Gastrointestinal Disorders

CHAPTER 7 Gastrointestinal Disorders

Section One Disorders of the Mouth and Esophagus

Stomatitis

Overview/Pathophysiology

Inflammatory and infectious diseases of the mouth are commonly overlooked in the debilitated hospitalized patient. Stomatitis (inflammation of the mouth and mucous membrane) is the term generally applied to a variety of mouth disorders characterized by mucosal cell destruction and disruption of the mucosal lining.

Assessment

Signs and symptoms/physical findings

Oral pain; sensitivity to hot, spicy foods; foul taste; oral bleeding or drainage; fever; xerostomia (dry mouth); burning sensation in the lips; difficulty chewing or swallowing; poorly fitting dentures.

The oral mucosa appears swollen, red, and ulcerated; the lymph glands may be swollen; and the breath is often foul smelling. The lips may have cracks, fissures, blisters, ulcers, and lesions; the tongue may appear dry and cracked and contain masses, lesions, or exudate.

History and risk factors

Typically occurs secondary to systemic disease and infection; nutritional and fluid deficiencies; poorly fitting dentures; neglect of oral hygiene; side effects of drugs; or exposure to oral irritants such as alcohol, smoking, or smokeless tobacco. Patients with leukemia or neoplastic disease of the head and neck are at increased risk for stomatitis. It is one of the major side effects of radiation therapy and cancer chemotherapy, and it occurs in more than 30% of this population. It also is commonly seen in patients older than 65 yr of age, patients in the ICU, and individuals with human immunodeficiency virus (HIV) infection.

Collaborative Management

Treatment varies, depending on the type of impairment and its cause.

Identification and attempt to control or remove causative factor(s)

If appropriate (e.g., if poor nutrition is the cause of stomatitis, the goal is to improve nutrition and follow through with other treatments that may be necessary, such as antibiotics).

Oral hygiene/mouth irrigations

Teeth should be brushed with a fluoride-containing dentifrice and a soft-bristle toothbrush. The tongue also should be lightly brushed and the mouth rinsed with sterile normal saline solution after brushing. Mouthwashes may be used to loosen debris, but use of commercial mouthwashes, especially those containing alcohol, should be avoided. The accepted mouthwash, in particular for immunosuppressed patients with stomatitis, is sodium bicarbonate with normal saline. A typical solution is made with 15 mL of sodium bicarbonate and 500 mL of normal saline. Oral hygiene should be repeated 4-5×/day or even more frequently, depending on degree of oral mucosal impairment.

Dietary management

Typically, a diet high in protein to promote wound healing, high in calories for protein sparing, and high in vitamins to correct the specific deficiency. Usually, hot and spicy foods are restricted, and consistency of the food ranges from liquid to regular, as tolerated. Fluids are encouraged. Severe cases necessitating hospitalization also may require treatment with nutritional support, that is, enteral feeding or total parenteral nutrition (TPN) if unable to insert feeding tube.

Cauterization of ulcerations

Dental restoration and repair

Adequate rest

For optimal tissue repair.

Nursing Diagnoses and Interventions

Impaired oral mucous membrane (stomatitis)

related to ineffective oral hygiene, dehydration, irritants, or pathologic condition

Desired outcomes

Patient demonstrates oral hygiene interventions and complies with the therapeutic regimen within 12-24 hr of instruction. Patient’s oral mucosal condition improves, as evidenced by intact mucous membrane, moist and intact tongue and lips, and absence of pain and lesions.

Nursing Interventions

⧫ Inspect mouth 3 ×/day for inflammation, lesions, and bleeding. Report significant findings to health care provider.

⧫ Administer analgesics; corticosteroids; anesthetics, and mouthwashes (described in the next list item) as prescribed. Avoid commercial mouthwashes. This is because they are high in alcohol. For mild stomatitis, provide mouth care after every meal and before bedtime. For moderate stomatitis, provide mouth care q4h; for severe stomatitis, provide mouth care q2h and twice at night or even hourly if indicated.

