Archive for August, 2008

Crohn’s Disease – DIFFERENTIAL DIAGNOSIS

Posted by Alex

Patients with irritable bowel syndrome rarely present with “inflammatory” features. Persistent symptoms despite therapy for presumed irritable bowel syndrome (especially in the presence of weight loss), bleeding attributed to “hemorrhoids,” or a family history of IBD deserve a more comprehensive evaluation to exclude IBD. Most enteric infections are self-limited. Viral gastroenteritis typically lasts 1 to 4 days without rectal bleeding or fecal leukocytes. Most bacterial pathogens produce self-limited disease lasting less than 7 to 14 days, despite intermittent rectal bleeding, fevers, fecal leukocytes, and a mucosal appearance that may be indistinguishable from that of UC or CD. Occasionally, Campylobacter jejuni produces protracted symptoms and Clostridium C. difficile toxin-induced colitis can mimic the symptoms, signs, and endoscopic appearance of UC or CD. When a patient with IBD presents with new or exacerbated symptoms, stool cultures for enteric pathogens and studies for C. difficile toxin should be obtained, especially if the patient has been recently treated with antibiotics. In Northern Europe and Canada, Yersinia enterocolitica infection can mimic terminal ileitis. If the clinical suspicion warrants, cultures and serologic studies for Yersinia should be obtained. Similarly, tuberculosis of the gastrointestinal tract may mimic CD in geographic areas where intestinal tuberculosis is edemic, and, rarely, Actinomycosis simulates fistulizing CD.

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Crohn’s Disease – RADIOGRAPHY

Posted by Alex

Radiographic examination should begin with a supine and upright view of the abdomen. Associated findings of nephrolithiasis, cholelithiasis, or arthritis of the spine or sacroiliac joints may be identified. Intestinal dilatation or air-fluid levels suggesting obstruction preclude aggressive barium studies until the patient’s clinical condition is stabilized. In colitis, a plain view of the abdomen often demonstrates a tubular, ahaustral segment of colon in the presence of distal UC with fecal matter proximal to diseased mucosa. Intestinal edema, ulceration, or thumb-printing may give a gross estimate of disease activity. Air-contrast barium studies of the colon reveal diffuse, contiguous granularity, superficial ulceration, and absent haustration in active UC. Pseudopolyps or a tubular-appearing “lead pipe” colon may be found in chronic UC. Focal, asymmetric ulceration with linear or fissuring ulcers, the presence of fistulas, rectal sparing, or a diseased terminal ileum with reflux of the barium define the radiographic extent and severity of colonic CD. A small bowel follow-through or enteroclysis (small bowel enema) demonstrates the extent of small intestinal involvement in CD and is normal in the absence of backwash ileitis in UC.

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Crohn’s Disease – ENDOSCOPY

Posted by Alex

Patients presenting with colitic symptoms of rectal bleeding, cramping, tenesmus, mucopus, or watery diarrhea in conjunction with fecal leukocytes warrant a colonic examination. A proctoscopic examination or flexible sigmoidoscopy reveals the presence and pattern of distal colonic inflammation. In the absence of perianal disease, diffuse, continuous mucosal changes with a distinct upper boundary to adjacent normal-appearing mucosa are typical of ulcerative proctitis or proctosigmoiditis. Focal inflammation with aphthoid ulcers, linear or stellate ulcers with normal intervening mucosa, or inflammatory changes beginning above the rectum (rectal sparing) in previously untreated patients suggest CD. If the patient is not acutely ill, colonoscopy demonstrates more proximal colonic changes and allows examination and intubation of the ileocecal valve to evaluate terminal ileal findings. Patients with upper abdominal symptoms can be diagnosed with upper gastrointestinal endoscopy when typical mucosal changes of CD involve this area. Findings can be correlated with mucosal biopsy studies and radiographic evaluation of the small and large intestine.

Crohn’s Disease – DIAGNOSIS

Posted by Alex

There are no pathognomonic clinical, endoscopic, or histologic features of the idiopathic IBD’s. The physician must therefore consider the entire clinical picture and the evolution of the illness. It is particularly important to exclude other disorders that may mimic the broad range of IBD symptoms and findings. First it is important to establish the presence of intestinal inflammation. A cardinal feature is the exudation of inflammatory cells into the lumen, manifested by fecal leukocytes or red blood cells on stool examination. Symptoms of rectal bleeding, tenesmus associated with the passage of pus, nocturnal pain and diarrhea, fever, night sweats, weight loss, or extraintestinal symptoms or signs generally exclude an uncomplicated “irritable bowel syndrome.” The presence of anemia, electrolyte disorders, hypoalbuminemia, or an elevated erythrocyte sedimentation rate of C-reactive protein is sufficient, but not necessary, to suggest IBD. On physical examination, evidence of significant weight loss or extraintestinal signs, a palpable abdominal mass or tenderness, or significant perianal disease suggests IBD. When suspicion of the diagnosis warrants, endoscopic and radiographic studies, in conjunction with histologic interpretation of biopsy specimens, confirm the diagnosis; the degree of illness at presentation should determine the aggressiveness of the diagnostic workup. Acutely ill patients should be stabilized before invasive studies are pursued.

