Inflammatory Bowel Disease

Inflammatory Bowel Disease By Dr. Osman Bukhari

-Includes ulcerative colitis (UC) & Crohns disease( CD).
-There is overlap between or they are spectrum of the same disease.
-In 10% of colitis it is difficult to differentiate between them.
-Common in the west. Peak age is20-40 y. M=F.
-Remission & relapses.
Aetiology
-Genetic & enviromental factors.
-Familial:10% with high concordance in id. twins

-Genetics: HLAB27. Association with autoimmune diseases.
-High sugar & low residue diet and smoking are associated with CD.
-Transmissible agent in CD( measles & T.b.)
-Multiangiitis leading to infarction.
-Bact. Endotoxins release NO causing damage.
-Immune response to luminal Ag.( bacterial product or diet) leading to inflammation through cytokins & free O2 radicals with activation & attraction of polymorphs, plasma cells & lymphocytes causing inflmm.& ulcers .

Pathology
-In CD whole GIT is involved. Terminal ileum & ascending colon being commonly affected. Rectal disease is rare. In UC proctitis is invariable & back wash ileitis is rare.
-Macroscopically : In CD small bowel is thickened & narrowed. The lesions are skipped deep ulcers with enlarged L.nodes, abscesses, fissures & fistulae. Toxic colonic dilatation can follow fulminant colitis.
-In UC colitis is continuous with ulceration & is more distally. Pseudopolyps are common.

toxic dilatation can follow fulminant colitis.
-Microscopically: In CD there is transmural non casiating granuloma with normal goblet cells & infrequent crypt abscesses. In UC inflamm. is superficial with chronic inflamm. infiltrates, loss of goblet cells, frequent crypt abscesses. Displasia & Ca are more common.
Clinical features of CD
- presentation is variable depending on the severity & extent of the disease. Mild cases lead normal life with repeated admission in severe cases.

-Major symptoms of abd. Pain, diarrhoea (80%) & weight loss. Abd. Pain is due to peritoneal involvement or obstruction. 10% present wuth acute pain in RIF. Diarrhoea is bloody in colitis & steatorrhoeic in small bowel disease
-Constitutional symptoms of anorexia, N, V, general illhealth & fatigue ( Anemia due to malabsorption of Fe, FA,& B12).
-Abdominal ex.=normal or tender or masses in the RIF ( Inflm. Loops of bowel or abscesses).

-PR =perianal abscess, skin tags, fissures & fistulae sp. with colitis.
-Sigmoidoscopy= rectum may be spared or may be indistinguishable from UC. Take biopsies.
Clinical feature of UC
-Presentation is variable depending on the extent & severity of the disease.
-Bloody diarrhea with mucus & occasionally only blood &mucus. Lower abdominal pain.
-Urgency & tensmus in proctitis without constitutional symptom.

-Anorexia ;nausea & lethargy in total colitis.
-Slight abdominal distension & tenderness.
-PR= normal or tender with blood in the examining finger.
-Mild colitis=up to 4 motions per day.
-Mod. Colitis=4-6 motions per day.
-Severe Colitis = more than 6 motions per day, patient very ill temp. >37.5, pulse >90, Hb <10 g./dl., ser. Albumin <30 g./l. & under nutrition.
Anorexia, nausea

* Fulminent colitis may cause toxic megacolon with perforation or septicemia.
Extra-intestinal manifestations of IBS
(Related to disease activity & more in UC.)
-Clubbing of fingers, E. nodosum, pyoderma gangrenosum & oral aphthus ulcers.
-Episcleritis, conjunctivitis, iritis & uveitis.
-Monoarthritis, sacro-ilitis & ankylosing spondylitis.
-Fatty liver, chronic hep., cirrhosis, autoimmune hep. scl.cholanhitis, cholanioCa.

-Portal pyaemia &liver abscess.
-Auto-immune hemolytic anemia, vasculitis & thrombosis of portal & mesenteric veins.
-Amyloidosis.
* *** Relapses in UC are precipitated by:- Stress, intercurrent infection, G.E, antibiotics & NSAIDs.
Investigations in IBD.
-anemia( multifactorial), raised WBC, ESR & CRP.
-stools ex. To exclude bacterial ,protozal & helmithic infections.