⧫ Prepare a solution containing 15 mL of sodium bicarbonate and 500 mL of normal saline. Instruct patient to rinse mouth with the solution (as often as indicated by assessments described earlier). This is to provide local relief and promote healing. Warm saline solution may be used. This provides some heat and aids in cleansing mucous membranes. Avoid solutions containing hydrogen peroxide.

⧫ Instruct patient to brush teeth after meals and at bedtime, with a soft-bristle toothbrush and nonabrasive toothpaste. Patients with severe stomatitis who have dentures should remove them until the oral mucosa has healed. Dietary alterations may be necessary (e.g., changing to a full liquid or pureed diet). This will reduce the irritation. A dietary or nutritional consultation may be helpful.

⧫ Use disposable foam swabs to stimulate gums and clean the oral cavity. Avoid use of lemon and glycerin swabs. This is because glycerin is hydrophilic and will cause excessive drying of oral membranes. If platelet levels are at least as high as 50,000/mm³, encourage gentle flossing of teeth twice daily, using unwaxed floss.

⧫ Advise patient to use lip emollients, such as lanolin or any nonpetroleum surgical lubricant. This will keep the lips lubricated and avoid drying and cracking.

⧫ Advise patient to avoid irritants, including alcohol; tobacco products; and foods that are hot, spicy, and rough in texture.

⧫ Offer ice or flavored ice pops. This is to help anesthetize the mouth.

Deficient knowledge

related to disease process, treatment, and factors that potentiate oral bleeding

Desired outcome

Within the 24-hr period before hospital discharge, patient verbalizes knowledge about the cause, preventive measures, and treatment of stomatitis and factors that potentiate oral bleeding.

Nursing Interventions

⧫ Assess patient’s facility with language; engage an interpreter or provide language-appropriate written materials if necessary.

⧫ Describe causes of patient’s stomatitis, and remind patient that the best treatment is prevention.

⧫ Explain importance of meticulous, frequent oral hygiene and periodic dental examinations.

⧫ Advise patient to avoid substances such as alcohol; tobacco; hot, spicy, and rough foods. This is because they can be irritating to the mouth lesions.

⧫ Teach importance of discontinuing flossing when platelet count drops below 50,000/mm³, or as suggested by health care provider, and discontinuing brushing when count drops below 30,000/mm³, or per health care provider’s instructions, to avoid possible bleeding. Instead, instruct patient to perform oral hygiene using mouth irrigation technique described in Impaired oral mucous membrane, immediately preceding.

Imbalanced nutrition: less than body requirements

related to inability to ingest food secondary to discomfort with chewing and swallowing

Desired outcome

At least 24 hr before hospital discharge, patient exhibits adequate progress toward optimal nutrition, as evidenced by stable weight, serum protein 6-8 g/dL, serum albumin 3.5-5.5 g/dL, and a balanced or positive N state.

Nursing Interventions

⧫ Assess patient’s ability to chew and swallow.

⧫ Monitor I&O. Unless contraindicated, ensure patient has optimal hydration (at least 2-3 L/day) and a diet that is high in protein, calories, and essential vitamins and minerals. Drinks high in calories and protein are especially helpful. Consider adding Polycose to beverages and powdered milk or protein powder to food preparations. Alert health care provider if need for IV or nasogastric (NG) tube feedings becomes apparent.

⧫ Provide any special equipment such as straws, nipples, or syringes. This is to facilitate ingestion.

⧫ Encourage intake of soft foods (e.g., cooked cereals, soups, gelatin, ice cream). This is to reduce mouth pain.

⧫ Encourage mouth care after every meal or more frequently. This is to minimize risk of infection caused by nonintact oral mucosa.

