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7
Anterior
The rectum andanal canal 275
Anterior stulas
open directly
A
3
A
Posterior
(a) (b)
Arrangement of
haemorrhoids
Figure28.1 Distribution of different conditions around the anal canal.
Anal ssure (c) Goodsall's rule for
Perianal haematoma
(d)
P
Posterior tear
90% men
70% women
A
P
Table28.1 Rectal bleeding
Blood Pain
Haemorrhoids Bright red blood on paper and in the
toilet bowl. May prolapse.
Fissure Bright red blood on paper and outside
of stool.
Colon and rectal cancer Blood often mixed in with stool, especially
if proximal tumour.
Diverticular disease Large volume of blood in the pan. Painless.
Ulcerative colitis Blood and mucus mixed with loose,
frequent stool.
Painless, unless prolapsed and/or thrombosed.
Painful; pain during and lasting long after
passing stool.
Usually painless, unless distally placed
in rectum or in anal canal, when causes
tenesmus.
Painless, unless co- existent fissure.
P
Posterior stulas
open in midline
stula in ano
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Classication
Haemorrhoids (or piles; the words are synonymous)
may be classified according to their relationship to the
anal orifice into internal, external and interoexternal.
Internal haemorrhoids are congested vascular cushions with dilated venous components draining into
the superior rectal veins. External haemorrhoids is a
term that covers multiple different pathologies including perianal haematoma (‘thrombosed external pile’),
the ‘sentinel pile’ of anal fissure and anal skin tags.
Strictly speaking, internal piles that prolapse should
be termed ‘interoexternal haemorrhoids’, but this term
is seldom used in clinical practice. In this chapter, the
terms ‘external’ and ‘interoexternal’ haemorrhoids
will not be used further.
Pathology
Internal haemorrhoids are abnormal anal cushions,
usually congested as a result of straining at stool and/
or pregnancy, and traumatized by the passage of hard
stool. The anal cushions are particularly prominent in
pregnancy owing to the venous congestion caused by
the large gravid uterus and the laxity of the supporting
tissues caused by the influence of progesterone. With
the patient in the lithotomy position, the usual
arrangement is that three major haemorrhoids occur
at 3, 7 and 11 o’clock.
Occasionally, anorectal varices, similar in
appearance to oesophageal varices, co- exist with
haemorrhoids in patients with portal hypertension
since the anorectal area is the site of a portosystemic
anastomosis between the superior and inferior rectal
veins (see Chapter34).
Clinical features
Rectal bleeding is almost invariable; this is bright red
and usually occurs at defaecation. In the case of firstdegree haemorrhoids, this is the only symptom. Some
haemorrhoids prolapse and may produce a mucus
discharge and itching (pruritus ani). The prolapsed
haemorrhoids may result in soiling.
Note that pain is not a feature of internal haemorrhoids except when these undergo thrombosis (see
later in this chapter). When a patient complains of ‘an
attack of piles’, it often means that some acute painful
condition has developed at the anal margin. The most
common and dramatic is strangulation of prolapsing
haemorrhoids leading to thrombosis; apart from this,
acute pain may be due to the following:
• Anal fissure.
• Perianal haematoma.
• Perianal or ischioanal abscess.
•
Tumour of the anal margin.
• Proctalgia fugax: benign episodic, short- lived pain
felt up inside the rectum.
Grading haemorrhoids
• First- degree haemorrhoids are confined to the anal
canal– they bleed but do not prolapse.
•
Second- degree haemorrhoids prolapse on defaeca-
tion, then reduce spontaneously.
• Third- degree haemorrhoids prolapse outside the
anal margin on defaecation; they need to be manually pushed back inside by the patient.
• Fourth- degree haemorrhoids remain prolapsed
outside the anal margin at all times.
Predisposing factors
Most haemorrhoids are idiopathic, but they may
beprecipitated or aggravated by factors that produce
congestion of the superior rectal veins. These
include compression by any pelvic tumour (of which
the most common is the pregnant uterus), lots of
regular heavy lifting, chronic constipation and
straining to pass a stool.
