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Inflammatory Bowel Disease Nursing CE Course for RNs and LPNs

1.5 ANCC Contact Hours

About this course:

This learning activity aims to increase nurses' knowledge of inflammatory bowel disease (IBD), including the difference between ulcerative colitis and Crohn's disease. This includes the pathophysiology, clinical manifestations, risk factors, diagnostic testing, and treatment options for both types of IBD.

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Inflammatory Bowel Disease

Disclosure Statement

This learning activity aims to increase nurses' knowledge of inflammatory bowel disease (IBD), including the difference between ulcerative colitis and Crohn's disease. This includes the pathophysiology, clinical manifestations, risk factors, diagnostic testing, and treatment options for both types of IBD.


After completing this module, learners will be able to:

  • identify the differences between ulcerative colitis and Crohn's disease
  • describe the pathophysiological changes that occur in ulcerative colitis and Crohn's disease
  • recognize the clinical manifestations of IBD
  • explain the risk factors and comorbidities for IBD
  • summarize the diagnostic criteria and treatment options for IBD


Background 

Inflammatory bowel disease (IBD) is a chronic inflammatory disease that affects the gastrointestinal (GI) tract. The cause of IBD is thought to be an inappropriate immune response to the normal microflora found within the GI tract. The exact cause of IBD remains unknown as no one cause can universally explain disease development in all individuals (McDowell et al., 2022).

 

Risk Factors

Many risk factors increase an individual's risk of developing IBD, and diagnosis is more common in non-Hispanic Whites and those of Ashkenazi Jewish background. Other risk factors include the presence of susceptible genes, exposure to environmental factors, alterations in the function of epithelial cells, and an altered immune response to normal microflora in the intestines (McCance & Huether, 2019).

Unknown environmental causes or infections are thought to change the function of the mucosal epithelium, promote a loss of tolerance by the immune system to normal flora, and increase the uptake of luminal antigens, which are vital to gut function and immunity. The immune system loses the ability to differentiate between normal microflora and harmful pathogens. This leads to dendritic cells' activation and transport to the mesenteric lymph nodes. Once at the lymph nodes, the dendritic cells promote the differentiation of naïve T cells into T helper cells. The production of proinflammatory cytokines and chemokines, interleukins, interferon-gamma, and oxygen-free radicals damage the intestinal epithelium. This damage and resulting changes to the intestinal mucosa can lead to colon cancer over 30 to 35 years (McCance & Huether, 2019).

Based on aggregate data from the National Health Interview Survey (NHIS) from 2016 and 2018, it is estimated that 3.1 million Americans have a current diagnosis of IBD, with approximately 80,000 new diagnoses each year. This equates to a lifetime prevalence of 1.3%. Specific characteristics either increase or decrease the lifetime prevalence of IBD for certain individuals. The prevalence of IBD is higher among females (1.5%) versus males (1.0%). There are also age-specific increases in the prevalence of IBD. Those aged 45 years and older have the highest prevalence, 1.7%, versus those aged 18 to 24 (0.5%) or 25 to 44 (1.0%). IBD is most prevalent in non-Hispanic White adults (1.4%), followed by non-Hispanic Black adults (0.6%) and other non-Hispanic adults (0.8%). The prevalence of IBD decreases as an individual's highest level of education increases. Those with less than a high school education have a prevalence of 1.6% compared to those with at least a bachelor's degree (1.1%). Marital status also seems to impact the prevalence of IBD, with divorced, separated, or widowed individuals experiencing a lifetime prevalence of 2.3% versus those married or cohabitating at 1.1% (McDowell et al., 2022; Xu et al., 2018). Other characteristics that influence an individual's likelihood of developing IBD include:

  • unemployed (1.6%) versus employed (1.1%)
  • US-born (1.2%) versus non-US-born (0.8%)
  • adults living in small metropolitan areas (1.4%) versus those living in large metropolitan areas (1.1%; Xu et al., 2018)


Of those diagnosed with IBD, certain lifestyle factors have an increased prevalence (Xu et al., 2018). These include:

  • sleeping less than 7 hours per day (38.2%)
  • sedentary lifestyle (50.4%)
  • smoking history (26%; Xu et al., 2018)


Comorbidities

A diagnosis of IBD is associated with comorbid conditions. These are often related to the systemic, GI, and immune changes that occur with IBD (Terlizzi et al., 2021). Individuals with IBD are more likely to have comorbidities, including:

  • cardiovascular disease
  • colorectal cancer
  • diabetes
  • arthritis
  • liver disease (Terlizzi et al., 2021)


Symptoms

Common symptoms experienced by patients with IBD include fatigue (91%), abdominal cramps and pain (81%), joint pain or inflammation (74%), an urgent need to have a bowel movement (74%), bloating (68%), and a feeling of fullness in the abdomen (63%). Specific symptoms differ based on the type of IBD that is present. These different types and accompanying symptoms are discussed in the following sections (Crohn's and Colitis Foundation of America [CCFA], 2014; McCance & Huether, 2019).