Hiatal Hernia, Gastroesophageal Reflux Disease, and Barrett’s Esophagus

Overview/Pathophysiology

Hiatal hernia is a herniation of the esophagogastric junction and a portion of the stomach into the chest through the esophageal hiatus of the diaphragm. Hernias are classified as acquired or congenital. Acquired hernias include sliding, paraesophageal, and mixed as the most common classifications. In a sliding hernia, intraabdominal pressure increases, enabling a portion of the lower esophagus and stomach to rise up into the chest. In paraesophageal hernias, the esophagogastric junction remains in place and the stomach fundus or greater curvature squeezes into the chest through the esophageal hiatus. Complications of hiatal hernia include aspiration of reflux contents; ulceration; hemorrhage; stricture; gastritis; and in severe cases, strangulation of the herniated tissue. The most common type of hiatal hernia is the sliding hernia, which accounts for most of adult hiatal hernias. The incidence of hiatal hernia increases with age.

Diagnosis of diaphragmatic hernia is often suspected on the basis of reflux symptoms. However, gastroesophageal reflux disease (GERD) is not caused by any one abnormality. The multiple factors that determine whether GERD is present include (1) efficacy of the antireflux mechanism, (2) volume of gastric contents (in the stomach), (3) potency of refluxed material, (4) efficiency of esophageal clearance, and (5) resistance of the esophageal tissue to injury and the ability for tissue repair. By definition, however, the patient must have several episodes of reflux for reflux disease to be present. Barrett’s esophagus is a condition caused by chronic gastric reflux that injures the esophageal squamous epithelium. Abnormal columnar epithelium replaces the injured squamous epithelium. Seen predominantly. The incidence of Barrett’s esophagus is increasing. It is predominantly seen in white males. Complications include esophagitis, strictures, and ulcers. Although not all patients develop esophageal adenocarcinoma, GERD and Barrett’s esophagus are the most important risk factors.

Assessment

Signs and symptoms/physical findings

Many individuals are asymptomatic unless esophageal reflux is present. Reflux often occurs 1-4 hr after eating and while sleeping or reclining, with stress, and with increased intraabdominal pressure. Heartburn (often worse with recumbency), belching, regurgitation, vomiting, retrosternal or substernal chest pain (dull, full, heavy), hiccups, mild or occult bleeding in vomitus or stools, and mild anemia also may occur. Dysphagia can occur and is associated with advanced disease and greater potential for complications. The older adult often presents with symptoms of pneumonitis caused by aspiration of reflux contents into the pulmonary system. Peptic stricture of the esophagus is a serious sequela of aggressive reflux esophagitis. Barrett’s esophagus can cause additional signs and symptoms, including chronic cough and hoarseness. Some patients have few symptoms, possibly from desensitized esophageal tissue.

Physical assessment

Auscultation of peristaltic sounds in the chest, presence of palpitations, abdominal distention. These findings are not diagnostic, nor are they usually helpful in making the diagnosis.

History and risk factors

History and causative factors for acquired hernias include degenerative changes (aging), trauma, kyphoscoliosis (a curvature of the spine), increased intraabdominal pressure, and surgery. Increased intraabdominal pressure can occur with coughing, straining, bending, vomiting, obesity, pregnancy, trauma, constricting clothing, ascites, and severe physical exertion. GERD is the result of incompetence of the lower esophageal sphincter (LES) that allows regurgitation of acidic gastric contents into the esophagus. Chronic gastric reflux is found in patients with Barrett’s esophagus. Male gender and older age are also risk factors for esophageal problems.

Diagnostic Tests

For most patients with reflux, obtaining a complete history is sufficient for starting therapy without the necessity of comprehensive diagnostic tests.

Barium swallow

The most specific diagnostic test for revealing hernias and gastroesophageal and diaphragmatic abnormalities. With fluoroscopy, a hiatal hernia appears as a barium-containing outpouching at the lower end of the esophagus. It may be necessary for the patient to be in Trendelenburg’s position for the hernia to appear on x-ray film. Although gastric barium moves into the esophagus with reflux, the degree of esophagitis is not easily demonstrated radiographically. Scintigraphic techniques using a technetium-99m–labeled solid meal have been used to quantify the degree of esophageal reflux.

