Inflammatory Bowel Disease

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36 Inflammatory Bowel Disease

James Ahn

image      Key Points

• Acute exacerbations of inflammatory bowel disease are characterized by abdominal pain, nausea, vomiting, diarrhea, and gastrointestinal bleeding.

• Life-threatening complications include bowel obstruction, hemorrhagic shock, toxic megacolon, malabsorption, abscess formation, and sepsis.

• Treatment with analgesics, intravenous hydration, antiemetics, and electrolyte replacement should occur in parallel with appropriate diagnostic imaging and laboratory studies.

• Antibiotics, steroids, and immunosuppressant therapies can be used in conjunction with specialty consultation.

• Hypersensitivity reactions may result from long-term immunomodulator and antiinflammatory therapies.

• Patients receiving immunosuppressant therapy have increased susceptibility to opportunistic infections.

Perspective

Approximately 1 million people in the United States suffer from inflammatory bowel disease (IBD). The two major forms of IBD are Crohn disease and ulcerative colitis (UC). The incidence of both disease processes is similar, although Crohn disease appears to be increasing.1 Each disease may relapse and remit, with exacerbations that often require emergency care and hospitalization.

IBD has a familial predilection, with an absolute risk of 7% among first-degree relatives.2,3 Up to a fifth of patients with IBD have an affected first-degree family member. Ashkenazi Jewish populations continue to have the highest documented incidence per capita of any group in the world. Hispanic and African American populations have a lower incidence of IBD than the Caucasian population does.4

The age at onset of IBD is bimodal. The greatest numbers of new cases are diagnosed in patients 15 to 35 years of age. Classically, a second peak is observed during the sixth decade of life.5 Advances in diagnostic testing have probably contributed to an overall rise in the number of new cases of IBD, as well as to the identification of the disease in younger patients.

Pathophysiology

Crohn Disease

Pathology

Crohn disease is characterized by segmental, transmural, granulomatous inflammatory changes that can occur anywhere along the gastrointestinal tract from the mouth to the perianal area. Disease of the terminal ileum is present in 80% of patients with Crohn disease, and 50% of patients have ileocolitis. Approximately 33% and 20% of patients demonstrate only ileal and colonic involvement, respectively. The finding of skip lesions between areas of normal bowel and cobblestoning of the intestinal mucosa is classic for Crohn disease. Chronic inflammation commonly leads to bowel stenosis.

Epidemiology

The yearly incidence of Crohn disease is between 3 and 14 cases per 100,000 people in North America, with a disease prevalence of 26 to 201 cases per 100,000. The incidence rate of Crohn disease has risen steadily, with the highest incidence found in North America and northern Europe. Crohn disease is more common in Caucasian and Latino people in the United States than in African Americans, Native Americans, and Asian Americans. Women have a 20% to 30% higher incidence than men do.

The cold chain hypothesis suggests that the rise in incidence of Crohn disease has been associated with the development of home refrigeration techniques. Bacteria that thrive in refrigerated foods, such as Yersinia and Listeria, are thought to play a role in stimulation of the immune and inflammatory responses that ultimately lead to Crohn disease.6 Exacerbations of Crohn disease may be worsened during periods of higher physiologic or mental stress.7 Other environmental factors such as cigarette smoking, use of nonsteroidal antiinflammatory drugs (NSAIDs), increased refined sugar intake, increased dietary fat, and decreased fiber intake have been linked to the development of Crohn disease.8–11

Genetic mutations and chromosomal variants have also been linked to the development of Crohn disease. Specific alterations in the NOD2 gene are associated with a 20-fold increase in the likelihood of Crohn disease with ileal predilection.12–15 Patients with Crohn disease may also be HLA-B27 positive.

Clinical Presentation

Patients with Crohn disease typically have abdominal pain, fever, diarrhea, and weight loss. Because Crohn disease involves the entire gastrointestinal tract, patients may suffer from oral ulcers, odynophagia, dysphagia, and symptoms of gastric outlet obstruction. Sinus tracts may develop and lead to common complications such as abscesses and fistula formation. Patients with Crohn disease can also have gastrointestinal bleeding, though to a lesser extent than patients with UC. Other complications include bowel obstruction, fissures, malignancy, malabsorption, malnutrition, and hypocalcemia.

