What is Crohns Disease?

Crohns disease is a type of inflammatory bowel disease, characterized by

transmural granulomatous inflammation, in which the body launches an
autoimmune attack on the bowel. It most commonly affects the terminal ileum,
however it can affect any part of the gastrointestinal tract, from the mouth to the
anus.
It is characterized histologically by transmural granulomatous inflammation. The
prevalence is thought to be around 30 per 100,000, with males and females
equally at risk.
Like many autoimmune diseases its onset is usually in early adult life (teens to
early twenties) and as a result it has a huge psychological and physical impact on
an individuals quality of life and ability to function in society.
Cause
Crohns disease is caused by a combination of genetic and environmental factors,
which provide the necessary environment for the development of disease.
Over 30 gene mutations have been associated with an increased risk of Crohns
disease
(e.g. NOD2/CARD15).
Many of the genes are involved in the regulation of immune response.
Siblings of those with Crohns disease are up to 30 times more likely to develop the
disease as compared to the general population, suggesting a strong genetic
component.
It was thought that Crohns disease at its core was a disease related to T-cell
autoimmunity, however other research suggests that it may be a disease related to
impaired innate immunity, which prevents individuals from being able to clear
microbes from the bowel wall, causing over activity of adaptive immunity (T-cell
response) leading to a sustained inflammatory response to the bowel tissue.
Risk factors
1.
2.
3.
4.
5.

Family history of disease

Smoking increases risk by 3 fold
increased intake of animal & milk protein
Less in Asian
NSAIDs may exacerbate the disease.

Symptoms
1. Abdominal pain
2. Urgency/ Diarrhea (smells so bad) may or may not be bloody
Wakes up at nightMay go 4-5 times a day or in hours
3. Weight loss / Failure to thrive
4. Fever

5. Malaise
6. Anorexia
7. Nausea & Vomiting can occur due to strictures / bowel obstruction
(smells so bad)
8. Perianal Discomfort itching, pain due to fistulas / abscesses
9. Mouth / Aptheous ulcers
10.
Patient may say I can feel fine for a minute and terribly ill in
the second.
Signs
1. Abdominal tenderness
2. Abdominal masses most commonly right iliac fossa (terminal
ileum)
3. Perianal abscesses / skin tags
4. Fistulas
5. Rectal / Anal strictures may be noted on PR
6. Aptheous ulcer
Extra-intestinal Features of Crohns
Clubbing skin eye joint problems
1.
2.
3.
4.
5.
6.
7.
8.

Finger clubbing
Aptheous ulcer
Episcleritis / Uveitis inflammation of the episclera or uvea
Seronegative Spondylarthropathy inflammation of axial skeleton Rh
factor -ve
Erythema Nodosum red tender nodules which are usually located over
the shins
Pyoderma Gangrenosum necrotic deep ulcers, often on the legs
Deep Vein Thrombosis
Autoimmune haemolytic anaemia antibody mediated lysis of RBCs

Complications
1. Malabsorption often resulting in significant weight loss, electrolyte
disturbances
2. Fistula formation entero-cutaneous, colo-vesicular, bowel to bowel, PeriAnal, colo-vaginal
3. Perforation
4. Rectal Hemorrhage
5. Fatty liver
6. Primary Sclerosing Cholangitis
7. Cholangiocarcinoma
8. Renal stones
9. Osteomalacia
10.
Malnutrition
11.
Amyloidosis
12.Abscess formation (abdominal pelvic or ischiorectal)
13.Small bowel obstruction vomiting, abdominal distension, dilated bowel
loops on AXR, absolute constipation

14.Toxic Megacolon can lead to perforation (usually at the caecum) leading

to peritonitis (less common than in UC)
15.Colonic carcinoma continuous inflammation increases the risk of
malignant changes

