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Crohn’s Disease

In 1932 Crohn, Ginsburg and Oppenheimer described it as inflammatory disease of the terminal part of the ileum in adults, hence popularly known as “regional ileitis”, but later scientists described it as the inflammatory process throughout the entire GIT tract hence better termed as “regional enteritis”.

Etiology:
The cause is not well understood but the process is undoubtedly one of the non-specific inflammations. There are different views:
  • Due to Streptococci, B. Coli or dysenteric organisms
  • Due to acid fast bacilli
  • Type of sarcoidosis
  • Due to Lymphatic blockage
  • Due to foreign body reaction to silica or other irritants. This is the most popular view
Pathology:
Pathology usually occurs in the terminal ileum involving limited segment, usually about 12 inches. Distally the pathology stops at the ileocecal valve. Proximal to lesion there is healthy gut but still proximal to it, there is usually a small lesion i.e. a skip lesion. It is believed that further skip lesion often microscopic do exist and re the cause of recurrence after the resection of affected loop (50-60%). There are two forms of the disease: Acute and Chronic.

In acute form:
  • the loop is grossly congested and somewhat oedematous
  • The mesentery is congested and contains enlarged soft nodes
  • There is no evidence of caseation anywhere
In chronic form:
  • There is grossly thickening of the wall by the granulomatous and fibrous tissue deposits particularly in submucosal and subserosal coats. Hypertrophying wall makes the lumen irregularly narrow and gut becomes stiff like a hose pipe with loss of capacity to contract. The granulomatous tissue doesn’t show signs of caseation but there is giant cell system. The mucous membrane shows patchy ulceration
  • The adjacent mesentery is grossly thickened and edematous. It contains enlarged and fleshy lymph nodes, which never caseate or calcify
  • Subsequently multiple strictures develop in the gut
  • Still later dense adhesions, abscesses and fistula formations are likely to develop
Clinical Features:
Acute Form:
It is very similar to acute appendicitis excepting that instead of constipation diarrhoea occurs.

Chronic Form:
It has four stages:
  1. The inflammatory stage, when the mass is palpable in the right iliac region
  2. The colitis stage, when diarrhea, anemia, fever and weight loss is present
  3. Stenotic stage, when picture of bowel obstruction supervenes
  4. Fistula formation stage internal or external – communicating with sigmoid colon, bladder, cecum, etc.
Investigations:
Stool examination is useful to detect the presence of blood, mucus and often steatorrhoea. Barium enema provides the diagnosis:

In non-stenoting stage:
  • Lack of segmentation with loss of peristalsis
  • Strengthening of vulvulae conniventes
  • The oedematous mucosa in between ulcers produce multiple filling defects (it gives a cobble stone appearance) seen after evacuation of meals.
When stenosis sets in:
There is gross irregular narrowing of the lumen, which in its extreme stage shows barium as narrow as string (string sign of Kantor).

Treatment:
Acute:
No treatment is required. It usually subsides itself and appendectomy should not be performed by mistake.

Chronic:
    Medical:
    • Sulphasalazine or antibiotics
    • Cortisone
    Surgical treatment:
    Surgical treatment is indicated when:
    • Failure with medical treatment
    • Presence of intestinal obstruction
    • Fistula formation
    In such cases right hemicolectomy is performed. “Defunctioning ileo-transverse anastomosis” is done due to skip lesions.
Click here to see the differences between Crohn's Disease and Ulceratice Colitis.

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This article has been written by Dr. M. Javed Abbas.
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21:01 21/12/2002