32 years old male presented with complaint of loose stools with blood

for 3 months and abdominal pain for 2 months. Initially stool

frequency was 2 to 3 per day but for last 2 weeks it has become 6 to 8
per day. Abdominal pain is in the lower abdomen, colicky in nature and
relieved by defecation. There is also complaint of right knee joint pain
for last 1 month with no overlying swelling or redness.
Inflammatory Bowel
Disease
Definition

• Inflammatory bowel disease (IBD) is a term for two conditions

(Crohn’s disease and ulcerative colitis) that are characterized by
chronic inflammation of the gastrointestinal (GI) tract.

• A crucial distinction is that ulcerative colitis only involves the colon,

while Crohn’s disease can involve any part of the gastrointestinal tract
from mouth to anus.
• The incidence of inflammatory bowel disease (IBD) varies widely
between populations.

• In the West, the incidence of ulcerative colitis is stable at 10–20 per

100,000, with a prevalence of 100–200 per 100 000, while the
incidence of Crohn’s disease is increasing and is now 5–10 per
100,000, with a prevalence of 50–100 per 100 000.
• Life expectancy in patients with IBD is similar to that of the general
population.

• Both diseases most commonly start in the second and third decades
of life, with a second smaller incidence peak in the seventh decade.
Pathophysiology

• Inflammatory bowel disease has both environmental and genetic

components.

• It is thought that IBD develops because these genetically susceptible

individuals mount an abnormal inflammatory response to
environmental triggers, such as intestinal bacteria.
• This leads to inflammation of the intestine with release of
inflammatory mediators, including TNF, IL-12 and IL-23, which cause
tissue damage.

• In both diseases, the intestinal wall is infiltrated with acute and

chronic inflammatory cells but there are important differences
between the conditions in the distribution of lesions and in histological
features.
Ulcerative colitis
• Inflammation invariably involves the rectum (proctitis) and spreads
proximally in a continuous manner to involve the entire colon in some
cases (pancolitis).

• In long-standing pancolitis, the bowel can become shortened and post-

inflammatory ‘pseudopolyps’ develop; these are normal or hypertrophied
residual mucosa within areas of atrophy.

• The inflammatory process is limited to the mucosa and spares the deeper
layers of the bowel wall.
• Both acute and chronic inflammatory cells infiltrate the lamina
propria and the crypts (‘cryptitis’).

• Crypt abscesses are typical. Goblet cells lose their mucus and, in long-
standing cases, glands become distorted.
• Dysplasia, characterised by heaping of cells within crypts, nuclear
atypia and increased mitotic rate, may herald development of colon
cancer.
Crohn’s disease

The sites most commonly involved are, in order of frequency,

• Terminal ileum and right side of colon

• Colon alone

• Terminal ileum alone

• Ileum and jejunum

• The mesenteric lymph nodes are enlarged and the mesentery
is thickened.

• Crohn’s disease has a patchy distribution and the inflammatory process is

interrupted by islands of normal mucosa.

• On histological examination, the bowel wall is thickened with a chronic

inflammatory infiltrate throughout all layers
Clinical Features
Ulcerative colitis

• The cardinal symptoms are rectal bleeding with passage of mucus and
bloody diarrhoea.

• The presentation varies depending on the site and severity of the

disease as well as the presence of extra-intestinal manifestations.
• The first attack is usually the most severe and is followed by relapses
and remissions.

• Emotional stress, intercurrent infection, gastroenteritis, antibiotics

or NSAID therapy may all provoke a relapse.

• Proctitis causes rectal bleeding and mucus discharge, accompanied by tenesmus.

• Some patients pass frequent, small volume fluid stools, while others pass pellety
stools due to constipation upstream of the inflamed rectum.

• Constitutional symptoms do not occur. Left-sided and extensive colitis causes bloody
diarrhoea with mucus, often with abdominal cramps.

• In severe cases, anorexia, malaise, weight loss and abdominal pain occur, and the
patient is toxic, with fever, tachycardia and signs of peritoneal inflammation.
Crohn’s disease

• The major symptoms are abdominal pain, diarrhoea and weight loss.

• Ileal Crohn’s disease may cause subacute or even acute intestinal obstruction.

• The pain is often associated with diarrhoea, which is usually watery and does
not contain blood or mucus.