Chest x-ray examination

Reveals large hernias that look like air bubbles in the chest; infiltrates will be seen in lower lobes of the lungs if aspiration has occurred.

Upper endoscopy and biopsy

Used as initial evaluation when symptoms persist, are refractory to treatment, or worsen. These methods aid in differentiating between hiatal hernia and gastroesophageal lesion, exclude the possibility of neoplasm, and assess type and severity of esophagitis. They are the primary diagnostic tools for Barrett’s esophagus. Patients diagnosed with Barrett’s esophagus should be screened with esophagogastroduodenoscopy (EGD) and biopsy from yearly to every 5 yr.

Esophageal motility studies

Identify primary and secondary motor dysfunction before surgical repair of the hernia is performed. Included are manometry, which graphically records resting pressures and peristaltic wave pressures, and pH probe, which shows a low (acidic) value in the presence of gastroesophageal reflux.

Gastric analysis

Assesses bleeding, which can occur if ulceration is present.

CBC

May reveal anemic condition if bleeding ulcers are present.

Stool occult blood test

Positive if bleeding has occurred.

ECG

Rules out cardiac origin of pain.

Collaborative Management

Conservative medical management, which is successful in most cases, is preferred over surgical intervention. The goal is to prevent or reduce gastric reflux caused by increased intraabdominal pressure and increased gastric acid production.

Dietary management

Small, frequent meals; bland foods; weight reduction for obese individuals; food restriction 2-3 hr before reclining; refraining from fatty foods, acidic foods, chocolate, and alcohol. Meals low in fat and high in protein increase LES tone and decrease reflux. Restricting intake of irritants such as caffeine, nicotine, and nonsteroidal antiinflammatory drugs (NSAIDs) is important. Restricting tight clothing around the waist may also help. The cornerstone for many patients with reflux is a change in lifestyle.

Elevation of head of bed (HOB)

Using 4- to 6-inch blocks to prevent postural reflux at night, depending on reflux severity.

Pharmacotherapy

Proton pump inhibitors (PPIs) (e.g., omeprazole, lansoprazole, pantoprazole, esomeprazole, rabeprazole)

Provide significant remission of symptoms in many patients and are prescribed most often for their healing properties.

Histamine H₂-receptor blockers (e.g., cimetidine, ranitidine, famotidine, nizatidine)

Work by suppressing acid secretion in the stomach. Over-the-counter (OTC) use should not continue for more than 1-2 wk before consultation with a medical professional.

Antacids

Do not add to the effectiveness of the H₂-receptor blockers but may be useful when side effects of the H₂-receptor blockers preclude their use. Antacids should not be taken at the same time as PPIs and H₂-receptor blockers because antacids interfere with the effectiveness of these drugs.

Prokinetic agents (e.g., metoclopramide)

Augment peristalsis of the esophagus and stomach and increase LES pressure.

Antiemetics, cough suppressants, and stool softeners

Prevent increased intraabdominal pressure from vomiting, coughing, and straining with bowel movements.

Surgery

Indicated in some patients to restore gastroesophageal integrity and prevent reflux if symptoms do not resolve and complications (obstruction, bleeding, aspiration) occur. The most common procedure is a fundoplication, in which a portion of the upper stomach is wrapped around the distal esophagus and sutured to itself to prevent reflux from recurring. Typically, an abdominal rather than a thoracic approach is used. Laparoscopic approaches may also be used.

Postsurgical management

Includes chest physiotherapy to prevent respiratory complications; IV fluids and electrolytes until bowel sounds are present; a gradual increase in diet as tolerated after the return of peristalsis; and, in some cases, gastric tubes for decompression and feeding.

Nursing Diagnoses and Interventions

Deficient knowledge

related to disease process and treatment for hiatal hernia, GERD, or Barrett’s esophagus

Desired outcome

Within the 24-hr period before hospital discharge, patient verbalizes knowledge about the cause and therapeutic regimen for hiatal hernia, reflux disease, or Barrett’s esophagus.

