Crohn’s Disease – COMPLICATIONS

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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Crohn’s Disease – CLINICAL MANIFESTATIONS

The symptoms and signs of CD also are determined by the site and extent of inflammation. Gastroduodenal CD mimics peptic ulcer disease, with nausea, vomiting, and epigastric pain. Patients with small intestinal involvement have abdominal cramping, diarrhea, and abdominal tenderness. The pain and tenderness of CD are due to transmural inflammation. Transmural inflammation leads to fibrosis and narrowing of the intestinal lumen, which produce symptoms of obstruction: nausea, vomiting, waves of abdominal pain, and a reduced output of stool on physical examination. This is appreciated as a thickened, tender loop of bowel or an abdominal mass, if the mesentery is involved. Patients with colonic CD present with abdominal pain, cramping or localized pain, rectal bleeding, and diarrhea.

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PATHOLOGY OF CROHN’S DISEASE

CD involves any segment or combination of segments of the alimentary tract from the mouth to the anus. Unlike UC, microscopic changes often are identified distant from sites of macroscopic disease. These focal changes and the tendency of CD to recur after segmental resection suggest that subtle changes of CD exist throughout the alimentary tract. Most commonly the distal ileum and right colon are macroscopically inflamed (ileocolitis). The colon is involved, exclusively, in about 20% of patients (Crohn’s colitis or granulomatous colitis); approximately 15 to 20% have gross disease limited to the small bowel (ileitis or regional enteritis). The stomach or duodenum is involved in < 10% of patients and usually in association with more distal disease. Disease of the anal canal, including deep fissures, fistulas, and prominent “hemorrhoidal” skin tags, are common and distinguish CD confined to the colon from UC. Unlike UC, the mucosa in CD is involved in a focal, discontinuous manner, both microscopically and macroscopically. Rarely, lesions indistinguishable from those of CD occur in the skin or urogenital mucosal surfaces (miliary CD).

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Crohn’s Disease – PATHOGENESIS

The absence of an etiologic factor leaves a gap in our understanding of the pathogenesis of IBD. Although a number of potential factors may influence the initiation of the inflammatory response, a popular view is that a defect exists in the “down-regulation”

TABLE 104-1 — EPIDEMIOLOGY OF INFLAMMATORY BOWEL DISEASE

of immune events (see Part XIX), allowing persistent amplification of the tissue-damaging process. The inflammatory reaction in IBD closely mimics infectious enterocolitis with the exception of the failure to halt progressive tissue destruction. Subtle differences exist between the immunologic findings of UC and CD, such as the production of immunoglobulin heavy-chain allotypes or neutrophil-cytoplasmic antibodies; however, pathognomonic findings to classify these disorders remain elusive. Nosology is currently based on descriptive clinical, endoscopic, and histologic criteria, and misclassification often is recognized as the clinicopathologic process evolves over time. When the diagnosis changes, it is almost always from UC to CD and virtually never the converse.

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Crohn’s Disease – EPIDEMIOLOGY

CD occurs among all age groups but have a peak incidence in the second and third decades. CD incidence has risen over the past 20 years; CD has an incidence and prevalence rates of 5 per 100,000. The combined prevalence of the two diseases is approximately 100 per 100,000 population. CD are seen most commonly in Northern Europe and North America and in relatives of European immigrants in the cities of South Africa, Australia, and New Zealand. Inflammatory bowel disease (IBD) included Crohn’s disease and Crohn’s disease. IBD is rare in Central America, South America, Africa, the Middle East, and Asia. Although CD can be seen in all ethnic groups, there is an increased prevalence in Jews who have immigrated from Northern Europe. This Jewish predisposition is not seen in Sephardic (Mediterranean or Middle-Eastern) Jews. Although less common in the nonwhite population, more cases are being recognized in black, Hispanic, and Asian immigrants to western cities.

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Crohn’s Disease

Crohn’s disease is a recurrent segmental inflammatory disorder that may affect the any location in the gastrointestinal tract from the mouth to the anus. Crohn’s disease is of unknown etiology. Fifty percent of patients have involvement of both the small intestine and colon, whereas one third have disease limited to their small intestine and the remaining 20% have inflammation in the colon only. Perianal lesions and inflammatory conditions involving the skin, eyes, joints, and liver are common. The transmural inflammatory process and variable anatomic extent of disease contribute to diverse clinical presentations with unpredictable spontaneous exacerbations and remissions.

Multiple Myeloma – TREATMENT

About 10 percent of patients with myeloma will have an indolent course demonstrating only very slow progression of disease over many years. Such patients only require antitumor therapy when the serum myeloma protein level rises above 50 g/L (5 g/dL) or progressive bone lesions develop. Patients with solitary bone plasmacytomas and extramedullary plasmacytomas may be expected to enjoy prolonged disease-free survival after local radiation therapy to a dose of around 40 Gy. There is a low incidence of occult marrow involvement in patients with solitary bone plasmacytoma. Such patients are usually detected because their serum M component falls slowly or disappears initially only to return after a few months. These patients respond well to systemic chemotherapy.

The vast majority of patients with myeloma require therapeutic intervention. In general, such therapy is of two sorts: systemic chemotherapy to control the progression of myeloma, and symptomatic supportive care to prevent serious morbidity from the complications of the disease. All patients with stage II or III disease and stage I patients exhibiting Bence Jones proteinuria, progressive lytic bone lesions, vertebral compression fractures, recurrent infections, or rising serum M component should be treated with systemic combination chemotherapy. Therapy can prolong and improve the quality of life for myeloma patients.

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