Every patient presenting with a history suggestive of
internal haemorrhoids should be considered for the
following examinations:
1
Examination of the abdomen to exclude palpable
lesions of the colon or aggravating factors for
haemorrhoids, for example an enlarged liver or a
pelvic mass, including the pregnant uterus.
2 Rectal examination. Internal haemorrhoids are
not palpable but prolapsing haemorrhoids may be
immediately obvious on inspection. The presence
of prolapsing haemorrhoids does not exclude a
lesion higher in the bowel. Rectal examination
allows anal abscess, fissure and tumour to be
excluded.
3 Proctoscopy, which will visualize the internal
haemorrhoids.
4 Sigmoidoscopy (rigid or flexible) is performed to
eliminate a lesion higher in the rectum– proctitis,
polyp or carcinoma. Contrary to its name, the rigid
sigmoidoscope does not afford a view of the
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sigmoid colon, hence rigid sigmoidoscopy is more
correctly termed ‘rectoscopy’.
Colonoscopy is carried out when symptoms such
5
as a change in bowel habit or blood mixed in with
the faeces point to a more serious condition than
internal haemorrhoids. Computed tomography
(CT) colonography is carried out when colonoscopy is not readily available or appropriate.
Complications
• Iron deficiency anaemia: following severe or
continued bleeding. This is uncommon, and a
more serious cause of anaemia (colorectal or
oesophagogastric cancer) should be considered in
most cases.
• Thrombosis: this occurs when prolapsing haemorrhoids are gripped by the anal sphincter
(‘strangulated piles’). The venous return is
occluded and thrombosis of the haemorrhoid
occurs. The prolapsed haemorrhoids are swollen
often to the size of large plums, purplish- black
and tense, and are accompanied by considerable
pain and distress. Suppuration or ulceration may
occur. After 2–3 weeks, the thrombosed tissue
become fibrosed, often with spontaneous cure.
Haemorrhoidectomy can be considered acutely,
especially if there is any concern for necrosis, but
often surgery can be avoided in the acute phase
and subsequent treatment options, including
none, considered with the patient.
Treatment
Before commencing treatment, it is essential to
exclude either any predisposing cause or an associated and more important lesion, such as carcinoma of
the rectum.
Conservative management
Ideally, the patient should avoid straining at stool,
and spending too long sat on the toilet. A bulk laxative, together with advice on an adequate fluid and
fibre intake, are often required.
Sclerotherapy
This is suitable for some first- degree haemorrhoids;
2–3mL of 5% phenol in almond oil is injected above
each haemorrhoid as a sclerosing submucosal
perivenous injection. (The phenol sterilizes the oil,
which is the main sclerosant.) Because the injection is
placed high in the anal canal/distal rectum above the
dentate line, it is painless. One or more repeat injections may be required at intervals. This is now most
commonly used in patients taking medication that
predisposes to bleeding (e.g. warfarin, novel oral anticoagulants (NOACs)), as other interventions are likely
to be contraindicated in this setting.
Suction banding
Application of a small rubber band to areas of
protruding mucosa results in strangulation of the
mucosa, which falls away after a few days. It can be
successfully applied to firsthaemorrhoids, but care must be taken to position the
bands above the dentate line in order to avoid significant pain.
, second- and third- degree
Surgery
Surgery is generally considered for recurrent thirddegree and for fourth- degree haemorrhoids. There
are several options that can be considered:
Haemorrhoidectomy involves excising the haem-
1
orrhoids after first ligating the vascular pedicle.
This has the lowest recurrence rate of all operative
interventions, but is very painful for a week or two
afterwards.
Haemorrhoidal artery ligation (HALO) involves
2
using a Doppler probe to identify the haemorrhoidal arteries which are then ligated above the
dentate line. This may be combined with plication
of the prolapsing mucosa if causing symptoms.
Stapled haemorrhoidopexy uses a circular stapling
3
device to excise a band of mucous membrane
above the dentate line. It also interrupts the blood
supply to the haemorrhoids. This is less commonly considered now due to the very small risk
of serious septic complications.
