Inflamatory Bowel Disease Dr Shatdal

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INFLAMMATORY BOWEL DISEASE Dr. Shatdal Chaudhary Assistant Professor BP Koirala Institute of Health Sciences Dharan, Nepal Shatdalchaudhary@yahoo.com

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Inflammatory Bowel Disease (IBD) Definition:- Comprises those conditions characterized by a tendency for chronic or relapsing immune activation and inflammation within the GI tract. Types – Idiopathic - Crohn’s disease - Ulcerative colitis - Identified etiology - Diversion colitis - Bypass enteropathy - Radiation colitis - Drug induced colitides.

CROHN’S DISEASE : 

CROHN’S DISEASE Condition of Chronic inflammation potentially involving any location of the alimentary tract from mouth to anus but with a propensity for the distal small bowel and proximal large bowel. Often discontinuous along the logitudinal axis of the gut but may involve all layers from mucosa to serosa. Cardinal symptoms – Diarrhoea, abdominal Pain and often wt loss.

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Etiology and Pathogenesis Initiating Events: Proposed as the causative organism of Crohn’s disease Chlamydia, listeria monocytogenes, cell wall deficient Pseudomonas species , reo virus Paramyxovirus Mycobacterium Paratuberculosis Infamamation is kept in check through an active process of immune tolerance. Tolerance – mediated by CD4 + helper T cells. Immune response may be skewed toward cell mediated immunity or toward humoral immunity and production of cytokine profile by CD4 +T Cell.

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T helper 1 ( Th1) – IL - 2 and INF – r - Support cell mediated immunity and delayed hypersensitivity type response T helper 2 ( Th2) - IL-4, IL-5, IL-10 - Humoral immunity anf antibody production . In Crohn’s disease, CD4 + T cells have a clear cut Th 1 cytokine profile. b) Amplification and Tissue Reaction On activation, macrophages further shape and amplify the immune response by producing IL – 2 and the proinflammatory cytokines IL- 1 and TNF.

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C) Genetics. -First degree relatives is 14 to 15 times higher than general population - Roughly one of five patients with crohn’s disease will report having at one affected relatives. - Jews ( 2-4 fold) > Non Jews in Eastern European. - Monozygotic twin -67%

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d) Environment: - breast feeding ( Protective) - high socioeconomic status - oral contraceptive - NSAIDs - Increased intake of refined sugars and a paucity of fresh fruits and vegetables in the diet - increased dietary fiber intake. - smoking.

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Pathology: Macroscopic Features - affect any part of the G1 tract from mouth to anus. - Some, 30-40% - small bowel 40 to 55% - small and large intestines 15 to 25% - colitis alone - In the 75% of pts with small- intestine disease, the terminal ileum is involved in 90%. - Rectum is often spared in CD. - CD is segmental , with skip areas in the midst of diseased intestine.

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- Perirectal fistulas, fissures, abscesses, and anal stenosis are present in one-third of pts with CD, particularly those with colonic involvement. - CD may also involve the liver and the Pancreas. - Endoscopically – Aphthous or small superficial ulcerations characterize mild disease; in more active disease, stellate ulcerations fuse longitudinally and transversely to demarcate islands of mucosa that frequently are histologically normal – “ Cobblestone” appearance. - Pseudopolyps can form in CD.

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Crohn's Disease - Cobblestoning; This picture shows a small bowel opened longitudinally. The mucosal surface contains an irregular longitudinal ulcer running down the center and expanding toward the hemostat into broader ulcers. The end opposite the hemostat shows a "cobblestone" pattern in which the remaining edematous mucosa bulges up around the ulcers.

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- Acive CD is characterized by focal inflammation and formation of fistula tracts, which resolve by fibrosis and stricturing of the bowel. The bowel wall thickens and becomes narrowed and fibrotic, leading to chronic, recurrent bowel obstruction. b. Microscopic feature. - Earliest lesions are aphthoid ulcerations and focal crypt abscesses with loose aggregations of macrophages, which form non caseating granulomas in all layers of the bowel wall from mucosa to serosa. - Grannuloma can be seen in lymph nodes, mesentery, Peritoneum, liver and pancreas. - Granulomas are a pathognomic feature of CD. - Submucosal or Subserosal lymphoid aggregates.

