Crohn’s disease

55 Crohn’s disease




Overview/pathophysiology


Crohn’s disease (CD), also known as regional enteritis, granulomatous colitis, or transmural colitis, is a chronic inflammatory disease that can involve any part of the gastrointestinal (GI) tract from the mouth to the anus. Usually the disease occurs segmentally, demonstrating discontinuous areas of disease with segments of healthy bowel in between. In 45%-50% of cases, the end of the ileum and cecum/ascending colon are involved (ileocolitis); in 35% of cases, the terminal ileum is affected (ileitis); and in 20% of cases, the colon alone is affected (Crohn’s colitis). A small number of patients have involvement of the jejunum, duodenum, stomach, esophagus, and mouth; in these cases, the ileum, colon, or both are also involved. Approximately 30%-35% of patients have perianal fistulas, fissures, or abscesses. The disease affects all layers of the bowel: the mucosa, submucosa, circular and longitudinal muscles, and serosa, predisposing to intestinal strictures and fistulas. A family history of this disease or ulcerative colitis occurs in 15%-20% of affected patients.


The cause of CD is unknown, but theories include infection, immunologic factors, environmental factors, and genetic predisposition. In a genetically susceptible subject, an outside agent or substance, such as a bacterium, virus, or other antigen, interacts with the body’s immune system to trigger the disease or may cause damage to the intestinal wall, initiating or accelerating the disease process. The resulting inflammatory response continues unregulated by the immune system. As a result, inflammation continues to damage the intestinal wall, causing the symptoms of CD. It is a chronic disease that has no cure. However, there are effective treatments to aid in controlling the disease. Initial treatment is nonoperative, individualized, and based on symptomatic relief. Surgery is reserved for complications rather than used as a primary form of therapy.


Since the end of World War II, the incidence of CD has increased steadily, whereas that of ulcerative colitis (UC) has stabilized. This rise may reflect increased diagnostic awareness rather than increased incidence of CD. There is a 20-fold increase in risk of inflammatory bowel disease (IBD) in first-degree relatives of individuals with CD. CD is generally diagnosed between the ages of 15 and 35, but it also can occur in young children and in people 70 years of age or older. Prevalence is slightly higher in women than in men. CD, like UC, is seen more frequently in the Caucasian population and in Ashkenazi Jews than in nonwhite populations and in people of non-Jewish descent. It is more prevalent in urban, developed countries with temperate climates than in rural, more southern countries. However, increasing incidence is being observed in Japan and South America. Cigarette smoking has been shown to increase the risk of developing CD and is associated with resistance to medical therapy and recurrence of disease after surgery. There have been studies in the United Kingdom and the United States promoting the idea that CD is caused by a bacterium, raising important questions for further research.



Health care setting


Primary care, with possible hospitalization resulting from complications



Assessment




Signs and symptoms:


Clinical presentation varies as a direct reflection of the location of the inflammatory process and its extent, severity, and relationship to contiguous structures. Sometimes onset is abrupt, and the patient can appear to have appendicitis, UC, intestinal obstruction, or a fever of obscure origin. Acute symptoms include right lower quadrant (RLQ) pain, tenderness, spasm, flatulence, nausea, fever, and diarrhea. A more typical picture is insidious onset with more persistent but less severe symptoms, such as vague abdominal pain, unexplained anemia, and fever. Diarrhea—liquid, soft, or mushy stools—is the most common symptom. The presence of gross blood is rare. Abdominal pain is a common symptom, and it may be colicky or crampy, initiated by meals, centered in the lower abdomen, and relieved by defecation because of chronic partial obstruction of the small intestine, colon, or both. As the disease progresses, anorexia, malnutrition, weight loss, anemia, lassitude, malaise, and fever can occur in addition to fluid, electrolyte, and metabolic disturbances.