Thrombosed strangulated
haemorrhoids
Conservative management is generally instituted for
these. The patient may require several days of rest at
home. Analgesia, often in combination with stool softeners, is given for the pain, which is also eased by local
cold compresses. Often the thrombosed haemorrhoids
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fibrose completely with spontaneous cure. Acute
haemorrhoidectomy can generally be avoided, unless
there is a suggestion of tissue necrosis.
Specic complications
ofhaemorrhoid surgery
Acute retention ofurine
This is the result of acute anal discomfort
postoperatively.
Postoperative haemorrhage
This may be reactionary, usually on the night of the
operation, or secondary, on about the seventh or
eighth day. The bleeding may not be apparent externally, as the source of haemorrhage may be above the
anal sphincter, with the blood filling the large bowel
with only a little escaping to the exterior.
General treatment comprises blood transfusion if
haemorrhage is severe as evidenced by the general
appearance of the patient and the presence of tachycardia and hypotension.
Local treatment is carried out under general anaesthetic in the operating theatre. The blood is washed out
of the rectum with warm saline. Occasionally, in reactionary haemorrhage, a bleeding point is seen and can
be suture- ligated. More often, there is a general oozing
from the operation field and the anal canal requires
packing with gauze and removal 24 hours later.
Anal stenosis
This only occurs when excessive amounts of mucosa
and skin are excised at the time of a haemorrhoidectomy. It is important to leave a bridge of epithelium
between each excised haemorrhoid.
Anal Incontinence
This is an uncommon complication of haemorrhoidectomy, and is generally incontinence of gas. Patient
selection is paramount, with a history of previous
anal surgery, significant obstetric history and preexisting continence being carefully considered as part
of the consent and shared decision- making process
with the patient.
within the subcutaneous tissue of the perianal skin.
Unlike internal haemorrhoids, it is covered by squamous epithelium supplied by somatic nerves and is,
therefore, initially very painful when it occurs. The onset
is acute, often after straining at stool or after heavy lifting,
with sudden pain and the appearance of a lump at the
anal verge. Local examination shows a tense, smooth,
blue, cherry- sized lump at the anal margin.
dark-
Untreated, this perianal haematoma either subsides
over a few days, eventually leaving a fibrous anal skin
tag, or ruptures, discharging some clotted blood.
Treatment
In the acute phase, immediate relief is produced by
evacuating the haematoma through a small incision,
conveniently performed under local anaesthetic. This
is generally most effective when performed within
24 hours of symptom onset. If the patient is seen
when the haematoma is already discharging or
becoming absorbed, hot baths may help symptoms
and reassurance given that the symptoms will resolve
over several weeks.
Anal fissure
An anal fissure is a tear in the anal canal, which most
commonly follows the passage of a hard stool, but
sometimes follows a prolonged bout of diarrhoea.
The site is usually posterior in the midline (90% of
men, 70% of women), occasionally anteriorly in the
midline and rarely multiple. The posterior position of
the majority of fissures has traditionally been
explained by the anatomical arrangement of the
external anal sphincter; its superficial fibres pass forward to the anal canal from the coccyx, leaving a relatively unsupported V posteriorly. However, mucosal
tears are probably quite common and while most heal
spontaneously, those occurring posteriorly (or anteriorly) are slow to heal because of the relatively poor
blood supply to the anal mucosa in the midline.
Anterior fissures in women may be associated with
weakening of the pelvic floor following tears at
childbirth. Multiple fissures may be a presenting
feature of perianal Crohn’s disease
1
.
Perianal haematoma
This lesion, which is also sometimes incorrectly termed
a ‘thrombosed external pile’, is produced by thrombosis
1
Burrill Bernard Crohn (1884–1983), Gastroenterologist,
Mount Sinai Hospital, NewYork, USA. e disease was rst
described by Morgagni (1682–1771).
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Clinical features
Acute anal pain is characteristic. It is stinging in
nature and lasts for a while after the passage of stool,
sometimes several hours. Fissure is the most common cause of pain at the anal verge (see earlier in this
chapter). There is often slight bleeding and, because
of the pain, the patient is usually constipated. On
examination, the anal sphincter is in spasm, and
there may be a ‘sentinel pile’ protruding from the
anus, which represents the torn tag of anal epithelium. The fissure can usually be seen by gently pulling
open the anal verge. It may be impossible to do a rectal examination without anaesthetic; the fissure may
then be evident as a tear in the anal canal.