Crohn's Disease of the Terminal Ileum : 

Crohn's Disease of the Terminal Ileum Crohn's Disease of the Terminal Ileum

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Clinical Manifestations Disease location Predilection for the distal small bowel and proximal large bowel. 50% affecting both ileum and colon. 1/3 rd – small bowel primarily the terminal ileum Oesophagus, stmoach or duodenum – rare and almost always association with disease of the more distal small bowel or large bowel.

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B. Clinical Presentation - Compared with ulcerative colitis, abdominal pain is a more frequent and persistent complaint., intermittent and colicky in nature or sustained and severe. - delay in diagnosis - > 1 yrs. - Fecal ocult blood + in ½ pt. but gross rectal bleeding is uncommon. - constitutional symptoms – wt. loss, fever

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Typical Presentations. Disease of the ileum, often accompanied by cecum. - Small bowel obstruction ( Precipitated by impaction of indigestible foods such a raw vegetables or fruits) - intermittent colicky Pain, along with nausea & vomitting. - Fullness or tender mass in the right hypogastrium ( during obstruction) - Active inflammatory component – anorexia, loose or frequent stools, and wt. loss. - Malnutrition. - right lower quadrant pain mimicking appendicitis.

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2. Colonic disease primarily rt colon or extend distally to involve most or all of the colon. - typically presenting symptoms is diarrhoea, occasionally with passage of obvious blood. - severity of diarrhea – related with both the extent of colitis and severity of inflammation. - Abdominal pain. - wt. loss & malaise. 3. Perianal disease. - 24% - Skin lesion – maceration, superficial ulcers, and abscesses - Anal canal lesion – fissures, ulcers, stenosis. (more eccentrically) - Perianal fistulas.

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b) Unusual Presentations: 1. Upper G1 tract crohn’s disease. - Younger at the time of diagnosis - present with abd. Pain and malaise. - Gastroduodenal crohn’s disease presents as H. pylori- negative peptic ulcer disease, with dyspepsia or epigastric pain 2.Esophageal - rare - <2% - dysphagia, odynophagia, substernal chest pain, and heart burn. - wt. loss

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- Aphthous ulcer – mouth and posterior pharynx. - Esophageal stricture and even esophagobronchial fistula. 3. Jejunum & Ileum. - Frank malabsorption and steatorrhea 4. Appendix - resembles acute appendicitis and occasionally periappendicular abscess C. Disease Behavior Two categories 1. Fibrostenotic – obstructing pattern 2. Penetrating fistulous pattern.

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a) Fistula and Abscess. Fistula – Frequent manifestation. - release of proteases and matrix metalloproteinases – tissue destruction – sinus tract formation – penetration to adjacent tissue planes. Perianal fistula – common 15 – 35% (Also, scrotum, buttocks or things ii) Enteroenteric, enterocolonic, & colocolic fistula. -also coloduodenal or cologastric fistula. iii) Rectovaginal fistula - Enterovaginal fistula- who had a hysterectomy, permitting direct extension to the adjacent vaginal cuff.

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iv) Enterovesicular or colovesicular fistula. v) enterocutaneous fistula to ant. Abdomen. - enterocutaneous fistula after appendectomy for what had been presumed to the appendicitis. 2. Abscess – 1/4the will present with an intra abdominal abscess - classic presentation of intra abdonimal abscess spiking fever and focal abdominal tenderness or localized peritoneal signs

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b) Stricture. - represent long standing inflammation. - likely to recur, most often at the anastomosis. - Silent until the luminal caliber is small enough to cause relative obstruction. -Colicky post prandial abdominal pain and bloating - radiographic “string sign” marked narrowed bowel bowel segment. .