-Low serum albumin & abnormal LFT.
-Blood culture in suspected septicemia.
-Stool culture if diarrhea persist despite Tr.
-Plain abd. X-ray in toxic megacolon.
-Ba.enema : shortening, narrowing & loss of haustrations of colon, granular appearance of colon, pseudopolyps & filling defects. Avoided in acute cases.
-Sigmoidoscopy: engorged hyperemic mucosa which bleed spontaneously in severe cases.
-Colonoscopy: assesses extent & severity of disease

and take multiple biopsies to distinguish between UC & CD.
-Small bowel Ba. follow- through ( abn. Mucosal pattern, skipped lesions, deep ulcers & narrowing_string sign.)
- US fore masses & CT for abscesses & bowel thickening.
Diff. diag :
- Small bowel disease: chronic diarrhea, malabsorption & malnutrition, ileocecal Tb.,

actinomycosis, yersinia, appendicitis & append. Abscess, lymphoma &Ca caecum.
-Infective diarrhea :salmonella, shigella, campylobacter., E.coli hagic colitis, GN & Chlamydia proctitis, pseudomembraneous, herpes simplex & amebiasis.
-Noninfecive colitis: ischemic, radiation, diffuse lymphoma, behcet, NSAID, diverticulitis & colonic Ca.
Management of IBS.
Medical :well balanced diet with protein and energy. Maintain fluid & elect. balance.

-Low fat & milk if malabsorption. High fibre avoided in mall bowel disease, it is beneficial in proctitis & constipation. Iron, folic acid, B12,Vit. D & Ca supplements.
-Drugs: Mild CD treated symptomatically with antidiarrheal.In acute CD admit for induction of remission with Prednsolone 40-60 mg/ day for 2W & reduce to 10-20mg for 6-8 w. Azathioprin for maintenance of steroid induced remission or if Prednsolone fails. Sulphasalasine ( 5ASA) & mesalasine for maintenance of remiss. In colonic CD . Methotrexate, ciclosp & TNF Abs.for those who do not respond to a.m. drugs.

-Antibiotics & Metronidazole bacterial colonization & perianal disease.
-Surgery is required in 80% CD but should be avoided & conservative with minim. resection ( stricture & fistulae, abscess, perforation , toxic megacolon & severe extensive colonic disease if no response to med . TR..). Unlike UC surgery is not curative.
-Medical management in UC: In severe active colitis--- fluid & elect. correction, blood & plasma transfusion , nutrition, S/C heparin to prevent DVT, blood culture & antibiotics if septicemia is suspected.

-Parentral methylprednsolone or oral Prednsolone ( 40-60) for 2W to induce remission & maintain on (5ASA) to prevent relapse. If no response use azathioprin. If no response then surgery. Azathioprin is also used for patients who require high dose steroids for Maintaince.
-Steroid suppositories for proctitis & steroid enema for mild proctocolitis. If no response or if the patient can not retain enema; use systemic steroids. 5ASA can induce remission in mild & mod. colitis but less effective.

- Surgery for UC : Emergency proctocolectomy or colectomy Ist.& later proctosigmoidectomy for toxic dilatation, perforation & hage ,. Acue severe UC failing to med. TR , colonic abscess stricture & long standing total colitis & severe extra-intestinal not responding to med. TR are another indications.
Complications of IBS:
-Fistulae, fissures, abscess & local perforation in CD.
-Toxic colonic dilatation.
- Perforation in toxic dilt.

-Massive hage is rare.
-Ca colon (3-5%) specially in extensive colitis of > 10 years.
-Amyloidosis.
Course in IBS:
- R elapses & remiss. Mortality is twice as common as in normals in CD & is associated with surgery.
-Prognosis is good in proctitis & worse with severe colitis. Mortality 15-25 % in fulmin. colitis

-Low serum albumin & abnormal LFTs.
-Blood culture in suspected septicemia.
-Stool culture if diarrhea is persistent.
=In colitis plain in toxic dilatation of colon,
Ba enema : avoided in acute cases.There is narrowing, shoryening, loss of haustration , ulceration, pseudo polyps &granular appearance.
-Sigmoidoscopy :engorged hyperemic mucosa which bleeds spontaneously or or touch

-Colonoscopy: To assess extenty & severity of the disease, to distinguish between UC &CD & take multiple biopsies.
-Small bowel follow through in CD( skipped lesions, abnormal mucosa, deep ulcerations & narrowing ( string sign)
-CT for abscesses & bowel thickening & US for masses.
Diff. Diagnosis:
-CD of small bowel: chronic diarrhea, malabsorption, malnutrition, ileocecal Tb.,

actinomycosis, appendicitis &abscess, Yesinia ielitis, lymphoma & Ca cecum.
-Colitis: infective colitis ( salmonella, shigella, campylobacter, E. coli hemorrhagic colitis, G.N.& Chlamydia proctitis, pseudomembr.colitis & amebiasis.) AND noninfective colitis ( ischemic, radiation, Behcets, NSAIDs, Ca colon & diverticulitis )

IBD includes UC & CD:
-There is overlap between them & could be spectrum of the same disease & in 10% of colitis it is difficult to say which is which.
-Common in the west .F=M. 20-40 ys.
-Relapses & remissions.
Aetiology
Genetic & enviromental factors are implicated
-Familial
-Genetic associated with HLAB27.
- Dietary: low residue & high sugar diet.

- Smoking in CD. UC more common in non smokers.
-Transmissible agent e.g. measels-mycob.Tb.
-Multifocal angiitis—infarction.
-Bacterial endotoxins liberating NO3 causing damage.
-Luminal Ag. Evocing immune response causing inflammatory response through cytokins & free O2 radicals.