Treatment
Early small acute anal fissures may heal spontaneously. A local anaesthetic ointment together with a
stool softener may give relief. Application of 0.4%
glyceryl trinitrate (GTN) or 2% diltiazem ointment
relaxes the anal sphincter, allowing the torn epithelium to heal; these are indicated for chronic fissures,
i.e. it has been present for at least six weeks.
Injection of botulinum A toxin into the anal sphincter to create a chemical sphincterotomy appears to be
at least as effective as GTN or diltiazem ointment in
facilitating fissure healing, works faster but with a
small incidence of transient incontinence to gas
afterwards. The effects are more sustained than
topical creams, and last around 12weeks.
Intractable cases usually respond to dividing the
internal sphincter submucosally (lateral internal anal
sphincterotomy) under general anaesthetic. It is
important to take a detailed history of continence and
to assess the anal tone prior to performing a sphincterotomy, as incontinence may result, particularly in
patients who have suffered previous obstetric injury.
Anal stretch, once a common treatment of fissures,
has been abandoned because of the damage it caused
to the sphincter with associated incontinence, and
should no longer be performed.
A chronic recurring anal fissure may require excision and histological analysis to rule out malignancy.
Anorectal abscesses
Classication (Figure28.2)
• Perianal: likely resulting from infection of a hair
follicle, a sebaceous gland or perianal haematoma.
These may be submucosal or subcutaneous.
Intersphincteric: arising from between the internal
•
and external anal sphincter muscles.
•
Ischioanal: from infection of an anal gland leading
from the anal canal into the submucosa and intersphincteric space, and then traversing the external
Longitudinal
muscle
Levator ani
External
sphincter
Internal
sphincter
Figure28.2 The anatomy of anorectal abscesses.
Supralevator
abscess
Ischioanal
abscess
Intersphincteric
abscess
Perianal
(subcutaneous)
abscess
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anal sphincter to spread to the ischioanal fossa.
The abscess may occasionally form a track like a
horseshoe behind the rectum to the opposite
ischioanal fossa.
Supralevator: most commonly due to downward
•
extension from a pelvic source (e.g. diverticular
abscess) although this is a rare finding.
Treatment
Early surgical drainage.
Anal fistula
Denitions
• A fistula is an abnormal communication between
two epithelial surfaces, for example between a
hollow viscus and the surface of the body or
between two hollow viscera.
• A sinus is a granulating track leading from a source
of infection to an epithelial surface.
Aetiology
The term ‘anal fistula’ or ‘fistula in ano’ is applied to
fistulas in relation to the anal canal. The majority
result from an initial abscess likely forming in one of
the anal glands that pass from the intersphincteric
space of the anal canal to open within its lumen. Anal
fistulas are most commonly idiopathic, but they may
also be associated with Crohn’s disease and carcinoma of the anorectum (rarely, also, tuberculosis).
Anatomical classication
(Figure28.3)
Anal fistulas are classified according to their position
and relation to the internal and external anal
sphincters.
Submucosal/subcutaneous.
•
Intersphincteric.
•
• Transsphincteric.
•
Suprasphincteric.
• Extrasphincteric.
Subcutaneous or submucosal fistulas are superficial
tracks resulting from rupture, respectively, of subcutaneous and submucosal abscesses. They sometimes
form from a partially healed anal fissure. Intersphincteric
fistulas are examples of low anal fistulas, in which the
track is below the dentate line; they constitute the
majority of anal fistulas. Transsphincteric fistulas differ
in their penetration through the external sphincter, and
most are at a low level with the track passing through
the subcutaneous part of the sphincter, although some
may be classified as high if they traverse the majority of
Extrasphincteric
Transsphincteric
Intersphincteric
Submucosal/subcutaneous
Figure28.3 The anatomy of anal stulas.
Dentate line
Levator ani
Rectal venous
plexus
External anal
sphincter
Internal anal
sphincter
Suprasphincteric
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the external anal sphincter. Suprasphincteric fistulas
pass via the intersphincteric space to open into the
anus above the puborectalis and are high anal fistulas.
