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CHAPTER 11 Colorectal surgery
392
Ulcerative colitis
Key facts
• An acute and chronic infl ammatory disease originating in the colonic
columnar mucosa.
• Precise aetiology is unknown, but an environmental trigger combined
with a genetic predisposition (family history) are factors.
• Often precipitated by an apparent acute GI infection; peak age of
diagnosis is the late teens and twenties, but may present in late
adulthood.
• Commonest in white Anglo-Saxon Caucasians.
Pathological features
• Granular, hypervascular, and mildly oedematous mucosa with loss of
vascular pattern seen at endoscopy.
• Acute neutrophil infi ltration of the colonic mucosa and submucosa;
mucosal crypt abscesses with goblet cell mucin depletion.
• With more severe infl ammation, there are multiple aphthous ulcers,
which may become confl uent with only islands of infl amed mucosa and
granulation tissue remaining (‘pseudopolyposis’).
• Transmural infl ammation may occur in severe disease secondary to the
widespread loss of mucosa and subsequent severe infl ammation.
• Chronic ‘burnt-out’ disease leads to a pale, featureless, ahaustral
pattern to the colon.
• Disease tends to be present in the distal colon and rectum and spread
proximally with increasing extent of disease.
Clinical features
• Proctitis. Commonest presentation. Rectum ‘always’ involved unless
already on topical treatment. Symptoms of urgency and frequency of
defecation due to rectal irritability; bloody mucus mixed with loose
stools (frank bloody diarrhoea rare).
• Left-sided colitis. Disease up to the splenic fl exure. Symptoms of rectal
irritation plus extensive bloody mucus in stools, often leading to
bloody diarrhoea; mild associated systemic features.
• Pancolitis. Disease involving the entire colon. May be associated with
mild secondary infl ammation of the terminal ileum (‘backwash ileitis’).
Diarrhoea predominant feature; systemic features common (fever,
malaise, anorexia, tachycardia). May be associated with anaemia (due to
blood loss), hypoalbuminaemia, and hypokalaemia (due to mucus loss).
Diagnosis and investigations
Basic tests
i WCC and CRP; d Hb and albumin, especially during episodes of infl ammation. AXR may show oedematous colonic mucosa (‘thumbprinting’),
but is unreliable for diagnosis or extent of disease. Proctosigmoidoscopy
usually shows erythematous, granular, or frankly ulcerated rectal mucosa
with mucus and blood. Biopsies should be taken before starting treatment.
Always send stool M,C,&S and test for parasites and cysts in any acute
presentation to exclude infectious causes.
ULCERATIVE COLITIS
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Advanced tests
Extent of disease is best assessed with colonoscopy and biopsies; will also
usually exclude colonic Crohn’s disease.
Treatment
See b p. 418 for management of acute severe colitis.
Medical treatment
Principles are to reduce infl ammation and prevent complications. Acute
derangements in blood results should be corrected (e.g. blood transfusion
for severe anaemia, potassium supplementation, nutritional support for
hypoalbuminaemia).
Proctitis
• Topical steroids—Predsol
®
suppositories.
• Topical 5-aminosalicyclic acid (5-ASA) suppositories.
Left-sided colitis
• Topical steroids—Predsol
®
foam enemas (penetrate up as far as the
splenic fl exure).
• Topical 5-ASA foam enemas.
• May require systemic steroid treatment (prednisolone).
Pancolitis
• Topical steroids or 5-ASA treatments for local symptoms.
• Usually need systemic treatment, e.g. oral steroids (prednisolone),
5-ASA treatment.
• Oral immunosuppressives, e.g. azathioprine, 6-mercaptopurine.
• Systemic affectors of lymphocyte function, e.g. cyclosporin A,
anti-TNFα (infl iximab)
Surgical treatment
Surgery is indicated for acute colitis that fails to respond to treatment (see
b p. 418) and for chronic colitis when:
• Chronically symptomatic despite maximal medical therapy.
• Medical therapy controlling symptoms, but associated with
unacceptable side effects, e.g. osteoporosis, immunosuppression.
• Recurrent exacerbations affecting growth or development in
adolescents.
• Confi rmed diagnosis of either high grade dysplasia or dysplasia-
associated lesion or mass (DALM), or carcinoma of colon.
Surgical treatment may be:
• Proctocolectomy (removal of colon and rectum) with ileoanal pouch
formation (see b p. 402).
• Panproctocolectomy (removal of colon, rectum, and anus) with end
ileostomy formation (permanent).