Investigations
Bloods

FBC anemia inflamed / ulcerated bowel mucosa results in blood loss

ESR
U&E
LFT
INR
Ferritin
TIBC
CRP may be elevated, useful for monitoring response to treatment
Serum iron
B12 & Folate often deficient as mainly absorbed in terminal ileum, which
is commonly affected

Stool
Fresh blood
Microscopy & culture rule of infection (c.diff (CDT), salmonella, shigella,
campylobacter, E. coli, CMV, EBV)
Colonoscopy +/- biopsy allows direct visualization & histology of mucosa to be
assessed. Take rectal biopsy even if mucosa looks normal 20 % have microscopic
granulomas)
o

Skip lesions

Fistulas

Histology reveals loss of crypt architecture & full thickness mucosal

inflammation

Small bowel enema detects ileal disease

Barium Enema Rarely used (cobblestoning rose thorn ulcers +/- strictures
Capsule endoscopy
AXR look for small bowel dilatation obstruction
MRI assess pelvic disease and fistulas/ Site of strictures

CT Colonography often used instead of colonoscopy in more elderly / frail

patients
Differential Diagnosis
Ulcerative colitis
Infective colitis C.Diff / CMV / E-coli / Shigella Campylobacter
Ischemic colitis
Management

Assess severity T inc ,Pulse inc ,WCC inc, ESR inc,CRP inc, + decrease in albumin
Admit
Liver often switches to producing CRP type proteins rather than albumin
Specific options : Amino-salicylates, Steroids, Immuno-suppressants, TNF inhibitors,
Diet, Antibiotic, Supplements
First line mild disease

(Symptomatic but systemically well)

First presentation or a single inflammatory exacerbation in a 12 month

period (mild):
o

Prednisolone initial high dose with a stepwise decrease in dose over a

number of weeks

Budesonide or 5-aminosalicylate (5-ASA) are less effective alternatives for

those who cant tolerate prednisolone

Budesonide & 5-ASA are NOT to be used as first line management of severe
exacerbations

Elemental diet for 6 weeks to induce remission mainly used for children
with mild disease

Regular review in clinic

Second line / Severe flares (looks ill) Admit for IV steroids hydrocortisone
Second line therapy is considered if there are 2 or more inflammatory exacerbation
in a 12 month period or if tapering of corticosteroid treatment has failed.
o

Hydrocortisone treat rectal disease

Metronidazole

Monitor T, Pulse, BP, stool frequency and character

P/E daily and FBC ESR CRP U&E AXR

If (Hb <100g/L) transfuse + Parenteral nutrition

Consider adding Azathioprine or Mercaptopurine to first line corticosteroid

treatment

TPMT levels need to be assessed prior to starting these treatments TPMT

metabolises these drugs

Methotrexate can be used if Azathioprine / Mercaptopurine are not

tolerated or if TPMT levels are deficient

Azathioprine can cause neutropaenia closely monitor FBC & advise patient
to seek medical help if develops sore throat etc

Methotrexate can cause bone marrow suppression, liver toxicity and

pulmonary toxicity monitoring needed

Third Line Biologics

To be used in severe active Crohns disease which is unresponsive to 1st &
2nd line therapies
o

Infliximab and Adalimumab are monoclonal antibodies

Infliximab and Adalimumab target Tumor Necrosis Factor Alpha

Surgery
50-80% require surgery at some point in their life
Indications include
o

Failure to respond to medical therapy

Intestinal obstruction

Intestinal perforation

Fistulas & Abscesses

Surgery can involve:

o

Resection of heavily diseased bowel

Strictureplasy to resolve bowel obstruction caused by strictures

Treatment of fistulas between bowel segments

Risks of surgery:
o

Bleeding / Perforation / Infection

Poor wound healing

Small bowel syndrome inability to absorb nutrients due to extensive bowel

resection

Prognosis
Most patients live a normal life span, however this depends upon disease severity.
Patients are at a significantly increased risk of small bowel & colorectal carcinoma.