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Table. Vienna Classifacation of Crohn’s disease Age of onset A1 <40y A2 > 40 y 2. Location L1, terminal itlum L2, colon L3, ileocolon L4, upper gastrointestinal 3. Behaviour B1, nonstricturing , nonpenetrating B2, stricturing B3, Penetrating

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Diarrhoea  ed stool frequency and ed stool consistency arise through alteration in mucosal function & intestinal motility. i) Altered fluid and electrolyte absorption & secretion. ii) Increased mucosal permeablitiy iii) Imbalance in the luminal conc. of bile acids relative to dietary fat. iv) Bacterial overgrowth v) Drug – olsalazine & any of the 5 amino salicylate. Pathophysiology of common symptoms & sign

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3. Abdominal Pain - Stretch receptors in the bowel wall + as a food bolus passes through stenotic bowel – abd. Pain and possibly vomitting. - Visceral pain – result from inflammation of the serosa - substance p c. wt. Loss & malnutritions -Deficiencies in iron, folic acid, vit. B12, Ca, magnesium, Zn, and particularly in the setting of malabsorption from small bowel disease, fat soluble vitamins. - inadequate intestinal absorption

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-increased protein losses through exudation. - Medication –  Ca absorption – glucocorticord Malabsorption of fat, fat soluble vitamin & Ca – Cholestyramine Folate malabsorption – sulfasalazine - increased energy and protein requirement –catabolic state - poor oral intake – fear of eating due to pain. D. Anorexia, nausea & vomitting - contribute to wt. loss & poor nutrition. - TNF - Drugs – metronidazole, sulfasalazine, 6- mercaptopurine, azathioprine and methotrexate

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E. Fever – low grade IL-1, IL- 6 & TNF F. Anaemia – 1/3 rd Pt. - Primarily as a consequece of iron from losses. Macrocytic anaemia – Vit B12 deficiecny because of ileal disease or resection Folate dificiency because of proximal small bowel disease or sulfasalazine therapy. -  production of Interferon – Y, TNF or IL-1 – (-) erythropoietin Production.

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Extra intestinal manifestation - 1/4 the of Pt. ¼ the of those affected will have >1 manifestation. Nephrolithiasis resulting from oxalate malabsorption. 1.Musculoskeletal manifestation. - Disorders of the bone and Joints - Clubbing - Pauciarticular arthopathy. -Peripheral arthralgia – 16 to 20% - Accompanied by skin complication ( erythema nodosum) and eye (uveitis)

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- pts are seronegative for rheumatoid factor. -knee & ankles- often affected first. - Axial arthropathies – less common -Ankylosing spondylitis - Symmetic sacroilitis - Complicaton include granulomatous vasculitis, periostitis & amyloidosis - metabolic bone disease – osteopenia or osteporosis. 2. Mucocutaneous manifestations. - Pyoderma gangrenosum - Erythema nodosum

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3. Ocular manifestation – 6% - Episcleritis - scleritis - Uveitis. 4.Hepato biliary manifested - Gall stones – 25% - Asymptomatic and mild elevations of liver biochemical tests - primary sclerosing cholangitis – 4% - Peri cholangitis - Fatty liver and autoimmune hepatitis.

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5. Renal and genitourinary manifestations. Uric acid and oxalate stones ---result from volume depletion & hypermetabolic state Rare-membranous nephropathy, glomerulonephritis,& renal amyloidosis. 6.Coagulation and vascular complication - Prothrombotic tendency – venous thrombo embolism or less commonly arterial thrombosis.

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. - Circulating immune complexes,  levels of plasminogen activator inhibitors, ed levels of tissue plasminogen activator & spontaneous platelet aggregation. - Folate and Vit. B12 deficiency – linked to hyperhomocysteinemia – turn predisposes to thrombosis . 7. Other manifestation. - lung – subclincal - heart – cardiomyopathy, pleuropericarditis, myocarditis, endocarditis - pancrease- acute pancreatitis, granulomatous pancreatitis.