EXTRAINTESTINAL COMPLICATIONS – Crohn’s Disease

Posted by Alex

The extraintestinal manifestations of IBD can be divided into complications of gastrointestinal inflammation or diseases associated with IBD. The latter occur most often with “colitis” but can occur in either UC or CD when the colon is inflamed.

Nutritional and metabolic abnormalities occur with chronic disease, inadequate intake of calories, maldigestion, and malabsorption. Blood and protein loss contribute to iron deficiency anemia and hypoalbuminemia. Deficiencies of calcium, magnesium, or zinc are most often noted with small intestinal CD in the presence of active inflammation or extensive surgical resections. Calcium deficiency may be aggravated by milk-free diets or vitamin D deficiency. Deficiency of folic acid can be secondary to inadequate intake, proximal small bowel disease, or competitive inhibition of folate absorption by sulfasalazine. Treatments for these nutritional deficiencies require appropriate diagnosis, treatment of the underlying inflammation, and enteral or parenteral repletion. Deficiencies in fat-soluble vitamins (vitamin A, D, E, and K) are most often produced by ileal disease or resection. Low vitamin D levels can aggravate metabolic bone disease and calcium malabsorption. Vitamin B12 deficiency can be avoided by regular replacement intramuscular injections.

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Crohn’s Disease – CANCER

Posted by Alex

Cancer of the colon is a long-term complication of UC. Its development depends on two factors: the extent of mucosal involvement (pancolitis greater than left-sided colitis) and the duration of disease. Severity of the initial attack, subsequent course, and specific medical therapies are not related to the cancer risk. Colonic adenocarcinomas may occur in patients who have had quiescent UC for decades. Indeed, these may be the patients at highest risk. In Europe, where colectomy is performed earlier, the risk of cancer is reduced.

 
TABLE 104-2 – CANCER IN ULCERATIVE COLITISRisk factors
Extent of colon involved
Duration of disease after 10 years
Surveillance
Begin after 10 years
Increase frequency of surveillance with increased duration of disease
Warning
Indefinite dysplasia: requires follow-up 3-6 months and/or confirmation by experienced pathologist
Surgical indication
Confirmed dysplasia, or dysplasia-associated lesion or mass (DALM)

 

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Crohn’s Disease – COMPLICATIONS

Posted by Alex

INTESTINAL COMPLICATIONS

Rectal bleeding is a common manifestation of both UC and CD. In UC the superficial inflammation induces capillary hemorrhage, manifested as bright red coating of stool or blood-tinged mucopus. In severe UC the bleeding can be more prominent and on rare occasions is profuse. Iron deficiency anemia is a common secondary association due to the chronic blood loss. In CD, hemorrhage may be profuse as a result of deeper inflammation and ulceration into larger vessels. Recurrent bleeding occurs in a small subset of patients with CD and is rarely the single indication for surgery.

Toxic megacolon, once thought to occur only with UC, also occurs in CD and infectious colitis. Toxic megacolon develops in seriously ill individuals when transmural inflammation extends into the muscular layer, thinning the intestinal wall. The entire colon, or segments of the colon, can dilate as a result of disruption of the neural and muscular elements that maintain normal tone. Dilatation of the diameter of the colon on a plain abdominal radiograph to > 6 cm, associated with clinical symptoms of increasing abdominal pain, distention, rebound tenderness, and signs of fever, tachycardia, and dehydration, indicates the condition. Even without prominent dilatation, similar symptoms and signs are sufficient to diagnose severe colitis with an identical risk of perforation and the hazard of peritonitis. Precipitating circumstances include severe colitis, instrumentation with barium studies or endoscopic procedures in severe inflammation, potassium depletion, anticholinergic medications, or narcotics, which are thought to reduce neuromuscular activity of the gut. Associated laboratory findings include leukocytosis, hypokalemia, anemia, and hypoalbuminemia.

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