Types of Inflammatory Bowel Disease

Two main types of IBD affect adults: ulcerative colitis and Crohn's disease. Both disorders are considered chronic, relapsing inflammatory diseases of the bowel. Many differences help to differentiate between the two conditions, including the affected locations within the GI tract, duration of inflammation, and systemic effects; however, in 10% of patients, the clinical manifestations present in a way that makes it impossible to initially differentiate between them (Ignatavicius et al., 2018; McDowell et al., 2022).


Figure 1

Ulcerative Colitis versus Crohn's Disease 

(WolfpackBME, 2022)


Ulcerative Colitis

Ulcerative colitis is a form of IBD characterized by ulceration of the colonic mucosa and submucosa. It most commonly affects the rectum and sigmoid colon and is the most common type of IBD globally. Ulcerative colitis causes significant morbidity but has a low incidence of mortality. However, due to the chronic nature of the condition, there can be long-term effects on the patient's mental and physical well-being. In the US, ulcerative colitis accounts for over 250,000 provider visits and costs approximately 4 billion dollars annually (Lynch & Hsu, 2022; McCance & Huether, 2019; Rubin et al., 2019).


Epidemiology 

The prevalence of ulcerative colitis varies based on geographical location. The disease has increased prevalence in Northern America and Northern Europe. In these areas, ulcerative colitis has an estimated incidence of 9 to 20 per 100,000 and a prevalence of 156 to 291 cases per 100,000 individuals per year (McCance & Huether, 2019).


Pathophysiology

Ulcerative colitis lesions begin as inflammation at the base of the crypts of Lieberkuhn, which are glands found in the lining of the colon and rectum. Ulcerative colitis typically involves the rectum but can extend proximally to affect the entire colon. Only about 5% of patients with ulcerative colitis do not have rectal involvement. The lesions caused by ulcerative colitis are typically limited to the mucosa and are not transmural or include skip lesions (discussed in the Crohn's disease section). The inflammation seen with ulcerative colitis is caused by the release and infiltration of cytokines that a


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ctivate neutrophils, plasma cells, lymphocytes, macrophages, mast cells, and eosinophils. When macrophages are activated, they can lead to the presence of cytokines that cause fever during the acute phase of ulcerative colitis. The resulting inflammation damages the intestinal wall's mucosal barrier, which allows fluid to leak into the gut (McCance & Huether, 2019).

The mucosa can become hyperemic and edematous when mild inflammation is present, leading to a dark red and velvety appearance. The mucosa becomes hemorrhagic with small erosions that merge into ulcers if inflammation is severe. Abscesses can form in the crypts, and granulation tissue can develop due to necrosis and ulceration of the mucosa. Edema and thickening of the muscularis mucosa can lead to a narrowing of the affected colon. With chronic disease, inflammatory polyps may develop over time due to the rapidly regenerating epithelium (McCance & Huether, 2019). Figure 2 depicts the anatomy of the GI tract.


Figure 2 

Layers of the GI Tract 

(Goran tek-en, 2014)

 

 

Risk Factors

There are many risk factors specific to ulcerative colitis. Some of the risk factors are modifiable, while others are nonmodifiable. Examples of the risk factors for the development of ulcerative colitis include:

  • family history: this is the most critical risk factor and accounts for 8% to 14% of patients diagnosed with ulcerative colitis; individuals with a 1st-degree relative diagnosed with ulcerative colitis were four times more likely to be diagnosed themselves
  • ethnicity: there is a higher incidence of ulcerative colitis in Jewish populations; specifically those of Ashkenazi Jewish descent
  • age: ulcerative colitis has a bimodal pattern of presentation; the predominant age of onset is between 15 and 30 years old, with a smaller, later onset between 50 and 70 years old
  • gender: ulcerative colitis is more common in men than women, and men are more likely to experience later onset, with diagnosis in their 50s or 60s
  • having an appendix: having an appendectomy decreases the risk of developing ulcerative colitis
  • smoking history: ulcerative colitis occurs less frequently in current smokers; some evidence suggests smoking is a protective factor against the development of ulcerative colitis, but there is no confirmed link (CCFA, 2014; Lynch & Hsu, 2022)

 