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Establishing the diagnosis. -Diagnosis is established through a total assessment of the clinical presentation with confirmatory evidence from radiographic , endoscopic, and in most cases, pathologic finding. -History- key symptom and their severity and duration. Specific point-recent travel history, antibioiotic use, diet & sexual activity. -Family history -laboratory:-increases ESR and CRP -.Anaemia & hypoalbuminemia .

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-TLC –N or elevated. -Stool -for ova & parasite c/s. Cl.dfficile toxin Serology for E.histolylica Endoscopy – rectal sparing aphthous ulceration fistulas & skip lesion Barium enema- filling defect Radiographic - aphthous ulceration & thickened fold. - “ cobble stoning”. CT scan - mural thickenng > 2cm.

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Crohn's Disease: Aphthoid Ulcers. This is a portion of a colon opened longitudinally from a patient with acute activation of Crohn's disease. One of the earliest areas of breakdown in the mucosa can be seen as tiny pin-point erosions of the surface.

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Crohn's Disease, Barium Enema showing cobblestoning. This picture illustrates a portion of colon during a barium enema study. The barium is the white substance pooled in the dependent portions of the bowel. The cobblestoning pattern can be seen in the loop of bowel from which the barium has drained away leaving a very delicate picture of the mucosal pattern in that area.

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Serologic markers P ANCA – 5 to 10 % (general population – 2to 3% PANCA (+)) ASCA- 60to 70% CD (ASCA was associated e small bowel CD) sensitivity -50to 65% specificity – 85%

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*Differentiating crohn's disease from UC Feature CD UC Abd pain Frequent & prominent Preachy campy (occasionally) Diarrhea watery or voluminous stool usually; occasionally constipation Gross blood in stool occasionally frequently. Mucus in stool occasionally frequently Abd mass frequently rarely Abd tenderness frequently rarely Intestinal obstruction frequently rarely Perianal disease frequently rarely

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Perianal fistulas frequently No Rectovaginal fistula occasionally rarely Abscess occasionally No 12. Recurrence the surgery Yes No Toxic mega colon rare infrequent. Current smoker frequently rarely Former smoke rarely frequently Macrocytic anemia Occasionally rarely 17 PANCA 20% 70% 18. ASCA 65% 15%

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Endoscopy CD UC 19. Distribution of disease Involves any segment Contiguous Involvement of of GI tract colon from rectum proximal 20. Abnormalities proximal to terminal ileum Sometimes No 21. Abnormal terminal ileum Frequent Occasionally 22. Ileocecal valve narrowed normal 23. Rectal involvement 25-50% 95-100% 24. Continuous Colitis rarely Yes 25. Bowel wall thickening marked None or moderate 26. Cobblestone appearance Frequent rare

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Radiographic Stricture Frequently occasionally Asymmetric colitis Yes No Segmental colitis Yes No. Ulceration Depth- aphthous to deep Superficial Fistulas often Rarely Treatment A Goals of therapy. .No cure .Primary – to induce and maintain remission - -To achieve theses goals, the intention is to ameliorate symptoms and improve the quality of life.

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other goals - Specific to the problems or characteristics of the pt. such as healing a fistula or achieving normal growth in child. b). Therapy a. Active disease mild-moderate – 1. 5-ASA oral and/or enema 2. Metronidazole and / or ciprofloxacin. 3. Oral glucocorticoids 4. Infliximab 5. Budesonide Severe - 1. 5 ASA oral and/ or enema 2. Metronidazole and / or ciprofloxacin 3. Oral or IV glucocorticoids 4. Infliximab 5. TPN or elemental diet

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Perianal or fistulizing disease 1. Metronidazole and /or ciprofloxacin 2. Azathioprine or 6-MP 3. Infliximab 4. I.V. CSA b. Maintenance Therapy Inflammatory 1. 5 ASA oral and/ or enema 2. Anathioprine or 6-MP 3. Infliximab Perianal or fistulizing disease 1. Meteronidazole and / or ciprofloxacin 2. Azathioprine or 6 – MP 3. Infliximab