• Almost all patients lose weight because they avoid food, since eating provokes
pain.
• Weight loss may also be due to malabsorption, and some patients present with features
of fat, protein or vitamin deficiencies.

• Crohn’s colitis presents in an identical manner to ulcerative colitis, but rectal sparing and
the presence of perianal disease are features which favour a diagnosis of Crohn’s disease.

• Many patients present with symptoms of both small bowel and colonic disease.

• A few patients present with isolated perianal disease, vomiting from jejunal strictures or
severe oral ulceration.
• Physical examination often reveals evidence of weight loss, anaemia with
glossitis and angular stomatitis.

• There is abdominal tenderness, most marked over the inflamed area.

• An abdominal mass may be palpable and is due to matted loops of

thickened bowel or an intra-abdominal abscess.

• Perianal skin tags, fissures or fistulae are found in at least 50% of patients.
Complications
• Life-threatening colonic inflammation

• This can occur in both ulcerative colitis and Crohn’s colitis.

• In the most extreme cases, the colon dilates (toxic megacolon) and bacterial
toxins pass freely across the diseased mucosa into the portal and then
systemic circulation.

• An abdominal X-ray should be taken daily because, when the transverse

colon is dilated to more than 6 cm, there is a high risk of colonic perforation,
although this complication can also occur in the absence of toxic megacolon.
• Haemorrhage
Haemorrhage due to erosion of a major artery is rare but can occur in both
conditions.

• Fistulae
These are specific to Crohn’s disease. Enteroenteric fistulae can cause diarrhoea and
malabsorption due to blind loop syndrome. Enterovesical fistulation causes recurrent
urinary infections and pneumaturia.
An enterovaginal fistula causes a faeculent vaginal discharge. Fistulation from
the bowel may also cause perianal or ischiorectal abscesses, fissures and fistulae.
• Cancer
The risk of dysplasia and cancer increases with the duration and
extent of uncontrolled colonic inflammation.

• Thus patients who have long-standing, extensive colitis are at highest

risk. Oral mesalazine therapy reduces the risk of dysplasia and
neoplasia in ulcerative colitis.
• Azathioprine also seems to reduce the risk of colorectal cancer in ulcerative
colitis and Crohn’s colitis.

• This protective effect probably extends to any medical treatment

that results in sustained healing of the colonic mucosa.

• The cumulative risk for dysplasia in ulcerative colitis may be as high as 20%
after 30 years but is probably lower for Crohn’s colitis.
• The risk is particularly high in patients who have concomitant primary
sclerosing cholangitis for unknown reasons.

• Tumours develop in areas of dysplasia and may be multiple. Patients

with long-standing colitis are therefore entered into surveillance
programmes beginning 10 years after diagnosis
• Targeted biopsies of areas that show abnormalities on staining with
indigo carmine or methylene blue increase the chance of detecting
dysplasia and this technique (termed pancolonic chromo-endoscopy)
has replaced colonoscopy with random biopsies taken every 10 cm in
screening for malignancy.
• The procedure allows patients to be stratified into high-, medium- or
low-risk groups to determine the interval between surveillance
procedures.
• If high-grade dysplasia is found, panproctocolectomy is usually
recommended because of the high risk of colon cancer.
Extra-intestinal complications

• Extra-intestinal complications are common in IBD and may dominate

the clinical picture.

• Some of these occur during relapse of intestinal disease; others

appear unrelated to intestinal disease activity
Investigations

• Investigations are necessary to confirm the diagnosis, define disease

distribution and activity, and identify complications.

• Full blood count may show anaemia resulting from bleeding or

malabsorption of iron, folic acid or vitamin B12.

• Serum albumin concentration falls as a consequence of protein-losing

enteropathy, inflammatory disease or poor nutrition.
• The ESR and CRP are elevated in exacerbations and in response to
abscess formation.

• Faecal calproctectin has a high sensitivity for detecting gastrointestinal

inflammation and may be elevated, even when the CRP is normal.

• It is particularly useful in distinguishing inflammatory bowel disease

from irritable bowel syndrome at diagnosis, and for subsequent
monitoring of disease activity.
• Bacteriology
At initial presentation, stool microscopy, culture and examination for Clostridium
difficile toxin or for ova and cysts, blood cultures and serological tests should be
performed.

• These investigations may need to be repeated in established disease to exclude

superimposed enteric infection in patients who present with exacerbations of IBD.