Clinical Manifestations

The initial symptoms of ulcerative colitis are caused by inflammation of the rectum. These symptoms include bleeding, bowel movement urgency, and tenesmus (a feeling of rectal pressure that accompanies the need to have a bowel movement). Ulcerative colitis symptoms present intermittently, following a pattern of remission and exacerbation. The severity of intestinal damage influences symptoms. Changes leading to the loss of the absorptive mucosal surface and decreased transit time can result in large volumes of watery diarrhea. Destruction of the mucosal lining can lead to bleeding, abdominal cramping, and an increased urge to have a bowel movement. It is common for an individual to experience numerous episodes of bloody diarrhea accompanied by the passage of purulent mucus. When ulcerative colitis severity is mild, there is less mucosal involvement or involvement is limited to proctitis. Due to this decrease in intestinal damage, the prevalence of increased frequency of bowel movements, bleeding, and abdominal cramping are decreased. When the disease is severe, the entire colon can be affected. This can lead to additional symptoms, including fever, tachycardia, more than six bowel movements per day, urgency, bloody stools, severe continuous abdominal pain, dehydration, weight loss, and blood loss leading to anemia. Other complications that can occur with ulcerative colitis are systemic or affect specific areas outside the GI tract. These include cutaneous lesions, polyarthritis, sacroiliitis (inflammation of the sacroiliac joint), osteopenia and osteoporosis, oral ulcerations, episcleritis (inflammation of the episclera) or anterior uveitis of the eye (inflammation of the iris), sclerosing cholangitis of the liver, and increased incidence of cholelithiasis. The chronic inflammation that occurs with ulcerative colitis can also lead to changes in the coagulation pathway resulting in microthrombi or deep vein thrombosis (McCance & Huether, 2019).

There may be additional complications based on the areas affected, such as anal fissures, hemorrhoids, or a perirectal abscess. Although severe blood loss due to ulcerative colitis is rare, chronic blood loss can lead to hypotension and shock. The colon can sometimes become obstructed due to edema, strictures, or fibrosis. Although a rare complication, bowel perforation can occur (McCance & Huether, 2019). Table 1 outlines the most commonly experienced symptoms among patients with ulcerative colitis.


Table 1

Prevalence of Ulcerative Colitis Symptoms 

Symptom

Experienced Ever

Experienced within 30 days

Bowel movement urgency

76%

49%

Abdominal pain or cramps

73%

47%

Diarrhea (non-bloody)

72%

46%

Tiredness, exhaustion, or fatigue

71%

48%

Flatulence

67%

49%

Bloating

66%

47%

Bowel movement soon after eating

64%

37%

Anxiety or depression

53%

32%

Insomnia or sleeplessness

49%

30%

Back pain

47%

31%

(Elflein, 2021b)


Diagnostic Criteria

Any patient who presents with hematochezia (fresh, red blood in the stool) and bowel movement urgency should be suspected of having ulcerative colitis. An infectious cause of symptoms should be excluded, especially Clostridioides difficile (C. diff), Escherichia coli (E. coli), Salmonella, Shigella, Yersinia, Campylobacter, and parasitic infection (based on patient travel history or geographical location). A stool culture can eliminate an infectious cause of the patient's symptoms. Diagnosis of ulcerative colitis is based on the patient's medical history, clinical presentation, imaging, and biopsy results. When a colonoscopy is performed, the inflamed and hemorrhagic mucosa can be visualized. Radiology testing, using a computed tomography (CT) scan, can show the loss of the haustra (the pouches that give the colon a segmented appearance), the presence of ulceration, and irregular ulceration. Laboratory testing can also be performed to monitor hemoglobin, albumin, and potassium levels. Patients with ulcerative colitis have low hemoglobin, hypoalbuminemia, and hypokalemia. Other laboratory testing includes C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), which are both elevated with ulcerative colitis. Since the symptoms of ulcerative colitis overlap with Crohn's disease, the differential diagnosis can be challenging. A colonoscopy should be performed with intubation of the terminal ileum to confirm the diagnosis. Features seen upon endoscopic evaluation include a loss of vascular markings, erosion, and friability of the mucosa. When extensive inflammation is present, deep ulcerations and bleeding can be seen. Biopsies of affected and unaffected areas should be obtained and evaluated by a trained GI pathologist to confirm a diagnosis of ulcerative colitis. Biopsies of the unaffected areas are obtained since the disease may be present despite a normal presentation (McCance & Huether, 2019; Rubin et al., 2019).

Fecal calprotectin (FC) can be used as a noninvasive option to determine the extent of disease activity and response to therapy. FC is a neutrophil marker of inflammation that is often elevated in the presence of infectious or inflammatory colitis. However, FC is not elevated when the cause of symptoms is noninflammatory, such as irritable bowel syndrome (Rubin et al., 2019).

