Surgery : Crohn’s Disease
Also called regional enteritis
Chronic transmural inflammatory disease of GIT
Aetiology :
⁃ Immunological
⁃ Genetic factors - single strongest risk factor for development is a
relative with crohns
⁃ infectious - mycobacterium paratuberculosis, measles
⁃ Smoking - 3x increase
Pathology :
• starts in terminal ileum as ulceration
• Intense infiteration of mononuclear cells, Extensive inflammatory
oedema and mucosal ulcers
• Fibrous thickening of intestine results in hose pipe rigidity
• Segments of normal intestine in bw - skip areas (characteristic) +
cobble stone appearance
• Proximal bowel dilated and distal bowel collapsed
• Mesenteric nodes are enlarged and can get calcified
• As disease progresses , Non caseating circatrising granuloma in bowel
wall >> causes narrowing of lumen and intestinal obstruction (CASSEATION ABSENT)
• Once inflammation spread to serosa, adhesions develop between bowel
loops or other structures
Types :
1. Stricturing
2. Inflammatory
C/F:
Intermittent colicky lose abdominal pain , diarrhoea, wt loss common
Signs - pyoderma, clubbing, iritis, scleritis , aphthous ulcers
Depending on symptoms :
• Stage of ileocolitis
• Stage of intestinal obstruction
• Stage of fistula formation
• Perianal disease (anal fissure is the most common problem)
Dx :
1. Small bowel enema (enteroclysis) - MR enteroclysis
⁃ cobble stone reticulation due multiple ulcers and island of normal
⁃ Abcent peristalsis in terminal ileum
⁃ String sign of Kantor in terminal ileum due to narrow lumen
⁃ Multiple structures and dilated segments
2. Sigmoidoscopy and colonoscopy - inflamed mucosa (patchy inflammation)
with discrete aphthoid ulcers (ulcer surrounded by Edema produces target sign) ,
• fissure ulcers (rose thorn appearance),
• nodular pattern due to submucosal Edema of Vili
• Cobble stone appearance
• straightening of mesenteric border, saculations of anti mesenteric
border
3. Loss of layering, Doppler shows mucosal hyper vascularity
Also called regional enteritis
Chronic transmural inflammatory disease of GIT
Aetiology :
⁃ Immunological
⁃ Genetic factors - single strongest risk factor for development is a
relative with crohns
⁃ infectious - mycobacterium paratuberculosis, measles
⁃ Smoking - 3x increase
Pathology :
• starts in terminal ileum as ulceration
• Intense infiteration of mononuclear cells, Extensive inflammatory
oedema and mucosal ulcers
• Fibrous thickening of intestine results in hose pipe rigidity
• Segments of normal intestine in bw - skip areas (characteristic) +
cobble stone appearance
• Proximal bowel dilated and distal bowel collapsed
• Mesenteric nodes are enlarged and can get calcified
• As disease progresses , Non caseating circatrising granuloma in bowel
wall >> causes narrowing of lumen and intestinal obstruction (CASSEATION ABSENT)
• Once inflammation spread to serosa, adhesions develop between bowel
loops or other structures
Types :
1. Stricturing
2. Inflammatory
C/F:
Intermittent colicky lose abdominal pain , diarrhoea, wt loss common
Signs - pyoderma, clubbing, iritis, scleritis , aphthous ulcers
Depending on symptoms :
• Stage of ileocolitis
• Stage of intestinal obstruction
• Stage of fistula formation
• Perianal disease (anal fissure is the most common problem)
Dx :
1. Small bowel enema (enteroclysis) - MR enteroclysis
⁃ cobble stone reticulation due multiple ulcers and island of normal
⁃ Abcent peristalsis in terminal ileum
⁃ String sign of Kantor in terminal ileum due to narrow lumen
⁃ Multiple structures and dilated segments
2. Sigmoidoscopy and colonoscopy - inflamed mucosa (patchy inflammation)
with discrete aphthoid ulcers (ulcer surrounded by Edema produces target sign) ,
• fissure ulcers (rose thorn appearance),
• nodular pattern due to submucosal Edema of Vili
• Cobble stone appearance
• straightening of mesenteric border, saculations of anti mesenteric
border
3. Loss of layering, Doppler shows mucosal hyper vascularity