• Total abdominal colectomy (removal of colon) with ileostomy (used
when the patient is too unwell for major pelvic surgery, e.g. for acute
severe colitis).
393
CHAPTER 11 Colorectal surgery
394
Crohn’s disease
Key facts
• A chronic infl ammatory non-caseating, granulomatous disease affecting
any part of the GI tract.
• Associated with several extraintestinal disorders (see Box 11.1).
• Precise aetiology is unknown, but products from the bacterial fl ora
combined with a genetic predisposition (family history) are factors.
• Peak age of onset of symptoms is the teens and early twenties, but
diagnosis is often several years later.
• Commonest in white Anglo-Saxon Caucasians.
Pathological features
• Commonly focused in the terminal ileum and caecum, but may affect
the anus, colon, or entire small bowel.
• Anal Crohn’s disease is not common, but may be severe and
associated with active small bowel disease.
• Colonic Crohn’s disease is a long-term risk factor for colorectal cancer
formation.
• Affected bowel looks blue-grey, thickened, with spiral surface vessels
and encroachment of the mesenteric fat around the bowel (‘fat
wrapping’).
• Transmural infl ammation in the form of lymphoid aggregates,
particularly in the subserosal tissues (‘Crohn’s rosary’), mucosal crypt
ulceration, and fi ssuring ulceration.
• Mucosal thickening and serpiginous longitudinal ulceration combine to
give the appearance of ‘cobblestoning’.
• Perforation, fi stulation, and abscess formation are occasional
‘fi stulizing’ sequelae of transmural infl ammation.
• Extensive fi brosis and smooth muscle hyperplasia may occur, giving
rise to stenosis.
Clinical features
• Infl ammatory features. Fever, malaise, abdominal pain (often RIF),
change in bowel habit (usually diarrhoea without blood), and weight
loss. Children and adolescents may have failure to thrive or have
retarded growth. Rectal bleeding is rare except in Crohn’s colitis.
• Fistulizing features. Para-enteric abscess formation often with a tender
abdominal mass, fi stula formation (ileocolic, ileoileal, ileocutaneous);
rarely free perforation with features of peritonitis.
• Stenosing features. Colicky abdominal pain, weight loss due to poor
food intake (‘food fear’), palpable or visible distended small bowel
loops.
• Anal disease. Atypical severe anal fi ssures, fi stula in ano, anal mucosal
thickening, and discoloration.
CROHN’S DISEASE
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Diagnosis and investigations
Basic tests
i WCC and CRP; d Hb and albumin, especially during episodes of
infl ammation.
Advanced tests
• In acute presentations, an abdominal CT may show an infl ammatory
mass, abscess formation, localized or free perforation.
• In subacute or chronic presentations, small bowel disease may be
shown by a small bowel contrast study (shows mucosal irregularity and
narrowing) or a white cell scan showing ileal ‘hot spots’.
• Crohn’s colitis is diagnosed by endoscopy and biopsy.
• Anal disease may require, EUA, anal ultrasound, or MRI scanning for
assessment.
• OGD and biopsies may show features of Crohn’s in gastric mucosa.
Treatment
Medical treatment
Principles are to reduce infl ammation and control complications. Acute
derangements in blood results should be corrected.
• Systemic (5-ASA) drugs are fi rst-line acute and long-term treatment.
• Systemic steroids (hydrocortisone, prednisolone) control acute
exacerbations of infl ammation and steroids with very high fi rst pass
metabolism (budesonide) can be used chronically.
• Immunosuppressives (azathioprine, 6-mercaptopurine) are used as
maintenance therapy and anti-TNFA antibodies (infl iximab) may be
effective in fi stulizing complications.
• Dietary manipulation (elemental diet) may reduce infl ammatory
factors.
Surgical treatment
Principles are to deal with septic complications, relieve signifi cant bowel
obstruction, and remove as little bowel as possible. Indications for
surgery include the following.
• Acute. Free perforation, severe haemorrhage, acute severe colitis,
complete intestinal obstruction.
• Subacute. Infl ammatory mass, subacute obstruction, abscess formation,
symptomatic fi stulation.
• Chronic. Steroid dependency or complications, growth retardation,
cancer treatment or prevention.
395
Box 11.1 Extraintestinal manifestations of Crohn’s
disease
Associated with disease activity Independent of disease activity
• Pyoderma gangrenosum • Ankylosing spondylitis
• Erythema nodosum • Polyarthritis
• Primary biliary cirrhosis • Chronic active hepatitis
CHAPTER 11 Colorectal surgery
396
Other forms of colitis
Key facts and pathological features
Various insults of widely differing origin may give rise to colitis other then
idiopathic infl ammatory bowel disease.
