eMedicine Specialties > Emergency Medicine > Gastrointestinal

Inflammatory Bowel Disease: Follow-up

Author: William Shapiro, MD, Consulting Staff, Department of Urgent Care and Emergency Medicine, Scripps Clinic and Research Foundation
Contributor Information and Disclosures

Updated: Apr 25, 2008

Follow-up

Further Outpatient Care

  • Nutritional support in CD includes supplementation with trace metals, fat-soluble vitamins, and medium-chain triglycerides.
  • A low-oxalate diet with citrate supplementation helps reduce the risk of nephrolithiasis.
  • Oral calcium or cholestyramine may serve as an intestinal oxalate binder.
  • Encourage the patient to join an IBD support group, such as the Crohn's and Colitis Foundation of America (386 Park Avenue South, 17th Floor; New York, NY 10016; 1-800-932-2423).

Complications

  • Perforation and toxic megacolon are the most dreaded complications of UC. Perforation can occur in the presence of fulminating disease, even in the absence of toxic megacolon.
    • The mortality rate is 50% if perforation occurs.
    • Suspect toxic megacolon in a patient with fulminant UC, especially if the number of daily stools has declined sharply without a corresponding improvement in symptoms. The abdomen is typically distended, tender, and tympanitic. Toxic megacolon can be precipitated by antidiarrheal agents, hypokalemia, narcotics, cathartics, and enemas, including barium enemas. The best method of diagnosing toxic megacolon is through the use of plain radiography. Toxic megacolon occurs predominantly in the transverse colon, probably because air collects there in the supine position. The transverse colon is dilated, usually more than 8 cm. Dilation more than 6 cm is considered to be abnormal. A colectomy is required if no improvement occurs within 24-48 hours.
  • Strictures usually are benign but can lead to obstruction.
  • Fistulas and abscesses are much more common in CD, but they are observed in about 20% of patients with UC.
    • Fistula types include enterovesical (leading to recurrent urinary tract infections and pneumaturia), enteroenteric, enteromesenteric, enterocutaneous, rectovaginal, and perianal.
    • Additional problems include stenosis and obstruction.
    • Perianal complications occur in 90% of patients with CD.
    • In CD, obstructive hydronephrosis may result from a right lower quadrant inflammatory mass, leading to external compression of the right ureter.
  • Massive hemorrhage occurs in fewer than 1% of patients.
  • Cancer concerns are as follows:
    • UC carries a 10- to 30-fold increase in development of carcinoma of the colon.
    • Risk increases with extent and duration of the disease.
    • Cumulative risks of cancer after 15, 20, and 25 years are 8%, 12%, and 25%, respectively.
    • Perform periodic colonoscopies with biopsies, especially in patients with pancolitis. Most authors recommend beginning surveillance approximately 10 years after onset of disease and repeating surveillance at 1- to 2-year intervals. Evidence currently does not support the need for cancer surveillance in CD.
    • The risk of cancer in CD may be equal to that of UC if the entire colon is involved. Hence, screening may be beneficial for patients with CD who have pancolitis. The risk of small intestinal malignancy in CD is increased. However, the malignancy is as likely to arise in a normal as in an inflamed area, and no screening protocol has ever been demonstrated to be effective against small bowel CD.
  • Extraintestinal complications occur in approximately 20% of patients with IBD. In some cases, they may be more problematic than the bowel disease itself.
    • Arthritic
      • Peripheral arthritis, usually migratory and monoarticular, tends to parallel disease activity but may antedate it.
      • Ankylosing spondylitis is associated with human leukocyte antigen-B27 (HLA-B27).
    • Ocular
      • Episcleritis manifests with burning eyes and scleral injection (see Image 3) and is observed in 3-4% of IBD cases. Episcleritis parallels the course of the disease and resolves with treatment of the IBD. Topical steroids may be administered.
      • Iritis, which manifests as an acute painful red eye with photophobia and conjunctival injection, often runs a course independent of intestinal disease. It can progress to blindness. Treatment is with topical or systemic steroids.
      • Cataracts are associated with long-term steroid use. Patients taking long-term steroids should have an annual slit-lamp examination.
    • Dermatologic
      • Erythema nodosum is characterized by painful, tender, raised red or violaceous subcutaneous nodules, usually found over the extensor aspects of the arms and the legs, especially the anterior tibia. Activity usually follows that of the intestinal disease and often heralds onset of increased bowel activity.
      • Pyoderma gangrenosum is characterized by ulcerating relatively painless lesions that correlate with bowel activity in about 50% of patients (see Image 4). Although ulcers may exhibit purulent drainage, culture to the present time, the treatment of pyoderma gangrenosum has involved the use of corticosteroids and cyclosporine. Reports have indicated that, not only does the condition respond to infliximab, but this drug should probably be considered the drug of choice against pyoderma gangrenosum.
      • Aphthous ulcers are more common in patients with IBD than in the general population.
    • Other
      • Additional extraintestinal manifestations include pericholangitis, chronic active hepatitis, cirrhosis, primary sclerosing cholangitis, and bile duct carcinoma. Pericholangitis is the most common hepatic complication of IBD and is usually asymptomatic. Look for elevations of the alkaline phosphatase, less often bilirubin. Primary sclerosing cholangitis can progress to cirrhosis, in which case liver transplantation is the treatment of choice. However, it can recur in the transplanted liver.
      • Gallstones occur in about one third of patients with CD, resulting from increased lithogenicity of the bile due to impaired ileal absorption of bile acids.
      • A hypercoagulable state can occur, leading to deep venous thromboses, pulmonary embolism, and arterial thromboses. Additionally, portal or hepatic vein thrombosis, stokes, retinal venous thrombosis, gonadal vein thrombosis, and mesenteric venous thrombosis have been reported. The incidence of thrombotic complications may be as high as 39%. The hypercoagulable state correlates with the activity of the disease. Its cause is unclear, but it may be related to increased levels of plasminogen activator inhibitor, factors V and VIII and fibrinogen or to decreased levels of factor V Leiden, antithrombin III, and proteins C and S.