Crohn disease is associated with an increased risk for demyelinating diseases, as well as a higher incidence of inflammatory processes such as asthma, arthritis, bronchitis, psoriasis, and pericarditis.16,17 Approximately 20% of patients with Crohn disease experience one or more of the following extraintestinal manifestations of disease during their lifetimes: ankylosing spondylitis, uveitis, episcleritis, hepatitis, cholelithiasis, pancreatitis, primary sclerosing cholangitis, cholangiocarcinoma, nephrolithiasis, and erythema nodosum (Fig. 36.1; Box 36.1).

image

Fig. 36.1 Computed tomography scan showing terminal ileitis (arrow) in a patient with Crohn disease.

Box 36.1 Differential Diagnosis

Colitis

Inflammatory bowel disease:

– Crohn disease
– Ulcerative colitis
– Indeterminate colitis

Infectious colitis:

– Shigella
– Amoeba
– Giardia
– Escherichia coli O157:H7
– Yersinia
– Campylobacter
– Entamoeba histolytica
– Viral infections
– Mycotic infections

Pseudomembranous colitis (Clostridium difficile):

Diverticulitis
Sarcoidosis
Tuberculosis

Proctitis (including sexually transmitted causes):

Collagenous colitis
Irritable bowel syndrome
Food intolerance

Ulcerative Colitis

Pathology

UC is a recurring inflammatory disease confined to the mucosal layer of the colon and rectum only. Areas of inflammation are continuous, not segmental; patients commonly experience ascending disease from the rectum to the colon. Isolated rectal involvement is present in a minority of patients.

Epidemiology

The yearly incidence of UC is relatively constant—in the United States it is 8 per 100,000 people, with a disease prevalence of 246 cases per 100,000 people.18,19 The etiology of this disease is unknown, although certain risk factors have been identified. UC is most commonly found in North American and northern European Caucasian populations. In addition, similar to Crohn disease, development of UC has been linked to the use of NSAIDs, increased refined sugar intake, increased dietary fat, and decreased fiber intake.9–11 However, cigarette smoking appears to lessen the risk for development of UC.20

Clinical Presentation

Although UC has variable findings, bloody, purulent, and mucoid diarrhea is considered to be the classic manifestation. Fever, weight loss, dehydration, anemia, and hypoalbuminemia are common. Patients may be categorized as having mild disease (60%), moderate disease (25%), or severe disease (15%). Severe disease is defined as six or more bowel movements per day.

Significant lower gastrointestinal bleeding is the most common complication, with 3% of patients with UC having massive hemorrhage. Patients may also have toxic megacolon as a complication of fulminant colitis. Toxic megacolon causes a loss of colonic muscular tone that results in luminal diameters larger than 6 cm—pathologic changes that increase the risk for perforation and mortality. Long-term complications of UC include bowel strictures and the development of colon cancer.

Patients with UC may have extraintestinal complications such as concurrent arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, and progressive liver disease (Fig. 36.2; Table 36.1).

image

Fig. 36.2 Computed tomography scan showing colonic wall thickening in a patient with ulcerative colitis.

Table 36.1 Features of Crohn Disease and Ulcerative Colitis

FINDING CROHN DISEASE ULCERATIVE COLITIS
Location
Colonic Common Common
Rectal Common Common
Extracolonic Common Never
Ileal Common Never
Signs and Symptoms
Fever Common Common
Diarrhea Common Common
Vomiting Variable Occasional
Abdominal pain Common Variable
Hematochezia Variable Common
Weight loss Common Common
Perianal disease Common Never
Pathologic Findings
Continuity Discontinuous Continuous
Inflammation Transmural Mucosal
Oral ulcers Variable Never
Fissures Common Never
Fistulas Variable Rare
Cobblestoning Common Never
Strictures Common Rare
Laboratory Findings
Perinuclease-staining antineutrophil cytoplasmic antibody (p-ANCA) positivity Uncommon Common
Anti–Saccharomyces cerevisiae antibody (ASCA) positivity Common Uncommon