Acute infective colitis
• Typically caused by pathological variants of normal enteric organisms,
e.g. enteropathogenic E. coli; only rarely progresses to acute severe
colitis.
• Typhoid colitis (Salmonella typhi) (rare in the UK). Typifi ed by acute
bloody diarrhoea, but few if any colonic mucosal neutrophils on biopsy
due to bone marrow suppression.
Clostridium (C.) diffi cile-related colitis
Caused by C. diffi cile infestation. Associated with antibiotic use, particularly
third generation cephalosporins (even a single dose), prolonged inpatient
stay. Toxin A produced by the organism causes acute severe infl ammation
in the mucosa.
Clinical picture may be varied.
• C. diffi cile diarrhoea. Foul green liquid without bloody stools.
• Acute C. diffi cile colitis. Caused by progressive rapid mucosal loss, acute
neutrophil infi ltration, and infl ammation
• Pseudomembranous colitis. Exudate and slough forms grey-white
‘plaques’ of material on the denuded colonic surface called
pseudomembranes. May rapidly progress to acute severe ‘invasive’
colitis, especially in the immunocompromised or acutely unwell.
Typifi ed by secondary infections associated with mucosal loss.
Neutropenic colitis
Occurs in the severely immunocompromised with neutropenia and/or
neutrophil dysfunction. Caused by multiple, normally non-pathogenic,
enteric organisms colonizing the colonic mucosa.
Radiation colitis
Acute, transient colitis caused by mucosal injury secondary to external
beam radiotherapy. May progress to chronic mucosal damage, haemorrhagic telangectasia, and possible stricturing after months or years.
Ischaemic colitis
Commonest in the upper left colon where the collateral blood supply
between the middle and inferior colic arteries is poorest. Usually precipitated by an acute occlusion of part or all of the inferior mesenteric
artery. May progress to infarction, but often presents with acute onset
bloody diarrhoea and abdominal pain; may settle spontaneously although
occasionally forms an ischaemic stricture.
Clinical features
Broadly similar, independently of the underlying cause. Typical features are
vague abdominal pain, mild fever (absent in neutropenic colitis), diarrhoea
(may be bloody, especially in ischaemic, radiation, severe pseudomembranous, and typhoid colitis). Cessation of diarrhoea, except with treatment,
OTHER FORMS OF COLITIS
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suggests acute severe colitis is developing and should be investigated
urgently.
Diagnosis and investigations
Depending on the suspected cause:
• Stool sent for C. diffi cile toxin (CDT), three samples.
• Stool for M,C,&S (if atypical infective causes possible, also send for
cysts, parasites, and ova (C,P,&O)).
• Plain abdominal radiograph may show thickened colonic haustrae.
• CT abdomen often shows typical mucosal thickening in colitis and may
be diagnostic for pseudomembranous colitis.
• Flexible endoscopy (usually fl exible sigmoidoscopy) with biopsy.
Treatment
Medical treatment
• Acute infective colitis. Antibiotics only if severely symptomatic.
• C. diffi cile diarrhoea/colitis. Oral vancomycin up to 200mg PO
daily or metronidazole 400mg PO tds; treatment may be as for
pseudomembranous colitis if severe.
• Pseudomembranous colitis. Oral vancomycin up to 200mg PO daily or
metronidazole 400mg PO tds; adjuvant systemic treatment may be
added in severe cases, e.g. IV vancomycin or tigicycline.
• Neutropenic colitis. Broad-spectrum antibiotics, bone marrow support.
• Radiation colitis. Symptomatic treatment only; anti-diarrhoeals.
• Ischaemic colitis. Supportive treatment; anticoagulation may be
appropriate if the underlying cause is thromboembolic.
Surgical treatment
Rarely indicated. Any form of colitis may progress to acute severe colitis
and require emergency colectomy (see b p. 418). Indications are:
• Failure to respond to maximal medical therapy with life-threatening
colitis (usually requires perioperative ITU support).
• Complications of colitis. Uncontrollable bleeding, perforation
(especially in ischaemic or neutropenic colitis).
397
Key revision points—colorectal resections
Anastomosis of the colon/rectum may be in several ways.
• Hand sewn. Either end to end or end to side, usually single layer of
sutures (dissolvable), either interrupted or continuous.
• Stapled colonic. By mechanical stapler (‘linear stapler’), usually side
to side.
• Stapled colorectal. By mechanical stapler (‘endoluminal stapler’), end
to end.