Prognosis

  • UC
    • A small percentage of patients have a single attack and no recurrence. Typically, however, remissions and exacerbations are characteristic of UC, with acute attacks lasting weeks to months.
    • Twenty percent of patients require colectomy, which is curative.
    • Long-term morbidity primarily results from complications of medical therapy, especially long-term steroids.
  • CD
    • Prognosis depends on the site and extent of disease.
    • Periodic remissions and exacerbations are the rule.
    • Approximately 50% of patients require surgical intervention; 50% of patients undergoing surgery require a second operation; of these patients, 50% have a third operation.
    • Rate of recurrence is 25-50% within 1 year for patients who have responded to medical management. This rate is higher for patients who require surgery.
    • Overall, the quality of life with CD generally is lower than with UC. Death usually occurs as a consequence of surgery, pulmonary embolus, or sepsis.
    • Intestinal cancer may become a more important long-term complication in patients with CD because of longer survival.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Failure to obtain early surgical consultation for suspected obstruction, peritonitis, or fulminant disease
  • Failure to consider diagnosis of IBD, especially CD, in patients presenting with perianal disease: Look for fistulous openings, induration, redness, or tenderness near the anus.
  • Failure to recognize unusual presentations, such as sciatica resulting from a terminal ileal abscess with right iliopsoas extension
  • Failure to recognize that steroids may mask the clinical severity of illness: The febrile patient on steroids may be harboring a serious bacterial infection or abscess.
  • Failure to consider concomitant enteric infection (eg, C difficile) as the cause of an exacerbation
  • Use of antidiarrheals, anticholinergics, and narcotics in fulminant disease, which should be avoided
  • Overzealous use of steroids in the presence of an undrained abscess or when symptoms are due to a stricture or fibrotic process, rather than active inflammation
  • Failure to perform endoscopic examination: Remember that all patients with new-onset rectal bleeding should undergo an endoscopic evaluation of the colon, unless an infectious etiology seems likely. For a young patient with apparent distal rectal bleeding (red blood on toilet paper and coating the stool), a flexible sigmoidoscopy may suffice.
  • Prescribing NSAIDs: Beware of prescribing NSAIDs because they can lead to disruption of GI mucosal integrity and cause a flare of IBD.
  • Failure to consider the diagnosis of Crohn disease in a patient with seemingly refractory gastric or duodenal ulcer disease.