Diagnostic Testing

Imaging Modalities

Most cases of IBD diagnosed in the emergency department (ED) are found via computed tomography (CT) of the abdomen in patients with severe, unexplained abdominal pain. A presumptive diagnosis of IBD can be based on typical CT findings coupled with the appropriate signs and symptoms. CT enterography has been shown to have 100% sensitivity and 95% specificity for detection of small bowel lesions associated with Crohn disease.21 CT enterography is superior to standard CT of the abdomen and pelvis in patients with a high pretest probability of Crohn disease (i.e., first-degree family members of patients with IBD). Confirmation of the diagnosis is made by histologic examination of tissue biopsy specimens obtained via inpatient endoscopy or surgery.

Patients seen in the ED with an exacerbation of known IBD do not always require CT. Plain films are generally sufficient to exclude complications such as bowel obstruction and rare perforations. CT should be used to identify abscesses or other intraabdominal disease in patients with peritoneal findings or sepsis.

Other imaging modalities are best used outside the ED. Barium and air-contrast radiographic studies frequently demonstrate classic radiographic evidence of IBD; they are useful tests for obese patients who exceed the weight limit for standard CT scanners. Upper and lower endoscopy allows direct visualization and biopsy of suspected lesions. Technology that enables patients to swallow endoscopic cameras as capsules represents a promising, minimally invasive method to visualize the bowel mucosa.

Laboratory Tests

Laboratory studies have limited value in the ED evaluation of IBD. Most tests serve to exclude complications or alternative diagnoses. A complete blood count can provide a baseline hemoglobin level. Leukocytosis is a nonspecific finding in patients with chronic IBD; marked elevations in the white blood cell count may correlate with new abscess formation, toxic megacolon, sepsis, or corticosteroid therapy. A serum chemistry panel is needed to exclude hypokalemia, hypocalcemia, and electrolyte imbalances in patients with severe vomiting and diarrhea. Hypoalbuminemia is often detected with liver function tests. The erythrocyte sedimentation rate and C-reactive protein levels add little value for guiding ED therapy.

Serologic markers may be used to differentiate Crohn disease from UC. The presence of p-ANCAs (perinuclease-staining antineutrophil cytoplasmic antibodies) is sensitive and predictive of UC, whereas detection of ASCA (anti—Saccharomyces cerevisiae antibodies) markers probably predicts Crohn disease. These serologic tests are not indicated for use in the ED.

Treatment

General Management

Exacerbations of IBD are often marked by significant pain, fever, diarrhea, gastrointestinal bleeding, anorexia, and dehydration; severity is most pronounced in patients with chronic disease who seek treatment in the ED because of exacerbations. Management of symptoms should be done in parallel with diagnostic testing. Analgesics, antiemetics, and intravenous hydration should be administered on arrival of the patient. In the setting of refractory emesis or bowel obstruction, nasogastric tube decompression may provide substantial relief. Identification and treatment of electrolyte imbalances, concurrent infections, and hemorrhage should precede hospital admission.

Immunomodulator, antiinflammatory, and antibiotic agents should be given in consultation with the patient’s gastroenterologist. Because these medications often require long-term administration and dose adjustments, complex drug regimens are typical. Treatment algorithms for Crohn disease and UC are summarized in Figures 36.3 and 36.4.

image

Fig. 36.3 Treatment algorithm for Crohn disease.

5-ASA, 5-Aminosalicylic acid; IV, intravenous; TPN, total parenteral nutrition.

(From Goldman L, Ausiello D, editors. Cecil’s textbook of medicine. 22nd ed. Philadelphia: Saunders; 2003.)

image

Fig. 36.4 Treatment algorithm for ulcerative colitis.

5-ASA, 5-Aminosalicylic acid.

(From Goldman L, Ausiello D, editors. Cecil’s textbook of medicine. 22nd ed. Philadelphia: Saunders; 2003.)