There are different categories of ulcerative colitis based on areas of involvement (Rubin et al., 2019). One standard used to classify the location of ulcerative colitis is the Montreal classification system. This classification system is outlined as follows:

  • proctitis: affected areas are within 18 cm of the anal verge and distal to the rectosigmoid junction
  • left-sided colitis: affected areas extend from the sigmoid colon to the splenic flexure
  • extensive colitis: affected areas extend beyond the splenic flexure (Rubin et al., 2019)


There are also classification systems for the severity of ulcerative colitis. One of these classification systems is the Truelove and Witts system (Rubin et al., 2019). Initially published in 1955, this system outlines the severity of ulcerative colitis based on the following:

  • mild colitis: less than four bowel movements per day, hemoglobin greater than 11 g/dL, ESR less than 20 mm/hr, and no changes to temperature or heart rate
  • severe colitis: more than six bowel movements per day in the presence of fever, tachycardia, anemia, and elevated ESR (Rubin et al., 2019)

Complications

Since ulcerative colitis is a chronic disease, complications can develop as the disease progresses. Common complications include a leak from anastomosis, the development of a pelvic abscess, enterocutaneous fistulas, fecal incontinence, sexual dysfunction, colon or rectal cancer, toxic megacolon, and pouch prolapse. The risk of colorectal cancer increases as the time since diagnosis increases. After 10 years, the risk is 2%, increasing to 8% after 20 years and 20% to 30% after 30 years. Over time, ulcerative colitis can lead to bowel perforation due to the weakened intestinal wall resulting from chronic inflammation. Severe inflammation can also lead to a rapid enlargement of the colon, known as toxic megacolon, a rare but deadly complication of ulcerative colitis (CCFA, 2014; Lynch & Hsu, 2022; Skomorochow & Pico, 2022).


Surgical Management

Since ulcerative colitis is typically restricted to the colon, a colectomy is considered a curative treatment. A colectomy is indicated in patients who have not achieved remission despite medication management or experience intolerable adverse effects due to medication management. Surgical intervention is also indicated for patients with toxic megacolon, bowel perforation, bleeding, strictures, intractable fulminant colitis, or cancer. The standard surgical treatment is a restorative proctocolectomy with ileal pouch-anal anastomosis (RPC-IPAA). An RPC-IPAA is a 2-step procedure. During the first step, the colon and most of the rectum are removed, leaving the anus and anal sphincter untouched. Then, a surgical pouch is created using the last 1.5 feet of the small intestine. A temporary loop ileostomy is created to allow the surgically created pouch to heal. The second stage involves reversing the temporary loop ileostomy. This can occur in as little as 1 to 2 months after stage 1. Some patients may not be good candidates for an RPC-IPAA. In these cases, a total proctocolectomy with permanent ileostomy is indicated. During this procedure, the colon, rectum, and anus are removed, and the anus is surgically closed. The end of the ileum is then diverted through the abdominal wall, creating a stoma (Ignatavicius et al., 2018; Lynch & Hsu, 2022).

 

Crohn's Disease

Crohn's disease is a type of IBD that affects the GI tract at any point from the mouth to the anus; however, it most commonly affects the distal portion of the small intestine and the proximal portion of the large intestine. It is an idiopathic disorder of unknown etiology. Crohn's disease develops slowly and progresses unpredictably. The disease affects multiple areas of the intestine, with the presence of normal, unaffected regions in between. This disease pattern is known as skip lesions and appears as a cobblestone pattern. The symptoms of Crohn's disease occur in a waxing and waning pattern with periods of active disease and remission (Ignatavicius et al., 2018).

 

Epidemiology

Approximately 1 million individuals are living with Crohn's disease in the US. Globally, Canada has the highest incidence of Crohn's disease. Of those with Crohn's disease, 35% have involvement of the ileum only (ileitis), 45% have involvement of the ileum and colon (ileocolitis), with more involvement on the right side of the colon, and 20% have involvement of the colon only (granulomatous colitis) without the involvement of the rectum (Walfish & Companioni, 2022a).


Pathophysiology

Crohn's disease begins with inflammatory lesions in the intestinal submucosa and spreads sporadically, which, as discussed above, is known as skip lesions. The progression of Crohn's disease is unpredictable, and one side of the small intestine may be affected while the other may not. Progression involves neutrophils infiltrating the crypts, resulting in the development of abscesses and the destruction of the crypts. Ulcerations caused by Crohn's disease appear as longitudinal and transverse fissures that can extend into the lymphoid tissue. The typical presentation of Crohn's disease lesions is a granuloma surrounded by areas of ulceration (McCance & Huether, 2019).