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Nutritional therapy:- Purposes- Repletion of nutrients and treatment of the primary disease Protein calorie malnutrition – enteral supplement. Lactose intolerant (many)- calcium supplement TPN – with severe malnutrition before surgery or selected pts with severe disease. Surgical Therapy -At least one operation in their life time . -80% chance of requiring surgery-small bowel disease 50% chance of requiring surgery-colitis

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-Small intestine disease Types:-a) surgical resection of the diseased segment b) strictureplasty- Indications-1. Stricture and obstruction unresponsive to medical therapy. 2.Massive hemorrhage 3.Refractory fistula 4.Abscess. Colorectal disease Precedures-1.Temporary loop ileostomy 2. Resection of segments of diseased colon or even the entire colon and rectum. 3.Diverting colostomy 4.Total protocolectomy and ileostomy.

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Indications:-1.Intractable disease 2.Fulminant disease 3.Perianal disease unresponsive to medical therapy. 4.Refractory fistula 5.Colonic obstruction 6.Cancer prophylaxis 7Colon dysplasia or cancer. Sexuality,fertility,and pregnancy :- Sexuality- In men and women,decreases libido from symptoms such as diarrhea, abdominal pain, fatigue or dyspareunia from rectovaginal fistula .

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.Fertility- decreases Pregnancy – depends on the status of the disease at conception. “one third rule – 1/3rd -improve - 1/3rd -worse - 1/3rd -unchanged - Postpartum relapses are uncommon and tend to be mild. - Small number –still birth, spontaneous abortion or premature labor, 2/3rd had active disease during the pregnancy.

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Prognosis Morbidity - 1st yr,,relapse rate 50%,with 10% had chronic relapse course Cancer - colorectal cancer - if large bowel involves – increases risk of colorectal cancer. - increases risk of small bowel adenocarcinoma. - Association betn Hodgkin’s and Non-Hodgkin’s lymphoma. -Squamous cell carcinoma Mortality:- -highest in the first 4 or 5yr after diagnosis. -15yrs survival rate -93.7% -proximal small bowel disease –higher risk of mortality.

Ulcerative Colitis : 

Ulcerative Colitis Definition:- Ulcerative colitis is an inflammatory disorder that affects the rectum and extends proximally to affect a variable extent of the colon. History:- Samuel wilks – Guy’s Hospital – Recognized Sir Arthur Hurst – Complete description

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Epidemiology Worldwide disorder United kingdom, USA, Northern Europe and Australia Among Whites, incidence 3-15 / 100000 yrs. A. Age and Sex: All age Primarily young adults (20 to 40 yr.) Secondary Peak – elderly Women > men. B. Ethnic Variation - In USA, Jews more prone than non- Jews C. Urban – Rural Differences - more in Urban D. Socioeconomic factors: - Higher incidence among higher salaried or better educated members.

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Genetics:- Familial association noted in first degree relatives. Younger age of onset in offspring – inheritance from parents. Concordance rates – monozygotic twins – 13% -Dyzygotic twins – 2% Chromosome 2, 3 , 6 ,7 and 12 HLA – DR 2 ( DR B1 * 502 ) – Disease susceptibility in Japanese and Jewish HLA- DR1 ( DR B1* 0103) – Severe disease. P-ANCA marker for the DRB* 1502 allele of HLA – DR. (Among Jewish) Non Jewish, antibody associated with the HLA –DR3 DQ2 – TNF < 2 haplotype.