Nursing Interventions

⧫ Assess patient’s facility with language; engage an interpreter or provide language-appropriate written materials if necessary.

⧫ Assess patient’s knowledge about the disorder, its treatment, and methods used to prevent symptoms and their complications. Provide instructions as appropriate. The main treatment for these disorders is lifestyle change, so patient needs to understand the methods for making those changes.

⧫ Explain the following methods of dietary management: eating a low-fat, high-protein diet; eating small, frequent meals; eating slowly; chewing well to avoid reflux; avoiding extremely hot or cold foods; limiting stimulants of gastric acid, such as alcohol, caffeine, chocolate, fatty or spicy foods, peppermint, citrus fruit/juices, and nicotine; and losing weight if appropriate. These interventions will help reduce symptoms of the disease and may prevent surgery.

⧫ Advise patient to drink water after eating. This is to cleanse the esophagus of residual food, which can irritate esophageal lining.

⧫ Advise patient to avoid smoking. It may increase aerophagia, acid exposure, and belching.

⧫ Explain the following alterations in body positions and activities: avoiding supine position for 2-3 hr after eating; sleeping on right side with HOB elevated on 4- to 6-inch blocks to promote gastric emptying; for 2-3 hr after eating, avoiding bending, coughing, lifting heavy objects, straining with bowel movements, strenuous exercise, and clothing that is too tight around waist.

⧫ Stress importance of following prescribed pharmacologic regimen: PPIs, H₂-receptor blockers, antacids, sucralfate, or prokinetic agents. It is important to continue with the prescribed medications even if symptoms no longer are persistent.

⧫ Explain chronic nature of these conditions, including follow-up, support, education, and adherence to pharmacologic therapy. This is because the disease management is a life-long process.

Acute pain, nausea, or feeling of fullness

related to gastroesophageal reflux and increased intraabdominal pressure

Desired outcomes

Patient’s subjective perception of discomfort decreases within 1 hr of intervention, as documented by pain scale. Nonverbal indicators, such as grimacing, are absent or diminished.

For Patients with a Fundoplication

Ineffective breathing pattern

related to guarding secondary to pain of thoracic incision or chest tube insertion

Desired outcome

Patient’s respiratory rate (RR) is 12-20 breaths/min with normal depth and pattern (eupnea) within 1 hr after pain-relieving intervention.

Nursing Interventions

⧫ If a thoracic rather than abdominal approach was used, chest tubes may be present. Assess insertion site and suction apparatus for integrity, patency, function, and character of drainage. Tape all chest tube insertion sites.

⧫ Be alert for dyspnea, cyanosis, sharp chest pain. These are indicators of a pneumothorax. (See “Pneumothorax/Hemothorax,” p. 75, for care of the patient with a chest tube.)

⧫ Encourage and assist patient with coughing, deep breathing, incentive spirometry, and turning q2-4h, and note the quality of breath sounds, cough, and sputum.

⧫ Teach patient how to splint incision with hands, a folded blanket, or pillow. This is to facilitate coughing and deep breathing.

⧫ Medicate patient about ¹/₂ hr before major moves such as ambulation and turning. This is to enhance compliance with postoperative routine. If patient-controlled analgesia (PCA) is available, advise its use accordingly. Be aware that opioid analgesics will depress respirations.

⧫ Reassure patient that sutures and tubes will remain intact with coughing and deep breathing.

Patient-Family Teaching and Discharge Planning

When providing patient-family teaching, include verbal and written information about the following:

⧫ Importance of dietary management and activity (see Deficient knowledge, p. 446).

⧫ Medications, including drug names, dosage, schedule, purpose, precautions, and potential side effects. Also discuss drug/drug, herb/drug, and food/drug interactions.

⧫ Indicators that signal recurrence of hernia or reflux (which happens only rarely after surgery): dysphagia, hematemesis, increased pain.

