an abdominal mass
Case 71: A patient with bowel obstruction
2828
https://t.me/medicina_free
The rectum andanal canal
Justin Davies
Learning objectives
✓ To know the causes and treatment of rectal bleeding.
✓ To know the presentation and management of benign and malignant
anorectal conditions.
The distribution around the anal canal of various
common conditions is shown in Figure28.1.
Bright red rectal bleeding
( Table28.1)
The passage of bright red blood per anum is a common symptom, which the patient usually attributes to
haemorrhoids, commonly known as ‘piles’; indeed,
haemorrhoids are by far the most common cause of
rectal bleeding. It is important, however, to bear in
mind a list of other possible causes of this symptom.
General causes
Bleeding diatheses (rare).
Local causes
• Haemorrhoids.
• Anal fissure.
• Tumours of the colon and rectum:
– Benign.
– Malignant.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
• Diverticular disease.
• Ulcerative colitis.
• Infective colitis.
• Ischaemic colitis.
•
Trauma.
• Angiodysplasia of the colon.
• Rarely, massive haemorrhage from higher up the
alimentary canal – even a bleeding duodenal
ulcer, may produce bright red blood per anum
instead of the usual melaena, although such cases
are commonly accompanied by haematemesis.
Haemorrhoids
Functional anatomy
Continence is mainly a function of the anal sphincters
but also partly a consequence of the anal cushions.
The anal cushions comprise highly vascular tissue
lining the anal canal, with a rich blood supply from
the rectal arteries, which anastomose with the draining veins both through capillaries and through direct
arteriovenous shunts. The draining veins form saccules, commonly just below the dentate line, which
then drain via the superior rectal vein. The venous
saccules are supported by smooth muscle to form the
cushions. Apposition of these subepithelial vascular
cushions makes some contribution to continence of
flatus and liquid.
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