The small intestine ANATOMY - PowerPoint Presentation

Slide1

The small

intestine

ANATOMY

The

length of the small bowel varies

from 300

to 850

cm.

B

etween

the duodenojejunal (DJ) flexure

to the

ileocaecal

valve.

The

proximal 40% of the small intestine is referred to

as the

jejunum; the remainder is the ileum.

There

is no

clear demarcation

between jejunum and

ileum.

The

jejunum tends to have a wider diameter and

a thicker

wall, with more prominent mucosal folds (

valvulae conniventes).

T

he

ileum has a thicker, more fatty

mesentery with

more complex arterial arcades.

I

t also contains

larger aggregates of lymph nodes (Peyer’s patches

).

The blood

supply,

derived from

the superior mesenteric

artery.

T

he

venous drainage

is via

the portal venous system, into which the superior

mesenteric vein

drains blood rich in nutrients after a meal.

Slide2

This

arrangement facilitates processing of the nutrients by the liver, into which the portal vein drains in turn.

The lymphatic drainage of the small intestine follows the arterial supply.

The small intestine has a rich autonomic innervation arising from the splanchnic nerves, which contribute a dense network of sympathetic fibres around the superior mesenteric artery and its branches.

Referred pain from the small intestine is usually felt in the periumbilical region (T10).

The blood and nerve supply to the small intestine runs in the attached mesentery, which originates on the posterior abdominal wall and runs obliquely downwards to the right between the duodenojejunal flexure to the left of the second lumbar vertebra and the right sacroiliac joint.

Slide3

PHYSIOLOGY OF THE

SMALL INTESTINE

The principal function of the small intestine is the

digestion of

food and the absorption of nutrients, water and electrolytes.

Carbohydrates

and

proteins

are broken down in

the intestinal

lumen by pancreatic

enzymes,

after

which they

are absorbed.

Fats

are digested

by the actions

of pancreatic

lipase and bile salts.

The

products of fat

digestion, (fatty

acids and

monoglycerides),

separate from bile salts in

the jejunum

and are absorbed for further processing.

The jejunum is

the principal site for digestion and absorption of fluid,

electrolytes, iron

, folate, fat, protein and

carbohydrate

.

The absorption

of bile salts and vitamin B12 only occurs in

the terminal ileum

.

Slide4

If the jejunum is resected, the ileum can assume all the required absorptive functions.

Resection of the terminal ileum will result in a diminished bile salt pool, B12 deficiency and may lead to deficiency of the fat-soluble vitamins A, D, E and K.

The small intestine plays an important role in the metabolism of plasma lipoproteins, as it is the main site of synthesis of high-density, low-density and very low-density

lipoproteins (HDL

, LDL, VLDL).

These particles transport most of the absorbed dietary fat to the systemic circulation via the lymph.

The small bowel also synthesises intestinal hormones such as glucagon-like peptides GLP-1 and 2, peptide YY and motilin, which interact with the enteric nervous system to modulate intestinal function, growth and differentiation.

Slide5

INFLAMMATORY

BOWEL DISEASE

It is a

conditions characterised by the presence

of idiopathic

intestinal

inflammation.

Crohn’s

disease (regional enteritis)

CD

is characterised by

a chronic

full-thickness inflammatory process that can

affect any

part of the gastrointestinal tract from the lips to the

anal margin

.

It

is most common in North America and

Northern Europe

with an annual incidence of 8 per 100 000.

Over

the last four decades, the incidence appears to

have increased

three-fold, thought to possibly be a

consequence of;

E

nvironmental factors

I

mproved

diagnostic

modalities

B

oth.

Slide6

It is slightly more common in women than in men, and is most commonly diagnosed between the ages of 25 and 40 years.

There is a second peak of incidence around the age of 70 years.

In those countries with high prevalence of CD, the groups with the highest prevalence seem to be Caucasian, notably American Whites and Northern Europeans, whereas it is less common, even in high prevalence countries, in those originating from Central Europe and less prevalent still in those originating from South America, Asia and Africa.

CD seems to be especially prevalent (three- to five-fold higher) in the Ashkenazi Jewish population, although interestingly, the prevalence of CD in the Jewish population in Israel is lower than that in Europe or the United States, suggesting that environmental factors are also important.

Slide7

Aetiology

I

s

incompletely understood

T

hought to

involve a complex interplay of genetic and

environmental factors.

N

o

causative organism has ever been

demonstrated.

Smoking

increases the relative risk of

CD three-fold

.

Smoking

cessation has a beneficial effect on

disease activity.

Genetic

factors are also clearly extremely important.

10% of patients have a first-degree

relative with

the disease,

and

50% in monozygotic twins.

Inheritance

is

thought to

involve multiple genes with low penetrance.

The NOD2/ CARD15

gene

have

strong associations with CD.

The

vast majority of individuals with CD have no abnormalities of these genes.

Since these genes are involved in intracellular recognition of bacteria, their discovery provides potentially valuable insight into the pathogenesis of CD, as a disease in which the

relationship between

the gut mucosa and the normal gut bacteria becomes deranged, resulting in uncontrolled intestinal inflammation

.

Slide8

Pathogenesis

I

ncreased

gut mucosal permeability appears

to develop

at

a

early stage of the disease.

This lead

to increased passage of luminal antigens, which

then induce

a cell-mediated inflammatory response.

This results in

the release of proinflammatory cytokines, such as

interleukin- 2

and tumour necrosis factor, which coordinate local

and systemic

inflammatory responses.

It

has been suggested

that CD

is associated with a defect in suppressor T-cells,

which usually

act to prevent escalation of the inflammatory process.

I

ncrease

in

gut permeability

,

combined with

an abnormal immune-mediated

response to

colonisation of the gut with some subspecies of the

normal enteric

microflora, may initiate the disease.

Slide9

Pathology

The terminal ileum is most commonly involved (65%),

either in

isolation or in combination with colonic disease.

Colitis alone

occurs in up to a one-third of cases and the

remainder are

patients with more proximal small bowel

involvement.

The

stomach and duodenum are affected in around 5

%, but

perianal lesions are common, affecting up to 50–75%

of patients.

Macroscopically,

resection specimens show fibrotic

thickening of

the intestinal wall with narrowing of the lumen

and fat

wrapping (encroachment of mesenteric fat around

the bowel).

There

is usually dilated bowel just proximal to the stricture and deep mucosal ulcerations with linear or snake-like patterns in the strictured area itself.

Oedema in between the ulcers gives rise to a cobblestone appearance of the mucosa.

The transmural inflammation (which is a characteristic feature of CD) may lead to segments of bowel becoming adherent to each other and to surrounding structures, inflammatory masses with mesenteric abscesses and fistulae into adjacent organs

.

.

Slide10

The

serosa is usually opaque, with thickening of the mesentery and enlarged mesenteric lymph nodes.

CD is characteristically discontinuous, with inflamed areas separated by normal intestine, so-called ‘skip’ lesions.

Microscopically,

there are focal areas of chronic inflammation involving all layers of the intestinal wall with lymphoid aggregates.

Non-caseating giant cell granulomas are found in 60% of patients and when present clearly allow a confident diagnosis of CD.

They are most common in anorectal

disease Multifocal

arterial occlusions are found in the muscularis propria, which is thickened.

There may be nerve cell hyperplasia and there is deep, fissuring ulceration within affected areas.

Characteristically, and unlike in UC, there may be completely normal areas immediately next to areas of severe inflammation

Slide11

Clinical

features

Occasionally, CD

presents acutely with ileal inflammation and

symptoms and

signs resembling those of acute

appendicitis or

even

with free

perforation of the small intestine, resulting in a local

or diffuse

peritonitis.

M

ay

present with fulminant

colitis.

M

ore

commonly presents with features of chronicity.

Small bowel CD is often characterised by abdominal

colicky pain

, which may be postprandial, and mild diarrhoea

extending over

many months occurring in bouts.

A

tender mass

may be

palpable in the right iliac fossa.

Intermittent

fevers,

secondary anaemia

and weight loss are common.

After months of

repeated attacks

of acute

inflammation,

the affected

area of intestine begins to narrow with fibrosis,

causing more

chronic obstructive symptoms

.

Slide12

Children developing the illness before puberty may have retarded growth and

sexual development

.

With progression of the disease, adhesions and transmural fissuring, intra-abdominal abscesses and fistulae may develop.

Fistulation may occur into adjacent loops of bowel (enteroenteric or interloop fistulae).

Occasionally

, the (healthy) sigmoid loop may become adherent to the affected terminal ileum, resulting in ileosigmoid fistulation.

The fistula tracks in such cases are usually small and the profuse diarrhoea that results from ileosigmoid fistulation is

due

to bacterial overgrowth (attributable to colonisation of

the small

bowel with colonic flora) rather than passage of small bowel content into the colon.

Fistulation

may also occur into the bladder (ileovesical) or the female genital tract and,

less commonly

, the duodenum.

Slide13

Fistulation

into the

abdominal wall

(enterocutaneous fistulation) may also develop

spontaneously, or more

commonly occurs as a complication

of abdominal surgery.

Colonic

CD presents with symptoms of colitis and

proctitis as

described for

UC,

although toxic

megacolon is

much less common.

Many patients with CD present with perianal

problems.

In

the presence of active disease, the perianal skin

appears bluish

.

Superficial

ulcers with undermined edges are

relatively painless

and can heal with bridging of epithelium.

Deep cavitating ulcers

are usually found in the upper anal canal;

they can

be painful and cause perianal abscesses and fistulae,

discharging around

the anus and sometimes forwards into

the genitalia

.

Fistulation

through the posterior wall of the

vagina may

lead to rectovaginal fistula and continuous leakage of

gas and/or

faeces per vaginam.

Slide14

The rectal mucosa is often spared in CD and may feel normal on rectal examination.

If it is involved, however, it will feel thickened, nodular and irregular.

Perianal

disease is frequently associated with dense, fibrous stricturing at the anorectal junction.

Incontinence may develop as a result of destruction of the anal sphincter musculature because of inflammation, abscess formation, fibrotic change and repeated episodes of surgical drainage.

In

severe cases, the perineum may become densely fibrotic, rigid and covered with multiple discharging

openings.

Each

patient with CD should have their disease phenotype (manifestations) classified according to the Montreal classification.

This is important as it allows an overview of disease progression in the individual patient over time, and it enables group comparisons and evaluations.

The Montreal classification specifies age of onset, location and behaviour.

T

he

behaviour of CD can be dominated by inflammation without stricturing or penetration, stricturing or penetration (causing phlegmons, abscesses and fistulae).

Slide15

Montreal classification for Crohn's disease

Montreal

Age at diagnosis

A1

below 16 y

A2

between 17 and 40

y

A3

above 40 y

Location

L1

ileal

L2

colonic

L3

ileocolonic

L4

isolated upper disease*

Behaviour

B1

non‐stricturing, non‐penetrating

B2

stricturing

B3

penetrating

p

perianal disease modifier

†

----------------------------------------------------------------------------------------------------------

*L4 is a modifier that can be added to L1–L3 when concomitant upper gastrointestinal disease is present.

†“p” is added to B1–B3 when concomitant perianal disease is present.

Slide16

Investigations

LABORATORY

A full blood count should be performed, as

anaemia

is

common and

usually multifactorial.

It

may result from the

anaemia of

chronic

disease

.

From

iron deficiency as a result of

blood loss

or malabsorption.

Vitamin

B12 deficiency may occur

as a

consequence of terminal ileal disease

or resection

.

Folate deficiency

may also result from diffuse small bowel disease

or resection

.

Active

inflammatory disease is usually

associated with

a fall in serum albumin, magnesium, zinc and

selenium.

Acute

phase protein measurements (C-reactive

protein)

and the erythrocyte sedimentation rate

may correlate

with disease activity.

Finding an elevated concentration in the stools of

calprotectin

, a

specific marker of

inflammation.

M

ay

support

a diagnosis

of CD in patients with new onset of persistent

gastrointestinal symptoms

.

It

can also be used to monitor

disease activity

in the long-term management of established CD.

Slide17

ENDOSCOPY

M

ay

be normal or show

patchy inflammation

.

Characteristically

, there are areas of

normal mucosa

in between areas of inflammation that are

irregular and

ulcerated, with a mucopurulent exudate.

The earliest findings

are of aphthous ulcers surrounded by a rim of

erythematous mucosa

.

These

become larger and deeper

with increasing

severity of disease.

There

may be stricturing,

and it

is important to exclude malignancy at these sites by

multiple and

often repeated mucosal biopsies.

An

irregular

Crohn’s stricture

with polypoid mucosa may be almost

macroscopically indistinguishable

from malignancy.

The

terminal

ileum may

be ulcerated and strictured

.

Slide18

In patients who have had previous ileocaecal resection and anastomosis, recurrent disease usually presents first with aphthous ulceration just proximal to the anastomosis.

Interval colonoscopy is therefore important in the follow-up after surgery for CD.

Upper gastrointestinal symptoms may

require

upper

gastrointestinalendoscopy

, which may reveal deep longitudinal ulcers and cobblestoning of mucosa in the duodenum,

stomach or

, rarely, in the oesophagus.

Enteroscopy

may reveal jejunal ulceration and stricturing.

Capsule endoscopy

should not be undertaken where there is a suspicion of stricture, because of the possibility of the capsule becoming stuck in the narrow segment.

Slide19

IMAGING

High-resolution ultrasound

can demonstrate inflamed

and thickened bowel loops, as well as fluid

collections and

abscesses.

The

small intestine is traditionally

imaged by

a

small bowel

enema

.

This

is performed

by instilling

contrast into the small bowel via a

nasoduodenal tube

, and will show up areas of stricturing and

prestenotic dilatation

.

The

involved areas tend to be narrowed,

irregular and

, sometimes, when a length of terminal ileum is

involved, there

may be the ‘string sign’ of

Kantor.

Computed tomography (CT) scans

with oral

contrast are

widely used in the investigation of abdominal

symptoms and

can demonstrate fistulae, intra-abdominal abscesses

and bowel

thickening or dilatation.

Slide20

Magnetic resonance imaging (MRI)

is useful in assessing complex perianal disease and, more recently, has been shown to be an excellent method for investigating the small bowel.

MR enterography (oral contrast) or enteroclysis (contrast administered via nasoduodenal tube) is particularly effective at demonstrating small bowel stricturing and avoids the need for repeated exposure to large doses of ionising radiation in young patients

.

A labelled white cell scan

is occasionally of value to determine whether or not a segment of bowel is actively inflamed and guide decisions on medical treatment.

In patients with enterocutaneous fistulae,

fistulography

will be required to demonstrate the anatomy and complexity of the fistulae and allow adequate planning for future surgery.

Slide21

Treatment

MEDICAL TREATMENT

Steroids

are the traditional method for

inducing remission

in CD, and remain important when rapid

remission is

required.

They

induce remission in 70–80% of

cases with

moderate to severe disease.

They

should be used

in short

courses only and tapered when a response has

been achieved

.

They

reduce inflammation and are therefore

ineffective in

fibrostenotic disease, where the symptoms

relate mainly

to obstruction.