• During acute flares necessitating hospital admission, three separate stool samples
should be sent for bacteriology to maximise sensitivity.
• Endoscopy
Patients who present with diarrhoea plus raised inflammatory markers or
alarm features, such as weight loss, rectal bleeding and anaemia, should
undergo ileocolonoscopy.

• Flexible sigmoidoscopy is occasionally performed to make a diagnosis,

especially during acute severe presentations.

• In ulcerative colitis, there is loss of vascular pattern, granularity, friability

and contact bleeding, with or without ulceration.
• In Crohn’s disease, patchy inflammation, with discrete, deep ulcers,
strictures and perianal disease (fissures, fistulae and skin tags), is typically
observed, often with rectal sparing.

• In established disease, colonoscopy may show active inflammation with

pseudopolyps or a complicating carcinoma.

• Biopsies should be taken from each anatomical segment (terminal ileum, right
colon, transverse colon,left colon and rectum) to confirm the diagnosis and define
disease extent, and also to seek dysplasia in patients with long-standing colitis.
• In Crohn’s disease, wireless capsule endoscopy is useful in the
identification
of small bowel inflammation but should be avoided in the presence of
strictures.

• Enteroscopy may be required to make a histological diagnosis of small

bowel Crohn’s disease, when the inflamed segment is out of reach of
standard endoscopes.
• Radiology
Barium enema is a less sensitive investigation than colonoscopy in
patients with colitis and, where colonoscopy is incomplete, a CT
colonogram is preferred.

• Traditional contrast imaging by barium follow-through demonstrates

affected areas of the bowel as narrowed and ulcerated, often with
multiple strictures.
• MRI enterography, which does not involve exposure to radiation and
is a sensitive way of detecting extraintestinal manifestations and of
assessing pelvic and perineal involvement.

• A plainabdominal X-ray is essential in the management of patients

who present with severe active disease.
• Dilatation of the colon, mucosal oedema (thumb-printing) or evidence of perforation
may be found.

• In small bowel Crohn’s disease, there may be evidence of intestinal obstruction or

displacement of bowel loops by a mass.

• Ultrasound is a very powerful tool to detect small bowel inflammation and stricture
formation, but it is rather operator-dependent.

• The role of CT is limited to screening for complications, such as perforation or abscess

formation, in the acutely unwell
Management
• Management depends on establishing a multidisciplinary team-based
approach involving physicians, surgeons, radiologists, nurse specialists
and dietitians.

• The key aims of medical therapy are to

Treat acute attacks (induce remission) prevent relapses (maintain

remission).
Prevent bowel damage

Detect dysplasia and prevent carcinoma

Select appropriate patients for surgery

Ulcerative colitis
• Active proctitis.  Most patients with ulcerative proctitis respond to a
1 g mesalazine suppository but some will additionally require oral 5-
aminosalicylate (5-ASA) therapy.

• Topical corticosteroids are less effective and are reserved for patients
who are intolerant of topical mesalazine.

• Patients with resistant disease may require treatment with systemic

corticosteroids and immunosuppressants.
• Active left-sided or extensive ulcerative colitis. In mild to
moderately active cases, the combination of a once daily oral and a
topical 5-ASA preparation (‘top and tail approach’) is usually effective.

• The topical preparation (1 g foam or liquid enema) is typically

withdrawn after 1 month.

• The oral 5-ASA is continued long-term to prevent relapse and

minimise the risk of dysplasia.
• In patients who do not respond to this approach within 2–4 weeks,
oral prednisolone (40 mg daily, tapered by 5 mg/week over an 8-week
total course) is indicated.

• Corticosteroids should never be used for maintenance therapy.

• Severe ulcerative colitis.  Patients who fail to respond to maximal oral therapy
and those who present with acute severe colitis are best managed in hospital and
should be monitored jointly by a physician and surgeon:

• clinically: for the presence of abdominal pain, temperature, pulse rate, stool
blood and frequency

• by laboratory testing: haemoglobin, white cell count, albumin, electrolytes, ESR

and CRP

• radiologically: for colonic dilatation on plain abdominal X-rays

• Supportive treatment with intravenous fluids to correct dehydration, and
enteral nutritional support for malnourished patients.

• Intravenous corticosteroids (methylprednisolone 60 mg or hydrocortisone

400 mg/day) should be given by intravenous infusion or bolus injection.

