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INFLAMMATORY BOWEL
DISEASE
CROHN’S DISEASE
| Kowshalya Ram |
INTRODUCTION
• Crohn’s disease, chronic trans mural inflammatory disease
of the gastrointestinal tract.
• Although most commonly found in the terminal ileum,
may occur anywhere in the alimentary tract from the
mouth to the anus.
• It may be confined to the large bowel or there may be
involvement of both the small and large intestine.
It was called regional
ileitis because the disease
was first reported in the
terminal ileum.
Epidemiology
• ‘Crohn’s disease’ became
attached to a chronic
inflammatory disease of the
ileum by Burrill Crohn and
colleagues in 1932.
• Incidence in North America and
Northern Europe is 5 in 1L .
• Prevalence in UK 50 in 1L.
Women > Men
Caucasians ,
Jews > Asians,
Africans
Commonly
seen
(1st peak)
Young
patients
b/w the
ages of
25&40
years.
(2nd peak)
around the
age of 70
years.
Aetiology
• The aetiology of Crohn’s
disease is exactly not known.
• But it is an complex interplay
of genetic & environmental
factors.
Infectious
agents
Immunologic
factors
Genetic
factors
Smoking
Race
• INFECTIOUS AGENTS:- No causative organism has ever
been demonstrated.
An intriguing similarity to Johne’s disease of cattle, a
chronic inflammatory enteropathy resulting from infection with
Mycobacterium paratuberculosis, suggests that CD in man may
share a common aetiology.
• Immunologic factors:-Similar to UC, Focal ischemia due
to autoimmune reaction has also been considered.
• Genetic factors:-Mutations within the NOD2/CARD15
gene in chromosome 16q12 have recently been shown to be
associated with Crohn's disease.
• Race:- Relatively high incidence is found in Ashkenazi Jews
& Caucasians.
• Smoking:-It increases the risk of Crohn's disease threefold
unlike its protective effect against ulcerative colitis.
Pathogenesis
Defect in suppressor T cells
Granuloma formation with linear snake like ulcers
Cell-mediated inflammatory response
The release of pro-inflammatory cytokines  IL-2 and TNF
Local and systemic inflammatory responses .
As in UC, it is thought to be an increased permeability of the
mucous membrane.
Increased passage of luminal antigens
Fistula formation
Adhesions
Thickening of the bowel wall (Hose pipe pattern)
Cicatrisation
Pathology
• Skip lesions
• Mouth to anus with relative rectal sparing
• Earliest lesion – superficial aphthous ulcer
• Transmural inflammation
• Commonly ileum and ascending colon
• Fibroses common
• Cobblestone appearance
• Noncaseating granulomas common
• Submucosa is widened
Clinical features
Pain : can be mild or
severe in the abdomen,
joints, lower abdomen, or
rectum .
Gastrointestinal: bloating,
bowel obstruction,
diarrhoea, nausea,
Vomiting .
Whole body: fatigue,
fever, or loss of appetite.
Abdominal: cramping or
tenderness
Anal: fissures or bleeding
Also common: depression,
apthous ulcer, or weight
loss.
EXTRAINTESTINAL COMPLICATIONS
• Skin: Erythema nodosum,
pyoderma gangrenosum—
most common
• Eyes: Iritis, uveitis
• Joints: Arthritis, ankylosing
spondylitis
• Sclerosing cholangitis
• Nephrotic syndrome
• Pancreatitis
• Amyloidosis
• Blood: Anaemia,
thrombocytosis, DVT,
arterial thrombosis.
Differential Diagnosis
• Ulcerative colitis
• Crohn’s disease
• Infective diarrhoea
• Diverticulitis
• Tuberculosis
• Intestinal obstruction
Treatment
INVESTIGATIONS
• Complete blood count (CBC): to rule out anaemia ( RBC),
infection ( platelet)
• C-reactive protein: looks for this protein, which is a sign of
inflammation.
• Iron and B12 levels: These can be low if your small
intestine isn’t absorbing nutrients like it should.
• Active inflammatory disease:- usually associated with In
albumin, magnesium, zinc and selenium.
Endoscopy
• Patchy inflammation.
• 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 structuring.
Radiologic Tests
X-RAY:-
A barium X-ray where barium sulphate
suspension is ingested and fluoroscopic images
of the bowel are taken to check inflammation
and narrowing of the small bowel.
Identifying anatomical abnormalities when
strictures of the colon are too small for a
colonoscope to pass through, or in the
detection of colonic fistulae.