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ETIOLOGY A. Infection E. coli B. Food allergy Milk C. Environmental factors Smoking - common among nonsmokers - relative risk in nonsmoker -2 to 6 -high for exsmoker(exheavy smoker > ex light smoker)esp. within the first 2 years -decrease mucus production -alter colonic mucosal blood flow - decreases mucosal permeability Oral contraceptives

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IMMUNOPATHOGENESIS A. Humoral responses -increases in plasma cells -Ig G1 and Ig G3 - associated with autoimmune disorder(eg. Thyroid disease ,DM ,pernicious anemias ) -P-ANCA – 60 to 80% -within lamina propria and IgG1 subclass B. Cellular responses -T-cell - CD8+cells -Macrophages –IL-1beta,TNF,and IL-6 (+) acute phase response - Interferon gamma - permiability TGF-beta, IL-1, IL-6 -- (+)collagen synthesis PSYCHOSOCIAL FACTORS -illness or death in family -divorce or separation -interpersonal conflict ,major loss

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Pathology:- Macroscopic features:- - Approxi – 20% total colitis 30 to 40% - extending beyond the sigmoid but not involving the whole colon 40 to 50% - limited to rectum and rectosigmoid. With mild inflammation - mucosa – hyperemic, edematous & ranular severe disease – mucosa – hemorrhagic , edematous & ulcerated.

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Ulcerative Colitis. This is a close-up picture of the mucosal surface of a bowel with active ulcerative colitis. The important features to note here are multiple shallow ulcers and intense hyperemia of mucosa between them.

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ulcer - irregular with overhanging edges - linear along the line of the teniae coli - In long standing , inflammatory poly( pseudopolyp) – exuberant generation of the epithelium . - In many years of disease , it appears atrophic and featureless and entire colon becomes narrowed and shortened . - Fulminant disease – develop a toxic colitis or megacolon - may lead to perforation .

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Microscopic features :-- Limited to the mucosa and superficial submucosa, with deeper layers unaffected except in fulminant disease. - Mucosal vascular congestion with edema and focal hemorrhage, and inflammatory cell filtrate of neutrophils, lymphocyte , plasma cell and macrophage. - Neutrophils invade the epithelium – usually in crypts – cryptitis – crypt abscess

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CLINICAL FEATURES - Major symptoms – diarrhea , rectal bleeding, the passage of mucus and abdominal pain. - weeks or even months . - slow , insidious onset . A) Rectal bleeding :- - hemorrhagic proctitis – passing fresh blood, either separately from the stool or streaked on the surface of a normal or hard stool. - Blood usually mixed with stool or grossly bloody diarrhea- if extends beyonds the rectum. - Severe disease – liquid stool containing blood , pus, and fecal mater.

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B) Diarrhea :- - not always present - Post prandial diarrhea –common. - Urgency , with feeling of in complete evacuation. - Diarrhea associated with passing large quantities of mucus, often with blood and pus - Failure to absorb salt and water is perhaps the predominant factor. - reduced Na/ k – ATPase pump - increase permeability - altered membrane phospholipids .

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C) Abdominal pain :- - not a prominent symptom - vague lower abdominal discomfort, an ache in left iliac fossa, or mild central abdominal cramping . - increase tension with in the inflamed colonic wall. D) Other symptom :- - anorexia - nausea, vomitting - wt loss & hypoalbuminemia protein loss through inflamed mucosa hypercatabolism down regulation of albumin synthesis

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-Fever -breathlessness, ankle swelling and fatigue – Anaemia -Sec. to blood loss - Bone marrow suppression (from Chr. Inflamation). - Drugs ( 6-mercaptopurine, azathioprine, sulfasalazine.) SIGNS: Tender anal canal and blood on rectal examination Digital examination – mucosa feel “Velvety” and edematous Tachycardia Sign of iron deficiency. Dependent edema Oral candidiasis or aphthoid ulceration of the oral mucosa Clubbing

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Ulcerative Colitis: Disease Presentation MILD - 1. <4per day bowel movement 2. small blood in stool 3.No fever 4.No tachycardia 5.Mild anemia 6.ESR < 30 mm 7.Endoscopic – erythema, decreased vascular pattern, fine granularity MODERATE 1. 4-6per day bowel movements 2. Moderate amount of blood in stool.