⧫ Importance of follow-up care; reconfirm date and time of next medical appointment.

⧫ Care of incision, including dressing changes. Ensure that patient verbalizes indicators of infection (e.g., increasing pain, local warmth, fever, purulent drainage, swelling, foul odor).

⧫ Procedure for enteral feedings and care of tubes if appropriate. Initiate a visiting nurse referral for follow-up as needed.

⧫ Community resources for weight reduction and smoking cessation. Refer patient to a smoking cessation program as appropriate. Additional resources, including free brochures, can be found at:

Agency for Health Care Policy and Research (AHCPR): www.ahrq.gov or www.ahrq.gov/consumer. Select the links listed under “Quit Smoking.”

National Cancer Institute: www.nci.nih.gov. A link to the stop smoking website is available or can be accessed directly at www.smokefree.gov.

Section Two Disorders of the Stomach and Intestines

Overview/Pathophysiology

Peptic ulcers are erosions of the upper gastrointestinal (GI) tract mucosa that may extend through the muscularis mucosa and into the muscularis propria. They may occur anywhere the mucosa is exposed to the erosive action of gastric acid and pepsin. Commonly, ulcers are gastric or duodenal, but the esophagus, surgically created stomas, and other areas of the upper GI tract may be affected. Autodigestion of mucosal tissue and ulceration are associated with increased acidity of the stomach juices or increased sensitivity of the mucosal surfaces to erosion. Erosions can penetrate deeply into the mucosal layers and become a chronic problem, or they can be more superficial and manifest as an acute problem resulting from severe physiologic or psychologic trauma, infection, or shock (stress ulceration of the stomach or duodenum). Both duodenal and gastric ulcers can occur in association with a high-stress lifestyle, smoking, or use of irritating drugs, as well as being secondary to other diseases. Ulceration may occur as a part of Zollinger-Ellison syndrome, in which gastrinomas (gastrin-secreting tumors) of the pancreas or other organs develop. Gastric acid hypersecretion and ulceration subsequently occur. However, the most common causes of peptic ulcer disease are use of nonsteroidal antiinflammatory drugs (NSAIDs) and infection with Helicobacter pylori (H. pylori).

H. pylori, a gram-negative, spiral-shaped bacterium with four to six flagella on one pole, was first isolated from gastric biopsy material in 1983. H. pylori can reside below the mucosa of the stomach because it produces the enzyme urease, which hydrolyses urea to ammonia and carbon dioxide and provides a buffering alkaline halo. Infection can go undetected for years because there may be no symptoms until gastric or duodenal ulceration or gastritis occurs. Transmission of H. pylori has been determined to be by fecal-oral and oral-oral routes of transmission. A high duodenal acid load is one of the characteristics of duodenal ulcer disease inasmuch as it reduces concentration of bile acids that normally inhibit growth of H. pylori. Gastric ulcers tend to occur on the lesser curvature of the stomach. Ulcers in both locations are characterized by slow healing leading to metaplasia. In turn, greater colonization with H. pylori causes slow healing and results in a vicious cycle.

Serious and disabling complications, such as hemorrhage, GI obstruction, perforation, peritonitis, or intractable ulcer pain, are common. With treatment, ulcer healing usually occurs within 4-6 wk (gastric ulcers can take as long as 12-16 wk to heal), but there is potential for recurrence at the same or another site.

Assessment

Signs and symptoms/physical findings

Burning, gnawing, dull pain typically with onset 1-3 hr after eating. Discomfort occurs more often between meals and at night. With duodenal ulcer, eating usually alleviates discomfort; with gastric ulcer, pain often worsens after meals. Older persons have less sensory perception in the stomach and may not experience pain as a symptom. In addition, 40% of patients with active ulcers deny abdominal pain. However, on examination there may be findings of ulceration, gastritis, and other conditions. Even so, pain symptoms warrant further investigation.