Special Concerns

  • Children
    • Approximately 15-30% of patients with IBD are younger than 20 years.
    • Presentation can include growth failure from malnutrition and delayed sexual maturation. Many of these children also have depression.
    • Sulfasalazine may be used as in adults, but administer steroids on an alternate day regimen, if possible, to diminish adverse effects.
    • Although immunosuppressives have been used in children, concern for adverse reactions is high; the possibility of malignancy exists in view of potential for longer exposure.
  • Pregnancy
    • Outlook generally is favorable; however, IBD is associated with an increased frequency of adverse pregnancy outcomes, especially if the disease is active at the time of conception.
    • Fertility in women with IBD is normal or only minimally impaired. The incidence of prematurity, stillbirth, and developmental defects in IBD are similar to those of the general population.
    • If the IBD is inactive at time of conception, it is likely to remain inactive during pregnancy. If IBD is active at the time of conception, UC tends to worsen. In two thirds of patients who have active CD at the time of conception, the degree of activity remains the same; in the other third, some have improvement and others have deterioration.
    • Sulfasalazine and steroids may be administered during pregnancy. Sulfasalazine can be taken throughout pregnancy; however, it interferes with folate absorption, and pregnant women have an increased requirement for folic acid. Hence, women taking sulfasalazine should also take 1 mg of folate twice a day. The use of steroids during pregnancy has not been associated with an increased rate of activity; thus, the risks of treatment with sulfasalazine or corticosteroids in pregnant women with IBD are less significant than the risks of allowing disease activity to go untreated.
 


More on Inflammatory Bowel Disease

Overview: Inflammatory Bowel Disease
Differential Diagnoses & Workup: Inflammatory Bowel Disease
Treatment & Medication: Inflammatory Bowel Disease
Follow-up: Inflammatory Bowel Disease
Multimedia: Inflammatory Bowel Disease
References

References

  1. Bayless TM, Hanaeur SB. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: BC Decker. 2000.

  2. Bell S, Kamm MA. Antibodies to tumour necrosis factor alpha as treatment for Crohn's disease. Lancet. Mar 11 2000;355(9207):858-60. [Medline].

  3. Brooklyn TN, Dunnill MG, Shetty A. Infliximab for the treatment of pyoderma gangrenosum: a randomised, double blind, placebo controlled trial. Gut. Apr 2006;55(4):505-9. [Medline].

  4. Buhner S, Buning C, Genschel J. Genetic basis for increased intestinal permeability in families with Crohn's disease: role of CARD15 3020insC mutation?. Gut. Mar 2006;55(3):342-7. [Medline].

  5. Cattaneo M, Vecchi M. Inflammatory bowel disease and the risk of thrombosis. Gastroenterology. Jul 1999;117(1):280-1. [Medline].

  6. Cheung O, Regueiro MD. Inflammatory bowel disease emergencies. Gastroenterol Clin North Am. Dec 2003;32(4):1269-88. [Medline].

  7. Cho J. Update on inflammatory bowel disease genetics. Curr Gastroenterol Rep. Dec 2000;2(6):434-9. [Medline].

  8. Compton RF, Sandborn WJ, Yang H. A new syndrome of Crohn's disease and pachydermoperiostosis in a family. Gastroenterology. Jan 1997;112(1):241-9. [Medline].

  9. Dieckgraefe BK, Korzenik JR. Treatment of active Crohn's disease with recombinant human granulocyte-macrophage colony-stimulating factor. Lancet. Nov 9 2002;360(9344):1478-80. [Medline].

  10. Eaden JA, Abrams KR, Mayberry JF. The risk of colorectal cancer in ulcerative colitis: a meta-analysis. Gut. Apr 2001;48(4):526-35. [Medline].

  11. Fagan B TN, Lavine J, Taylor S. Evaluation of serologic testing for inflammatory bowel disease (IBD) in children. Digestive Disease Week. 2001;Abstract Book; 2001 May 20-23.