Steroids

can also be used as

topical agents

in the rectum where the benefits include reduced

systemic bioavailability

, but long-term use can still cause

adrenal suppression.

More recently, oral steroid formulations

such as

budesonide have been devised, to ensure that the

steroid moiety

is removed in the portal circulation, reducing

systemic side

effects.

Steroids

should not be used for maintenance

therapy for

CD and are usually replaced with

immunomodulatory agents

in order to minimise the risk of side

effects associated

with long-term steroid use.

Slide22

Aminosalicylates

Colonic symptoms can be treated by 5-ASA agents in a similar manner to that in UC.

These agents

have limited efficacy in small bowel CD.

Antibiotics

Metronidazole

and ciprofloxacin may be used, particularly for periods of a few weeks at a time, especially in perianal disease.

Long-term

use of metronidazole is to

be especially

avoided, as there is a risk of peripheral neuropathy.

Ciprofloxacin

also has significant side effects when used in the long term, such as Achilles tendinitis and tendon rupture

.

Antibiotics may also be used to decrease systemic symptoms resulting from an inflammatory mass or an abscess.

In

general

,

abscess should be treated by percutaneous drainage and/or surgery as antibiotics alone will not treat a Crohn’s mass effectively.

Slide23

Immunomodulatory

agents

Azathioprine is used for

its additive

and steroid-sparing effects and currently

represents standard

maintenance therapy.

It

is a purine analogue,

and

works

by inhibiting

cell-mediated immune responses.

6-MP (6-Mercaptopurine) may be given

directly for the same

effects.

Cyclosporin

also acts by inhibiting cell-mediated

immunity.

Short-course

intravenous cyclosporin treatment is

associated with

80% remission; however, there is relapse

after completion

of treatment in many cases.

Monoclonal

antibody therapy

monoclonal antibodies

targeting tumour necrosis factor alpha and

other key

pro-inflammatory mediators.

Infliximab, a murine chimeric monoclonal antibody,

was the

first available monoclonal antibody for the treatment

of CD.

This needs to be administered as an intravenous

infusion and

is typically given every 8 weeks for maintenance of remission.

Adalimumab

, an entirely human monoclonal

antibody, is

an alternative to

infliximab.

This

is administered

subcutaneously every

1–2 weeks, depending on response, and

most patients

can self-administer this agent.

Slide24

Third-generation monoclonal antibody therapies

include integrin

antibodies vedulizumab and etrolizumab.

Both prevent leucocyte

migration

in

the

gastrointestinal tract

and may therefore have fewer side effects than the

earlier monoclonal antibodies.

The

roles of monoclonal antibodies have expanded

from initially

being used exclusively in the most severe cases of

CD when

other therapies failed, to having a more central role

in the

management of moderate to severe CD.

They

are

currently widely

used for induction and maintenance of remission.

Slide25

There is evidence that early and aggressive use of these agents in patients at high risk for early recrudescent disease after surgery (for example, penetrating phenotype, early mucosal inflammation or aphthous ulceration at follow-up colonoscopy) may reduce the need for subsequent surgery.

These agents also appear to be effective treatments for perianal disease.

Recent studies have suggested, however, that while they may reduce the inflammation associated with the process of fistulation and can achieve healing of fistula openings, the fistula tracks may remain patent and cessation of therapy is usually associated with a high risk of

reactivation of

the fistulae.

Monoclonal antibodies are expensive forms of treatment that are associated with a small but definable risk of overwhelming bacterial infection and specific malignancies over the long term.

Active

infection, tuberculosis and a past history of malignancy are specific contraindications

.

Slide26

Nutritional

support

Patients

with moderate nutritional

impairment will

require nutritional supplementation and

severely malnourished

patients may require enteral tube or even

intravenous feeding

.

Anaemia

, hypoproteinaemia and

electrolyte, vitamin

and metabolic bone problems must all be

addressed.

Elemental

diet or parenteral nutrition can induce

remission in

up to 80% of patients, an effect comparable to steroids.

However, almost all patients relapse rapidly after cessation of therapy

.

Principles

of management of Crohn’s disease (CD)

●

Close liaison between physician and surgeon is crucial

●

Medical therapy should always be considered as

an alternative

to surgery, although surgery should not be

delayed when

a clear indication for surgery exists

●

Patients must be optimised as far as possible prior to

surgery, and

this may require preoperative total parenteral nutrition

●

CD is a chronic relapsing disease with a high likelihood

of reoperation

; the surgeon must take every reasonable effort

to

preserve

bowel length and sphincter function

Slide27

ENDOSCOPIC DILATATION IN CROHN’S DISEASE

S

tricturing

may be

amenable to

endoscopic treatment, provided the strictures can

be reached

with an

endoscope.

This may be accomplished by enteroscopy or

colonoscopy, depending

on the site of the stricture.

Dilatation

of

an inflamed

or ulcerated stricture is contraindicated because

of the

risks of perforation, but balloon dilatation of

fibrostenotic disease

may result in substantial symptomatic

improvement and

obviate the need for surgery in selected cases.

Slide28

INDICATIONS FOR SURGERY

Surgical resection will not cure CD.

Surgery therefore focuses on managing the complications of the disease.

As many of these indications for surgery may be relative, joint

management by

an aggressive physician and a conservative surgeon is ideal.

CD is a complicated condition and decisions regarding management are best made jointly

by members

of a

team

.

Complications or manifestations of CD for which surgery is usually appropriate include the following

:

Recurrent

intestinal obstruction;

Persistent

or, less commonly, massive acute bleeding;

Free

perforation of the bowel;

Failure

of medical therapy;

Steroid

dependent disease;

Intestinal

fistula;

Perianal

disease (abscess, fistula, stenosis);

Malignant

change (notably in the colon and less commonly as a complication of small bowel disease).

Slide29

TOP-DOWN APPROACH TO MANAGEMENT

OF CROHN’S

DISEASE

A

ctive

ileocolic CD may be treated

initially with

a thiopurine, adding steroids and then a

monoclonal antibody

only if and when required.

Some

centres

instead advocate

a top-down approach, where rapid remission

is obtained

by initiating therapy with a monoclonal

antibody agent

(unless contraindicated), often in combination with

a thiopurine

.

Studies

suggest advantages mainly in the form

of rapid

remission, steroid sparing and increased rates of

mucosal healing

.

Slide30

Intra-abdominal septic

complications are

more common if one or more of the following risk factors are present:

● Current

high-dose steroid therapy (≥10 mg prednisolone for ≥4 weeks before surgery);

● Current

preoperative monoclonal antibody therapy;

● Preoperative

significant weight loss (>10% premorbid weight);

● Pre-existing

abdominal sepsis (notably abscess or fistula);

● Serum

albumin <32 g/L.

If any these risk factors are present (and particularly if more than one risk factor is present as the risks appear to be additive), one should consider exteriorising the bowel and planning a delayed anastomosis when the risk factor has been corrected

.

Slide31

A range of operations is performed for CD, depending on the pattern of disease – the most common are outlined below

:

● Ileocaecal resection is the usual procedure for terminal ileal disease, with a primary anastomosis between the ileum and the ascending or transverse colon, depending on the extent of the disease.

● Segmental resection of short segments of small or large bowel strictures can be performed.

● Colectomy and ileorectal anastomosis may be undertaken for colonic CD with rectal sparing and a normal anus.

● Subtotal colectomy and ileostomy for Crohn’s colitis accounts for 8% of such procedures for acute colonic disease.

● Temporary loop ileostomy.

This

can be used either in patients with acute distal CD, allowing remission and later restoration of continuity, or in patients with severe perianal or rectal disease.

Slide32

●

Proctectomy and proctocolectomy. Many patients

with severe

anal disease failing to respond to medical

treatment will

eventually require a permanent colostomy. When

this occurs

in a setting of severe colonic disease,

proctocolectomy and

permanent ileostomy may be required.

●

Strictureplasty.

Strictured

areas of CD

can be

treated by strictureplasty, a local widening

procedure, to

avoid small bowel resection and is thus an

important bowel

sparing technique

Strictureplasty is

particularly useful for the treatment of

fibrostenotic disease

, when there is little or no active

inflammation in

the involved segment. Multiple strictureplasties

can be

performed and strictureplasty can be combined

with resection

.

.

Slide33

Anal disease should be treated conservatively by simple drainage of abscesses and the use of setons through fistulae to avoid sphincter injury.

Infliximab or adalimumab therapy may be combined with seton insertion in the early phase of management of perianal fistulae.

Once the fistula has dried up, typically after 2–3 doses, the seton can be removed.

Laying open of fistulae (fistulotomy), commonly performed for fistulae resulting from the common cryptoglandular perianal abscess, should be avoided in CD as the wound edges heal very slowly or not at

all.

Slide34

Extraintestinal manifestations of Crohn’s disease

●

Related to disease activity

Erythema nodosum

Pyoderma gangrenosum

Arthropathy

Eye complications (iritis/uveitis)

Aphthous ulceration

Amyloidosis

●

Unrelated to disease activity

Gallstones

Renal calculi

Primary sclerosing cholangitis

Chronic active hepatitis

Sacroiliitis

Slide35

Differences between ulcerative colitis (UC)

and Crohn’s

disease (CD)

●

UC affects the colon; CD can affect any part of

the gastrointestinal

tract, but particularly the small and

large bowel

●

UC is a mucosal disease, whereas CD affects the

full thickness

of the bowel wall

●

UC produces confluent disease in the colon and

rectum, whereas

CD is characterised by skip lesions

●

CD more commonly causes stricturing and fistulation

●

Granulomas may be found on histology in CD, but not in UC

●

CD is often associated with perianal disease, whereas this

is unusual

in UC

●

CD affecting the terminal ileum may produce

symptoms mimicking

appendicitis, but this does not occur in UC

●

Resection of the colon and rectum cures the patient with

UC, whereas

recurrence is common after resection in CD

Slide36

INFECTIVE ENTERITIS

Campylobacteriosis

Infection with Campylobacter jejuni (a gram-negative rod

with a distinctive spiral shape) is the most common form of bacterial gastroenteritis

in the UK, typically acquired from

eating infected

poultry.

It

causes diarrhoea and abdominal pain

and may

mimic an acute abdomen.

Severe

cases may

resemble UC

, with rectal bleeding and colorectal ulceration,

causing diagnostic

difficulty.

The

organism is very sensitive and

may take

several days to isolate on stool culture.

Toxic dilatation and

even disintegrative colitis have rarely been reported

to occur

.

Treatment

is generally supportive as the condition

usually resolves

without antibiotics.

It

is a notifiable disease

.

Slide37

Yersiniosis

Yersinia enterocolitica is a gram-negative rod that can infect the terminal ileum, appendix, ascending colon and mesenteric lymph nodes, and can cause a granulomatous

inflammatory process

that mimics CD.

Yersinia

typically causes a fever and gastroenteritis, but may persist and cause a terminal ileitis, which, on occasion, may perforate.

The diagnosis may

be made on stool culture, but is more often confirmed serologically

.

If discovered at laparotomy, the terminal ileum and mesenteric nodes will look thickened and inflamed and

a lymph

node biopsy can be taken for diagnostic purposes.

The

disease is normally self-limiting, but responds to treatment with cotrimoxazole or chloramphenicol.

Slide38

Salmonellosis, typhoid

and paratyphoid

Salmonella are a family of gram-negative rods that can

cause a

range of enteric infections.

Salmonella

gastroenteritis is

typically caused

by S. enteritidis from poultry, and is most

often a

self-limiting illness comprising headache, fever and

watery diarrhoea

.

When

severe,

antibiotics, hospitalisation and intravenous

fluids may be needed.

The

diagnosis is based

on stool

culture.

Shigella

and enteropathogenic strains of E.

coli may

cause similar diarrhoeal illnesses.

Typhoid fever is caused by S. typhi and presents with

fever and

abdominal pain after an incubation period of 10–20

days.

Over

the next week, the patient can develop distension,

diarrhoea, splenomegaly

and characteristic ‘rose spots’ on

the abdomen

caused by a vasculitis.

Typhoid

is a systemic

infection and

diagnosis of typhoid is confirmed by culture of

blood or

stool.

Treatment

is by antibiotics, usually chloramphenicol.

A number of surgical complications can result, including

paralytic ileus

, intestinal haemorrhage, free ileal perforation

and cholecystitis

.

Slide39

I

nvasion

of the systemic circulation,

which is

a characteristic feature of salmonellosis, may cause

severe gram-negative

sepsis, resulting in septic shock.

Some patients develop

metastatic sepsis, including septic arthritis and

osteomyelitis, meningitis

, encephalitis, disseminated

intravascular coagulation

and pancreatitis.

Perforation of a typhoid ulcer characteristically

occurs during

the third week of the illness, although it is

sometimes the

first clinical sign of the disease.

The

ulcer is parallel

to the

long axis of the gut and is usually situated in the

distal ileum

.

Perforation

requires surgery to wash out and close

the ulcer

and intestinal resection is usually avoided.

In unstable patients

, notably with evidence of septic shock, the

bowel should

be exteriorised and the perforation closed after

recovery.

Paratyphoid

infection (with S. paratyphi)

resembles typhoid

fever and is treated in a similar manner.

Slide40

Tuberculosis of the intestine

Tuberculosis,

can

affect any part of the gastrointestinal tract from the mouth to the anus.

The

sites affected most often are the ileum, proximal colon and peritoneum.

The disease presented as

;

Ulcerative tuberculosis

Ulcerative tuberculosis develops secondary to pulmonary tuberculosis and arises as a result of swallowing tubercle bacilli.

Multiple

ulcers, lying transversely,

in

the

terminal ileum

and the overlying serosa is thickened, reddened and covered in tubercles.

Patients

typically present with diarrhoea and weight loss, although subacute obstruction

and even

local perforation and fistula formation can occur.

A

barium follow-through or CT examination fails to show filling of the lower ileum, caecum and the ascending colon as a

result of

narrowing of the ulcerated

segment.

A

course of antituberculous chemotherapy usually leads to cure, provided the pulmonary tuberculosis is adequately treated.

Surgery

is usually undertaken only in the rare event of a perforation or complete intestinal obstruction.

Slide41

Hyperplastic

tuberculosis

This is caused by the ingestion of Mycobacterium

tuberculosis by

patients with a high resistance to the organism.

The infection usually

occurs in the ileocaecal region, although

solitary and

multiple lesions in the lower ileum are also

sometimes seen

.

The

infection establishes itself in lymphoid

follicles, and

the resulting chronic inflammation causes thickening

of the

intestinal wall and narrowing of the lumen.

There

is

early involvement

of the regional lymph nodes, which may

caseate.

A

bscess

and fistula formation are rare.

Patients usually present with attacks of abdominal

pain and

intermittent diarrhoea.

There

is incomplete ileal

obstruction, leading

to stasis and bacterial overgrowth.

This

in

turn causes

steatorrhoea, anaemia and loss of weight.

Patients may present

with a mass in the right iliac fossa and vague ill health.

The differential diagnosis is that of an appendix mass,

lymphoma, carcinoma

of the caecum, CD, tuberculosis or actinomycosis

.

Slide42

A barium follow-through or small bowel

enema will

show a long narrow filling defect in the terminal

ileum.