• Defunctioning (loop) ileostomy typically for rectal anastomosis
when:
Below the peritoneal refl ection.•
Comorbidities (diabetes, age, previous DXT, acute illness).•
CHAPTER 11 Colorectal surgery
398
Colorectal polyps
‘Polyp’ is a purely descriptive term and any growth from the lining of the
large bowel can be described as a polyp. Polyps may be predominantly
raised with a stalk attachment (pedunculated), fl at and spreading over
the surface of the bowel wall (sessile), or occasionally a combination of
the two.
Key facts and pathological features
Polyps may arise for many different reasons.
Juvenile polyps
Mucin-fi lled cystic swellings of the lower rectal mucosa. Rarely part of
a hereditary syndrome (juvenile polyposis) with multiple juvenile polyps
throughout the colon; small increased risk of colorectal cancer.
Hamartomatous polyps
Polyps containing excessive amounts of the normal architectural components of the bowel wall, usually isolated. May be part of a hereditary
syndrome (Peutz–Jeghers syndrome, with polyps characterized by extensive branched growth of the muscularis mucosa); small increased risk of
colorectal and other GI cancers.
Hyperplastic polyps
Small sessile polyps formed from normal elongated mucosal crypts.
Only associated with risk of colorectal cancer if numerous (‘hyperplastic
polyposis’).
Adenomatous polyps
• True neoplastic polyps formed by excessive growth of the colorectal
epithelium; divided by the morphology of the glandular tissue into
tubular, tubulovillous, and villous types.
• May be sessile, pedunculated, or mixed.
• Thought to be the precursor of most colorectal cancers; the risk of
cancerous change within an adenomatous polyp increases with size
(particularly >1cm), villous morphology, and sessile form.
• Majority are sporadic (either isolated or in small numbers), although
occasionally part of a hereditary syndrome.
Familial adenomatous polyposis (FAP)
Caused by an autosomal dominant defect in the APC gene on chromosome 5. Characterized by between dozens and thousands of adenomatous
polyps in the colorectum and an increased risk of polyp formation in the
stomach and duodenum. The risk of cancerous transformation in any given
polyp is similar to that in normal polyps, but the overall risk is very high
due to the vastly increased number present.
Associated with:
• Desmoid formation, particularly in the abdominal tissues.
• Multiple osteomata, fi bromata, and thyroid infl ammation (called
Gardner’s syndrome).
COLORECTAL POLYPS
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Hereditary non-polyposis colorectal cancer (HNPCC)
A range of abnormalities of the mismatch repair (MMR) genes that
predispose adenomas to acquire multiple genetic defects and so progress
more rapidly than normal to cancer, although the overall rate of
adenoma formation is similar to that in normals.
Clinical features
Most polyps are asymptomatic, although symptoms may occur with increasing size and with proximity to the anus. Typical symptoms are:
• Bleeding. Usually low volume, dark red, often fl ecks or mixed with
stool.
• Mucus discharge. White, clear, or watery; commonest with large villous
adenomas and may cause hypokalaemia and hypoproteinaemia if the
villous adenoma is large with copious mucus discharge.
• Prolapse. If pedunculated and low in the rectum polyps, may prolapse
out of the anus.
Diagnosis and investigations
• Most polyps are diagnosed by colonoscopy.
• Most patients with polyps require further follow-up investigations
to keep them under surveillance for future polyp formation; the
frequency and length of follow-up depends on the number, size, and
histology of the polyp.
1
• Hereditary polyposis syndromes may be investigated by genetic
mutation analysis.
Treatment
Medical treatment
• Colonoscopic polypectomy (see b p. 36). Simple, is carried out for
pedunculated polyps larger than 1–2mm; others may be removed by
EMR/ESD (see b p. 403).
• Patients with FAP require regular gastroscopy and upper GI
surveillance to identify premalignant polyps.
Surgical treatment
• Surgical excision is required for polyps that are too large or unsuitable
for colonoscopic removal and in which there is a risk of current or
future malignant change; for colonic polyps this means either resection
or open excision.
• Rectal polyps may be removed by transanal microsurgery (see b p. 403).
• FAP is usually treated by proctocolectomy (usually with ileoanal
pouch formation) or colectomy and ileorectal anastomosis before
early adulthood; other polyposis syndromes may also be treated by
prophylactic colectomy.
Reference
1 Atkin WS, Saunders BP (2002). Surveillance guidelines after removal of colorectal adenomatous
polyps. Gut 51 (Suppl. V), v6–v9.