• Response to therapy is judged over the first 3 days. Patients who do not
respond promptly to corticosteroids should be considered for medical
rescue therapy with ciclosporin (intravenous infusion or oral) or infliximab
(5 mg/kg).
• Patients who develop colonic dilatation (> 6 cm), those whose clinical
and laboratory measurements deteriorate and those who do not
respond after 7–10 days’ maximal medical treatment usually require
urgent colectomy.

• Subtotal colectomy can also be performed laparoscopically, given

sufficient local expertise.
• Maintenance  of  remission

• Life-long maintenance therapy is recommended for all patients with left-

sided or extensive disease but is not necessary in those with proctitis

• Once-daily oral 5-aminosalicylates are the preferred first-line agents.

• Sulfasalazine can be considered in patients with coexistent arthropathy.

• Patients who frequently relapse despite aminosalicylate drugs should be

treated with thiopurines.
• Crohn’s disease
Principles  of  treatment.  Crohn’s disease is a progressive condition
which may result in stricture or fistula formation if suboptimally treated.

• It is therefore important to agree long-term treatment goals with the

patient; these are to induce remission and then maintain corticosteroid-
free remission with a normal quality of life.

• Treatment should focus on monitoring the patient and ensuring that

mucosal healing is achieved.
• Induction  of  remission.  Corticosteroids remain the mainstay of treatment for
active Crohn’s disease.

• The drug of first choice in patents with ileal disease is budesonide.

• A typical regimen is 9 mg once daily for 6 weeks, with a gradual reduction in dose
over the subsequent 2 weeks when therapy is stopped. If there is no response to
budesonide within 2 weeks, the patient should be switched to prednisolone,
which has greater potency.
• This is typically given in a dose of 40 mg daily, reducing by 5 mg/week
over 8 weeks, at which point treatment is stopped.

• Oral prednisolone in the above dose regimen is the treatment of

choice for inducing remission in colonic Crohn’s disease.

• Calcium and vitamin D supplements should be co-prescribed in

patients who are on corticosteroids.
• Some patients with severe colonic disease require admission to
hospital for intravenous corticosteroids.

• In severe ileal or panenteric disease, induction therapy with an anti-

TNF agent (Infliximab and Adalimumab) is appropriate, provided that
acute perforating complications, such as abscess, have not occurred.
• Maintenance  therapy

• Immunosuppressive treatment with thiopurines (azathioprine and

mercaptopurine) forms the core of maintenance therapy, but methotrexate is also
effective and can be given once weekly.

• Women of childbearing potential who are prescribed methotrexate must use a

robust contraceptive method, since it is teratogenic.

• Combination therapy with an immunosuppressant and an anti-TNF antibody is the

most effective strategy but costs are high and there is an increased risk of serious
adverse effects.
• Careful monitoring of disease activity is the key to maintaining
sustained remission and preventing the accumulation of bowel
damage in Crohn’s disease.

• Cigarette smokers should be strongly counselled to stop smoking at

every possible opportunity.
• Fistulae and perianal disease

• Fistulae may develop in relation to active Crohn’s disease and are

often associated with sepsis.

• Surgical exploration by an examination under anaesthetic is usually

then required.

• Corticosteroids are ineffective. For simple perianal disease,

metronidazole and/or ciprofloxacin are first-line therapies.
• Thiopurines can be used in chronic disease but do not usually result in
fistula healing.

• Infliximab and adalimumab can heal fistulae and perianal disease in

many patients.
Surgical treatment
• Ulcerative colitis

Up to 60% of patients with extensive ulcerative colitis eventually

require surgery. The indications are

• Surgery involves removal of the entire colon and rectum, and cures

the patient. One third of those with pancolitis undergo colectomy

within 5 years of diagnosis.

• The choice of procedure is either panproctocolectomy with ileostomy,

or proctocolectomy with ileal–anal pouch anastomosis.

• Crohn’s disease
The indications for surgery are similar to those for ulcerative colitis.

• Operations are often necessary to deal with fistulae, abscesses and perianal
disease, and may also be required to relieve small or large bowel obstruction.

• In contrast to ulcerative colitis, surgery is not curative and disease recurrence is

the rule.

• The only method that has consistently been shown to reduce post-operative
recurrence is smoking cessation. Antibiotics are effective
in the short term only.
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