CT will also

demonstrate the narrowed segment with proximal

distension and

the associated lymphadenopathy.

When

the

diagnosis is

clear and the patient has not yet developed

obstructive symptoms

, treatment with chemotherapy is advised and

may be

curative.

Where

obstruction is present, or the possibility

of CD

or lymphoma require clarification, ileocaecal resection

is often

required.

Slide43

Actinomycosis

Abdominal actinomycosis is rare.

It is caused by infection with Actinomyces israelii and infection usually develops several weeks after an apparently straightforward perforated appendicitis.

An

abscess develops and spreads to the retroperitoneal tissues and the adjacent abdominal wall, eventually becoming the seat of multiple indurated discharging sinuses.

At

first,

the discharge

from the sinuses is thin, watery and inoffensive, but it may later become thicker and malodorous.

Secondary

fistulation may occur and the tissues may become

extensively indurated

and woody.

M

esenteric

lymph nodes are not involved and the lumen of the intestine is not narrowed.

Haematogenous

spread via

the portal

vein may lead to multiple liver abscesses.

Pus should be sent for bacteriological examination, which will reveal the characteristic sulphur granules.

Penicillin

or cotrimoxazole treatment is required and should be

prolonged and

in high dosage.

Slide44

Human immunodeficiency virus

Human immunodeficiency virus (HIV) infection is

associated with

a number of proctological

problems.

Intestinal

complications are common

after the

development of AIDS when opportunistic organisms

can cause gastroenteritis.

HIV

may

also cause

a specific enteropathy.

Treatment

is directed towards

the relevant

organism and surgery should be avoided if possible.

Opportunistic

intestinal infections in patients with AIDS

●

Bacteria

Salmonella

Shigella

Yersinia

Campylobacter

Mycobacterium avium intracellulare (MAI)

●

Viral

Cytomegalovirus

●

Protozoa

Cryptosporidium

Giardia

●

Fungal

Candida albicans

Slide45

TUMOURS OF THE

SMALL INTESTINE

Small bowel tumours are rare and in total account for

less than

10% of gastrointestinal neoplasia

.

Benign

The majority of small bowel neoplasms are benign,

comprising adenomas

, lipomas, haemangiomas and neurogenic

tumours.

They

are frequently asymptomatic and identified

incidentally, but

can present with intussusception, small bowel

obstruction and

bleeding that may cause anaemia or may even be

overt.

Where

these lesions do cause anaemia, the cause can be

difficult to

diagnose, as CT or small bowel contrast studies do

not show

them easily.

Capsule

endoscopy or small bowel

endoscopy has

been used successfully where the facilities exist.

Symptomatic lesions can be treated by small bowel

resection and

anastomosis

.

Slide46

Peutz–Jeghers syndrome

This is an autosomal dominant disease characterised by melanosis of the mouth and lips, with multiple hamartomatous

polyps

in the small bowel and

colon.

Melanin

spots can also occur on the digits and perianal skin.

The

gene STK11 on chromosome 19 has been found in a proportion of patients with this condition.

Long-term

follow-up of the original family described by Peutz has shown reduced survival as a consequence of complications of bowel obstruction and the development of a range of cancers

.

Slide47

It is logical to perform regular colonic surveillance and encourage female patients to attend breast and cervical screening.

Despite the increased risk of malignancy in general, malignant change in the polyps themselves rarely occurs and the polyps can be left alone unless they are the cause of symptoms.

Resection may be indicated, however, for heavy and persistent or recurrent bleeding or intussusception.

Polyps may be removed by enterotomy or, at laparotomy, snared via a colonoscope introduced via an enterotomy.

Heavily involved segments of small intestine may occasionally be resected.

Slide48

Malignant

Small bowel malignancy is rare and classically presents

late, most

often diagnosed after surgery for small bowel

obstruction.

Four

types will be considered, which account for

over 99

% of small bowel malignancies:

Adenocarcinoma

C

arcinoid tumours

L

ymphomas

M

esenchymal

tumours (

gastrointestinal stromal

tumours [

GIST]

Adenocarcinoma

Small

bowel adenocarcinoma is more often found in the

jejunum than

the ileum and although the aetiology is

unknown, it

is more common in patients with CD, coeliac disease,

familial adenomatous

polyposis, hereditary non-polyposis

colon cancer

and Peutz–Jeghers syndrome.

Slide49

The tumours

present

with anaemia, overt gastrointestinal bleeding, intussusception or obstruction.

Prognosis

is poor, particularly in patients with CD, in whom these tumours often present late, because the symptoms are commonly mistaken for those of CD and treated conservatively.

When suspected, the advised surgical

treatment

is a resection of 5 cm of non-involved bowel either side of the lesion and the affected mesentery.

A right hemicolectomy is likely to be required for tumours of the distal ileum.

Slide50

Carcinoid tumours

These

neuroendocrine tumours

occur throughout the gastrointestinal tract, most commonly in the appendix, ileum and rectum in decreasing order of frequency.

Appendicular carcinoid tumours

are commonly noted as an incidental finding at appendicectomy, and are said to occur in approximately 2% of appendices removed surgically.

The

tumour arises from Kulchitsky cells at the base of intestinal crypts (of Lieberkuhn).

The

primary is usually small, although

significant lymph

node metastases can occur.

In

up to one-third of cases of small bowel carcinoids, the tumours are multiple.

They may

produce dense fibrosis in the surrounding tissues, resulting in distortion and scarring of the bowel and associated mesentery, giving them a characteristic radiological appearance.

Slide51

Carcinoid

tumours can produce a number of

vasoactive peptides

, most commonly 5-hydroxytryptamine (serotonin

), but

also histamine, prostaglandins and kallikrein.

When they metastasise

to the liver, the ‘carcinoid

syndrome’ can become evident

, because the vasoactive substances escape the

filtering actions

of the liver.

The

clinical syndrome itself

consists of

reddish-blue cyanosis, flushing attacks, diarrhoea,

borborygmi, asthmatic

attacks and, eventually, pulmonary

and tricuspid stenosis.

Slide52

Classically, the flushing attacks are induced by alcohol.

Surgical resection is usually sufficient for patients with primary disease, but the incidence of recurrence is significant.

The extent of disease can be assessed preoperatively using

octreotide scanning

, which may detect otherwise clinically unapparent primary and secondary tumours.

Plasma markers of tumour bulk, such as

chromogranin A

concentrations, may be useful markers of disease recurrence, as well as of prognostic value.

Slide53

Hepatic resection can be carried out in patients with metastatic disease.

The

treatment

has been transformed by the use of octreotide (a somatostatin analogue), which

reduces both

flushing and diarrhoea, and octreotide cover is usually used in patients with a carcinoid syndrome who have surgery to prevent a carcinoid crisis resulting from liberation

of vasoactive

substances following handling of the tumour.

Carcinoid

tumours generally grow more slowly than most metastatic malignancies and patients may live with the syndrome of metastatic disease for many years.

They

are not usually sensitive to chemo- or radiotherapy

Slide54

Lymphoma

primary or, secondary

The

incidence

is

increased in patients with CD and

immunodeficiency syndromes

.

It

is rare for Hodgkin’s lymphoma

to affect

the small bowel and most western-type lymphomas

are

non-Hodgkin’s

B-cell lymphomas.

They

usually present

with anaemia

, bleeding, perforation, anorexia and weight loss

.

T-cell lymphoma

develops in patients with coeliac

disease.

It

usually presents with worsening of the patient’s

diarrhoea, pyrexia

of unknown origin and local obstructive

symptoms.

Mediterranean

lymphoma

is found mostly in North

Africa and

the Middle East and is often widespread at

diagnosis.

Burkitt’s

lymphoma

can aggressively affect the

ileocaecal region

, particularly in children

.

The

treatment

for

these conditions is chemotherapy; however, surgery

may be

required for obstruction, perforation or bleeding.

Slide55

Gastrointestinal stromal

tumours (

GISTs)

A

re mesenchymal tumours

and the distinction between benign or

malignant types

is difficult even on histological examination

.

Increased size

and high levels of c-kit (CD117) staining are

associated with

malignant potential.

GISTs

are found most

commonly in

the stomach, but can be found in other parts of the gut.

They occur most commonly in the 50- to 70-year age

group.

Although

the cause is unknown, patients with

neurofibromatosis have

an increased risk of developing these

types of

tumour.

Patients

may be asymptomatic and the

tumour may

present as an incidental mass on a CT scan.

Symptoms include

lethargy, pain, nausea, haematemesis or melaena.

Surgery

is

the most effective way of treating GISTs, as the

tumour is

radioresistant and is not sensitive to conventional

chemotherapy.

Glivec

® (imatinib) is a tyrosine kinase inhibitor

that has

been shown to be effective in advanced cases and

may also

have a role in adjuvant treatment

.

Slide56

CONNECTIVE TISSUE DISORDERS

Intestinal diverticulae

Diverticulae (hollow out-pouchings) are a common structural abnormality that can occur from the oesophagus to the rectosigmoid junction (but not usually in the rectum).

Small

bowel diverticulae may be congenital or acquired.

Congenital diverticulae

A

ll

three coats of the bowel are present in the wall of

the diverticulum

(e.g. Meckel’s diverticulum

).

Acquired diverticulae

These

develop

in the jejunum and arise from the mesenteric side of the bowel as a result of mucosal herniation at the point of entry of the blood vessels.

There

is thus no muscularis layer present in the wall.

Jejunal

diverticulae can vary in size and are frequently multiple.

They

are commonly asymptomatic and present as an incidental finding at surgery or on radiological

imaging.

However

, they can result in malabsorption, as a result of bacterial stasis, or present as an acute abdominal emergency if they become inflamed or perforate.

Bleeding

from a jejunal diverticulum is a rare complication (compared with sigmoid diverticular disease).

Slide57

Elective

resection of an affected small bowel

segment that

is causing malabsorption can be effective, provided

there is

only a limited amount of jejunum affected by the

condition.

If

perforated jejunal diverticulitis is found at

emergency laparotomy

, a small bowel resection should be performed

and a

decision made between anastomosis and stoma

formation.

This

will depend on the degree of contamination,

physiological stability

and local resources for managing a patient with

a high

output

jejunostomy.

Complications

resulting from extensive jejunal

diverticulosis can

be extremely difficult to treat.

In

severe cases,

much of

the proximal small intestine may be involved,

effectively precluding

resection.

Prolonged

antibiotic therapy for

bacterial overgrowth

may be preferable, and antibiotics (

metronidazole, ciprofloxacin

, rifaximin) are frequently rotated in

an attempt

to avoid the development of antibiotic

resistance.

.

Slide58

Meckel’s diverticulum

A Meckel’s diverticulum is a persistent remnant of the

vitellointestinal duct

and is present in about 2% of the

population.

It

is found on the antimesenteric side of the ileum,

commonly approximately

60 cm from the ileocaecal valve and is

classically 5

cm

long.

A

Meckel’s diverticulum

is a

congenital diverticulum.

It

contains all three coats of

the bowel

wall and has its own blood supply.

It

may be

vulnerable to

obstruction and inflammation in the same way as

the appendix

; indeed, when a normal appendix is found at

surgery for

suspected appendicitis, a Meckel’s diverticulum

should be

looked for by examining the small bowel, particularly

if free

fluid or pus is found

.

In approximately 20% of cases,

the mucosa

of a Meckel’s diverticulum contains heterotopic

epithelium of

gastric, colonic or pancreatic type.

The presence of

heterotopic mucosa may predispose to the development

of complications

.

The

vast majority of Meckel’s diverticulae

are asymptomatic

and Meckel’s diverticulum is notoriously

difficult to

see with contrast radiology

.

Slide59

Meckel’s diverticulum may, however, present clinically in the following ways:

●

Haemorrhage

. If gastric mucosa is present, peptic ulceration can occur and present as painless dark rectal bleeding or melaena. If the stomach, duodenum and colon are excluded as a source of bleeding by endoscopy, radioisotope scanning with technetium-99m may demonstrate aMeckel’s diverticulum.

●

Diverticulitis

. Meckel’s diverticulitis presents like appendicitis, although if perforation occurs the presentation may resemble a perforated duodenal ulcer.

●

Intussusception.

A Meckel’s diverticulum can be the lead point for ileoileal or ileocolic intussusception.

●

Chronic ulceration

. Pain is felt around the umbilicus, as the site of the diverticulum is midgut in origin.

●

Perforation

.

When

found in the course of abdominal surgery, a Meckel’s diverticulum can safely be left alone, provided it has

a wide

mouth and is not thickened. When there is doubt, it can be resected. The finding of a Meckel’s diverticulum in an inguinal or femoral hernia has been described as ‘Littre’s hernia’.

Slide60

Meckel’s

diverticulectomy

A broad-based Meckel’s diverticulum should not

be amputated at

its base and invaginated (as for an appendix

), as

there is the risk of stricture and of leaving heterotopic

epithelium behind

.

It

is safer simply to excise the

diverticulum, either

by resecting it and suturing the defect at its base,

or with

a linear stapler-cutter.

If

the base of the diverticulum

is indurated

, it is on balance more logical to perform a

limited small

bowel resection of the involved segment followed

by an

anastomosis.

Slide61

VASCULAR ANOMALIES OF

THE INTESTINE

Mesenteric ischaemia

Classified to;

A

cute intestinal ischaemia

– with or without

venous occlusion

Chronic arterial ischaemia, central

or peripheral.

The

superior mesenteric

vessels

A

re

the visceral vessels most likely to be affected by

embolisation or

thrombosis, with the former being most common.

Occlusion at the origin of the superior mesenteric

artery (SMA

) is almost invariably the result of thrombosis,

whereas emboli

tend to lodge at the origin of the middle colic

artery.

Inferior

mesenteric

vessels

I

nvolvement

is usually clinically

silent because

the collateral circulation is better

.

Slide62

Possible sources for embolisation of the SMA

include;

T

he

left atrium in atrial fibrillation,

T

he

left ventricle after mural myocardial infarction,

V

egetations

on mitral and aortic valves associated with endocarditis

A

theromatous

plaque from an aortic aneurysm.

Primary thrombosis is associated with atherosclerosis and vasculitides, including conditions such as thromboangitis obliterans and polyarteritis nodosa.

Primary

thrombosis of the superior mesenteric veins may occur in association

with;

F

actor V Leiden

P

ortal hypertension

P

ortal pyaemia

S

ickle cell disease

W

omen taking the oral contraceptive pill.

A specific form of ‘non-occlusive mesenteric ischaemia’ may complicate critical illness, possibly due to alterations in splanchnic blood flow

.

Slide63

Irrespective of whether the occlusion is arterial or

venous, haemorrhagic

infarction occurs.

The

mucosa is

especially sensitive

to ischaemic injury because of its high

metabolic activity

.

The

intestine and its mesentery become

swollen and

oedematous, especially with venous occlusion.

Bloodstained fluid

exudes into the peritoneal cavity and

bowel lumen

.

The

changes develop rapidly and irreversible

injury, ranging

in severity from mucosal necrosis and sloughing,

to full-thickness infarction

usually occurs within a few hours

at most.