Risk Factors

There are many modifiable and nonmodifiable risk factors associated with Crohn's disease. Some risk factors overlap with those seen with ulcerative colitis, while others are distinct. Risk factors for the development of Crohn's disease include:

  • family history
  • smoking history
  • ethnicity: Crohn's disease is more common in those with an Ashkenazi Jewish background
  • geographical location: those living in urban areas are more at risk of developing Crohn's disease
  • gender: women are affected slightly more than men
  • age: onset usually occurs before the age of 40
  • history of an appendectomy: having the appendix surgically removed increases an individual's risk of developing Crohn's disease
  • gene mutation: there is a strong association between Crohn's disease and alterations in the nucleotide-binding-oligomerization-domain-containing protein 2 (CARD15/NOD2) gene found on chromosome 16 (CCFA, 2014; McCance & Huether, 2019)


Clinical Manifestations

Typically, in the early stages of Crohn's disease, individuals have no other symptoms besides reports of an irritable bowel. Symptoms associated with Crohn's disease can be localized to the GI tract or systemic. The symptoms are similar to those seen with ulcerative colitis but can vary depending on the area of the affected intestine and the disease's extent. The most common symptom of Crohn's disease is chronic diarrhea. Other GI symptoms include abdominal pain, unintentional weight loss, and anal pain. Anal pain can be attributed to anal fissures, ulcers, fistulas, or stenosis. Additional symptoms and complications may include fatigue, aphthous stomatitis (oral ulcerations), joint pain, osteonecrosis, cholelithiasis, and uveitis or scleritis. A diagnosis of Crohn's disease can also be associated with other immune-mediated disorders, including asthma, pericarditis, psoriasis, celiac disease, multiple sclerosis, rheumatoid arthritis, and chronic bronchitis (Lichtenstein et al., 2018; McCance & Huether, 2019). Symptoms of Crohn's disease are patient-dependent. Table 2 lists the most commonly experienced symptoms. The presence of symptoms is broken down into those experienced at any point during the disease compared with those experienced in the last 30 days (Elflein, 2021).


Table 2

Prevalence of Crohn's Disease Symptoms 

Symptom

Experienced Ever

Experienced within 30 days

Diarrhea (non-bloody)

79%

58%

Abdominal pain or cramps

77%

53%

Bowel movement urgency

75%

52%

Tiredness, exhaustion, or fatigue

73%

56%

Nausea and vomiting

71%

39%

Bloating

70%

52%

Bowel movement soon after eating

69%

46%

Flatulence

69%

52%

High stool frequency

62%

37%

Anxiety or depression

58%

37%

(Elflein, 2021a)


Diagnostic Criteria

The diagnosis of Crohn's disease is similar to ulcerative colitis. It is based on clinical presentation and endoscopic, pathologic, and histologic results. Laboratory testing may also be performed to assess for inflammation, anemia, dehydration, and malnutrition. Laboratory results typically show a decrease in hemoglobin and an increase in platelets. CRP is elevated due to the inflammation that occurs with Crohn's disease. ESR may also be elevated due to inflammation; however, it will not differentiate between Crohn's disease and another disorder that causes inflammation. Approximately 40% of patients with Crohn's disease will have a normal CRP and ESR (Lichtenstein et al., 2018).

Endoscopic testing can be completed via a colonoscopy or through the use of an ingestible camera. Abdominal X-rays may also be performed and can show a narrowing of the intestine and the presence of ulcerations, strictures, and fistulas. Magnetic resonance enterography (MRE) can also assess bowel motility. An abdominal ultrasound or CT scan may demonstrate the extent of the disease. An FC test should be performed to differentiate between IBD and IBS, and the patient should be tested for an infectious cause of symptoms (Ignatavicius et al., 2018).

Complications

Complications related to a diagnosis of Crohn's disease are similar to those associated with ulcerative colitis. While hemorrhage is possible with Crohn's disease, it is less common. The most common complication is malabsorption due to changes in the small intestine. Cancer of the colon or small intestine is rarer in Crohn's disease but may occur after the disease has been present for at least 15 to 20 years. Fistula development is more likely with Crohn's disease than ulcerative colitis. A fistula can develop between segments of the intestine, as a perirectal abscess, opening in the skin, or as an extension to another organ structure (e.g., the vagina or bladder). The thickened lining that results from chronic inflammation can lead to the development of strictures that can cause a bowel obstruction (Ignatavicius et al., 2018). Other complications of Crohn's disease may include:

  • ankylosing spondylitis
  • episcleritis or iritis
  • cholelithiasis
  • anemia; due to vitamin B12 deficiency because of malabsorption
  • hypercoagulable state
  • osteoporosis; due to deficiencies in vitamin D and calcium due to malabsorption
  • renal calculi
  • erythema nodosum (a condition characterized by red bumps on the shins)
  • pyoderma gangrenosum (a condition that results in large, painful leg ulcers; Ranasinghe & Hsu, 2022)

 

Treatment of Inflammatory Bowel Disease

Treatment options are based on disease severity and patient presentation. Guidelines for treatment consider patient-reported outcomes, including normalizing bowel habits or decreased bleeding. Treatment guidelines also change based on the inflammatory burden, extent and severity of inflammation, disease course, whether hospitalization or steroids are indicated, if there is a failure in conservative treatment options, and disease impact on the patient's quality of life. Treatment should also be guided by the specific diagnosis, disease severity, and prognosis (Rubin et al., 2019; Walfish & Companioni, 2022b).