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3.<37.5 C mean 4.< 90 mean pulse 5.> 75% -anemia 6 Endoscopic -marked erythema, coarse granularity ,absent vascular markings, contact bleeding, no ulcerations SEVERE 1.> 6 per day 2.severe blood in stool 3.>37.5 C mean 4.> 90 mean pulse 5.<75% - anemia 6.endoscopic – spontaneous bleeding, ulceration.

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Laboratory Data  acute phase reactants in serum (CRP, orosomucoid), plat. Count & ESR.  Hb and s. albumin. Neutrophilic leukocytosis. P/s – band cells (young neutrophil) – severe attacks. DIAGNOSIS Stool samples -contain many pus cells, RBC and frequently eosinophils. - C/S to rule out salmonella spp. And shigella spp. Campylobacter spp. Cl difficile

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Sigmoidosopic Appearance - best performed in the unprepared bowel. - Earliest sigh – blaring or loss of the vascular pattern with hyperemia and edema of the mucosa. - Pseudopolyp ( long standing) Colonoscopy - not necessary for diagnosis in most pts. - Especially useful for assesing pts whose symptoms seem out of proportion to the known radiologic extern of disease .

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D. Radiology : - Plain supine film of abdomen. - margin of the colon becomes edematous irregualar. - for detecting the presence of fecal material . - if the diagnosis in doubt , an “instant” enema can be performed. - Double contrast barium enema – fine mucosal granularity The mucosal line becomes irregular . Superficial ulcer - “en face”. Deep ulcer- “Collar stand” or “ Collar- button” - loss of haustration- long standing disease. esp. Ascending and transverse colon. - Shortening and narrowing of colon. Biopsy - Rigid sigmoidoscopy- taken on the posterior wall within 10cm of the anal canal to minimize the risk of perforation

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Chronic Ulcerative Colitis. This is an air contrast barium enema study in which a barium enema was evacuated and then the colon was insufflated with air. This is an excellent way to see the contour of the internal mucosal surface of the bowel. Notice that in this picture the haustral markings of the normal colon have disappeared and the colon appears to be a fairly straight rigid tube. Also, the distribution of barium over the mucosal surface is irregular and there is apparent pooling of the barium, possibly in small ulcers and erosions. Pseudopolyps can be seen as dark dots surrounded by a ring of white. The dark dots would be the pseudopolyp projecting up above the surface where the barium has pooled. This is almost a mirror image of the apthoid ulcers which appear as a solid white dot of barium pooled in a pit in the mucosal surface

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F. Laboratory date - Iron deficient (0.5g of elemental iron can be lost during the attack). Microcytic hypochromic anaemia -Thrombocytosis , leukocytosis . - eosinophilia , monocytosis. - hypokalemia , hypoalbuminaemia & increases serum gamma 2 globulin levels . - minor increases in aspartate aminotrasferase or alkaline phosphates . - Serum immunoglobulin -increases – active diseasa - fall in remission .

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D/D:-

Extraintestinal manifestations of UC: : 

Extraintestinal manifestations of UC: Related to activity of colitis - peripheral arthropathy - Erythema nodosum - Episcleritis - Apthous ulceration of the mouth. - Fatty Liver B. Usually related to activity of colitis - pyoderma gangrenosum - Anterior Uveitis.

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C. Unrelated to colitis - Sacroilitis - Ankylosing spondylitis - Primary sclerosing Cholangitis D. Rare - Pericarditis - Acute febrile neutrophilic dermatosis ( sweet’s syndrome) - Amyloidosis

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Treatment Regimens - Medical - Surgery Medical Active disease Mild Prednisolone 20mg orally/ daily Topical glucocorticoids 4 weeks then tapered if remission has occurred 5-ASA compound before glucocorticoids

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2. Moderate - oral glucocorticoids, Prednisolone 40—60 mg/daily. 20 mg over 2 to 3 weeks - Then, as mild disease. 3. Severe Disease. - Admitted hospital - IV fluids. - IV glucocorticoids (eg. Hydrocortisone 100mg iv 6 hrly or methylprednisolone 16mg iv 6 hrly) together with rectal glucocorticoids twice daily. - A rectal drip of Hydrocortisone 100 mg in 100 ml water given over 20 to 30 minutes.