If the main trunk of the SMA is involved, the

infarction usually

covers an area from just distal to the DJ

flexure to

the splenic flexure.

Usually

, a branch of the main trunk

is implicated

and the area of infarction is less.

Slide64

Clinical

features

S

udden

onset of severe

abdominal

pain in a patient with atrial fibrillation or atherosclerosis.

The pain is

typically in the central

abdomen.

Persistent

vomiting and defaecation occur early, with the subsequent passage of altered blood.

Abdominal tenderness may be mild initially, with rigidity being a late feature.

Shock

, with features of both hypovolaemia and sepsis, rapidly ensues.

Investigation

A

profound neutrophil leucocytosis

A

bsence

of gas in the lumen of the thickened small intestine on abdominal radiographs

and

CT scans.

Gas

may be present within the intestinal wall and occasionally in the mesenteric and portal veins.

Slide65

Treatment

F

ull resuscitation

L

aparotomy

with embolectomy

via the

ileocolic artery or revascularisation of the SMA by

vascular bypass

may be considered in early cases.

Anticoagulation should

be implemented early in the postoperative

period.

However

, the condition is usually diagnosed late in the

disease process

and the mortality rate is extremely high.

In

the

young, all

affected bowel should be resected, whereas in the elderly

situation

may

be incurable

.

After

extensive enterectomy, it is usual for patients

to require

intravenous alimentation.

The

young, however,

may sometimes

develop sufficient intestinal digestive and

absorptive function

to lead relatively normal lives.

In

selected

cases, consideration

may be given to small bowel transplantation

.

Slide66

Chronic small intestinal ischaemia

A

lmost

invariably results from atherosclerosis and affects the proximal superior mesenteric and coeliac vessels.

Patients

classically present with symptoms of severe central abdominal pain that comes on within 30–60 minutes of eating (mesenteric angina).

Weight

loss and diarrhoea due to malabsorption may also occur.

The

condition may be difficult to diagnose and is often overlooked initially, the symptoms being mistaken for those of peptic ulcer disease or irritable bowel syndrome.

The

presence of significant vascular disease on visceral angiography is common in elderly patients and in those with severe vascular

disease, and

should not necessarily be assumed to indicate that abdominal symptoms are attributable to chronic ischaemia.

Treatment

By

selective visceral angiography, with

stenting/angioplasty

If not

possible

, so

bypass surgery.

Smoking

cessation in

imperative.

P

atients

are usually anticoagulated.

Slide67

STOMAS

A colostomy (or ileostomy)

stoma;

I

s

an artificial

opening made

in the colon (or small intestine) to divert faeces

and flatus

out-side the abdomen where they can be collected

in an

external appliance.

A

stoma may

be;

Temporary

Permanent

Loop ileostomy

;

I

s often used

for defunctioning a low

rectal anastomosis

or an ileal pouch.

A

knuckle of ileum is exterio-rised through a skin trephine in the right iliac fossa.

An incision is

made in the distal part of the knuckle, and this is

then pulled

over the top of the more proximal part to create a

spout on

the proximal side of the loop with a flush distal side

still in

continuity

.

Slide68

This allows near perfect defunctioning, but also the possibility of restoration of continuity, by taking down the spout and reanastomosing the partially divided ileum.

The advantages of a loop ileostomy over a loop colostomy are the ease with which the bowel can be brought to the surface and the relative absence of odour.

Care

is needed when the ileostomy is closed, so that suture line obstruction does not occur.

Closure

of a loop ileostomy can be a technically challenging procedure, particularly if there are dense adhesions resulting from previous surgery.

Slide69

End ileostomy

Is

formed after a subtotal colectomy without anastomosis, when it may later be reversed, or may be permanent after a panproctocolectomy.

The

ileum is

normally brought

through the rectus abdominis muscle.

Careful

attention to the terminal ileal mesentery should be taken to ensure that it is not too bulky.

The

use of a spout was

should project some 2–4 cm from the skin

surface.

A

disposable appliance is placed over the ileostomy so that it is a snug fit at skin level.

Slide70

There may be an ‘ileostomy flux’ while the ileum adapts to the loss of the colon.

A

consistent ileostomy output in excess of 1.5 litres is usually associated with dehydration and sodium depletion in the absence of intravenous therapy.

The

stools thicken in a few weeks and are semisolid in a few months.

The help and

advice of the stoma care nurse specialist are essential.

Modern

appliances have transformed stoma care, and skin problems are

unusual.

Stoma

bags and appliances

Stoma output is collected in disposable adhesive bags.

Ileostomy appliances tend to be drainable bags, which are leftin place for 48 hours, while colostomy appliances are simply changed two or three times each day.

A wide range of such bags is currently available.

Many now incorporate an adhesive backing, which can be left in place for several days.

In most hospitals, a stoma care service is available to offer advice to patients

Slide71

Stoma complications

● Skin

irritation ●

Prolapse

●

Retraction ●

Ischaemia

●

Stenosis ●

Parastomal hernia

●

Bleeding ●

Fistulation

Complications

of

stomas are common.

On

occasion,

require

surgical

revision.

Sometimes

, this can be achieved with an incision

immediately around

the stoma, but on occasion reopening the

abdomen and

freeing up the stoma may be necessary.

Repair of parastomal

hernias is particularly technically challenging

and the

recurrence rate is high.

Simple

suture of the

parastomal hernia

is associated with an almost 100% risk of

recurrence and it may need to either;

T

ransfer

to the opposite side of the

abdomen

.

I

nsertion of

a piece of prosthetic material within the abdominal

wall around

the stoma may be necessary

.

Slide72

CONDITIONS

CAUSING MALABSORPTION

Coeliac

disease

I

s

the most common cause of

malabsorption in

the UK with a stated prevalence of

1:1800.

It is characterised by a

hypertrophic small

bowel mucosa with atrophic villi and deep crypts.

It is thought

that the loss of surface area and brush border

enzymes results

in malabsorption.

I

s

caused by an abnormal immune

response to gluten.

There

is a genetic component, as the

disease is

more common in first-degree relatives and has an

association with

HLA B8.

In

children, coeliac disease presents

with steatorrhoea

and growth retardation.

In

adults, it may

result in

diarrhoea and weight loss but many patients simply

present with

an iron deficiency anaemia

.

Slide73

Some patients develop a characteristic skin rash (dermatitis herpetiformis)

The

diagnosis is usually made after an endoscopic duodenal biopsy allows pathological examination of mucosa.

The

antiendomysial antibody tests have a very high sensitivity and specificity for coeliac disease, but a duodenal biopsy is usually indicated to confirm the diagnosis.

The

biopsy usually shows flattening of the mucosa, marked inflammatory changes and characteristic findings of intraepithelial lymphocytes.

Patients

with coeliac disease may develop an acute inflammatory condition of the small intestine (ulcerative jejunoileitis) and have an increased risk of small bowel

lymphoma and

adenocarcinoma.

The

main treatment for coeliac disease is the

withdrawal of

gluten from the diet by avoiding wheat, rye and barley.

Surgery

does not usually play a role in the management of coeliac disease and is primarily reserved for resection of malignancy

.

Slide74

Bacterial overgrowth

The

small intestine can become colonised with bacteria

normally confined

to the colon if there is stasis resulting in

delayed bacterial

clearance (blind loop

syndrome).

Similar complications may result from chronic small

bowel obstruction

, jejunal diverticulosis and ileosigmoid

fistulation.

If

overgrowth occurs in the upper small

intestine, the

defect is chiefly of fat absorption; if in the lower

intestine, there

is vitamin B12 deficiency.

There

is usually

relatively little

effect on carbohydrate or protein metabolism.

Stasis results

in an abnormal bacterial flora, which prevents

adequate breakdown

of

fat.

Sometimes

, the only manifestation

is anaemia

, resulting from vitamin B12 deficiency but, if

steatorrhoea occurs

, other serious malabsorption features may

follow, including

glossitis, osteomalacia, paraesthesia and

peripheral neuropathy

.

Improvement normally follows after intermittent

therapy with

oral antibiotics; metronidazole, ciprofloxacin,

tetracycline and

rifaximin are commonly used.

Definitive treatment is

surgical when the anatomical abnormality can be

corrected, but

this is not always possible.

Slide75

ENTEROCUTANEOUS FISTULA

An abnormal connection between the small intestine and

the skin

can occur as a result of fistulating CD, radiotherapy

or abdominal

trauma, but the condition most commonly

follows a

surgical complication – either a leak from an anastomosis

or an

inadvertent enterotomy during dissection.

At

least 50%

of small

bowel enterocutaneous fistulae develop after surgery

in which

no small bowel has been resected, as a result of injury

to the

intestine following division of adhesions.

The

frequency

of this

complication has been shown to increase with the number

of

previous laparotomies.

Management

of patients

with enterocutaneous

fistulae can be very challenging,

especially when

the fistula output is high (usually defined as >500

mL of

effluent/day).

The

majority of fistulae can be expected

to heal

spontaneously, provided there is no distal obstruction

or disease

at the fistula site.

Reasons

for failure of

spontaneous healing

also include epithelial continuity between the

gut and

the skin and an associated complex abscess.

Slide76

The management of fistulas

An

early return to theatre to try and treat the problem definitively in a septic, malnourished patient is doomed to failure.

Infected

collections are best identified at

CT

and can be drained percutaneously.

Skin

protection is important, as small bowel effluent is caustic.

Nutritional

support must include fluid and electrolytes, which can be

lost in

high quantities from a proximal fistula, as well as carbohydrates, protein, fat

and vitamins

.

Judgements

have to be made between enteral and parenteral feeding – enteral feeding

has advantages

but if the fistula is proximal or high output,

total parenteral

nutrition will be

required.

Defining

anatomy is best done after

a

sequence of contrast studies (follow-through, fistulogram and enema) may well be required to define bowel length and plan a surgical strategy.

Surgery

can be extremely technically demanding, and an anastomosis should not be fashioned in the presence of continuing intra-abdominal sepsis or when the patient is hypoalbuminaemic (<32 g/dL).

Slide77

SHORT BOWEL SYNDROME

Intractable diarrhoea with impaired absorption of

nutrients following

resection or bypass of the small intestine,

ultimately leading

to progressive malnutrition, is referred to

as ‘short

bowel syndrome’.

The

most common causes of

short bowel

syndrome

are;

R

esection

resulting from the

management of

CD and its complications (which accounts for almost

half of

cases

)

M

esenteric

vascular

thrombosis

R

adiation enteritis

Tumours

The

features

are usually appear

when there is less than 200 cm of small

bowel length

and nature of the remaining

intestine.

In general, diseases which result in short bowel

syndrome tend

to preferentially affect the distal small

intestine, and

there is some evidence that the ileum, with its

tighter intercellular

junctions and consequently better fluid

absorptive capacity

, can assume the functions of a missing

jejunum, but

not vice versa

.

Slide78

T

he

ileocaecal valve used to be considered important with regard to preservation of absorptive

function, of the distal ileum and right colon.

Patients

with an intact colon are relatively protected

from the

effects of massive small bowel resection because of the ability of the colon to absorb not only fluid and electrolytes, but a modest amount of nutrient energy.

Patients

with as

little as

100–200 cm of jejunum anastomosed to an intact colon may therefore be able to maintain satisfactory macronutrient, fluid and electrolyte status, although they will, of course, be

at risk

of fat-soluble and B12 vitamin deficiencies and will also generally need oral nutritional supplements of trace elements, vitamins and minerals.

Some

(but not all) patients with50–100 cm of small intestine and an intact colon will need long-term parenteral nutrition, as will almost all patients with 50 cm or less of jejunum anastomosed to an intact colon.

In

contrast, most patients with less than 200 cm of small intestine ending in a jejunostomy will require regular infusions of parenteral fluid and electrolytes, and almost all of those with less than 100 cm of small bowel ending in a jejunostomy will require long-term parenteral nutrition

.

Slide79

Medical

management

The

use of antidiarrhoeal agents (

loperamide and

codeine phosphate), drugs to reduce diarrhoea

related to

bile-salt malabsorption

and enteral, parenteral vitamin

and trace element supplements.

Although there

has also been interest in the use of drugs to

promote intestinal

adaptation, such as growth hormone,

glutamine and

, most recently, glucagon-like peptide 2 agonists, the

mainstay of

treatment for short bowel

syndrome.

H

ome parenteral nutrition

(HPN

)

is, however, expensive and

demanding.

The patients

with short bowel syndrome receiving HPN are at

risk from

catheter-related complications

(sepsis

and occlusion), as well as

metabolic

complications

(fibrotic

liver disease, gallstones, metabolic bone disease

and kidney

stones).

Slide80

Surgical

treatment

procedures

designed to improve the surface area or reduce the speed of transit of the remaining small intestine (and thus improve absorptive capacity) have shown some promise in children, but their place in managing adults with established short bowel syndrome is currently unclear.

In

some patients, the loss of venous access resulting from the complications of long-term intravenous feeding or the development of progressive liver dysfunction may represent indications for

small bowel transplantation

.

The

results of small bowel transplantation have progressively improved and 5-year patient survival now exceeds 80% in some centres.

Slide81

Quiz 1

In

patients with short bowel syndrome

receiving Home

parenteral nutrition

(HPN)

are at risk

of metabolic and catheter-related complications. Enumerate these complications.

Slide82

The large

intestine

ANATOMY

OF THE

LARGE INTESTINE

The large intestine begins at the ileocaecal valve and

extends to

the anus.

It

is divided into the caecum, ascending

colon, hepatic

flexure, transverse colon with attached greater

omentum, splenic

flexure, descending colon, sigmoid and

rectum.

The

large intestine is approximately 1.5 m long, but can

be straightened

at endoscopy so the caecum can be reached

with 70

cm of colonoscope.

The

colon is distinguished from the small bowel by

having fat-filled

peritoneal tags known as appendices

epiploicaem and

the taenia coli.

These

are three flat bands of

longitudinal muscle

that run from the appendix base to the

rectosigmoid junction

.

Slide83

They act to pull the colon into its sacculated state,producing a series of haustrations.

Distended

small and large intestine can be distinguished on an abdominal radiograph as the small bowel has complete transverse markings caused by the valvulae conniventes, while the colon has incomplete lines from the sacculation caused by the taeniae.

The

important posterior relations of the caecum and ascending colon are the right ureter, right gonadal vessels and

duodenum and

these must be protected at surgery.

The

left ureter, left gonadal vessels and tail of the pancreas must be protected when operating on the left colon.

The

blood supply of the large intestine is derived from branches of the superior mesenteric artery from the

caecum to

the distal transverse colon and the inferior mesenteric artery and its branches more distally.

Adjacent

branches anastomose so there is usually a complete vascular supply along the colon, named the marginal

artery.

Slide84

This vessel is often the key blood supply to the

vascular arcades

, ensuring adequate perfusion of a colonic

anastomosis, but

blood flow in the ‘watershed’ area of the

splenic flexure

representing the junction between the superior

and inferior

mesenteric supply may be tenuous.

Sudden occlusion of

the inferior mesenteric artery may leave the area

of the

splenic flexure poorly perfused, leading to an

ischaemic colitis

.