Extrasphincteric fistulas, fortunately rare, extend
through the levator ani to open above the anorectal
junction, are a very challenging form of high anal
fistula.
Fistulas with external openings posterior to the
meridian in the lithotomy position usually open in
the midline of the anus, whereas those with anterior
external openings usually open directly into the
anus– Goodsall’s law
rule is not absolute.
2
(see Figure28.1); however, this
Clinical features
There is usually a story of an initial perianal abscess,
which discharges or requires surgical drainage.
Following this, there are recurrent episodes of perianal infection with persistent discharge of pus.
Examination reveals the external opening of a fistula.
The internal opening may be felt per rectum, but
probing of the track is painful and should generally be
deferred until the patient is under anaesthesia.
Accurate assessment of the extent of the fistula track,
in particular its relation to the anal sphincter, is crucial. Where doubt exists, and certainly when the fistula is recurrent, magnetic resonance imaging (MRI)
can demonstrate the anatomy of a fistula very clearly,
with endoanal ultrasound also useful.
High fistulas (suprasphincteric and transsphinc-
teric): sphincter-
considered. These include injection with fibrin
glue, placement of a bioprosthetic ‘fistula plug’ that
is passed along the track or use of an ‘over the
scope’ clip to close the internal opening. If these
sphincterloose draining seton may be required, comprising a
absorbable strong suture (e.g. Ethibond),
nonpassed through the track and left in place. The
seton may need to be replaced every 5 years or so.
Advancement flaps may be considered, but do have
potential implications for continence, and an alternative approach is ligation of the intersphincteric
tract (LIFT). Newer sphincterments include use of laser technology and also
assisted fistula surgery, but longer- term out-
videocome data are awaited.
Recurrent fistulas that are associated with Crohn’s
disease may respond to longadditional medical treatment with an anti- tumour
necrosis factor antibody such as infliximab, in addition to immunosuppressive therapy with azathioprine, in combination with drainage of any abscess
and loose draining seton(s) placement. The role of
stem cells in the treatment of Crohn’s diseaserelated anal fistulas is the subject of ongoing
research.
conserving procedures may be
preserving treatments fail, a long- term
preserving treat-
term antibiotics and
Treatment
Superficial and low anal fistulas may be laid open and
allowed to heal by secondary intention. When no
sphincter needs to be divided, there is no loss of anal
continence. If a few fibres of internal sphincter might
need to be divided, then careful assessment of preoperative continence, prior anal surgery and an accurate obstetric history are required, along with a fully
informed consent process as there will be a small risk
of permanent flatus incontinence and staining of
underwear. Careful clinical assessment, often augmented with information from the MRI scan, is,
therefore, important in this shared decisionprocess, and the final decision lies with the patient.
2
David Goodsall (1843–1906), Surgeon, St Mark’s Hospital,
London, UK.
making
Stricture ofthe anal canal
Classication
• Congenital.
•
Iatrogenic, particularly postoperative, after too
radical excision of the skin and mucosa in
haemorrhoidectomy.
• Inflammatory: lymphogranuloma inguinale
(mostly female), Crohn’s disease.
• Post- radiotherapy.
• Malignant tumour.
Treatment
Depends on the underlying pathology and may call
for repeated dilation, plastic surgery reconstruction,
defunctioning colostomy or, in the case of malignant
disease, excision of the anorectum.
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Prolapse ofthe rectum
This may be partial or complete.
•
Partial (mucosal) prolapse is confined to the
mucosa, which prolapses 2–5 cm from the anal
verge. Palpation of the prolapse between the finger and thumb reveals that there is no muscular
wall within it. It may occur in infants who are usually otherwise perfectly healthy. Treatment of
these infants requires nothing more than reassurance of the parents that the condition is selflimiting. In adults, it usually accompanies
prolapsing haemorrhoids or sphincter incompetence, and may present with pruritus ani and
mucus discharge.
Full- thickness prolapse involves all layers of the rec-
•
tal wall. It most commonly occurs in elderly, multiparous women. Apart from the discomfort of the
prolapse, there is associated incontinence owing to
the stretching of the sphincter muscles and mucus
discharge from the prolapsed mucosal surface.