Common Medications

Sulfasalazine is a first-line oral agent used for the treatment of mild to moderate IBD. Colonic bacteria cleave the drug into 5-aminosalicylic acid (5-ASA) and sulfapyridine. 5-ASA acts directly on intraluminal lesions without systemic absorption. Although its mechanism of action is still unclear, 5-ASA probably inhibits leukocyte chemotaxis, as well as prostaglandin and leukotriene production. Sulfapyridine is a toxic by-product responsible for a variety of dose-related adverse effects (nausea, vomiting, diarrhea, headache, abdominal pain, arthralgias) and hypersensitivity reactions (rash, bone marrow suppression, fever, pancreatitis, liver disease, nephrotoxicity). Sulfasalazine at doses of 4 g or more per day should produce a clinical response within 3 to 4 weeks. Oral, enema, and suppository preparations of sulfasalazine are available.

Oral steroids improve mild to moderate IBD symptoms within days to weeks and are used in patients who do not improve with 5-ASA agents. Prednisone, 40 mg/day, is an acceptable starting dose; equivalent parenteral administration should be reserved for severe disease or for patients who cannot tolerate oral medications. Long-term corticosteroid therapy at a low maintenance dose is often required. Patients with small bowel obstruction secondary to terminal ileitis may have a response to early treatment with steroids, thereby reducing the need for surgical intervention (Fig. 36.5).

image

Fig. 36.5 Plain radiograph showing small bowel obstruction as a result of terminal ileitis.

Patients with Crohn disease can benefit from maintenance therapy with azathioprine or its active metabolite 6-mercaptopurine (6-MP). These immunomodulator drugs inhibit lymphocytic proliferation and subsequent activation of the inflammatory cascades. Their onset of action is 3 to 5 months in most cases. 6-MP is reserved for patients with disease refractory to other medications. Adverse effects include pancreatitis, leukopenia, hepatitis, and lymphoma. Methotrexate is another immunosuppressant that is used for Crohn disease refractory to 6-MP or in patients exhibiting Crohn disease–related arthritis. Adverse effects of methotrexate include leukopenia, anemia, thrombocytopenia, hepatobiliary complications, pericarditis, and thrombosis.

Infliximab (Remicade) is an inhibitor of tumor necrosis factor that is administered intravenously for the control of severe, refractory Crohn disease. Complications of infliximab therapy are sepsis, hepatotoxicity, pneumonia, lupuslike syndrome, hypersensitivity reactions, lymphoma, leukopenia, and demyelinating disease. Infliximab, as well as cyclosporine, may be beneficial in the treatment of patients awaiting surgical intervention. Because of the strong immunosuppressant nature of certain IBD therapies, a high index suspicion for opportunistic infections must be maintained.

Antibiotics may be needed to treat patients with Crohn disease. Antibiotics are indicated for active Crohn disease and pouchitis; promising results have been shown for fistulizing Crohn disease.22–25 The antibiotics most commonly used are a combination of metronidazole and ciprofloxacin. The utility of these agents for UC has not been proved.

Surgery

Seventy-five percent of patients with Crohn disease require surgery within the first 20 years after diagnosis. Emergency consultation should be obtained for patients with complications of IBD-related surgery or for patients with suspected life-threatening complications, including massive hemorrhage, abscess formation, obstruction, toxic megacolon, and perforation. Intravenous hydration, nasogastric decompression, and broad-spectrum antibiotic therapy should be given in preparation for surgery.

Disposition

Hospital admission is required for moderate to severe exacerbations of IBD. Patients with severe dehydration, systemic infection, abscesses, or potentially life-threatening complications such as hemorrhage, toxic megacolon, perforation, and bowel obstruction must be managed as inpatients. Discharge should be reserved for patients with mild disease in whom oral hydration and pain control are easily attained. Changes in medication and disposition should be decided in consultation with a gastroenterologist.

Suggested Readings

Podolsky DK. Inflammatory bowel disease. N Engl J Med. 2002;347:417–429.

Rothfuss KS, Strange EF, Herrlinger KR. Extraintestinal manifestations and complications in inflammatory bowel diseases. World J Gastroenterol. 2006;12:4819–4831.