  12. Fraga XF, Vergara M, Medina C, et al. Effects of smoking on the presentation and clinical course of inflammatory bowel disease. Eur J Gastroenterol Hepatol. Jul 1997;9(7):683-7. [Medline].

  13. Hanauer SB, Dassopoulos T. Evolving treatment strategies for inflammatory bowel disease. Annu Rev Med. 2001;52:299-318. [Medline].

  14. Hanauer SB, Sandborn WJ, Kornbluth A. Delayed-release oral mesalamine at 4.8 g/day (800 mg tablet) for the treatment of moderately active ulcerative colitis: the ASCEND II trial. Am J Gastroenterol. Nov 2005;100(11):2478-85. [Medline].

  15. Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2000;21(9):291-5. [Medline].

  16. Kaditis AG, Perrault J, Sandborn WJ. Antineutrophil cytoplasmic antibody subtypes in children and adolescents after ileal pouch-anal anastomosis for ulcerative colitis. J Pediatr Gastroenterol Nutr. Apr 1998;26(4):386-92. [Medline].

  17. Kane S. Inflammatory bowel disease in pregnancy. Gastroenterol Clin North Am. Mar 2003;32(1):323-40. [Medline].

  18. Katz J. The course of inflammatory bowel disease. Med Clin North Am. Nov 1994;78(6):1275-80. [Medline].

  19. Kefalides PT, Hanaeur SB. Ulcerative colitis: diagnosis and management. Hospital Physician. 2002;38(6):53-63.

  20. Kornfeld D, Cnattingius S, Ekbom A. Pregnancy outcomes in women with inflammatory bowel disease--a population-based cohort study. Am J Obstet Gynecol. Oct 1997;177(4):942-6. [Medline].

  21. [Best Evidence] Korzenik JR, Dieckgraefe BK, Valentine JF. Sargramostim for active Crohn's disease. N Engl J Med. May 26 2005;352(21):2193-201. [Medline].

  22. Legnani PE, Kombluth A. Difficult differential diagnosis in IBD: ileitis and indeterminate colitis. Semin Gastrointest Dis. 2001;12(4):211.

  23. Lichtenstein GR, Yan S, Bala M. Infliximab maintenance treatment reduces hospitalizations, surgeries, and procedures in fistulizing Crohn's disease. Gastroenterology. Apr 2005;128(4):862-9. [Medline].

  24. Maltz C. Crohn's Disease. Emerg Med. June 2001;47-49.

  25. Maltz M. Ulcerative Colitis. Emerg Med. 2002;34(6):43-48.

  26. Marks DJ, Harbord MW, MacAllister R. Defective acute inflammation in Crohn's disease: a clinical investigation. Lancet. Feb 25 2006;367(9511):668-78. [Medline].

  27. Med Lett Drugs Ther. Infliximab (Remicade) for Crohn's disease. Med Lett Drugs Ther. Feb 26 1999;41(1047):19-20. [Medline].

  28. Med Lett Drugs Ther. Budesonide (Entocort EC) for Crohn's disease. Med Lett Drugs Ther. Jan 21 2002;44(1122):6-8. [Medline].

  29. Med Lett Drugs Ther. Oral balsalazide (Colazal) for ulcerative colitis. Med Lett Drugs Ther. Jul 23 2001;43(1109):62-3. [Medline].

  30. Peppercorn, MA. Crohn's Disease and Ulcerative Colitis. In: Cayten GC, et al, eds; Schwartz GR, chief ed. Principles and Practice of Emergency Medicine. 3rd ed. Philadelphia, Pa: Lea & Febiger;1992:1748-1759. [Medline].

  31. Rachmilewitz D, Karmeli F, Okon E, et al. Hyperbaric oxygen: a novel modality to ameliorate experimental colitis. Gut. Oct 1998;43(4):512-8. [Medline].

  32. Rubin DT, Hanauer SB. Smoking and inflammatory bowel disease. Eur J Gastroenterol Hepatol. Aug 2000;12(8):855-62. [Medline].

  33. Rutgeerts P, Sandborn WJ, Feagan BG. Infliximab for induction and maintenance therapy for ulcerative colitis. N Engl J Med. Dec 8 2005;353(23):2462-76. [Medline].