Computerised Tomography:-
• CT is less sensitive than barium studies in detection of early
mucosal changes (i.e ulceration).
• CT is more sensitive than barium studies in detection of
extra luminal changes (mural or extra intestinal).
MRI :-
• MRI scanning for assessing complex perianal disease.
Treatment goals:-
• to reduce inflammation
• to relieve symptoms of pain, diarrhoea, and bleeding
• to eliminate nutritional deficiencies
MEDICAL TREATMENT:-
-Cessation of smoking
-Bed rest, protein and vitamin supplementations. Often
nasogastric tube nutrition is required.
Anti-inflammatory drugs:-Corticosteroids
(prednisone and budesonide) can help reduce inflammation &
induces remission of the disease in initial phase.
• Immunomodulatory agents (Azathioprine) - used for
maintenance therapy. It inhibits the cell mediated immunity.
• Monoclonal antibody (infliximab)- used in severe refractory
cases which act against TNF.
• Antibiotics (Metronidazole and ciprofloxacin)- useful in
controlling sepsis in fistula, colitis.
• Nutritional support:- Elemental diet or parenteral nutrition
can induce remission in up to 80 per cent of patients.
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
• The main surgical principle is to preserve gut length and
maintain adequate function.
• Resection is not the aim of surgery but it may have to be
done in cases of obstruction, perforation, intra-abdominal
abscesses, internal fistulae, bleeding and malignancies.
• Laparoscopic surgery is possible for Ileocaecal or colonic resections.
• A great range of operations is performed for Crohn’s disease
depending on disease pattern – the most common are
Ileocaecal resection-most common type, removes the
terminal ileum and the caecum.
Colectomy and ileorectal anastomosis-surgical removal of
the colon & connecting terminal ileum to rectum.
Subtotal colectomy and ileocolonic anastomosis - resection
of part of the colon & damaged part of the ileum is removed and
the cut end are attached.
• Segmental resection-Resection of short segments of small or
large bowel strictures can be performed.
Temporary loop ileostomy- a loop of small intestine is pulled
out through a cut (incision) in abdomen. This section of intestine is
then opened up and stitched to the skin to form a stoma.
Proctocolectomy- surgical removal of the rectum and all or part
of the colon.
Strictureplasty-Multiple strictured areas of CD can be treated
by a local widening procedure.
CROHN'S DISEASE

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CROHN'S DISEASE

  • 2. INTRODUCTION • Crohn’s disease, chronic trans mural inflammatory disease of the gastrointestinal tract. • Although most commonly found in the terminal ileum, may occur anywhere in the alimentary tract from the mouth to the anus. • It may be confined to the large bowel or there may be involvement of both the small and large intestine.
  • 3. It was called regional ileitis because the disease was first reported in the terminal ileum.
  • 4. Epidemiology • ‘Crohn’s disease’ became attached to a chronic inflammatory disease of the ileum by Burrill Crohn and colleagues in 1932. • Incidence in North America and Northern Europe is 5 in 1L . • Prevalence in UK 50 in 1L. Women > Men Caucasians , Jews > Asians, Africans Commonly seen (1st peak) Young patients b/w the ages of 25&40 years. (2nd peak) around the age of 70 years.
  • 5.
  • 6. Aetiology • The aetiology of Crohn’s disease is exactly not known. • But it is an complex interplay of genetic & environmental factors. Infectious agents Immunologic factors Genetic factors Smoking Race
  • 7. • INFECTIOUS AGENTS:- No causative organism has ever been demonstrated. An intriguing similarity to Johne’s disease of cattle, a chronic inflammatory enteropathy resulting from infection with Mycobacterium paratuberculosis, suggests that CD in man may share a common aetiology. • Immunologic factors:-Similar to UC, Focal ischemia due to autoimmune reaction has also been considered.
  • 8. • Genetic factors:-Mutations within the NOD2/CARD15 gene in chromosome 16q12 have recently been shown to be associated with Crohn's disease. • Race:- Relatively high incidence is found in Ashkenazi Jews & Caucasians. • Smoking:-It increases the risk of Crohn's disease threefold unlike its protective effect against ulcerative colitis.
  • 10.
