Small and large bowel Dr. - PowerPoint Presentation

Slide1

Small and large bowel

Dr.

Firas

majeed

Slide2

Anatomy of the small and large intestine

■

Small intestine

Comprises jejunum and ileum

Has

valvulae

conniventes

Blood supply from superior mesenteric artery

■

Large intestine

Comprises caecum, ascending, transverse, descending and sigmoid colon

Has appendices

epiploicae

and

taenia

coli

Blood supply from branches of superior and inferior

mesenteric arteries

Marginal artery runs round the length of the colon

Slide3

Slide4

Slide5

PHYSIOLOGY OF THE SMALL AND

LARGE INTESTINES

Small intestine

The main function of the small intestine is the digestion of food

and the absorption of nutrients and fluid. Carbohydrates and

proteins are broken down by pancreatic enzymes, but the final

hydrolysis takes place at the brush border of the jejunum after

which they are absorbed. 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, but the absorption

of bile

salts and vitamin B12 occurs in the terminal ileum where there

are specific transporters.

Slide6

Large intestine

The

principal function of the colon is absorption of

water;1000

mL of

ileal

contents enter the caecum every 24 hours

of which

only about 150–250 mL is excreted as

faeces

.

Sodium absorption

is efficiently accomplished by an active

transport system

, while chloride and water are absorbed passively following gradients established by the sodium

pump .

Slide7

INFLAMMATORY BOWEL DISEASE

ULCERATIVE COLITIS

Ulcerative colitis is a disease of the rectum and colon

with

extraintestinal

manifestations. The incidence is 10 per 100

000 in

the UK with a prevalence of 160 per 100 000. The prevalence of UC is stable (unlike

Crohn’s

disease, which is increasing)

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

more common in the United States and

Western

Europe especially in

jewish

, but relatively

rare in the Far East and the Tropics

Slide8

Aetiology

The cause of UC is unknown. There is clearly a genetic contribution as 10–20 per cent of patients with UC have a

first-degree relative

with inflammatory bowel disease. UC is more

common in

Caucasians than in the

Afro-Caribbean

or Asian population.

No

causative link with any specific organisms has been

identified

Unlike

Crohn’s

disease, smoking seems

to have

a protective effect in UC and has even been the basis of

therapeutic trials of nicotine therapy.

Patients

often

comment that

relapses are associated with periods of stress, but personality and psychiatric profiles in patients with UC are the same

as those

of the normal

population

Slide9

Pathology

In virtually all cases, the disease starts in the rectum

and extends

proximally in continuity.

Colonic inflammation in UC

is diffuse, confluent and superficial, primarily affecting

the mucosa

and superficial

submucosa

. In very severe cases,

the inflammation

may extend full thickness through the wall

of the

colon, making interpretation difficult

Chronic mucosal ulceration

is associated with formation of granulation

tissue and

regeneration, leading to a polyp-like appearance, ‘

pseudopolyposis

’, which occurs in almost one-quarter of cases.

Stricturing

in UC is very unusual

and also irregular

mucosal swellings (

dysplasia-associated lesions

or mass,

DALMs)

should

prompt

urgent assessment

because of the possibility of coexisting carcinoma

Slide10

Histological examination

reveals

an increase

in inflammatory

cells in the lamina

propria

,

the

walls of the crypts

of

Lieberkuhn

are infiltrated

by inflammatory

cells and

there are

crypt abscesses.

There

is depletion of goblet cell

mucin.With

time, precancerous changes can develop (dysplasia).

The precise

incidence of dysplasia in UC is unclear. It seems

to increase

with time and may range from 2 per cent, up to

18 per

cent at 30 years.

Slide11

Symptoms

Clinical

presentation depends in large part on the extent

of disease

and the presence

of complications

The

disease remains

confined to

the rectum in 90 per cent of cases but proctitis may

spread proximally

over time. If confined to the rectum (proctitis

), there

is usually no systemic upset and extra-alimentary manifestations are rare. The main symptoms will be rectal

bleeding,

tenesmus

and mucous discharge

.

Colitis is almost always associated

with bloody

diarrhoea

and urgency that can be incapacitating.

Pain is

unusual. Children with poorly controlled colitis may

have impaired

growth.

The

more extensive the disease, the

more likely

extraintestinal

manifestations systemic

illness,

characterised

by

malaise, loss of appetite and fever.

Diarrhoea

may be profuse and bloody, resulting in

anaemia

,

hypoproteinaemia

and electrolyte

disturbance

Slide12

Slide13

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

characterised

by fewer than four stools

daily, with

or without bleeding. There are no systemic signs

of toxicity

, and a normal erythrocyte sedimentation rate (ESR).

•

Moderate disease corresponds to more than four stools daily,

but with few signs of systemic illness. There may be

anaemia

(but

not sufficient to require transfusions).