Treatment
Treatment of mucosal prolapse in adults comprises
excision of the redundant mucosa, or suction banding (see earlier in this chapter). In children, as already
mentioned, selffortunate rule.
Repair of a fullperformed by either a transabdominal or transperineal approach, the former being preferred in
younger and fitter patients, the latter in more elderly
and co- morbid patients.
Transabdominal rectopexy, whereby the mobilized
rectum is secured to the presacral fascia, relies on the
resultant brisk fibrous reaction to fix the rectum to the
pelvic tissues. Mesh is less commonly used now to
facilitate this apposition due to potential meshrelated complications such as erosion. The classic
perineal approach was anal encirclement with a
Thiersch wire,
passed around the anal orifice to narrow it and keep
the prolapse reduced. This was complicated by
obstruction and erosion of the wire and has largely
3
Karl iersch (1822–1895), Professor of Surgery, Erlangen
then Leipzig, Germany. He also devised the split skin graft.
cure without active treatment is the
thickness rectal prolapse may be
3
in which a wire or nylon suture is
fallen from favour. Today, a less traumatic approach
involves excision of a sleeve of prolapsing rectal
mucosa and pleating of the underlying muscle to
form a doughnutwhich holds the rectum in the pelvis rather as a ring
pessary may control vaginal prolapse. An alternative
is the Altemeier
which a fullwith coloanal anastomosis is performed.
Pruritus ani
There are four principal causes of pruritus ani.
Local causes within the anus or rectum. Any factor
1
that causes moisture of the anal skin, for example
poor anal hygiene, excessive sweating, leakage of
mucus from haemorrhoids, proctitis, colitis, anal
fistula, anorectal neoplasm or threadworms.
Skin diseases: psoriasis, scabies, pediculosis,
2
fungal infections, such as Candida albicans.
3
General diseases associated with pruritus: diabe-
tes mellitus, Hodgkin’s disease, obstructive
jaundice.
Idiopathic: Often the original cause has disap-
4
peared but the pruritus persists because of continued scratching and trauma of the anal region by
the patient.
like ring (Delorme’s procedure
5
perineal proctosigmoidectomy, in
thickness resection of prolapsing rectum
Treatment
Directed to the underlying cause. The idiopathic
group often responds dramatically to attention to
local hygiene, stopping the use of topical treatments
and dietary changes.
Faecal incontinence
This is characterized by lack of anal control to flatus,
liquid and/or solid stool, and is more common with
increasing age. Other risk factors include vaginal delivery, prior anal surgery and cauda equina syndrome.
The incontinence may be urge or passive in nature.
4
Edmond Delorme (1843–1929), Chief of Surgery in the
French Army.
5
William Arthur Altemeier (1910–1983), Professor of
Surgery, Cincinnati, Ohio.
4
),
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Treatment
This is most commonly non- operative, and includes
measures to firm the stool and reduce gas production,
such as a low fibre diet and regular loperamide, and
measures to improve the strength and function of the
sphincter complex (sphincter strengthening exercises
and biofeedback therapy). In addition, use of suppositories, enemas and rectal irrigation can help to
keep the rectum empty and reduce leakage; input
from specialist nurse practitioners is valuable in this
regard.
Surgery is uncommonly indicated, and only when
operative measures have been exhausted and
nonafter discussion by a pelvic floor multidisciplinary
team. Surgical approaches include external anal
sphincter repair (anal sphincteroplasty), radiofrequency therapy and sacral nerve stimulation/
neuromodulation. A colostomy is generally only
considered when all other appropriate treatment
options have not been successful.
Tumours
Pathology
Benign
• Adenoma.
•
Papilloma.
• Lipoma.
• Endometrioma.
Malignant
1 Primary:
A Adenocarcinoma.
B Anal squamous cell carcinoma.
C Melanoma.
D
Neuroendocrine tumour.
E Lymphoma.
2
Secondary: invasion from prostate, uterus or pel-
vic peritoneal deposits.
Rectal polyps
Rectal polyps may be classified according to
histology:
1 Hyperplastic: these are small, 2–3 mm, sessile
lesions. Often multiple and always benign, this is
an incidental finding on sigmoidoscopy.