  34. Sandborn WJ, Faubion WA. Clinical pharmacology of inflammatory bowel disease therapies. Curr Gastroenterol Rep. Dec 2000;2(6):440-5. [Medline].

  35. Sands BE. Therapy of inflammatory bowel disease. Gastroenterology. Feb 2000;118(2 Suppl 1):S68-82. [Medline].

  36. Solem CA, Loftus EV, Tremaine WJ. Venous thromboembolism in inflammatory bowel disease. Am J Gastroenterol. Jan 2004;99(1):97-101. [Medline].

  37. Sorensen HT, Fonager KM. Myocarditis and inflammatory bowel disease. A 16-year Danish nationwide cohort study. Dan Med Bull. Sep 1997;44(4):442-4. [Medline].

  38. Stein RB, Lichtenstein GR. Medical therapy for Crohn's disease: the state of the art. Surg Clin North Am. Feb 2001;81(1):71-101, viii. [Medline].

  39. Stenson WF. Inflammatory Bowel Disease. In: Alpers DH, et al, eds; Yamada T, chief ed. Textbook of Gastroenterology. 2nd ed. Philadelphia, Pa: Lippincott;1995:1748-1806. [Medline].

  40. Stotland BR, Stein RB, Lichtenstein GR. Advances in inflammatory bowel disease. Med Clin North Am. Sep 2000;84(5):1107-24. [Medline].

  41. Swain P. Wireless capsule endoscopy and Crohn's disease. Gut. Mar 2005;54(3):323-6. [Medline].

  42. Targan SR, Hanauer SB, van Deventer SJ, et al. A short-term study of chimeric monoclonal antibody cA2 to tumor necrosis factor alpha for Crohn''s disease. Crohn''s Disease cA2 Study Group. N Engl J Med. Oct 9 1997;337(15):1029-35. [Medline].

  43. Thirlby RC, Sobrino MA, Randall JB. The long-term benefit of surgery on health-related quality of life in patients with inflammatory bowel disease. Arch Surg. May 2001;136(5):521-7. [Medline].

  44. Vasiliauskas EA, Plevy SE, Landers CJ. Perinuclear antineutrophil cytoplasmic antibodies in patients with Crohn''s disease define a clinical subgroup. Gastroenterology. Jun 1996;110(6):1810-9. [Medline].

  45. Vecchi M, Cattaneo M, de Franchis R. Risk of thromboembolic complications in patients with inflammatory bowel disease. Study of hemostasis measurements. Int J Clin Lab Res. 1991;21(2):165-70. [Medline].

  46. Vecchi M, Bianchi MB, Calabresi C. Long-term observation of the perinuclear anti-neutrophil cytoplasmic antibody status in ulcerative colitis patients. Scand J Gastroenterol. Feb 1998;33(2):170-3. [Medline].

Further Reading

Keywords

IBD, ulcerative colitis, UC, Crohn disease, Crohn's disease, CD, regional enteritis, terminal ileitis, granulomatous ileocolitis, inflammation of the colon, colitis, irritable bowel syndrome, mucous colitis, rubor, spastic colon, chronic inflammatory diseases of the GI tract, pancolitis, backwash ileitis

perianal fistulas, perianal abscesses, strictures, gallstones, calcium oxalate kidney stones, fat malabsorption, enteric hyperoxaluria, iritis, episcleritis, arthritis, pericholangitis, sclerosing cholangitis, peritonitis with sepsis, thromboembolic disease, toxic megacolon, chronic anemia, malnutrition

growth retardation, bloody diarrhea, nonbloody diarrhea, rectal urgency, tenesmus, arthralgias, grossly bloody stools, gastric outlet obstruction, irregular bowel habits, uveitis, liver disease, perianal fissures, rectal prolapse

Contributor Information and Disclosures

Author

William Shapiro, MD, Consulting Staff, Department of Urgent Care and Emergency Medicine, Scripps Clinic and Research Foundation
William Shapiro, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, Department of Emergency Medicine, New York University School of Medicine; Consulting Staff, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eugene Hardin, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles R Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King, Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.