Diagnosis and treatment

Several procedures may be used in the diagnosis of CD. Ileocolonoscopy with biopsy specimens systematically obtained from each anatomical segment is a common procedure, except in patients with fulminant colitis.2 In contrast to ulcerative colitis, CD can involve the entire gastrointestinal tract, although the lesions are limited to the colon in 20% of patients. About half of patients have involvement of the terminal ileum and colon. A patchy, cobblestone pattern may be noted in the terminal ileum of patients with CD. Granulomas are also characteristic of CD but are not evident in all cases. Biopsies help differentiate between the transmural inflammation of CD and the mucosal inflammation of ulcerative colitis. Additional diagnostic examinations include magnetic resonance imaging, computed tomography, and transabdominal sonography. 

The treatment of CD is complex and depends on numerous factors, such as the location and severity of the disease (Table 1). Treatment is not curative, and recurrence is common after remission has been achieved. Several approaches are used, including steroids, immunomodulators, anti-TNF therapy, and surgery (Tables 2 and 3).7 The therapy for CD differs from that for ulcerative colitis, although some medications may be used in both conditions. Surgery is usually performed to manage complications such as strictures, fistula, abscess, and perforation. Extraintestinal manifestations and nutritional deficiencies also require adequate management.


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Click to enlarge Table 3.

Carlos A. Salazar, MSN, ARNP, FNP-BC, is a student nurse anesthetist at Florida International University and a field nurse practitioner for Altegra Health in Miami, Florida.

References

  1. Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel disease: an overview. Surg Clin North Am. 2007;87(3):575-585. 
  2. Engel MA, Neurath MF. New pathophysiological insights and modern treatment of IBD. J Gastroenterol. 2010;45(6):571-583.
  3. Vasseur F, Gower-Rousseau C, Vernier-Massouille G, et al. Nutritional status and growth in pediatric Crohn’s disease: a population-based study. Am J Gastroenterol. 2010;105(8):1893-1900. 
  4. Mayer L. Evolving paradigms in the pathogenesis of IBD. J Gastroenterol. 2010;45(1):9-16. 
  5. Rioux JD, Xavier RJ, Taylor KD, et al. Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis. Nat Genet. 2007;39(5):596-604. 
  6. Caprilli R, Lapaquette P, Darfeuille-Michaud A. Eating the enemy in Crohn’s disease: an old theory revisited. J Crohns Colitis. 2010;4(4):377-383. 
  7. Burger D, Travis S. Conventional medical management of inflammatory bowel disease. Gastroenterology. 2011;140(6):1827-1837.
  8. Hanauer SB, Sandborn W; Practice Parameters Committee of the American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol. 2001;96(3):635-643. 
  9. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of the American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol. 2009;104(2):465-483.

All electronic documents accessed February 4, 2016.