First-line treatment for ulcerative colitis is a class of medications known as aminosalicylates (5-ASAs). These drugs are also used for maintenance therapy. Although 5-ASAs are used to treat mild to moderate Crohn's disease, they are not approved by the US Food and Drug Administration (FDA) for this indication. Some guidelines recommend utilizing antibiotics as first-line treatment, whereas others suggest delaying antibiotic initiation until the completion of 4 weeks of treatment with a 5-ASA with no improvement. However, other guidelines consider corticosteroids the first-line treatment of Crohn's disease, with 5-ASA drugs reserved for those who do not see improvement in symptoms or cannot tolerate corticosteroid use (CCFA, 2022; Rubin et al., 2019; Walfish & Companioni, 2022a, 2022b).

The 5-ASA class of drugs includes sulfasalazine (Azulfidine), mesalamine (Asacol HD, Pentasa, Lialda, Apriso, Delzicol), olsalazine (Dipentum), and balsalazide (Colazal). These drugs work by decreasing inflammation in the GI tract. They are most effective in the colon and can be administered rectally via an enema or suppository or orally as an extended-release formulation. Rectal formulations can be used in addition to oral therapy as acute or maintenance treatment (CCFA, 2022; Rubin et al., 2019; Walfish & Companioni, 2022b).

Due to the presence of sulfa, sulfasalazine (Azulfidine) has the most adverse effects. These include nausea, dyspepsia, fever, rash, nervousness, sensitivity to sunlight, and headache. Taking the medication with food can decrease some of these effects. Sulfa can also disrupt folate absorption (folic acid) and cause hemolytic anemia, agranulocytosis, hepatitis, pneumonitis, or myocarditis. Sulfasalazine (Azulfidine) can also cause decreased sperm count and motility; this adverse effect has been reported in 80% of men but is reversible following treatment discontinuation. Side effects of the other 5-ASA medications include malaise, headache, hair loss, colitis, and pancreatitis. Olsalazine (Dipentum) can cause watery diarrhea in approximately 15% of individuals and occurs more frequently in those with pancolitis (Chiefetz & Cullen, 2022; Walfish & Companioni, 2022b).

Individuals diagnosed with Crohn's disease may need to be treated with antibiotics to treat the presence of bacterial infection in the GI tract. Infections associated with Crohn's disease may include abscesses and fistulas involving the anal canal and vagina. Examples of antibiotics commonly prescribed to treat infections in patients with Crohn's disease include metronidazole (Flagyl), ciprofloxacin (Cipro), and rifaximin (Xifaxan; CCFA, 2022).


When patients do not experience remission following treatment with a 5-ASA medication, switching to an alternative 5-ASA medication is not recommended. Instead, a corticosteroid may be added to the treatment regimen. Corticosteroids are also indicated in moderate to severe Crohn's disease. Examples of corticosteroids used in the treatment of ulcerative colitis are prednisone (Deltasone), hydrocortisone (Cortef), methylprednisolone (Medrol), and budesonide (Entocort, Uceris; CCFA, 2022; Rubin et al., 2019).

Symptoms should begin improving after 5 to 7 days of treatment. Adverse effects include edema, gastritis, hypertension, fluid and electrolyte imbalances, immunosuppression, increased appetite, weight gain, insomnia, psychosis, hyperglycemia, and cushingoid symptoms. Corticosteroids must be used cautiously in patients with renal disease, hypertension, osteoporosis, seizures, heart failure, psychosis, and emotional instability (CCFA, 2022; Rubin et al., 2019; Woods, 2023).

If remission is not achieved after adding a corticosteroid, a thiopurine or biological drug can be added to the treatment regimen. Thiopurines are immunosuppressants. These drugs suppress the body's immune response to prevent and reduce inflammation. Examples of thiopurines include azathioprine (Imuran) and 6-mercaptopurine (Purinethol). Azathioprine (Imuran) and its metabolite 6-mercaptopurine (Purinethol) can inhibit T-cell function as part of the immune response and may even induce T-cell apoptosis. These medications can be effective in the long-term management of IBD and may decrease the need for corticosteroids. These drugs can help maintain remission for multiple years and achieve clinical benefits in as little as 1 to 3 months (CCFA, 2022; Lynch & Hsu, 2022; Walfish & Companioni, 2022b). The most common adverse effects of these medications are nausea, vomiting, and malaise. Other adverse effects include pancreatitis and hepatotoxicity (Walfish & Companioni, 2022b).