Abdominal pain

may occur. Inflammatory markers, including ESR

and C-reactive

protein (CRP) are often raised.

Slide14

•

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 and an ominous finding.

•

Fulminant disease

is associated with more than ten

bowel

movements daily, fever, tachycardia, continuous bleeding,

anaemia

,

hypoalbuminaemia

, abdominal tenderness and

distension, blood transfusion requirement 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 immediate surgery if colonic

perforation is to be avoided.

Slide15

Extraintestinal

manifestations

Arthritis

occurs in around 15 per cent of patients and is of

the large joint

polyarthropathy

type, affecting knees,

ankles,elbows

and wrists

.

Sacroiliitis

and

ankylosing

spondylitis

Sclerosing

cholangitis

is associated with UC and can progress to

cirrhosis and

hepatocellular failure. Patients with UC and

sclerosing

cholangitis

are also at a 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 get better with

good colitis

control.

The

eyes can also be affected with uveitis and

episcleritis

.

Slide16

Acute colitis

Around 5 per cent of patients present with severe acute (fulminant) colitis

characterised

by frequent bloody

diarrhoea

,

weight loss

and dehydration.

Intensive

medical treatment and

fluid resuscitation

leads to remission in 70 per cent, but the rest

will require

urgent surgery.

Toxic

dilatation should be suspected

in patients

with active colitis ,

severe

abdominal pain and,

a

plain abdominal radiograph of

colon with a diameter of more than 6 cm (

megacolon

)

abdominal

radiographs should be obtained daily in patients with

severe colitis, and a progressive increase in diameter in spite of

medical therapy is an indication for surgery

.

Colonic perforation in UC is a grave complication with a mortality rate of

40 per

cent.

Slide17

Cancer risk in colitis

The

risk of cancer in ulcerative colitis increases with

duration of

disease. At ten years from diagnosis, it is around 1 per

cent. This

increases to 10–15 per cent at 20 years and may be as

high as

20 per cent at 30 years.

most

patients with

pancolitis

of

more than

ten years’ duration should be entered

into screening

programmes

to detect clinically silent

dysplasia

,

which is

predictive of increased cancer risk

Carcinomatous

change, often atypical

and high

grade, may occur at many sites at

once

Colonoscopic

surveillance

with multiple biopsies is advised to detect

dysplasia and carcinoma.

Slide18

Investigations

Endoscopy and biopsy

Rigid/flexible

sigmoidoscopy

the

mucosa is

hyperaemic

and bleeds on touch, and there

may be

a purulent exudate.

pseudopolyps

.

Later

, tiny ulcers may be seen that

appear to

coalesce. This is quite different from the picture of

amoebic

dysentery

, in which there are large, deep ulcers with

intervening normal

mucosa.

Slide19

Colonoscopy and biopsy has a key role in diagnosis and management:

• to establish the extent of inflammation;

• to distinguish between UC and

Crohn’s

colitis

•

to monitor the response to treatment;

• to assess long-standing cases for malignant change.

Slide20

Slide21

Resection specimen from a patient with

long-standing ulcerative

colitis showing a narrow tubular colon with areas of cancerous change in the rectum and sigmoid

Slide22

Radiology

(1)

: A

plain abdominal film may indicate the severity of disease

development

of toxic

megacolon

in acute cases .

Faeces

are present

only in parts of the colon that are normal

Mucosal

islands can sometimes be seen.

Slide23

Supine abdominal radiograph in toxic

megacolon

.

The transverse

colon is dilated (7 cm), there is no formed residue in

the colon

, and large mucosal islands are present in the ascending

colon and

hepatic flexure. No

haustration

is present in the transverse colon,

Slide24

(2) :

Barium

enema

loss

of

haustra

, especially in the

distal colon

,

pseudopolyps

a

narrow,

featureless, shortened

‘hosepipe’

colon

in chronic cases

(3):

CT

findings

in

pancolitis

may show significant thickening of the colonic wall,

as well

as inflammatory stranding in the colonic

mesentery

Slide25

Double-contrast barium enema showing left-sided ulcerative colitis with a tubular left colon compared with a normal right colon

Slide26

Bacteriology

A stool specimen should be sent for microbiology

analysis

to exclude infective

colitides,notably

Campylobacter

,

Shigella

and

amoebiasis

.

Pseudomembranous

colitis occurs

in hospital

patients on antibiotic treatment and, occasionally,

those on non-steroidal anti-inflammatory drugs (NSAIDs).

The causative

organism is

Clostridium

difficile

.

Immunocompromised patients

are at risk of infective proctocolitis from cytomegalovirus and

cryptosporidia

.

Slide27

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

(COX) enzyme

system.

They can be used long term as

maintenance therapy

.

Corticosteroids

are the mainstay of treatment for

any ‘flare

up’, 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.