Venous

and lymphatic drainage of the colon

follows the

arterial supply and venous drainage is into the

portal system

.

High

ligation of the artery supplying a segment

of colon

will therefore also remove the draining lymph

nodes, a

key technical point in cancer surgery.

The

nerve

supply to

the large intestine is derived from the splanchnic

nerves via

a dense sympathetic plexus surrounding the superior

and inferior

mesenteric arteries.

Visceral

pain from the part

of the

colon supplied by the superior mesenteric artery is

thus felt

, like that of the small intestine, in the

periumbilical region

, while pain from the colon distal to that point is

felt suprapubically

.

Slide85

PHYSIOLOGY OF THE LARGE INTESTINE

The principle function of the colon is absorption of water; 1000 mL of ileal content enters the caecum every 24 hours, of which only approximately 200 mL is excreted as faeces.

Sodium

absorption is

by

an active transport system, while chloride and water are absorbed passively.

Fermentation

of dietary fibre in the colon by the normal colonic microflora leads to the generation of short chain fatty acids, which are an important metabolic fuel for the colonic mucosa.

Diversion

of the faecal stream may lead to inflammatory changes in the colon downstream (diversion colitis).

Absorption

of nutrients including glucose, fatty

acids, amino

acids and

vitamins.

Colonic

motility is variable.

In

general, faecal residue reaches the caecum 4 hours after a meal and the rectum after 24 hours.

Passage

of stool is not orderly because of mixing within the colon, so it is not uncommon for residue from a single meal to still be passed 4 days later

.

Slide86

TUMOURS OF THE

LARGE INTESTINE

Benign

The

‘

polyp’

is

any protrusion

of the

mucosa

.

Polyps

can

occur;

S

ingly

Small

numbers

A polyposis syndrome

Adenomatous

polyps

A

tubular

adenoma

T

he

villous

adenoma

A

flat spreading

lesion

Villous

tumours can cause

diarrhoea, mucus

discharge and, occasionally hypokalaemia and

hypoalbuminaemia.

The

risk of malignancy developing in an

adenoma increases

with size; there is a 10% risk of cancer in

a 1-cm

diameter tubular adenoma, whereas almost one-third

of large

(>3 cm) colonic adenomas will have an area of

invasive malignancy

within them.

Slide87

Adenomas larger than 5 mm in diameter are usually excised because of their malignant potential.

Snare

polypectomy is usually possible for

colonic polyps

but larger sessile polyps may require endoscopic mucosal resection after infiltration of a solution containing dilute adrenaline

.

Larger rectal adenomas may require transanal resection or, where the adenoma is too high, transanal endoscopic microsurgery or resection via transanal placement of laparoscopic instruments.

Extensive

villous lesions of the rectum may require argon beam ablation when the patient is frail but symptomatic.

Slide88

Classification of intestinal polyps.

Inflammatory

Inflammatory polyps (pseudopolyps in UC)

Metaplastic

Metaplastic

or hyperplastic polyps

Hamartomatous

Peutz–Jeghers

polyp

Juvenile

polyp

Neoplastic

Adenoma Tubular

Tubulovillous

Villous

Adenocarcinoma

Carcinoid

tumour

UC,

ulcerative colitis

.

Slide89

Familial adenomatous

polyposis (

FAP)

D

efined clinically by

the presence of more than 100 colorectal adenomas, but is also characterised by duodenal adenomas and

multiple extraintestinal manifestations.

Over

80% of cases come from patients with a positive family history.

The

remainder arise as a result of new mutations in the adenomatous polyposis coli (APC) gene on the short arm of chromosome 5.

FAP

is inherited as an autosomal dominant condition and is consequently equally likely in men and women.

The

lifetime risk of colorectal cancer is 100% in patients with FAP.

FAP

can also 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 spread locally to involve the intestinal mesentery and, although non-metastasising, they may become

unresectable.

Up

to 50% of patients with FAP have congenital hypertrophy of the retinal pigment epithelium (CHRPE), which can be used to screen affected families if genetic testing is unavailable.

Slide90

CLINICAL FEATURES

Polyps are usually visible on sigmoidoscopy by the age of

15 years

and will almost always be visible by the age of 30

years.

Carcinoma

of the large bowel develops 10–20 years after

the onset

of the polyposis

.

If there are no adenomas by the

age of

30 years, FAP is unlikely.

If

the diagnosis is made

during adolescence

, surgery is usually deferred to the age of 17

or 18

years unless symptoms develop.

Malignant

change is

rare before

the age of 20 years

.

Examination of blood

relatives, including

cousins, nephews and nieces, is essential; a

family tree

should be constructed and a register of affected

families maintained.

Referral to a medical geneticist is essential.

If over

100 adenomas are present at colonoscopy, the

diagnosis can

be made

confidently.

Slide91

TREATMENT

The aim of surgery in FAP is to prevent the development of colorectal cancer.

The

surgical options are:

Colectomy

with ileorectal anastomosis (IRA);

Restorative

proctocolectomy with an ileal pouch–anal anastomosis (RPC);

Total

proctectomy and end ileostomy.

The patient is almost always young and likely to prefer to avoid a permanent stoma and so the choice is normally between the first two options.

The

advantage of an IRA is that it avoids the temporary stoma frequently required for an RPC and avoids the potential compromise to sexual function accompanying proctectomy.

It

is also has a lower morbidity and mortality.

However

, the rectum requires regular surveillance

.

Even with optimal surveillance of the rectal remnant, up to 10% of patients will develop invasive malignancy within a 30-year follow up period.

Restorative

proctocolectomy has the advantage of removing the whole colon and rectum

.

Slide92

T

here

is a pouch failure rate of approximately10

%.

In addition, and particularly where a

stapled anastomosis

has been created, there remains a small but

definite incidence

of cancer developing in the small strip of rectal mucosa between the pouch and the dentate line.

Some

advocate

complete mucosectomy of the residual cuff

and a

transanal anastomosis, although this may result in

worse function

.

In

experienced hands a laparoscopic approach

to these

operations can be

successful.

Slide93

Extracolonic manifestations of FAP

●

Endodermal derivatives

Adenomas and carcinomas of the duodenum, stomach, small intestine, thyroid and biliary tree

Fundic gland polyps

Hepatoblastoma

●

Ectodermal derivatives

Epidermoid cysts

Pilomatrixoma

Congenital hypertrophy of the retinal pigment epithelium (CHRPE)

Brain tumours

●

Mesodermal derivatives

Desmoid tumours

Osteomas

Dental problems

Slide94

POSTOPERATIVE SURVEILLANCE

F

ollow-up is important

and takes the form of rectal/pouch

surveillance, with

biopsy of the cuff recommended yearly.

Gastroscopies

to

detect upper gastrointestinal

tumours (notably

duodenal adenomas).

L

ifespan

is

reduced because

of the development of duodenal and

ampullary Cancers and

complications of desmoid tumours

.

Hereditary

non-polyposis colorectal

cancer (Lynch

syndrome)

Hereditary non-polyposis colorectal cancer (HNPCC)

is characterised

by an increased risk of colorectal cancer

and also

cancers of the endometrium, ovary, stomach and

small intestine

.

It

is an autosomal dominant condition caused

by a

mutation in one of the DNA mismatch repair genes.

The most

commonly affected genes are MLH1 and MSH2.

The lifetime

risk of developing colorectal cancer is 80%, and

the mean

age of diagnosis is 45 years.

Most

cancers develop

in the

proximal colon.

Females

have a 30–50% lifetime risk

of developing

endometrial cancer

.

Slide95

DIAGNOSIS

HNPCC can be diagnosed by genetic testing or by

the Amsterdam

II criteria:

●

T

hree

or more family members with an

HNPCC-related cancer (colorectal, endometrial, small bowel, ureter, renalpelvis), one of whom is a first-degree relative of the other two;

●

T

wo

successive affected generations;

●

A

t

least one colorectal cancer diagnosed before the age of 50 years;

●

FAP excluded;

●

T

umours

verified by pathological examination.

Patients with HNPCC are offered regular endoscopic surveillance.

Slide96

Malignant – colorectal cancer

Epidemiology

In the UK, colorectal cancer is the second most common cause of cancer death.

In

the

UK, approximately

35 000 patients are diagnosed with colorectal cancer every

year.

Approximately

one-third of these tumours are in the rectum and two-thirds in the colon.

The

burden of disease is similar in men and women.

Colorectal

cancer occurs less frequently in the resource-poor world than in resource-rich countries.

Slide97

Aetiology

I

t

arises from adenomatous polyps after a sequence of genetic mutations influenced by environmental factors.

The

adenoma–carcinoma sequence is not a simple stepwise progression of

mutations but

a complicated array of multiple genetic alterations, ultimately resulting in an invasive tumour.

Mutations

of the adenomatous polyposis coli (APC) gene occur in two-thirds of colonic adenomas and are thought to develop early in the carcinogenesis pathway.

K-ras

mutations result in activation of cell signalling pathways and are more common in larger lesions,

suggesting

that they are later events in mutagenesis

.

Slide98

The

p53 gene is frequently mutated in

carcinomas but

not in adenomas and therefore thought to be a marker of invasion.

There is association between diet

and colon cancer.

Worldwide

, the prevalence of

colorectal cancer

is closely associated with intake of red meat

and particularly

processed meat products (haem and

N-nitroso compounds

).

These

adversely affect DNA in the

colorectal mucosa

.

A

protective effect of dietary fibre is also

suggested by

epidemiological studies.

The

hypothesis is that

increased roughage

is associated with reduced colonic transit times,

and this

in turn reduces the exposure of the mucosa to dietary

carcinogens.

Increased

risk for colorectal cancer has also been associated with dietary animal fat, smoking and alcohol.

Cholecystectomy

may marginally increase the risk of rightsided colon cancer and inflammatory bowel disease is a well-recognized risk

factor.

Slide99

Pathology

Macroscopically, the tumour may take one of four

forms.

Annular

Tubular

Ulcer

Cauliflower

The

annular variety tends to give rise to obstructive symptoms, whereas the others present more commonly with bleeding.

Most

large bowel cancers arise from the left colon, notably the rectum (38%), sigmoid (21%), and descending colon (4%).

Cancer

of the caecum (12%) and ascending colon (5%) are less common, but may be gradually increasing in incidence.

Cancer

of the transverse

colon (5.5

%), flexures (2–3%) and appendix (0.5%) are relatively uncommon.

Microscopically

, the neoplasm is a columnar cell adenocarcinoma.

Origin

from a benign polyp may be

evident in

early cases, before the benign architecture is destroyed by malignant infiltration.

Slide100

Spread

Colonic cancer can

spread:

locally

the lymphatics

bloodstream

across

the peritoneal

cavity

Direct

spread may be longitudinal or radial.

Radial spread may

be retroperitoneal into the ureter, duodenum and

posterior abdominal

wall muscles or intraperitoneal into

adjacent organs

or the anterior abdominal

wall.

In

general, involvement of the lymph nodes by the

tumour progresses

from those closest to the bowel along the

course of

lymphatics to central nodes.

Haematogenous

spread is most

commonly to

the liver via the portal vein.

One-third

of

patients will

have liver metastases at the time of diagnosis and

50% will

develop them at some point, accounting for the

majority of

deaths.

The

lung is the next most common

site

M

etastasis to

ovary, brain, kidney and bone is less common.

Colorectal cancer

can spread from the serosa of the bowel or via

subperitoneal lymphatics

to other structures within the

peritoneal cavity

, including peritoneum, ovary and omentum.

Slide101

Staging colon

cancer

Dukes

’

classification was

originally described

for rectal tumours but has been adopted for histopathological reporting of colon cancer.

Although

it is simple and widely

recognised the

more detailed

TNM

system is regarded as the international

standard.

Slide102

Dukes

’ staging for colorectal cancer

●

A: invasion of but not breaching the muscularis propria

●

B: breaching the muscularis propria but not involving

lymph nodes

●

C: lymph nodes

involved.

Dukes

himself never described a stage D, but this is often

used to

describe metastatic

disease

TNM

classification for colonic cancer

●

T Tumour stage

T1 Into submucosa

T2 Into muscularis propria

T3 Into pericolic fat or subserosa but not breaching serosa

T4 Breaches serosa or directly involving another organ

●

N Nodal stage

N0 No nodes involved

N1 1-3 nodes involved

N2 Four or more nodes involved

●

M Metastases

M0 No metastases

M1 Metastases

Slide103

Clinical features

Carcinoma of the colon typically occurs in patients over 50 years of age and is most common in the 8th decade of life.

Emergency

presentation occurs in 20% of cases and is associated with a considerably worse prognosis, even when matched for disease stage

.

A careful family history should be taken.

Those

with first-degree relatives who have developed colorectal cancer before the age of 45 years may be part of one of the colorectal cancer familial syndromes.

Tumours of the

left side of the colon usually present with a change in bowel habit or rectal bleeding, while proximal lesions typically present later, with iron deficiency anaemia or a

mass.

Patients

commonly present with metastatic disease.

Lesions

of the flexures may present with vague upper abdominal symptoms for many months before symptoms

suggestive of

colonic disease appear

.

Slide104

Investigation of colon cancer

SCREENING

Colon cancer is suited to screening as prognosis is better

for early

stage disease and polypectomy allows the

prevention of

cancer development.

In

the UK, a screening

programme has

been introduced based on

faecal occult blood testing

of people

aged 60–69 years, followed by colonoscopy in

those who

test positive.

A

guaiac-based test

is used, which

detects peroxidase-like

activity of faecal haematin

.

Studies

have suggested

a 15–20% reduction

in

colorectal cancer

specific mortality in

the screened population.

Flexible sigmoidoscopy

can

also be used as the initial screening tool, with a

similar reduction

in colorectal cancer

specific mortality

.

Slide105

ENDOSCOPY

The 60-cm, fibreoptic, flexible sigmoidoscope is increasingly being used in ‘one-stop’ rectal bleeding clinics.

The

patient is prepared with an enema and sedation is not usually necessary.

It is usually possible to assess the bowel up to the splenic flexure, which will detect up to 70% of cancers and almost all that cause fresh rectal

bleeding.

Colonoscopy

is the investigation of choice if colorectal cancer is

suspected.

It

has the advantage of not only picking up a primary cancer but also having the ability to detect

polyps

or other carcinomas, which occur in 3–5% of cases.

There

is a small risk of perforation (1:1000).

Slide106

RADIOLOGY

Double-contrast

barium enema

has traditionally been

used and

shows a cancer of the colon as a constant irregular

filling defect

, often described as looking like an

apple-core.

False

positives occur in 1–2% of cases and

false negatives

in 7–9% of cases.

It

has now been largely

replaced by

computed tomography (CT)

virtual colonoscopy,

which is

extremely sensitive in picking up polyps down to a

size of

6

mm.

It

has the advantage of being

less invasive than

colonoscopy but if a biopsy is required,

an endoscopy

will still be needed.

CT

is used as a diagnostic

tool in

patients with palpable abdominal masses.

Spiral

CT of

the chest

, abdomen and pelvis now represents the standard

means of

staging colorectal cancer, although

chest x-ray and

liver ultrasound

are alternatives if CT is not readily available.