  • 11. Defect in suppressor T cells Granuloma formation with linear snake like ulcers Cell-mediated inflammatory response The release of pro-inflammatory cytokines  IL-2 and TNF Local and systemic inflammatory responses . As in UC, it is thought to be an increased permeability of the mucous membrane. Increased passage of luminal antigens
  • 12. Fistula formation Adhesions Thickening of the bowel wall (Hose pipe pattern) Cicatrisation
  • 13. Pathology • Skip lesions • Mouth to anus with relative rectal sparing • Earliest lesion – superficial aphthous ulcer • Transmural inflammation • Commonly ileum and ascending colon • Fibroses common • Cobblestone appearance • Noncaseating granulomas common • Submucosa is widened
  • 15. Pain : can be mild or severe in the abdomen, joints, lower abdomen, or rectum . Gastrointestinal: bloating, bowel obstruction, diarrhoea, nausea, Vomiting . Whole body: fatigue, fever, or loss of appetite.
  • 16. Abdominal: cramping or tenderness Anal: fissures or bleeding Also common: depression, apthous ulcer, or weight loss.
  • 17. EXTRAINTESTINAL COMPLICATIONS • Skin: Erythema nodosum, pyoderma gangrenosum— most common • Eyes: Iritis, uveitis • Joints: Arthritis, ankylosing spondylitis • Sclerosing cholangitis • Nephrotic syndrome • Pancreatitis • Amyloidosis • Blood: Anaemia, thrombocytosis, DVT, arterial thrombosis.
  • 18. Differential Diagnosis • Ulcerative colitis • Crohn’s disease • Infective diarrhoea • Diverticulitis • Tuberculosis • Intestinal obstruction
  • 20. INVESTIGATIONS • Complete blood count (CBC): to rule out anaemia ( RBC), infection ( platelet) • C-reactive protein: looks for this protein, which is a sign of inflammation. • Iron and B12 levels: These can be low if your small intestine isn’t absorbing nutrients like it should. • Active inflammatory disease:- usually associated with In albumin, magnesium, zinc and selenium.
  • 21. Endoscopy • Patchy inflammation. • 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 structuring.
  • 22.
  • 23. Radiologic Tests X-RAY:- A barium X-ray where barium sulphate suspension is ingested and fluoroscopic images of the bowel are taken to check inflammation and narrowing of the small bowel. Identifying anatomical abnormalities when strictures of the colon are too small for a colonoscope to pass through, or in the detection of colonic fistulae.
  • 24.
  • 25. Computerised Tomography:- • CT is less sensitive than barium studies in detection of early mucosal changes (i.e ulceration). • CT is more sensitive than barium studies in detection of extra luminal changes (mural or extra intestinal). MRI :- • MRI scanning for assessing complex perianal disease.
  • 26. Treatment goals:- • to reduce inflammation • to relieve symptoms of pain, diarrhoea, and bleeding • to eliminate nutritional deficiencies MEDICAL TREATMENT:- -Cessation of smoking -Bed rest, protein and vitamin supplementations. Often nasogastric tube nutrition is required. Anti-inflammatory drugs:-Corticosteroids (prednisone and budesonide) can help reduce inflammation & induces remission of the disease in initial phase.
  • 27. • Immunomodulatory agents (Azathioprine) - used for maintenance therapy. It inhibits the cell mediated immunity. • Monoclonal antibody (infliximab)- used in severe refractory cases which act against TNF. • Antibiotics (Metronidazole and ciprofloxacin)- useful in controlling sepsis in fistula, colitis. • Nutritional support:- Elemental diet or parenteral nutrition can induce remission in up to 80 per cent of patients.
  • 28. 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
  • 29. • The main surgical principle is to preserve gut length and maintain adequate function. • Resection is not the aim of surgery but it may have to be done in cases of obstruction, perforation, intra-abdominal abscesses, internal fistulae, bleeding and malignancies.
  • 30. • Laparoscopic surgery is possible for Ileocaecal or colonic resections. • A great range of operations is performed for Crohn’s disease depending on disease pattern – the most common are Ileocaecal resection-most common type, removes the terminal ileum and the caecum.
  • 31. Colectomy and ileorectal anastomosis-surgical removal of the colon & connecting terminal ileum to rectum.
  • 32. Subtotal colectomy and ileocolonic anastomosis - resection of part of the colon & damaged part of the ileum is removed and the cut end are attached.
  • 33. • Segmental resection-Resection of short segments of small or large bowel strictures can be performed.
  • 34. Temporary loop ileostomy- a loop of small intestine is pulled out through a cut (incision) in abdomen. This section of intestine is then opened up and stitched to the skin to form a stoma. Proctocolectomy- surgical removal of the rectum and all or part of the colon.
  • 35. Strictureplasty-Multiple strictured areas of CD can be treated by a local widening procedure.