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Continued for 5 to 7 day if the pt continues to improve. Good Response Feel well No fever or tachycardia Colon not tender on a abdominal palpation Diarrhea <4 / day. Then – started on oral Prednisone (eg. 40 mg daily) Plus a 5 –ASA drug and a light diet) If deteriorates during the first few day – surgery I.V. cyclosporine (induce remission – who does not improve rapidly with iv glucocorticoid) 4 mg/kg continue oral cyclosporin (5 mg/kg), taper glucocorticoids over 6 to 8 weeks, and then stop the cyclosporine at 3 to 6 months. [ Also, add Azathioprin or cyclosporin + Azathioprin]

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Indicators of a Poor Prognosis (in severe UC) a. Clinical and laboratory parameters - No. of bowel movements>9 - Pulse > 100 / min. - Maximum temperature > 38 c - Serum albumin < 3 mg/dl. b. Radiologic Signs - Mucosal islands - Colonic dilatation - Small bowel distension. B. Chronic Active Disease. - Admitted - iv. Glucocorticoids - Immunosuppressive therapy can be used eg. Azathioprine and 6-MP- over 3 to 6 weeks if benefit - continued for several months ( 18 to 24 months)

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Maintenance Therapy - 5 – ASA drug eg. Mesalamine preparations, eg olsalazine and balsalazide - fewer adverse effects - as effective as sulfasalazine - used indefinitely because 5- ASA exerts its suppressive effect on the disease over many years. .

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B. Indication for surgery The indications for colectomy Severe attacks that fails to respond to medical therapy. Complications for severe attack (eg. Perforation, acute dilatation) Chronic continuous disease with an impaired quality of life. Dysplasia or carcinoma. Choice of Operation 1. Proctocolectomy with a permanent Brooke ileostomy – .for elderly person. . Impaired anal sphincter pressure. 2. Proctocolectomy with an ileoanal pouch – operation of choice. 3. Colectomy with an ileorectal anastomosis. – rarely performed.

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Complication Perianal Lesion - Anal fissure - perianal abscesses - Hemorrhoids 2. Massive Hemorrhage – 1% - if pts requires 6 to 8 units of blood within 24 to 48 hrs and are still bleeding , urgent colectomy 3. Perforation - most dangerous - 16% mortality. - malaise, tachycardia, reduced bowel sounds–only C/F. - urgent colectomy with in a few hours.

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4. Acute dilatation (Toxic Megacolon) - defined as a transverse colon diameter of > 6 cm with loss of haustration in a pt with a severe attacks of UC. - 5% - triggered by hypokalemia or the opiates. - iv. Glucocorticoids – no response than emergency colectomy 5. strictures. 6. Pseudopolyps - All parts of colon although rectum often spared.

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Figure 36. Ulcerative Colitis - Toxic Megacolon. This is a resected portion of colon with toxic megacolon opened longitudinally. The dilated portion is readily visible. The gross features of toxic megacolon are identical to those of ordinary ulcerative colitis except that the bowel appears dilated and perhaps a bit more hemorrhagic and severely involved than the usual ulcerative colitis.

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7. Colorectal cancer. - highest in pts with extensive or total colitis - disease for 10 yrs. - began at an early or chronic continuous course – higher risk. Course and Prognosis 80% of UC – intermittent attack Length of remission – from few weeks to many yrs. Extent of disease determines the severity and course of disease. UC in Pregnancy No difficulty conceiving No ed risk of spontaneous abortion. Glucocorticoids, sulfasalazine, and even Azathioprine – safe Relapses of the disease during Pregency must be treated aggressively if a quick remission is to be attained.