Rectal

cancer

usually requires additional staging for local

spread, using

magnetic resonance

imaging (MRI)

.

Slide107

Surgical treatment

PREOPERATIVE PREPARATION

Mechanical bowel preparation

has fallen out of favour in surgery for colon cancer, with little evidence of benefit and some of an increased rate of wound infection

.

It currently

remains in

use largely for low rectal resection, where unprepared bowel may be associated with a higher infection rate.

Antiembolism

stockings

should be fitted and the patient started on prophylactic subcutaneous

low molecular weight heparin

.

If

available,

manual compression boots

are used perioperatively.

Intravenous

prophylactic antibiotics

are given immediately before the start of surgery, to reduce the risk of surgical site infection.

A

single dose of antibiotics covering bowel organisms is as effective as multiple doses.

In

all cases where a stoma seems likely, careful preoperative counselling and marking of an appropriate site by an enterostomal therapist is

essential.

Slide108

OPERATIONS

The operations described are designed to remove the

primary tumour

and its draining locoregional lymph nodes.

It is

unusual to find unsuspected metastases at laparotomy (

or laparoscopy

) after CT staging, but the presence of

peritoneal metastases

may predicate a palliative strategy with a

segmental resection

and less aggressive lymphadenectomy.

The

use

of stapling

and hand-suturing techniques for colonic

anastomoses have

been compared, and there is probably little

difference in

leak rate.

It

is more important that healthy bowel, free

of tension

or distal obstruction, is used to construct an

anastomosis and

that patients are adequately nourished and

free from

active infection if anastomotic leakage is to be avoided.

Slide109

Right hemicolectomy

Carcinoma

of the caecum or ascending colon

is treated by right

hemicolectomy.

At open surgery the peritoneum lateral to the ascending colon is incised, and the incision is carried around the hepatic flexure.

The mesentery of the distal 20 cm of ileum and the mesocolon as far as the proximal third of the transverse colon is divided.

When

it is clear that there is an adequate blood supply at the resection margins, the right colon is resected, and an anastomosis is fashioned between the ileum and the transverse colon.

If the tumour is at the hepatic flexure the resection must be extended further along the transverse colon and will involve dividing the right branch of the middle colic artery.

Slide110

Extended right hemicolectomy

Carcinomas of the transverse colon and splenic flexure are most commonly treated by an extended right hemicolectomy.

The extent of the resection is from the right colon to the descending colon.

The mobilisation is as for a right hemicolectomy but dissection continues to take down the splenic flexure and the whole transverse mesocolon is ligated.

Some surgeons prefer to perform a left hemicolectomy for a splenic flexure cancer.

Slide111

Left hemicolectomy

This is the operation of choice for descending colon and sigmoid cancers.

The

left half of the colon is mobilised completely along the ‘white line’ that marks the lateral attachment of the mesocolon.

As the sigmoid mesentery is mobilised, the left ureter and gonadal vessels must be identified and protected.

The splenic flexure may be mobilised by extending the lateral

dissection from

below and completed by entering the lesser sac

.

The bowel and mesentery can then be resected to allow a tension-free anastomosis.

A temporary diverting stoma may be fashioned upstream, usually by formation of a loop ileostomy.

This is usually undertaken if the anastomosis is below the peritoneal reflection of the rectum, because healing is more likely to be impaired distally.

Slide112

Laparoscopic surgery

Laparoscopic surgery for colon cancer has been shown to have equivalent overall and cancer related outcomes to open surgery.

In the UK, the National Institute for

Health and

Care Excellence has stated that laparoscopic

colorectal surgery

should be offered to suitable patients.

Operation times are

longer but wound infection rates, blood loss and

postoperative pain

scores are lower than for open surgery.

The costs of

laparoscopic surgery are, however, generally higher and

this may

particularly relevant where funds are limited

.

Specimen retrieval and bowel anastomosis can then be performed via small incisions.

Training in laparoscopic colorectal surgery is important, as there is a relatively long learning curve.

Slide113

Emergency surgery

In the UK, 20% of patients with colonic cancer will present as an emergency, the majority with obstruction, but occasionally with haemorrhage or perforation.

If

the lesion is right sided, it is usually possible to perform a right hemicolectomy and anastomosis in the usual manner.

If

there has been perforation with substantial contamination or if the patient is unstable, it may be advisable to bring out an ileocolostomy rather than forming an anastomosis.

For

a left-sided lesion the decision lies between a Hartmann’s procedure or resection and anastomosis.

Where

endoscopic and radiological facilities are present an obstructing left-sided lesion can be treated with an expanding metal

stent.

This

has the advantage of converting an emergency operation with a high chance of a stoma to a situation that can be

managed semi-electively

by resection and anastomosis.

Although

early studies cast doubt on the benefits of colorectal stenting, more recently evidence has emerged that stenting leads to a

reduction in

stoma rates.

Slide114

Postoperative

care

After colonic surgery patients should be closely

monitored, as

there is a small incidence of postoperative bleeding.

Antithrombosis measures

should be continued

for 28

days postoperatively.

Wound infections are

relatively common after colonic surgery and

may well

be more frequent than the 10% usually quoted.

Anastomotic leaks

occur in 4–8% of ileocolic or colocolic anastomoses.

The possibility should be borne in mind in

any patient

not progressing as expected or with unexplained

cardiac abnormalities

, fever or worsening abdominal pain.

Early investigation

with contrast enhanced CT scan is

appropriate.

In

the presence of sepsis or peritonitis, early return to

theatre and

taking down the leaking anastomosis with the

formation of

stomas is usually advised.

Slide115

Prolonged nasogastric drainage, intravenous fluid therapy and cautious introduction of oral fluid and diet represented traditional postoperative practice.

Enhanced

recovery

programmes have

been shown to reduce length of hospital stay from 10–14 days to as little as 2–3 days, by modulating the surgical stress response and reducing post-operative ileus

.

It

is important to appreciate that these programmes require multiple interventions to be instituted and considerable time, effort and education from the surgical, anaesthetic and ward teams.

Adjuvant

therapy

In most patients with colon cancer there is little clear benefit of preoperative chemotherapy, although trials in selected patient groups with locally advanced disease are ongoing.

There is evidence that adjuvant chemotherapy improves outcome after surgery in patients with node-positive disease (Dukes C).

Slide116

Metastatic

disease

Hepatic metastases can be resected and series have

demonstrated 5-year

survival of over 30% in resectable disease.

Liver surgeons

are increasingly aggressive in treatment and the

only absolute

limitation on what can be resected relates to

leaving behind

sufficient functioning liver, although this

clearly has

to be moderated by patient factors.

It

is important not

to biopsy

potentially resectable hepatic metastases as this

may cause

tumour dissemination.

Imaging

will usually

correctly identify

colorectal metastases and assess patients suitable

for liver resection.

The

role of

chemotherapy and

the timing of colonic and hepatic surgery in

synchronous metastases

is still a matter of debate and such cases should

be carefully

discussed by a multidisciplinary team.

Isolated lung metastases

may occasionally be suitable for resection but

they are

more commonly accompanied by metastases

elsewhere.

In

patients with widespread disease, palliative

chemotherapy is

offered alongside symptomatic treatment and support by

a palliative

care team.

Slide117

Prognosis

Overall 5-year survival for colorectal cancer is approximately 50%.

The

most important determinant of prognosis is tumour stage and, in particular, lymph node status.

Patients

with disease confined to the bowel wall (Dukes stage A) will usually have cure by surgical resection alone and over 90% will have disease-free survival at 5 years.

Spread

beyond the bowel

wall (Dukes

B) reduces 5-year survival to approximately 60–70%. Patients with lymph node metastases (Dukes C) have a 5-yearsurvival of 30%, while fewer than 10% of patients

presenting with

metastatic disease at the outset will be alive 5 years later.

Slide118

Colorectal

cancer follow-up

Since the advent of safe liver resection for metastases

the outcome

benefit of follow-up has been clearly demonstrated.

Follow-up aims to identify synchronous bowel tumours (

present in

3%) that were not picked up at the time of

original diagnosis

due to emergency presentation or incomplete assessment.

Similarly, 3% of patients will develop a

metachronous (at

a different time) colonic cancer and surveillance

colonoscopy is

designed to diagnose these.

Up

to a half of all

patients with

colorectal cancer will develop liver metastases at

some point

and regular imaging of the liver (by ultrasound and

CT scan

) and measurement of carcinoembryonic antigen (

CEA) is

designed to diagnose this early, in order to allow

curative metastectomy

.

Trials

of the optimum follow-up pathway

have suggested

that CEA measurement alone can be as effective

as regular

imaging.

Slide119

Quiz 2:

What are the advantages

of

the ileorectal

anastomosis (

IRA)

over

the Restorative

proctocolectomy with an ileal pouch–anal anastomosis (RPC

)?

Slide120

INFLAMMATORY

BOWEL DISEASE

The term ‘inflammatory bowel disease’ is reserved for conditions characterised by the presence of idiopathic intestinal inflammation (i.e. ulcerative colitis [UC] and Crohn’s

disease [CD

].

Ulcerative

colitis

UC is a disease of the rectum and colon with extraintestinal manifestations.

The

incidence is 10 per 100 000 per year in the UK with a prevalence of 160 per 100 000 population.

UC

affects men and women equally in early life, although it is said to be more common in males in later life.

It

is most commonly diagnosed between the ages of 20 and 40.

UC

is far more common in the USA and Western Europe but relatively rare in the Far East and tropics.

Asians

who spent their childhood before the age of 14 in Asia have a much lower incidence of UC than Asians born and raised in the UK, suggesting an important effect of environmental exposure in childhood.

Slide121

Aetiology

The cause of UC is unknown.

There

is clearly a genetic

contribution, as

10–20% of patients have a first-degree

relative with

inflammatory bowel disease.

Patients

with severe

colitis have

a reduction in the number of anaerobic bacteria and

in the

variability of bacterial strains in the colon, but no

causative link

with any specific organism has been

identified.

Unlike

CD, smoking seems to have a protective effect in

UC and

has even been the basis of therapeutic trials of

nicotine.

Relapses

are occasionally said to be associated with periods

of stress

, but personality and psychiatric profiles in patients

with UC

are the same as those of the normal population

.

Slide122

Pathology

A

ll

cases the disease starts in the rectum and extends proximally in continuity.

Colonic

inflammation is diffuse, confluent and superficial, primarily affecting the mucosa and superficial submucosa

.

‘Pseudopolyposis’ occurs in almost one-quarter of cases.

Stricturing

in UC is very unusual (unlike CD) and should prompt urgent assessment because of the possibility of coexisting carcinoma.

A

small proportion of patients develop irregular mucosal swellings (

dysplasia associated

lesions or mass [DALMs]), which are highly predictive of coexisting carcinoma.

Histological examination reveals an increase in inflammatory cells in the lamina propria and the crypts of Lieberkuhn and there are ‘crypt abscesses’.

There

is depletion of goblet cell mucin.

With

time, precancerous changes can develop (dysplasia).

Slide123

High-grade

dysplasia is regarded as an

indication for

surgery as 40% of colectomy specimens in which

highgrade dysplasia

was detected will have evidence of a

colorectal cancer

.

In

contrast, optimum management of

low-grade dysplasia

is currently controversial.

Ten

to twenty per cent

of patients

with low-grade dysplasia will have a cancer at

colectomy.

The

progression rate of low-grade dysplasia to

invasive cancer

is unclear and many cancers in patients with

low-grade dysplasia

probably develop without high-grade dysplasia

.

.

Slide124

Symptoms

Clinical presentation depends in large part on the extent of disease.

If confined to the rectum (proctitis), there is

usually no

systemic upset and extra-alimentary manifestations are rare.

The main symptoms are rectal bleeding, tenesmus and mucous discharge.

The disease remains confined to the rectum in 90% of cases but proctitis may extend proximally.

Colitis

is almost always associated with bloody diarrhoea and urgency.

Severe and/or extensive colitis may result in anaemia, hypoproteinaemia and electrolyte disturbances.

Pain

is

unusual

Children with poorly controlled colitis may have impaired growth.

The

more extensive the disease the more likely extraintestinal manifestations are to occur.

Extensive

colitis is also associated with systemic illness, characterised by malaise, loss of appetite, and fever

.

Slide125

Classification

of colitis severity

The assessment of severity of UC is determined by

frequency of

bowel action and the presence of systemic signs of illness:

●

Mild disease

is characterized by fewer than four

stools daily

, with or without bleeding. There are no

systemic signs

of toxicity.

●

Moderate

disease

corresponds

to more than four

stools daily

, but with few signs of systemic illness. There may

be mild

anaemia. Abdominal pain may occur.

Inflammatory markers

, including erythrocyte sedimentation rate

and C-reactive

protein, are often raised.

●

Severe disease

corresponds to more than six bloody

stools a

day and evidence of systemic illness, with fever,

tachycardia, anaemia

and raised inflammatory markers.

Hypoalbuminaemia is common.

●

Fulminant disease

is associated with more than 10

bowel movements

daily, fever, tachycardia, continuous

bleeding, anaemia

, hypoalbuminaemia, abdominal tenderness

and distension

, the need for blood transfusion and, in the

most severe

cases, progressive colonic dilation (‘toxic megacolon’). This is a very significant finding, suggestive of

disintegrative colitis

, and an indication for emergency

surgery if

colonic perforation is to be avoided.

Slide126

Extraintestinal manifestations

Arthritis

occurs in around 15% of patients and is typically a large joint polyarthropathy, affecting knees, ankles, elbows and wrists.

Sacroiliitis

and ankylosing spondylitis are 20 times more common in patients with UC than the general population and are associated with the HLA-B27 genotype

.

Sclerosing cholangitis

is associated with UC and can progress to cirrhosis and hepatocellular failure.

Patients

with UC and sclerosing cholangitis are also at a significantly greater risk of development of large bowel cancer.

Cholangiocarcinoma

is an extremely rare association and its frequency is not influenced by colectomy.

The

skin lesions

erythema nodosum and pyoderma gangrenosum

are associated with UC and both normally resolve with good colitis control.

The

eyes can also be affected by

uveitis

and

episcleritis

.

Slide127

Acute

colitis

Approximately 5% of patients present with severe acute (

fulminant) colitis

.

Intensive

medical treatment leads to

remission in

70% but the remainder require urgent surgery.

Toxic dilatation

should be suspected in patients who develop

severe abdominal

pain and confirmed by the presence on a

plain abdominal

radiograph of a colon with a diameter of more

than 6 cm.

A

reduction in stool frequency is

not always

a sign of improvement in patients with severe UC,

and a

falling stool frequency, abdominal distension and

abdominal pain

(resulting from progression of the inflammatory

process through

the colonic wall) are strongly suggestive of

disintegrative colitis

and impending perforation.

Plain abdominal radiographs

should be obtained daily in patients with

severe colitis

, and a progressive increase in colon diameter

despite medical

therapy is an indication for urgent surgery.

Colonic perforation

is a grave complication with a mortality rate

of 40

%. Steroids may mask the physical signs.

Severe haemorrhage is

uncommon (1–2%) but may occasionally

require urgent

surgical intervention.