2
Adenomatous polyp: there are three histological
types of benign adenomatous polyp, all of which
may undergo malignant change. Multiple polyps
are present in familial adenomatous polyposis
(see Chapter27):
a Tubular adenoma– usually small and rounded,
the most common type of adenomatous polyp;
the epithelium is arranged in tubular fashion.
Villous adenoma: appears like an anemone
b
with many fronds growing from its base on
the rectal wall. May grow very large, and
produce large amounts of mucus. Greatest
potential for malignant change, so should be
completely removed.
c
Tubulovillous adenoma; histology that has an
element of both.
Hamartomatous, for example the juvenile polyp; a
3
developmental malformation which presents in
children and adolescents and which looks like a
cherry on a stalk. It is always benign, presents with
bleeding and may prolapse during defaecation.
4 Inflammatory (pseudopolyp): associated with coli-
tis; is not a true polyp but is oedematous mucosa
against a background of ulcerated, denuded bowel
wall.
Diagnosis is by histological analysis after removal.
Because of the propensity for malignant change of
adenomatous polyps, particularly villous adenomas,
these should always be excised in full to ensure that
no area of malignant change is missed. Although very
small polyps may be excised in the clinic, most polyps
require endoscopic excision. Surgical excision may
still be required for very large rectal polyps, and this
can usually be performed via a minimally invasive,
transanal approach.
Carcinoma ofthe rectum
Pathology
The sexes are equally affected. It occurs in any age
group from the twenties onwards, but is particularly common in the age range of 50–70 years. There
is a recent increase in the incidence of younger
onset of rectal cancer, with the precise reasons
remaining unclear. Carcinoma of the rectum
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accounts for approximately one- third of all tumours
of the large intestine. Predisposing factors (as with
carcinoma of the colon) are prefamilial adenomatous polyposis and inflammatory
bowel disease (both ulcerative and Crohn’s
colitis).
existing adenomas,
M1
Macroscopic appearance
The tumours may be classified as follows:
Papillomatous.
•
• Ulcerating (most common).
• Annular.
Stenosing (more commonly at rectosigmoid
•
junction).
Microscopic appearance
Rectal carcinomas are adenocarcinomas. At the anal
verge and canal, anal squamous cell carcinoma may
occur, but a malignant tumour protruding from the
rectum through the anal canal is more likely to be an
adenocarcinoma of the rectum invading the anal
canal. True squamous cell carcinoma of the rectum
is rare.
Spread
1 Local:
a Circumferentially around the lumen of the
bowel.
Invasion through the muscular wall.
b
c
Penetration into adjacent organs, for example
prostate, bladder, vagina, uterus, sacrum,
sacral plexus, ureters and lateral pelvic side
wall.
Lymphatic: to regional lymph nodes along the
2
inferior mesenteric vessels. At a later stage, there is
invasion of the lateral pelvic side wall and external
iliac lymph nodes and of the inguinal (groin)
lymph nodes for very low tumours involving the
anal canal and involvement of the supraclavicular
nodes via the thoracic duct.
3 Blood: via the superior rectal venous plexus,
thence via the portal vein to the liver and lungs.
4 Nerves: Perineural invasion is the process of neo-
plastic invasion of nerves.
5 Transcoelomic: seeding of the peritoneal cavity,
which is more common in higher rectal cancers
above the peritoneal reflection.
D
N2
C
B
B
A
Dukes’
stage
Figure28.4 Staging of rectal cancer by modied Dukes’
and TNM classications. Dukes’ A, conned to the bowel
wall; B, penetrating the wall; C, involving regional lymph
nodes; D, distant spread.
T1
N1
T4
T3
T2
TNM
stage
Staging
The extent of spread of rectal tumours was traditionally classified by Dukes
a stage for metastatic disease (Figure28.4).
The tumour is confined to the mucosa and
A
submucosa.
B There is invasion of the muscle wall.
C The regional lymph nodes are involved.
D Distant spread has occurred, for example to the
liver or invasion into the bladder.
6
Cuthbert Esquire Dukes (1890–1977), Pathologist, St Mark’s
Hospital, London, UK.
6
and later modified to include
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