Physical assessment:


In early stages, examination is often normal but may demonstrate mild tenderness in the abdomen over the affected bowel. In more advanced disease, a palpable mass may be present, especially in the RLQ with terminal ileum involvement. Persistent rectal fissure, large ulcers, perirectal abscess, or rectal fistula is the first indication of disease in 15%-25% of patients with small bowel involvement and in 50%-75% of patients with colonic involvement. Rectovaginal, abdominal, and enterovesical fistulas also can occur. Extraintestinal manifestations characteristic of UC do occur, but less commonly (10%-20%).



Diagnostic tests




Stool examination:


Usually reveals occult blood; frank blood may be noted in stools of patients with colonic involvement or with ulcerations and fistulas of the rectum. A few patients have presenting symptom of bloody diarrhea. Stool cultures and smears rule out bacterial and parasitic disorders. Specimens are also examined for fecal fat. Stool also is examined for the presence of white blood cells and certain proteins, the presence of which suggests inflammation.



Sigmoidoscopy:


Evaluates possible colonic involvement and obtains rectal biopsy. The finding of granulomas on mucosal biopsy argues strongly for the diagnosis of CD. However, because granulomas are more numerous in the submucosa, suction biopsy of the rectum provides deeper, larger, and less traumatized specimens for a better diagnostic yield than mucosal biopsy obtained through an endoscope.



Colonoscopy:


May help differentiate CD from UC. Characteristic patchy inflammation (skip lesions) rules out UC. However, colonoscopy usually does not add useful diagnostic information in the presence of positive findings from sigmoidoscopy or radiologic examination. When diagnosis is unclear and there is a question of malignancy, colonoscopy provides the means of directly visualizing mucosal changes and obtaining biopsies, brushings, and washings for cytologic examination. Colonoscopy also may assist in planning for surgery by documenting the extent of colonic disease. Note: Because of risk of perforation, this procedure may be contraindicated in patients with acute phases of Crohn’s colitis or when deep ulcerations or fistulas are known to be present.



Endoscopic ultrasonography:


Aids in diagnosis of perirectal fistula and abscesses and in detecting transmural depth of inflammation in the bowel or esophagus, using an endoscopically placed ultrasound probe.



Small bowel enteroscopy:


Permits visualization of the upper GI tract to identify areas of inflammation and bleeding to the level of the midjejunum.



Wireless capsule:


Permits visualization of the small intestine to identify abnormalities. The patient swallows a large capsule that contains a small disposable camera; images are transmitted to a receiver on the patient’s waist. Note: Use is contraindicated if strictures exist, because strictures can prevent the capsule from progressing through the intestine; surgical removal of the capsule may be required.



Barium enema and upper GI series with small bowel follow-through:


Contribute to diagnosis of CD. Involvement of only the terminal ileum or segmental involvement of the colon or small intestine almost always indicates CD. Thickened bowel wall with stricture (string sign) separated by segments of normal bowel, cobblestone appearance, and presence of fistulas and skip lesions are common findings. A double-contrast barium enema technique may increase sensitivity in detecting early or subtle changes. Note: Barium enema may be contraindicated in patients with acute phases of Crohn’s colitis because of risk of perforation. Upper GI barium series is contraindicated in patients in whom intestinal obstruction is suspected.



Computed tomography (CT) scan:


Complements information gathered via endoscopy and conventional radiography. In advanced disease, CT scanning clearly delineates extraluminal complications (e.g., abscess, phlegmon, bowel wall thickening, mesenteric inflammation). CT scan has been used also to percutaneously drain fistulas (colovesicular, enterovesicular, colovaginal, enterocolonic) and to evaluate perirectal disease, enterocutaneous fistula, and sinus tracts.



Serum antibody testing:


In difficult to diagnose cases, may be helpful in differentiating CD from UC.



Radionuclide imaging:


Intravenous (IV) indium-111– or technetium-99–labeled leukocytes migrate to areas of active inflammation and are then identified by scans performed after 4 and 24 hr. This procedure aids in differentiating CD from UC and evaluating abscess and fistula formation.