More

recently, monoclonal

antibodies;

infliximab and

adalimumab

both act

against

tumour

necrosis factor alpha, which has a central

role in inflammatory cascades.

Slide28

Proctitis

The majority of patients can be managed with rectal

steroids for

an acute attack and oral 5-ASA compounds to

maintain remission

.

Acute

colitis

mild attack (up to four motions a day) usually respond to a course of oral prednisolone given over

a 3-

to 4-week period.

+One

of the 5-ASA compounds

.

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 per

cent of

patients and are emergencies requiring

hospital

admission,Regular

assessment

of

(

vital signs, weight and the

abdomen),

A

stool chart

,

daily

plain abdominal radiograph

is taken

and

inspected for dilatation of

the transverse

colon

..

Fluid and electrolyte balance

is maintained

,

anaemia

corrected and adequate nutrition is provided, sometimes intravenously in severe cases

Slide29

The patient

is treated with

intravenous hydrocortisone

four

times daily

, as well as rectal steroids.

Some

gastroenterologists will use azathioprine,

cyclosporin

A or infliximab in severe

attacks to try and induce remission.

Slide30

Abdominal radiograph demonstrating gas in the wall of

the caecum

Slide31

Indications for

surgery

•

severe or fulminating disease failing to respond to medical

therapy

;

(

no improvement within

3–5 days

.)

•

chronic disease with

anaemia

, frequent stools, urgency and

tenesmus

;

•

steroid-dependent disease (here, the disease is not severe,

but remission

cannot be maintained without substantial doses of

steroids

);

•

inability of the patient to tolerate medical therapy

•

neoplastic

change

•

extraintestinal

manifestations;

•

rarely, severe

haemorrhage

or stenosis causing obstruction.

Slide32

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 rectal stump (really

rectosigmoid

)

is left long and can either be brought out as a mucous fistula

or closed

just beneath the skin.

Slide33

Elective surgery

The indications for elective surgery include:

•

failure of medical therapy/steroid dependence;

•

growth retardation in the young;

•

extraintestinal

disease (

polyarthropathy

and

pyoderma

gangrenosum

respond to colectomy);

•

malignant change.

In the elective setting, four operations are available:

1

Subtotal colectomy and ileostomy (as in an emergency)

2

Proctocolectomy

and permanent end ileostomy

3

Restorative

proctocolectomy

with

ileoanal

pouch

4

Subtotal colectomy and

ileorectal

anastomosis.

Slide34

Slide35

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 incidence of 5 per 100 000

.

more

common in women than in men, and is most

commonly diagnosed

in young patients between the ages of 25 and

40 years

.

Slide36

Aetiology

The

aetiology

of

Crohn’s

disease is incompletely

understood but

is thought to involve a complex interplay of genetic

and

environmental

factors

(chronic infection ,a

diet high in refined

foodstuff

)

Smoking

increases the relative risk of CD

threefold

Approximately

10 per cent of

patients have

a first-degree relative with the

disease

Pathogenesis

A global, and

potentially genetically

determined increase

in gut permeability, combined perhaps with an abnormal

immune-mediated response to

colonisation

of the gut with subspecies of the normal enteric

microflora

, may initiate the disease.

Slide37

Pathology

The

terminal ileum is most commonly involved (60 per cent

),either

in isolation or in combination with colonic

disease . Colitis

alone occurs in up to a third of cases and the

remainder are

patients with more proximal small bowel involvement.

The stomach

and duodenum are affected in around 5 per cent,

but perianal

lesions are common, affecting up to 50–75 per cent

of patients .

Perianal disease occurs in 25 per cent of patients

with small

bowel disease, but in 75 per cent of patients with

Crohn’s

colitis

.

Slide38

Macroscopically,

fibrotic thickening of the intestinal wall with a narrow lumen and

fat wrapping

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 the mucosa

between the ulcers gives rise to a

cobblestone appearance

.

The

transmural

inflammation (which is a key 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.

The

serosa is usually opaque, with thickening of the mesentery and

enlarged

mesenteric lymph nodes.

CD

is characteristically

discontinuous, with

inflamed areas separated from normal intestine,

so-called ‘skip

’ lesions.

Slide39

Microscopically

focal

areas of chronic inflammation involving all layers of the intestinal wall with

lymphoid aggregates.

Non-

caseating

giant cell granulomas

Multifocal arterial occlusions in

the

muscularis

propria

, which is thickened.

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.

Slide40

Clinical

features

CD

may presents

acutely with acute

ileal

inflammation and symptoms

and signs resembling those of acute appendicitis,

or even

free perforation of the small

intestine.

CD may present with fulminant colitis

but this

is considerably less common than

in UC.