Patients diagnosed with Crohn's disease who require corticosteroids to manage symptoms or have not had symptoms adequately managed despite corticosteroid use and have not responded to the initiation of azathioprine (Imuran) or 6-mercaptopurine (Purinethol) can benefit from treatment with methotrexate (Trexall). Side effects include nausea, vomiting, neurotoxicity, fatigue, dizziness, aphasia, fever, blurred vision, diarrhea, cirrhosis, arthralgia, rash, photosensitivity, and alopecia. Those individuals of reproductive age, and their partners, should utilize an effective form of birth control such as an intrauterine device, implant, or oral contraceptive. Before attempting to conceive, methotrexate (Trexall) should be discontinued for at least 3 months (Walfish & Companioni, 2022b).

Biological drugs are antibodies that inhibit proteins from causing inflammation, specifically tumor necrosis factor (TNF). Examples of biological drugs include infliximab (Remicade), adalimumab (Humira), certolizumab (Cimzia), and golimumab (Simponi). Infliximab (Remicade), adalimumab (Humira), and certolizumab (Cimzia). These drugs can be used in Crohn's disease to prevent recurrence following remission. Infliximab (Remicade), adalimumab (Humira), and golimumab (Simponi) can be used in patients with refractory or corticosteroid-dependent ulcerative colitis. Of the biological drugs, infliximab (Remicade) is the most commonly used to treat ulcerative colitis (CCFA, 2022; Lynch & Hsu, 2022; Walfish & Companioni, 2022b).


These medications can be used as monotherapy or with a thiopurine or methotrexate (Trexall). Adverse effects can include fever, chills, headache, nausea, and immediate or delayed hypersensitivity reactions presenting as a rash, pruritis, or anaphylactic reaction (Walfish & Companioni, 2022b).

Another treatment option includes vedolizumab (Entyvio) and natalizumab (Tysabri); both belong to a novel class of biological drugs that function as antibodies to leukocyte adhesion molecules and are therefore known as anti-adhesion molecule inhibitors. These drugs are FDA-approved to treat moderate to severe ulcerative colitis and Crohn's disease. Although administered intravenously, the effects of vedolizumab (Entyvio) are limited to the GI tract. Adverse effects include fatigue, headaches, arthralgia, cough, fever, sinusitis, and infection. Due to its higher incidence of systemic effects, natalizumab (Tysabri) is reserved for second-line treatment, following vedolizumab (Entyvio). Due to adverse effects, natalizumab (Tysabri) authorization is required as it is only available through a restricted prescribing program, and treatment should be reassessed every 6 months. Adverse effects include headaches, fatigue, arthralgia, depression, and the development of progressive multifocal leukoencephalopathy (PML; Walfish & Companioni, 2022b).

Ustekinumab (Stelara) is an anti-IL-12/23 antibody approved for use in individuals with moderate to severe ulcerative colitis or Crohn's disease that have failed treatment with conventional therapy. Adverse effects include depression, dizziness, fatigue, headaches, fever, diarrhea, nausea, vomiting, abdominal pain, and increased risk for infection (Walfish & Companioni, 2022b; Woods, 2023).

Individuals with moderate to severe ulcerative colitis can be treated with target synthetic small-molecule medications. These drugs have a molecular weight of less than 1 kilodalton, and they differ from monoclonal antibodies as they lack the same immunogenicity and can be administered orally. These drugs reduce inflammation by directly targeting specific steps in the immune response. Examples include tofacitinib (Xeljanz) and ozanimod (Zeposia; CCFA, 2022; Walfish & Companioni, 2022b).

Tofacitinib (Xaljanz) specifically inhibits Janus kinas 1-3. It is available in immediate-release and extended-release formulations. Adverse effects include hypercholesterolemia, diarrhea, headaches, rash, upper respiratory infection, and reactivation of herpes zoster in the form of shingles. There is a black box warning of the increased risk of pulmonary embolism and death in individuals with rheumatoid arthritis (CCFA, 2022; Walfish & Companioni, 2022b).

Ozanimod (Zeposia) is a sphingosine 1-phosphate (S1p) receptor modulator. Adverse effects include rash, urticaria, bradycardia, hypertension, orthostatic hypotension, atrioventricular (AV) block, dyspnea, and increased risk of infection (CCFA, 2022; Walfish & Companioni, 2022b).