Blood tests:


Are nonspecific for diagnosis of CD but help determine whether the inflammatory process is active and evaluate patient’s overall condition. Anemia may be present and may be microcytic because of iron deficiency from chronic blood loss and bone marrow depression secondary to chronic inflammatory process or megaloblastic because of folic acid or vitamin B12 deficiency (usually seen only in patients with extensive ileitis causing malabsorption). Increased white blood cell (WBC) count, sedimentation rate, and C-reactive protein reflect disease activity and inflammation. Hypoalbuminemia corresponds with disease activity and results from decreased protein intake, extensive malabsorption, and significant enteric loss of protein. Hypokalemia is seen in patients with chronic diarrhea; hypophosphatemia and hypocalcemia are seen in patients with significant malabsorption. Liver function studies may be abnormal secondary to pericholangitis.



Urinalysis and urine culture:


May reveal urinary tract infection secondary to enterovesicular fistula.



Tests for malabsorption:


Because patients with active, extensive disease (especially when it involves the small intestine) may develop malabsorption and malnutrition, the following tests are clinically significant: d-xylose tolerance test (for upper jejunal involvement); Schilling test (for ileal involvement); serum albumin, carotene, calcium, and phosphorus levels; and fecal fat (steatorrhea).





Nursing diagnoses:


Deficient fluid volume


Risk for electrolyte imbalance

related to active loss occurring with diarrhea or presence of GI fistula


Desired Outcomes: Patient is normovolemic within 24 hr of admission as evidenced by balanced intake and output (I&O), urinary output 30 mL/hr or more, specific gravity 1.010-1.030, blood pressure (BP) 90/60 mm Hg or higher (or within patient’s normal range), respiratory rate (RR) 12-20 breaths/min, stable weight, good skin turgor, and moist mucous membranes. Patient reports that diarrhea is controlled. Serum electrolytes potassium, sodium, and chloride are all within optimal values as outlined in first Rationales section, below.






















ASSESSMENT/INTERVENTIONS RATIONALES
Assess I&O and urinary specific gravity, weigh patient daily, and monitor laboratory values to evaluate fluid and electrolyte status. These assessments monitor for fluid loss and electrolyte imbalance. GI fluid losses (nasogastric [NG] suction, vomiting, diarrhea, fistula) can lead to hyponatremia, hypokalemia, and hypochloremia. Optimal values are serum K+ 3.5-5.0 mEq/L, serum Na+ 137-147 mEq/L, and serum Cl− 95-108 mEq/L. Critical values: K+ less than 2.5 or more than 6.5 mEq/L, Na+ less than 120 or more than 160 mEq/L, Cl− less than 80 or more than 115 mEq/L.
Assess frequency and consistency of stools. Keep a stool count, and measure volume of liquid stools. These assessments monitor for presence and amount of blood, mucus, fat, and undigested food, which occur secondary to the underlying inflammatory process.
Assess patient for the presence of thirst, poor skin turgor, dryness of mucous membranes, fever, and concentrated (specific gravity greater than 1.030) and decreased urinary output. These are indicators of dehydration.
Maintain patient on parenteral replacement of fluids, electrolytes, and vitamins as prescribed. Patients with involvement of the small intestine often require supplementation of vitamins and minerals, especially calcium, iron, folate, and magnesium secondary to malabsorption or to compensate for foods excluded from the diet. Patients with extensive ileal disease or resection often require vitamin B12 replacement, and if bile salt deficiency exists, cholestyramine and medium-chain triglycerides may be needed to control diarrhea and reduce fat malabsorption and steatorrhea. Vitamin D deficiency is common in these patients and may require replacement with cholecalciferol.
When patient is taking food orally, provide diet as prescribed. Assess tolerance to diet by determining incidence of cramping, diarrhea, and flatulence. Modify diet plan accordingly.
Bland diets low in residue, roughage, and fat but high in protein, calories, carbohydrates, and vitamins provide good nutrition and reduce excessive stimulation of the bowel. A diet free of milk, milk products, gas-forming foods, alcohol, and iced beverages reduces cramping and diarrhea.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Crohn’s disease

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