Pathogenesis
Involves activation of macrophages in response to dietary element or bacterial product with release of inflammatory cytokins with activation & attraction of polymorphs, plasma cells & lymphocytes leading to inflammation & ulceration.
Pathology
General:
-In CD whole GIT is involved sp. Terminal ileum &

ascending colon are commonly affected while proctitis is rare. In UC proctitis is invariable & backwash ileitis is rare.
Macroscopic:
-In CD small bowel is thickened with skipped lesions & deep ulcers. Aphthus ulcers, abscesses & fistulae are common. Fulminant colitis & toxic diltation can occur. In UC there is confluent colitis with extensive ulceration and pseudopolyps.

Microscopy
In CD there is transmural non casiating granuloma of the bowl &L. nodes with infrequent crypts abscesses & normal goblet cells. In UC there is superficial chronic inflammatory infiltrate, no granuloma with loss of goblet cells & crypt abscesses.
Clinical picture
In UC clinical picture is variable depending on the site, extent & severity of the disease.

-bloody diarrhoea with mucus. Occasionally only mucus & blood. There is lower abdominal pain, distension & tenderness.
-Urgency & tensmus without constitutional symptoms in proctitis.
-Anorexia, malaise & lethergy in total colitis with aphthoid ulcers.
*Mild colitis =Up to 4 motions/day.
*Mod. Colitis = 4-6 motions/day.
*Severe colitis=More than 6 motions/day. Pat. Is very ill , febrile, Hb < 10gm, pulse >90, albumin <30 gm & undernutrition. Fulminant colitis with diltation, perforation & septicaemia can occur. PR= tender with blood.

In CD clinical picture is variable depending on the extent & severity of disease ranging from mild disease to severe disease with repeated admission.
-Acute or chronic onset with abd. Pain & diarrhoea(80%) with constitutional symptoms of fever, fever,A, N,V, weight loss & fatigue. Colicky pain suggests obstruction. Pain RIF like acute appendicitis.
-Features of malabsorption with anaemia, weihgt loss & vitamin deficiency. Aphth. Ulcer
-Abd. Ex. Normal or tender with masses
-Colitis in CD is similar to UC.
-PR: skin tags, perianal abscesses, fissures & fistulae sp. In CD with colitis.

Extraintestinal manifestations of IBD.
-Clubbing ,E. nodosum, Py. Gangrenosum, Aphthus ulcers & amyloidosis.
-A spondylitis, S/ Ilitis & monoarthritis.
-Conjunctivitis, episcleritis, iritis & uveitis.
-Fatty liver ,chronic hepatitis, cirrhosis, Scler cholangitis, cholangioCa, autoimmune hepatitis, portal pyemia &liver abscess.
-Autoimmune hemolytic anemia, vasculitis, thrombosis including portal mesen. Thrombosis.

Investigations
Aimed at confirming diagnosis, defining disease extent & activity and identifying complications.
-Anemia: multifactorial, high ESR & CRP.
-Low serum albumin & abn. Liver biochemst.
-Stool culture to exclude infections & biood cultures in patients with IBD who develop fever.
-Plain abdominal XR if toxic dilatation & perforation are suspected.

-BA. E nema: narrow & short colon, loss of haustrations, granular appearance, pseudopolyps & filling defects. Ba. Avoided in active disease.
-Sigmoidoscopy: ranges from abnormal vascular pattern in mild colitis to engorged mucosa which may bleeds spontaneously or on touch. Take biopsies. Rectal sparing in CD.
-Colonoscopy: In UC the pathology is continuous, while in CD it I patchy, ulcers are deep & strictures are common. Take multiple biopsies

-Small bowel follow-through in CD shows skipped lesions, deep ulcers & narrow segments ( string sign).
-CT for bowel thickening & abscesses.
-US to detect masses.
Differential diagnosis
-CD should be differentiated from other causes of chronic diarrhoea, malabsosption & malnutrition, ileocaecal Tb., actinomycosis, yersinia, appendicitis & append. Abscess, lymphomas & Ca caecum.

-Colitis in UC & CD should be differentiated from infective colitis ( bacterial or amoebic, & pseudomembraneous colitis ) Or non infective colitis ( ischemic, radiation, lymphoma, behcet, Ca & diverticulitis,).
Management
A-Medical of CD:
-Fluid & electrolyte balance. Maintenance of nutrition with low fat & milk diet if there is malabsorption. Iron, folic acid, B12, vit. D & calcium supplements.

-Symptomatic treatment with antidiarrhoeals in mild cases.
-For severe acute attacks, Prednsolone 40-60 mg. for 1-2 weeks reduced to 10-20 mg. for 6-8 weeks ( Budesonide has less S.E.).

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Inflammatory Bowel Disease

by mohammed sediq on Oct 23, 2009

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