Crohn’s

disease more commonly presents with features

of chronicity

manifests as

mild

diarrhoea

extending over many months, occurring in

bouts accompanied

by intestinal colic. Patients may complain of

pain, particularly

in the right iliac fossa, and a tender mass may

be palpable

. Intermittent fevers, secondary

anaemia

and

weight loss

are common

Slide41

After

months of repeated attacks with

acute inflammation, the

affected area of intestine begins to

narrow with

fibrosis, causing obstructive

symptoms. 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

fistula tracts

may develop

.

e.g

(

ileovesical

,

enteroenteric

fistulae

,

enterocutaneous

fistulation

may also

develop

spontaneously

, but more commonly occurs as

complication of abdominal surgery).

Colonic

CD presents with symptoms of colitis and

proctitis

CD

present with perianal

problems

,

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.

Slide42

The rectal mucosa is often spared and may feel normal

on rectal

examination. If it is

involved

it will feel thickened, nodular and

irregular

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

Slide43

Differences between ulcerative colitis and

Crohn’s

disease

■

Ulcerative colitis affects the colon;

Crohn’s

disease 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

Slide44

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

Slide45

Investigations

Laboratory

A

full blood count should be performed, as

anaemia

is

commonand

usually multifactorial, it may result from the

anaemia

of chronic

disease, or 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.

Active

inflammatory disease is usually associated with a fall in serum

albumin, magnesium

, zinc

and selenium

.

Acute

phase protein measurements (C-reactive protein and

orosomucoid

)

Slide46

Endoscopy

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.

stricturing

, and it is important to exclude malignancy in

these

polypoid

mucosa

The

terminal

ileum may

be ulcerated and

strictured

. In patients who have had previous

ileocaecal

resection, recurrent disease usually presents

first with

aphthous

ulceration proximal to

the anastomosis

.

Upper

gastrointestinal symptoms may require

upper

gastrointestinal endoscopy, which may reveal deep longitudinal

ulcers and

cobblestone mucosa in the duodenum, stomach or,

rarely, in

the

oesophagus

Slide47

Imaging

High-resolution

ultrasound

in expert hands can

demonstrate inflamed

and thickened bowel loops, as well as fluid

collections and

abscesses

.

small bowel enema

. This will show 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

.

CT

scans with luminal contrast

can demonstrate

fistulae, intra-abdominal

abscesses and bowel thickening or dilatation

Magnetic resonance imaging (MRI)

is useful in

assessing complex perianal

disease

Slide48

Small

bowel enema examination showing a narrowed terminal ileum involved with

Crohn’s

disease – the ‘string’ sign of Kantor.

Slide49

TREATMENT

Medical treatment

Steroids

Steroids

are the mainstay of treatment for CD. They

induce remission

in 70–80 per cent of cases with moderate to

severe disease.

Aminosalicylates

Colonic symptoms can be treated by 5-ASA agents in a similar

manner to that in UC.

Antibiotics

Metronidazole and ciprofloxacin may be

used for few weeks,

particularly

for

especially in perianal

disease, and when

there is evidence of a mass or an abscess.

Immunomodulatory

agents

Azathioprine

is used for its additive and steroid-sparing effect

and is now standard maintenance therapy.

Cyclosporin

also acts by inhibiting cell-mediated immunity

.

Monoclonal antibody

monoclonal antibodies targeting

tumour

necrosis

factor alpha. Infliximab, the murine

chimaeric

monoclonal antibody

and

Adalimumab

(human monoclonal) are used

for patients

with severe, active disease who are refractory to

other forms

of treatment and who would otherwise be at high risk

of requiring

surgical

intervention

Nutritional support

Slide50

Non-operative management of

Crohn’s

disease

stricturing

may

be amenable

to endoscopic treatment, provided the strictures

can be

reached with

an endoscope .

Dilatation of

an inflamed

and 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

Slide51

Indications for surgery

Surgical resection will not cure CD.

Surgery therefore focuses on

the complications of the

disease. These

complications include:

• recurrent intestinal obstruction

• bleeding

• perforation

• failure of medical therapy

• intestinal fistula

• fulminant colitis

• malignant change

• perianal disease.

Slide52

Surgery

The main surgical principle is to preserve gut length and maintain adequate function

.

•

Ileocaecal

resection is the usual procedure for terminal

ileal

Crohn’s

with a primary anastomosis

•

Segmental resection of short segments of small or large bowel

strictures can be performed.

•

Colectomy and

ileorectal

anastomosis is commonly

performed for

colonic CD with rectal sparing and a normal anus.

•

Subtotal colectomy and ileostomy for

Crohn’s

colitis

•

Temporary loop ileostomy. This can be used either in

patients with acute distal

CD

•

Proctocolectomy

. Patients with colonic and anal disease

failing to respond to medical treatment will eventually

require a permanent ileostomy.

•

Strictureplasty

. Multiple

strictured

areas of CD

can be treated by a local widening procedure,

strictureplasty

, to avoid small bowel resection

Slide53

Strictureplasty