Slide128

Cancer risk in colitis

The risk of cancer in ulcerative colitis increases with duration of disease.

At

10 years from diagnosis it is approximately 1%, increasing to 10–15% at 20 years and 20% at 30 years.

Patients with pancolitis (defined as the presence of inflammation proximal to the splenic flexure) of more than ten years duration should be entered into screening programmes

in order

to detect clinically silent dysplasia, which is

predictive of

increased cancer risk.

The

value of screening programmes remains somewhat controversial, however, with most UC patients who develop cancer (approximately 3.5% of all patients) presenting with their tumours in-between attendances for screening colonoscopy.

Carcinoma

is more likely to occur if the whole colon is involved

or if the disease started early in life.

Malignant

change, often

atypical and

high grade, may occur at many sites at

once.

Colonoscopic

surveillance with dye-spray (chromo-endoscopy) or multiple biopsies every 10 cm is undertaken to look for

subtle mucosal abnormalities.

Slide129

Investigations

ENDOSCOPY

AND BIOPSY

Rigid/flexible sigmoidoscopy can detect proctitis in the

clinic; the

mucosa is hyperaemic and bleeds on touch, and

there may

be a purulent exudate.

Where

there has been

remission and

relapse, there may be regenerative mucosal nodules

or pseudopolyps

.

Later

, tiny ulcers may be

seen.

Colonoscopy

and biopsy has a key role in

diagnosis and

management:

T

o

establish the extent of inflammation, although

colonoscopy is

contraindicated in severe acute colitis because

of the

risk of colonic perforation;

T

o

distinguish between UC and Crohn’s

colitis;

To

monitor the response to treatment;

T

o

assess longstanding cases for malignant change.

Slide130

RADIOLOGY

A plain abdominal film

may indicate the severity of disease in the acute setting and is particularly valuable in demonstrating the development of toxic megacolon.

Barium

enema

has largely

been replaced by CT, although a contrast study will show a featureless colon.

CT

findings in pancolitis may show significant thickening of the colonic wall, as well as

inflammatory stranding

in the colonic

mesentery.

BACTERIOLOGY

A stool specimen should be sent for microbiological analysis when UC is suspected, in order to exclude infective colitides, notably Campylobacter, which may be very difficult to

distinguish from

acute severe UC.

Clostridium

difficile colitis may need to be considered in populations at risk of this

disease.

Slide131

Treatment

MEDICAL

TREATMENT

Medical therapy is based on anti-inflammatory agents.

The 5-aminosalicylic

acid (5-ASA) derivatives can be given

topically (per

rectum) or systemically.

They

act as inhibitors of

the cyclo-oxygenase

enzyme system and are formulated to

protect the

aspirin-related drug from degradation before reaching

the colon

.

They

can be used long term as maintenance therapy.

Corticosteroids

are the mainstay of treatment for ‘flareups

’, either

topically or systemically, and have a

widespread anti-inflammatory

action.

The

immunosuppressive drugs

azathioprine and

cyclosporin can be used to maintain

remission and

as ‘steroid-sparing’ agents.

The

monoclonal

antibodies infliximab

and adalimumab both act against

antitumour necrosis

factor alpha, which has a central role in

inflammatory cascades

.

Most recently, vedolizumab, which blocks integrins, has been used as ‘rescue therapy’ for severe colitis, to try and avoid emergency colectomy.

Slide132

ACUTE COLITIS

Patients with a mild attack usually respond to a course of oral prednisolone.

A

moderate attack often responds to oral prednisolone, twice-daily steroid enemas and 5-ASA. Failure to achieve remission as an outpatient is an indication for admission.

Severe

attacks of UC occur in up to 10% of patients and are emergencies, requiring hospital admission.

Regular assessment of

vital signs, weight and the abdomen is required.

A

stool chart should be kept and a plain abdominal radiograph is taken daily and inspected for dilatation of the transverse colon.

The

presence of mucosal islands or intramural gas on plain radiographs, increasing colonic diameter or a sudden increase in pulse and temperature may indicate a colonic perforation.

Fluid

and electrolyte balance is maintained, anaemia corrected and adequate nutrition is provided, sometimes intravenously in severe cases

.

Slide133

The

patient is treated

with intravenous

hydrocortisone four times daily, as well as

rectal steroids

.

If

there is failure to gain an improvement within

48 hours

of commencing high-dose intravenous steroids,

then surgery

should be considered and it is certainly advisable

if there

has been no improvement within 3–5 days.

Regular and joint

review by gastroenterologist and surgeon is essential

to identify

patients who are failing to make anticipated

progress and

to ensure that surgery is neither inappropriately

delayed nor

undertaken.

Gastroenterologists

will use

azathioprine, cyclosporin

or infliximab in severe acute attacks to

attempt to

induce remission.

Slide134

INDICATIONS FOR

SURGERY

●

S

evere

or fulminating disease failing to respond to

medical therapy

;

●

C

hronic

disease with anaemia, frequent stools,

urgency and

tenesmus;

●

S

teroid-dependent

disease – here, the disease is not

severe but

remission cannot be maintained without

substantial doses

of steroids;

●

I

nability

of the patient to tolerate medical

therapy required

to control the

disease;

●

N

eoplastic

change: patients who have severe dysplasia

or carcinoma

on review colonoscopy;

●

E

xtraintestinal

manifestations;

●

R

arely

, severe haemorrhage or stenosis causing obstruction.

Slide135

OPERATIVE TREATMENT FOR UC

Emergency

In

the emergency situation, (or for a patient who is malnourished or on steroids), the ‘first aid’ procedure is a subtotal colectomy and end ileostomy.

The

rectosigmoid stump is left long and can either be brought out as a mucous fistula or closed just beneath the skin.

This

operation has the advantages that the patient avoids a pelvic operation while unwell, that colonic histology can be assessed and restorative surgery can be contemplated at a later date when the patient is no longer on steroids and has fully recovered.

The

mesentery is divided close to the bowel and the omentum should be preserved if possible.

Dissection

of the left colon is continued to divide the sigmoid at a level that will comfortably reach the skin as a mucous fistula.

The

temptation to close the rectal stump and leave it stapled off in the pelvis should be avoided if at all possible

.

Slide136

The

diseased rectum may disintegrate,

causing a

pelvic abscess and severe sepsis, with potentially fatal

consequences.

Allowing

the rectal remnant to discharge

through the

mucous fistula not only minimises the risk of this

serious complication

but may also allow the delivery of a

high-dose topical

steroid or 5-ASA compound, via the mucous

fistula, into

the isolated rectum.

An

emergency subtotal

colectomy can

be performed laparoscopically, provided the surgeon

and theatre

team has adequate experience

.

Elective

surgery

The

indications for elective

surgery include

:

F

ailure

of medical therapy/steroid dependence;

G

rowth

retardation in the young;

E

xtraintestinal

disease (polyarthropathy and

pyoderma gangrenosum

respond to colectomy);

M

alignant

change

.

Slide137

In the elective setting four operations are available – all

of these

can be successfully performed laparoscopically in

experienced hands

:

S

ubtotal

colectomy and ileostomy (as in an emergency);

P

roctocolectomy

and permanent end ileostomy;

R

estorative

proctocolectomy with ileoanal pouch;

S

ubtotal

colectomy and ileorectal anastomosis

.

Segmental resections are not recommended as even

when the

right side is not obviously involved there is a high

recurrence rate

in the remaining colon.

Subtotal

colectomy

with ileostomy

is performed electively for a frail patient, a

patient who

cannot be weaned from steroids and when there is

doubt as

to whether the colitis may represent CD.

A

pouch, a

completion proctectomy

and even an ileorectal anastomosis

can be

considered at a future date

.

Slide138

Crohn’s

disease of the colon

Colonic

involvement is found in 30% of patients with

CD, frequently

in association with perianal disease and it

may coexist

with small bowel pathology.

Colonic

CD

presents with

symptoms of colitis and

proctitis.

Colonic

strictures may form just as are seen in

small bowel

CD.

Endoscopic

dilatation may be performed in

expert hands

as an alternative to surgical resection.

Distinguishing between

CD and UC is often difficult and requires

clinical and

pathological patterns to be combined.

The

presence

of skip

lesions, rectal sparing, non-caseating granulomas or

perianal disease

will point to CD.

Slide139

Colonoscopic examination may be normal or show patchy inflammation.

There will be areas of normal colon or rectum in between areas of inflamed mucosa that are irregular and ulcerated, with a mucopurulent exudate.

The earliest appearances are aphthous ulcers surrounded by a rim of erythematous mucosa.

These become larger and deeper with increasing severity of disease.

There may be stricturing, and it is important to exclude malignancy in these sites.

An irregular Crohn’s stricture with polypoid mucosa may be almost indistinguishable from malignancy.

Slide140

Treatment

Disease

activity can be controlled with 5-ASA compounds and flare-ups treated with steroids.

Rectal

agents

can be

particularly effective if the disease activity is localised to the rectum.

Immunomodulatory

agents are frequently used, particularly if there is evidence of CD activity in large

and small

bowel.

Although

CD is usually regarded as a contraindication to pouch surgery, the other options (panproctocolectomy or total colectomy with ileorectal anastomosis) are

frequently appropriate

and there may be considerable rectal sparing in CD, justifying the latter.

Where

the diagnosis of CD is firmly established, segmental rather than total colectomy may be appropriate.

Slide141

INFECTIONS

OF THE

LARGE INTESTINE

Campylobacter

Infection with Campylobacter jejuni (a gram-negative rod

with a

distinctive spiral shape) is the commonest form of

gastroenteritis in

the UK, typically acquired from eating

infected poultry.

It causes diarrhoea and abdominal pain.

Severe cases may

resemble UC.

The

organism may take several days

to isolate

on stool culture

.

Treatment

I

s

supportive as it

usually resolves

without antibiotics, but severe colitis and even

perforation may

occur

.

It is a notifiable disease

.

Slide142

Intestinal amoebiasis

Entamoeba histolytica has a worldwide distribution and is transmitted mainly in contaminated drinking water.

It can cause colonic ulcers, which are described as ‘bottlenecked’ because they have considerably undermined edges.

The ulcers typically also have a yellow necrotic floor, from which blood and pus exude.

In

the majority of cases they are confined to the distal sigmoid colon and the rectum.

Clinically amoebiasis can mimic UC, most commonly causing bloody diarrhoea, but more severe colonic complications can occur, including severe haemorrhage,

Slide143

A pericolitis

is not uncommon and results in adhesions and may cause intestinal obstruction.

Amoebiasis

may cause liver abscesses or an amoebic mass (‘amoeboma’) of the

caecum or

sigmoid which is difficult to distinguish from a carcinoma.

Surgery

is fraught with danger as the bowel is extremely friable.

Endoscopic

biopsies or fresh hot stools are examined to look for the presence of amoebae

.

It

is important to emphasise, however, that the presence of the parasite does not indicate that it is pathogenic.

It

is especially important to exclude amoebic infection in patients suspected of having UC.

Treatment

Is

by metronidazole in the acute setting, three times daily for 7–10 days.

Diloxanide

furoate is

effective against

chronic infections associated with the passage of

cysts in

stools.

Slide144

Salmonellosis

, typhoid

and paratyphoid

Salmonella are a family of gram-negative rods that can

cause a

range of enteric infections.

Salmonella

gastroenteritis is

typically caused

by S. enteritidis from poultry, and is most

often a

self-limiting illness comprising headache, fever and

watery diarrhoea

.

When

severe, antibiotics and indeed

hospitalisation and

intravenous fluids may be needed.

The

diagnosis

is based

on stool culture.

Shigella

and enteropathogenic

strains of

E. coli may cause similar diarrhoeal

illnesses.

Typhoid fever is caused by S. typhi and presents with fever and abdominal pain after a 10–20-day incubation period.

Over

the next week, the patient can develop

distension, diarrhoea

, splenomegaly and characteristic ‘rose spots’ on

the abdomen

caused by a vasculitis.

Slide145

In addition, invasion of the systemic circulation,

which is

a characteristic feature of salmonellosis, may cause

severe gram-negative

sepsis and septic shock may develop.

Some patients

may develop metastatic sepsis, including

septic arthritis

and osteomyelitis, meningitis, encephalitis and pancreatitis.

A

number of surgical complications can result:

● Paralytic ileus

;

● Intestinal haemorrhage;

●

Perforation;

● Cholecystitis.

Human immunodeficiency

virus (HIV

)

Intestinal complications are common after the

development of

AIDS when opportunistic organisms can cause

gastroenteritis.

HIV1

may also cause a

specific enteropathy

.

Treatment

is directed towards the

responsible organism

and surgery should be avoided.

Slide146

Opportunistic intestinal infections in patients with AIDS

●

Bacteria

Salmonella

Shigella

Yersinia

Campylobacter

Mycobacterium avium intracellulare (MAI)

●

Viral

Cytomegalovirus

●

Protozoa

Cryptosporidium

Giardia

●

Fungal

Candida albicans

Slide147

Clostridium difficile

Clostridium difficile is a toxin-producing gram-positive

bacillus that

is an increasing concern in many hospitals.

Although normally

present in around 2% of the population, it

proliferates after

antibiotic treatment (especially cephalosporins).

Clinically, C. difficile infection presents with

diarrhoea, abdominal

pain and fever

.

Infection may progress to

pseudomembranous colitis

, so called because on visualisation of

the bowel

, plaques of inflammatory exudate between

oedematous mucosa

are seen.

Diagnosis

is usually made by detection

of the

toxin in stool samples, rather than by culture.

Treatment

I

s

by metronidazole or vancomycin alongside supportive care

.

If the colitis does not settle, an emergency subtotal

colectomy and

ileostomy may be necessary.

Slide148

Colonic diverticula

Diverticula (hollow out-pouchings) are a common

structural abnormality

.

They

can be classified as:

1 Congenital

.

All

three coats of the bowel are present

in the

wall of the diverticulum (e.g.

Meckel’s diverticulum

).

2 Acquired.

There

is no muscularis layer present in

the diverticulum

(e.g. sigmoid diverticular disease).

Diverticula are found in the left colon in around

75% of

over 70 year olds in the Western world.

The condition is found

in the sigmoid but can affect

the whole

colon.

Interestingly

, in South-East Asia

right-sided diverticular

disease is more common.

Diverticula

are

most often

asymptomatic (diverticulosis) and found

incidentally, but

they can present clinically with sepsis or haemorrhage

.

Slide149

Aetiology

Epidemiological studies indicate that diverticular disease is

a consequence

of a refined Western diet, deficient in

dietary fibre

.

The

combination of altered collagen structure with

ageing, disordered motility and increased intraluminal pressure, most notably in the narrow sigmoid colon, results in herniation of mucosa through the circular muscle at the points where blood vessels penetrate the bowel wall.

The rectum has a complete muscular coat and a wider lumen and is thus very rarely affected.

Diverticular disease is rare in Africa and Asia where the diet is high in natural fibre.

Slide150

Complications of diverticular disease

Pain

and inflammation (

diverticuliti

s).

Perforation

:

most often contained leading to

pericolic abscess

formation but occasionally leading to

generalised peritonitis

.