Hematemesis, melena, dizziness, and syncope are associated with an actively bleeding ulcer. Sudden, severe epigastric pain, often radiating to the right shoulder, suggests perforation of an ulcer. Pain described as piercing through to the back suggests penetration of the ulcer into adjacent posterior structures in the abdomen.

Typically there is tenderness over the involved area of the abdomen. With perforation, there will be severe pain (see “Peritonitis,” p. 461, for more information) and rebound tenderness. With penetration, the pain is usually altered by changes in back position (extension or flexion).

History and risk factors

NSAID use; chronic or acute stress; smoking; use of irritating agents such as caffeine, alcohol, corticosteroids, salicylates, reserpine, indomethacin, or phenylbutazone; disorders of the endocrine glands, pancreas, or liver; and hypersecretory conditions, such as Zollinger-Ellison syndrome.

Diagnostic Tests

Barium swallow

Uses contrast agent (e.g., barium) to detect abnormalities. Patient should maintain nothing by mouth (NPO) status and not smoke for at least 8 hr before the test. Postprocedure care involves administration of prescribed laxatives and enemas to facilitate passage of the barium and prevent constipation and fecal impaction.

Endoscopy

Allows visualization of the stomach (gastroscopy), duodenum (duodenoscopy), both stomach and duodenum (gastroduodenoscopy), or the esophagus, stomach, and duodenum (EGD) via passage of a lighted, flexible fiberoptic tube. Patient is NPO for 8-12 hr before the procedure, and written consent is required. Before the test, a sedative is administered to relax the patient, and an opioid analgesic may be given to prevent pain. Local anesthetic may be sprayed into the posterior pharynx to ease passage of the tube. A biopsy may be performed as part of the endoscopy procedure. Biopsied tissue may be sent for histologic examination and for culture and sensitivity to identify H. pylori infection. Postprocedure care involves maintaining NPO status for hr; ensuring return of the gag reflex before allowing the patient to eat (if local anesthetic was used); administering throat lozenges or analgesics as prescribed; and monitoring for complications, such as bleeding or perforation (e.g., hematemesis, pain, dyspnea, tachycardia, hypotension).

Stool for occult blood

Positive if bleeding is present.

Other laboratory tests

CBC reveals a decrease in hemoglobin (Hgb), hematocrit (Hct), and RBCs when acute or chronic blood loss accompanies ulceration. Serum antigen identifies exposure to H. pylori infection. However, antibody test results remain positive many months after successful therapy and are not reliable for assessing therapy effectiveness. A breath test is available to identify H. pylori infection by detecting carbon dioxide and ammonia as byproducts of the action of the bacterium’s urease in the patient’s expired air. Histologic identification of the microorganism and culture are other direct tests for H. pylori. Direct testing and stool antigen assay require discontinuation of all drugs that suppress H. pylori for 2 wk before testing.

Collaborative Management

Conservative management is preferred over surgical intervention, with the therapy aimed at decreasing hyperacidity, healing the ulcer, relieving symptoms, and preventing complications.

Lifestyle alterations

Smoking cessation, decreased consumption of alcohol, avoidance of irritating drugs, and stress reduction therapies.

Activity as tolerated with adequate rest

So that tissue repair can occur. The patient who is anemic from bleeding ulcers requires activity limitations and more assistance with activities of daily living (ADL) because of fatigue.

Dietary management

Well-balanced diet with avoidance of foods that are not tolerated. Three meals per day are recommended, with elimination of bedtime snacks. Consumption of caffeine and alcohol should be reduced or eliminated. For acute episodes of upper GI hemorrhage, the patient is NPO and is given IV fluid and electrolyte replacement, with foods and fluids introduced orally after bleeding subsides.

Pharmacotherapy

Histamine H₂-receptor blockers (e.g., cimetidine, ranitidine, nizatidine, famotidine)

Administered by the oral (PO) or IV route to suppress secretion of gastric acid and facilitate ulcer healing. These drugs also can be used prophylactically for limited periods, especially in patients susceptible to stress ulceration. Because antacids can reduce their absorption, these medications should be administered with meals at least 1 hr apart from antacids.