399
CHAPTER 11 Colorectal surgery
400
Colorectal cancer
Key facts
Colorectal cancer (CRCa) is the second commonest tumour and commonest GI malignancy. One in 18 of the population will suffer CRCa; ♂:♀
8 3:1. Peak age of incidence 55–75y, but is increasing in younger ages.
Pathological features
The predominant type is adenocarcinoma (mucinous, signet ring cell, and
anaplastic subtypes). Classifi ed as well, moderately, or poorly differentiated. Predisposing factors include:
• Polyposis syndromes (including FAP, HNPCC, juvenile polyposis).
• Strong family history of colorectal carcinoma.
• Previous history of polyps or CRCa.
• Chronic ulcerative colitis or colonic Crohn’s disease.
• Diet poor in fruit and vegetables.
Morphology
CRCa may occur as a polypoid, ulcerating, stenosing, or infi ltrative tumour
mass. The majority (75%) lie on the left side of the colon and rectum
(rectum, 45%; descending-sigmoid, 30%; transverse, 5%; right-sided,
20%). Three to fi ve per cent have a synchronous carcinoma at time of
diagnosis.
Clinical features
Rectal location
• PR bleeding. Deep red on the surface of stools.
• Change in bowel habit. Diffi culty with defecation, sensation of
incomplete evacuation, and painful defecation (tenesmus).
Descending-sigmoid location
• PR bleeding. Typically dark red, mixed with stool, sometimes clotted.
• Change in bowel habit. Typically increased frequency, variable
consistency, mucus PR, bloating, and fl atulence.
Right-sided location
Iron defi ciency anaemia may be the only elective presentation.
Emergency presentations
Up to 40% of colorectal carcinomas will present as emergencies.
• Large bowel obstruction (colicky pain, bloating, bowels not open).
• Perforation with peritonitis.
• Acute PR bleeding.
Diagnosis and investigations
Elective diagnosis By PR examination or rigid sigmoidoscopy for rectal
carcinoma. Colonoscopy is the preferred diagnostic investigation (alternatives are barium enema and CT colonography).
Emergency presentations Commonly diagnosed by abdominal CT scan.
Single contrast enema may be used when the diagnosis of large bowel
obstruction is possible and CT scanning is unavailable. Acute PR bleeding
is sometimes investigated by urgent colonoscopy.
COLORECTAL CANCER
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Staging investigations
• Assessment of the presence of metastases (liver, lung, or para-aortic).
Thoracoabdominopelvic CT scanning is gold standard; CT PET scan
may be used to evaluate equivocal lesions.
• Assessment of local extent. For colonic carcinoma, CT scanning is
adequate; for rectal cancer, pelvic MRI and TRUS are commonly used.
• Assessment of synchronous tumours. If not diagnosed by colonoscopy
or barium enema, one of these two tests is usually performed to
identify synchronous tumours.
• Tumour marker (CEA) is of no use for diagnosis or staging, but can
be used to monitor disease relapse if raised at diagnosis and falls to
normal after resection.
Pathological staging
Duke’s (approx. % 5y survival) TNM
• A, confi ned to bowel wall only
(75–90)
• B, through bowel wall (55–70)
• C, any with +ve lymph nodes
(30–60)
• D, any with metastases (5–10)
• T1–4, stages of invasion of
bowel wall
• N0/1/2, no/up to 4/more than
4 lymph nodes involved
• M0/1, metastases not present/
present
Treatment
Potentially curative treatment
Suitable for technically resectable tumours with no evidence of metastases
(or metastases potentially curable by liver or lung resection).
• Surgical resection (with lymphadenectomy) is the only curative
treatment. Typical operations:
Right/transverse. Right/extended right hemicolectomy.•
Left. Left hemicolectomy.•
Sigmoid/upper rectum. High anterior resection.•
Lower rectum. Low anterior resection/abdominoperineal resection •
(APER).
Anorectal. APER.•
• Preoperative (neoadjuvant) chemoradiotherapy may be used in rectal
cancer to increase the chance of curative resection.
• Adjuvant chemotherapy (5-FU based) is offered for tumours with
positive lymph nodes or evidence of vascular invasion.
• Hepatic or lung resection may be offered to patients with suitable
metastases and a clear resected/resectable primary tumour.
Palliative treatment
For unresectable metastases or unresectable tumours.
• Chemotherapy may effectively extend life expectancy with a good
quality of life.
• Obstructing tumours may be endoluminally stented with self-
expanding metal stents or transanally ablated if rectal.
• Surgery reserved for untreatable obstruction, bleeding, or severe
symptoms.
401
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