References

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2 Tysk C, Lindberg E, Jarnerot G, et al. Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic and dizygotic twins: a study of heritability and the influence of smoking. Gut. 1988;29:990–996.

3 Orholm M, Munkholm P, Langhoz E, et al. Familial occurrence of inflammatory bowel disease. N Engl J Med. 1991;324:84–88.

4 Calkins BM, Lilienfeld AM, Garland CF, et al. Trends in incidence rates of ulcerative colitis and Crohn’s disease. Dig Dis Sci. 1984;29:913–930.

5 Ekbom A, Helmick C, Zack M, et al. The epidemiology of inflammatory bowel disease: a large, population-based study in Sweden. Gastroenterology. 1991;100:350–358.

6 Hugot JP, Alberti C, Berrebi D, et al. Crohn’s disease: the cold chain hypothesis. Lancet. 2003;362:2012–2015.

7 Vidal A, Gómez-Gil E, Sans M, et al. Life events and inflammatory bowel disease relapse: a prospective study of patients enrolled in remission. Am J Gastroenterol. 2006;101:1–7.

8 Silverstein MD, Lashner BA, Hanauer SB, et al. Cigarette smoking in Crohn’s disease. Am J Gastroenterol. 1989;84:31–33.

9 Tanner AR, Raghunath AS. Colonic inflammation and nonsteroidal anti-inflammatory drug administration. An assessment of the frequency of the problem. Digestion. 1988;41:116–120.

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11 Amre DK, D’Souza S, Morgan K, et al. Imbalances in dietary consumption of fatty acids, vegetables, and fruits are associated with risk for Crohn’s disease in children. Am J Gastroenterol. 2007;102:2016–2025.

12 Satsangi J, Welsh KI, Bunce M, et al. Contribution of genes of the major histocompatibility complex to susceptibility and disease phenotype in inflammatory bowel disease. Lancet. 1996;347:1212–1217.

13 Satsangi J, Parkes M, Louis E, et al. A genome-wide search identifies potential new susceptibility loci for Crohn’s disease. Inflamm Bowel Dis. 1999;5:271–278.

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15 Hugot JP, Chamaillard M, Zomali H, et al. Association of NOD 2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature. 2001;411:599–603.

16 Gupta G, Gelfand JM, Lewis JD. Increased risk for demyelinating diseases in patients with inflammatory bowel disease. Gastroenterology. 2005;129:819–826.

17 Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a population-based study. Gastroenterology. 2005;129:827–836.

18 Loftus EV, Silverstein MD, Sandborn WJ, et al. Ulcerative colitis in Olmsted County, Minnesota, 1940–1993: incidence, prevalence, and survival. Gut. 2000;46:336–343.

19 Loftus EV. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology. 2004;126:1504–1517.

20 Boyko EJ, Koepsell TD, Perera DR, et al. Risk of ulcerative colitis among former and current cigarette smokers. N Engl J Med. 1987;316:707–710.

21 Boudiaf M, Jaff A, Soyer P, et al. Small-bowel diseases: prospective evaluation of multi-detector row helical CT enteroclysis in 107 consecutive patients: CT enteroclysis is a fast, well-tolerated, and reliable imaging modality for the depiction of small-bowel diseases. Radiology. 2004;233:338–344.

22 Prantera C, Zannoni F, Scribano ML, et al. An antibiotic regimen for the treatment of active Crohn’s disease: a randomized controlled trial of metronidazole plus ciprofloxacin. Am J Gastroenterol. 1996;91:328–332.

23 Rahimi R, Nikifar S, Rezaie E, et al. A meta-analysis of broad-spectrum antibiotic therapy in patients with active Crohn’s disease. Clin Ther. 2006;28:1983–1988.

24 Cheifetz A, Itzkowitz S. The diagnosis and treatment of pouchitis in inflammatory bowel disease. J Clin Gastroenterol. 2004;38:S44–S50.

25 Thia KT, Mahadevan U, Feagan BG, et al. Ciprofloxacin or metronidazole for the treatment of perianal fistulas in patients with Crohn’s disease: a randomized double-blind placebo-controlled pilot study. Inflamm Bowel Dis. 2009;15:17–24.

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