Patient Education

The goals of IBD management include pain control and proper skin care. To decrease abdominal pain, the patient should administer analgesics as ordered and report changes in the effectiveness of the treatment regimen. The patient should keep a log or diary of all fluid and food intake to help determine if certain foods exacerbate symptoms. Although there is no direct relationship between diet and IBD, many patients report exacerbations following the ingestion of caffeine, alcohol, raw vegetables, foods high in fiber, and those containing lactose or gluten. It is also important that patients monitor their weight. Patients should be counseled on proper skin care to prevent breakdown, including washing the perineal area with mild soap and water after each bowel movement and patting the area dry. If irritation occurs, sitz baths followed by a thin application of A & D ointment may be beneficial. Patients should be encouraged to report changes in their elimination pattern, including altered frequency, amount, presence of blood, and consistency of bowel movements. Patients should be educated on the importance of follow-up care, the availability of community resources, and signs and symptoms to report to the HCP (Ignatavicius et al., 2018).


References

Cheifetz, A. S., & Cullen, G. J. (2022). Patient education: Sulfasalazine and the 5-aminosalicylates (Beyond the basics). UpToDate. Retrieved December 22, 2022, from https://www.uptodate.com/contents/sulfasalazine-and-the-5-aminosalicylates-beyond-the-basics

Crohn's and Colitis Foundation of America. (2014). The facts about inflammatory bowel diseases. https://www.crohnscolitisfoundation.org/sites/default/files/2019-02/Updated%20IBD%20Factbook.pdf

Crohn's and Colitis Foundation of America. (2022). Understanding IBD medications and side effects. https://www.crohnscolitisfoundation.org/sites/default/files/2022-09/understanding-ibd-medications-brochure-final-rev0822-3_1.pdf

Elflein, J. (2021a). Most common Crohn's disease symptoms among Crohn's patients worldwide as of 2019. https://www.statista.com/statistics/1208470/most-common-symptoms-for-crohns-disease-patients-worldwide

Elflein, J. (2021b). Most common symptoms among ulcerative colitis patients worldwide in 2019. https://www.statista.com/statistics/1208499/most-common-symptoms-ulcerative-colitis-among-worldwide-patients

Goran tek-en. (2014). Layers of the GI tract [Image]. https://commons.wikimedia.org/wiki/File:Layers_of_the_GI_Tract_english.svg

Ignatavicius, D. D., Workman, M. L., & Rebar, C. R. (2018). Medical-surgical nursing: Concepts for interprofessional collaborative care (9th ed.). Elsevier.

Lichtenstein, G. R., Loftus, E. V., Isaacs, K. L., Regueiro, M. D., Gerson, L. B., & Sands, B. E. (2018). ACG clinical guideline: Management of Crohn's disease in adults. American Journal of Gastroenterology, 113(4), 481-517. https://doi.org/10.1038/ajg.2018.27

Lynch, W. D., & Hsu, R. (2022). Ulcerative colitis. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK459282

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.

McDowell, C., Farooq, U., & Haseeb, M. (2022). Inflammatory bowel disease. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK470312

Ranasinghe, I. R., & Hsu, R. (2022). Crohn disease. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK436021

Rubin, D. T., Ananthakrishnan, A. N., Siegel, C. A., Sauer, B. G., & Long, M. D. (2019). ACG clinical guideline: Ulcerative colitis in adults. The American Journal of Gastroenterology, 114(3), 384-413. https://doi.org/10.14309/ajg.0000000000000152

Skomorochow, E., & Pico, J. (2022). Toxic megacolon. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK547679

Terlizzi, E. P., Dahlhamer, J. M., Xu, F., Wheaton, A., Greenlund, K. J., & National Center for Chronic Disease Prevention and Health Promotion. (2021). Health care utilization among U.S. adults with inflammatory bowel disease, 2015-2016. National Health Statistics Reports, 152. https://doi.org/10.15620/cdc:100471

Walfish, A. E., & Companioni, R. A. C. (2022a). Crohn disease. Merck Manual Professional Version. https://www.merckmanuals.com/professional/gastrointestinal-disorders/inflammatory-bowel-disease-ibd/crohn-disease

Walfish, A. E., & Companioni, R. A. C. (2022b). Drugs for inflammatory bowel disease. Merck Manual Professional Version. https://www.merckmanuals.com/professional/gastrointestinal-disorders/inflammatory-bowel-disease-ibd/drugs-for-inflammatory-bowel-disease

WolfpackBME. (2022). Inflammatory bowel disease [Image]. https://commons.wikimedia.org/wiki/File:Inflammatory_Bowel_Disease_MTK.jpg

Woods, A. D. (2023). Nursing2023 drug handbook (43rd ed.). Wolters Kluwer.

Xu, F., Dahlhamer, J. M., Zammitti, E. P., Wheaton, A. G., & Croft, J. B. (2018). Health-risk behaviors and chronic conditions among adults with inflammatory bowel disease - United States, 2015 and 2016. Morbidity and Mortality Weekly Report (MMWR), 67(6), 190-195. https://doi.org/10.15585/mmwr.mm6706a4

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