Intestinal

obstruction:

progressive fibrosis can cause

stenosis of

the sigmoid and large bowel obstruction or

loops of

small intestine can adhere to an inflamed

sigmoid, resulting

in small bowel obstruction.

Haemorrhage

: diverticular disease may present with

profuse and

recurrent) colonic haemorrhage due to erosion

of vessels

adjacent to a diverticulum.

Fistula

formation

(colovesical, colovaginal,

enterocolic, colocutaneous

): occurs in 5% of cases, colovesical

fistulation is

most commonly seen.

Slide151

Clinical

features

In mild cases, symptoms such as distension, flatulence and

a sensation

of heaviness in the lower abdomen may be

indistinguishable from

those of irritable bowel

syndrome.

Surgical

treatment is rarely

,

in the absence of complications

.

Diverticulitis typically presents as persistent lower abdominal pain, usually in the left iliac fossa.

There

may be accompanying diarrhoea or constipation.

The lower abdomen is tender, especially on the left, but occasionally also in the right iliac fossa if the sigmoid loop lies across the midline.

The sigmoid colon may be tender and thickened on palpation and rectal examination may reveal a tender mass if an abscess has formed.

Distinguishing between diverticulitis and

abscess formation

is difficult on clinical grounds alone and radiological imaging is essential.

Generalised peritonitis as a result of free perforation presents in the typical manner with systemic upset and generalised tenderness and guarding

.

Slide152

Haemorrhage from colonic diverticula is typically

painless and

profuse.

Bleeding

from the sigmoid will be bright red

with clots

, whereas right-sided bleeding will be darker.

D

iverticular

bleeding may persist

or recur

requiring transfusion and resection.

The presentation of

a

fistula

resulting from diverticular disease depends on

the site

;

The

most common

colovesical fistula

results in

recurrent urinary

tract infections and pneumaturia (flatus in

the urine

) or even faeces in the urine.

Colovaginal

fistulae

are more

common after hysterectomy.

Colocutaneous fistulation

is

rare in the absence

of prior intervention.

Rarely

, diverticular disease may perforate into

the retroperitoneum

, leading to a psoas abscess, and even

groin fistulation

.

Slide153

Radiology

Plain radiographs can demonstrate a pneumoperitoneum.

Spiral CT has excellent sensitivity and specificity for

identifying bowel

wall thickening, abscess formation and

extraluminal disease

and has revolutionised the assessment

of complicated

diverticular

disease.

On identification of

abscesses in stable patients, drainage may be

carried out

percutaneously, avoiding the need for laparotomy/laparoscopy.

Contrast studies and endoscopy are usually avoided

for 6

weeks after an acute attack for fear of causing perforation.

They are used subsequently, however, to exclude a

coexisting carcinoma

and assess the extent of diverticular disease.

Contrast examination

or CT can demonstrate a fistula

.

Slide154

Colonoscopy

Endoscopic assessment may demonstrate the necks of

diverticula within

the bowel

lumen.

A narrowed area

of diverticular disease may be impassable because of

the severity

of disease and there is a significant risk of

endoscopic perforation

.

Colonoscopy

in these circumstances

requires judgement

and experience.

Biopsies

may be taken if

possible and

corroboration with barium enema or CT virtual

colonoscopy is

required.

Excluding

a carcinoma may not always

be possible

and may represent an indication for resection

.

Hinchey classification of

complicated diverticulitis

.

Grade I

Mesenteric

or pericolic abscess

Grade II

Pelvic

abscess

Grade III

Purulent

peritonitis

Grade IV

Faecal

peritonitis

Slide155

Management

Patients are frequently recommended to take a high-fibre

diet and

bulk-forming laxatives, although the evidence for

their effectiveness

in diverticulosis or after an attack of

diverticulitis is

limited.

Antispasmodics

may have a role if

recurrent pain

is a problem.

Acute

diverticulitis is treated by

intravenous antibiotics

(to cover gram-negative bacilli and

anaerobes) alongside

appropriate resuscitation and analgesia.

Nil by

mouth to ‘rest the bowel’ and catheterisation to reduce

the risk

of colovesical fistulation are often advocated, but

there is

little evidence to support these practices.

A

CT scan

can confirm

the diagnosis and assess for complications.

After the acute

attack has subsided the bowel should be investigated

by endoscopy

, barium enema or CT virtual colonoscopy.

Some pericolic

abscesses can be drained percutaneously.

A diameter of

5 cm is frequently regarded as the cut off

between an

abscess likely to settle with antibiotics and one likely

to require

intervention.

Slide156

Principles of surgical management of

diverticular disease

●

Hartmann’s procedure is the safest option in

emergency surgery

●

Primary anastomosis can be considered in selected patients

●

Elective resection may be offered for recurrent attacks

●

Definitive treatment of colovesical fistula will require

resection

VASCULAR ANOMALIES OF

THE INTESTINE

Angiodysplasia

Angiodysplasia is a vascular malformation that

commonly causes

haemorrhage from the colon in patients over the

age of

60.

The

malformations consist of dilated tortuous

submucosal veins

.

Clinical features

In the majority of cases, the symptoms are subtle and

patients can

present with

anaemia

.

About

10–15% have

brisk

bleeds

, which may present as melaena or significant

rectal bleeding

.

Many

patients in whom rectal bleeding has

been attributed

to diverticular disease have probably bled

from angiodysplasia

.

There is an association with aortic

stenosis (Heyde’s

syndrome).

Slide157

Investigation

Colonoscopy

may show the characteristic lesion in the

right colon

.

The

lesions are only a few millimetres in size

and appear

as reddish, raised areas at endoscopy.

Selective superior and

inferior mesenteric

angiography

shows the site

and extent

of the lesion by a ‘blush’ of contrast, provided

bleeding is

above 1 mL/minute.

If

this fails, a

technetium-99m (99mTc

)-

labelled red cell scan

may confirm and localise

the source

of haemorrhage.

Treatment

The first principle is to stabilise the patient.

Following this, the

bleeding needs to be localised.

Colonoscopy

may

allow cauterisation

to be carried out and an argon laser can

be helpful

.

In

severe uncontrolled bleeding, surgery

becomes necessary

.

On-table

colonoscopy is carried out to

confirm the

site of bleeding

.

Angiodysplastic lesions are

sometimes demonstrated

by transillumination through the

caecum.

If

it is still not clear exactly which

segment of

the colon is involved, then a subtotal colectomy may

be necessary.

Slide158

Ischaemic colitis

Ischaemia of the colon typically results from thrombosis

or embolism

.

Sudden

embolic events present with severe

pain out

of proportion to the degree of peritonism, bloody

diarrhoea, haemodynamic

instability and shock.

Resuscitation and

laparotomy are required with resection of

gangrenous bowel

and exteriorisation of viable bowel ends.

Mortality

is extremely high.

Thrombotic occlusion usually occurs in the context of global atherosclerosis and the presentation tends to be less dramatic with abdominal pain and rectal bleeding.

A plain abdominal radiograph may show ‘thumb-printing’ and endoscopy may demonstrate haemorrhagic oedema.

The left colon and, in particular, the splenic flexure are usually the worst affected.

Symptoms usually settle spontaneously.

In some cases, ulceration at the splenic flexure associated with ischaemic colitis may heal with stricturing and present with subsequent large bowel obstruction.

Slide159

COLOSTOMIES

A colostomy (or ileostomy) stoma is a planned opening

made in

the colon (or small intestine) to divert faeces and

flatus to

the abdominal wall where they can be collected in

an external

appliance.

Depending

on the purpose for which

the diversion

has been necessary, a stoma may be temporary or permanent

.

Loop

colostomy

A

transverse loop colostomy has in the past been used

to defunction

an anastomosis after an anterior resection.

It is now

less commonly employed, as it is difficult to

manage and

potentially disrupts the marginal arterial supply to

the anastomosis

.

Loop

transverse colostomies are also

particularly prone

to prolapse.

A

loop ileostomy is now more

commonly used

.

Slide160

A loop left iliac fossa colostomy is still sometimes

used to

prevent faecal peritonitis developing following traumatic injury to the rectum, to facilitate the operative treatment of a high anal fistula, for incontinence and to defunction an obstructing low rectal cancer prior to long course chemoradiotherapy.

A

temporary loop colostomy is made by bringing a mobilised loop of colon to the surface, where it is held in place by a plastic bridge passed through a mesenteric window.

Once

the abdomen has been closed, the colostomy is opened, and the edges of the colonic incision are sutured to the adjacent skin

margin.

When

firm adhesion of the colostomy to the abdominal wall has taken place, the bridge can be removed.

Slide161

Following healing of the distal lesion for which the temporary stoma was constructed, the colostomy can be closed.

It

is usual to perform a contrast examination (

proctogram) to

check that there is no distal obstruction or continuing problem at the site of previous surgery.

Colostomy

closure is most easily and safely accomplished if the stoma is mature, typically after the colostomy has been established for at least 2 months.

Closure

is usually possible with a circumstomal incision, which avoids a full laparotomy, but it is important for patient and surgeon to consider the risks of closure carefully as it does involve a bowel anastomosis.

In

some cases, a full laparotomy may be required for safe closure of the stoma.

Slide162

End colostomy

This is formed after an abdominoperineal excision of

the rectum

or as part of a Hartmann’s procedure, bringing

the divided

colon through a left iliac fossa trephine in

rectus abdominis

and skin.

The

colonic margin is then sutured to

the adjoining skin.

The

point at which the colon is brought to the

surface must

be carefully selected to allow a colostomy bag to

be applied

without impinging on the anterior-superior

iliac spine

.

The

best site is usually through the lateral edge of

the rectus sheath.

Stoma bags and

appliances

Stoma output is collected in disposable adhesive bags

.

Colostomy appliances

are simply changed two or three times

each day

.

A

wide range of such bags is currently available.

In most hospitals

, a stoma care service is available to offer advice

to patients

, to acquaint them with the latest appliances and

to provide

the appropriate psychological and practical help.

Slide163

FUNCTIONAL

ABNORMALITIES

Constipation

There is no single definition of constipation; however, a

bowel frequency

of less than one every 3 days is commonly

considered to

be abnormal.

Constipation

is an extremely

prevalent complaint

in western society and some patients are

greatly disabled

by abdominal pain, distension, reliance on

laxatives and

difficulty with defaecation

.

Drugs and a range of illnesses can result in

constipation.

Altering

medication or

addition of

laxatives can be helpful for drug-related

constipation and

correction of underlying illness is clearly ideal where possible.

There

remains a group of patients with constipation

who do

not have any structural, pharmacological or other

pathology to

explain their symptoms.

Some

will have

obstructed defaecation

(a syndrome of impaired rectal emptying

associated with

pelvic floor dysfunction

).

Others

will have

slow colonic

transit, a disorder usually seen in women, which

may have

been present since childhood or may suddenly

follow abdominal

or pelvic surgery.

Some

patients have a

combination of

both conditions.

Slide164

Drugs

that can cause constipation

●

Benzodiazepines

●

Carbamazepine

●

Chlorpromazine

●

Cholestyramine

●

Iron

●

Opiates, particularly codeine and morphine

●

Tricyclic antidepressants

●

Statins

Illnesses associated with constipation

● Neurological conditions

● Parkinson’s disease

● Multiple sclerosis

● Diabetic nephropathy

● Spinal cord lesion

● Endocrine conditions

● Hypothyroidism

● Hypercalcaemia

Slide165

Investigation

It is important to exclude a structural abnormality (

notably large

bowel obstruction) by conventional investigation (

colonoscopy, CT

virtual colonoscopy or barium enema)

before diagnosing

a functional bowel

disorder.

Whole-gut

transit time can be measured by asking

the patient

to stop all laxatives and take a capsule

containing radiopaque markers.

Retention

of more

than 80

% of the shapes, 120 hours after ingestion, is abnormal.

Defaecating proctography may demonstrate impaired

pelvic floor

relaxation, rectal intussusception and/or rectocoele

if they

are causing obstructed defaecation.

Anorectal manometry may

confirm an abnormal pattern of straining in

patients with

obstructed defaecation, with failure to reduce (or

even inappropriately

increase) anal canal pressures on

bearing down

.

Slide166

Treatment of slow colonic transit

and obstructed

defaecation

Dietary fibre

This is the first-line treatment for mild constipation.

Constipation

only resolves after several weeks of therapy, which usually needs to be continued in the long term.

Laxatives

It is important that patients do not fall into a cycle of laxative abuse.

A

number of

types of agents

are available including bulk, osmotic and stimulant agents.

New

agents such as prucalopride, which selectively activates serotonin (5HT-4) receptors, may have a role in chronic constipation.

Rectal irrigation

Rectal irrigation may improve quality of life in some patients, who can be trained to do this for themselves using commercially available kits.

Slide167

Biofeedback

This

involves training in pelvic floor

function.

It

has been shown to be effective in up to 50% of

patients with

obstructed

defaecation

Sacral nerve stimulation

Although

primarily used for

the treatment

of faecal incontinence, sacral

neuromodulation has

recently been suggested to be of value in the treatment

of obstructed

defaecation.

Surgery

The

results of surgery are relatively poor.

Surgery is justified

only after careful evaluation and when

appropriate medical

options have been exhausted.

Total

colectomy

and ileorectal

anastomosis is the preferred procedure for slow

transit constipation

but the results are unpredictable.

Complications

I

nclude

intermittent small bowel

obstruction (60

%), further surgery (30%), constipation (25%),

diarrhoea (25

%) and incontinence (10%).

Patients

need to

be carefully

selected for surgery and psychological

evaluation may

be of benefit. An ileostomy may be required in

some cases

.

Slide168

Obstructed defaecation may be amenable to surgical

treatment if

there is evidence of rectal intussusception or a

sizeable rectocele

.

These

can be corrected by a ventral mesh

rectopexy and

repair (transrectal or transvaginal), respectively.

If there is

coexisting evidence of impaired pelvic floor relaxation,

the results

of surgical treatment tend to be disappointing.

Slide169

Irritable

bowel syndrome

The term irritable bowel syndrome (IBS) covers a range

of symptoms

with a functional basis.

Clinical

features are

variable but

abdominal discomfort, bloating, irregularity of

bowel habit

and passage of mucus are common.

By

definition,

the symptoms

of pain have to have been present for at least 3

days per

month for at least the 3 previous months in the

6-month period

prior to diagnosis (

Rome criteria

).

IBS

is

common and

symptoms have been said to occur in up to 20% of

the population

.

Colonic investigations are typically performed to rule

out organic

disease (colonoscopy, barium enema or CT

virtual colonoscopy

) but are, by definition, normal

.

Slide170

Treatment

D

ifficult

.

Many

patients benefit from

reassurance

and

symptomatic treatment

; dietary modifications, including fibre for constipation and avoidance of fermentable carbohydrates, reduction of caffeine and nicotine intake, may be of value.

Antidiarrhoeals and antispasmodic agents are commonly prescribed, but the evidence of benefit is poor.

There is some evidence of benefit for low-dose tricyclic

antidepressants.

Psychological treatments, including hypnotherapy and cognitive behavioural therapy, may be beneficial.

Surgery is contraindicated.

Slide171

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