Sucralfate

An antiulcer agent that coats the ulcer with a protective barrier so that healing can occur. However, it is now considered outmoded as primary therapy for ulcer disease.

Antacids

Administered orally or through nasogastric (NG) tube to provide symptomatic relief; not used as primary therapy.

Proton pump inhibitors (PPIs) (e.g., omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole)

Deactivate the enzyme system that pumps hydrogen ions (H⁺) from the parietal cells, thus inhibiting gastric acid secretion; used for short-term treatment of active duodenal and gastric ulcers and for long-term treatment of hypersecretory conditions.

Misoprostol

Synthetic prostaglandin E₁ analog that enhances the normal mucosal protective mechanisms of the body and decreases acid secretion. The drug is used in the healing and prevention of NSAID-induced ulcers but is not a first-line agent. Caution must be used when giving this drug to women of childbearing years who could be pregnant because the drug can cause abortion.

Eradication therapy for H. pylori:

Indicated for patients in whom H. pylori is cultured. Eradication may be obtained with any one of the following regimens: (1) a PPI, clarithromycin 500 mg twice daily, and either amoxicillin or metronidazole for 2 wk; (2) ranitidine, bismuth citrate, clarithromycin 500 mg twice daily, and amoxicillin, metronidazole, or tetracycline for 2 wk; or (3) a PPI, bismuth, metronidazole, and tetracycline for 1-2 wk. Giving PPIs with antimicrobials increases the intragastric pH needed for antimicrobials to be effective.

NSAID ulcer treatment

NSAIDs should be discontinued to enable the ulcer to heal. If patient is also infected with H. pylori, therapy for that cause is instituted. For patients with rheumatoid arthritis, prednisone may be used until the ulcer is healed.

NG tube with gastric lavage

For acute, severe GI bleeding, to clear blood from the stomach before endoscopy and to prevent accumulation of clotted blood. For this procedure, the patient should be in semi-Fowler’s position or higher. A large-bore NG tube or an Ewald tube is inserted. Gastric contents are aspirated, followed by instillation of 100-250 mL of room-temperature normal saline or tap water, as prescribed, and reaspiration. The process is repeated until returns are clear or light pink and clot free. IV vasopressin may be administered to diminish uncontrolled bleeding before surgery.

Surgical interventions

Indicated for hemorrhage, intractable ulcers, GI obstruction, and perforation. Common surgical procedures include the following, singly or in combination.

Pyloroplasty

Remodeling of the pyloric valve between the stomach and duodenum. This may involve enlargement to relieve obstruction and facilitate gastric emptying or tightening to reduce duodenal reflux into the stomach.

Subtotal gastrectomy

Removal of distal part of the stomach with anastomosis to the duodenum in a gastroduodenostomy (Billroth I for gastric ulcer and gastric outlet obstruction) or removal of part of the stomach and the duodenum with anastomosis to the jejunum in a gastrojejunostomy (Billroth II for duodenal ulcer). Vagotomy may accompany subtotal gastrectomy.

Postsurgical care

Involves temporary GI decompression with NG tube; analgesics for pain; IV fluid and electrolyte replacement; symptomatic relief of dumping syndrome (rapid gastric emptying characterized by abdominal fullness, weakness, diaphoresis, fatigue, tachycardia, palpitations, dizziness) with a low-carbohydrate, high-fat, high-protein diet, small meals without liquids, and supine position after meals; treatment of pernicious anemia (decreased production of intrinsic factor secondary to removal of that part of the stomach that contains the parietal cells) with vitamin B₁₂ injections; and treatment with iron supplements for iron-deficiency anemia (which might occur secondary to loss of blood or iron-absorbing surface in the GI tract). Prevention of hypoventilation (and subsequent atelectasis) and hypoxemia with deep-breathing exercises is especially important in patients who have had abdominal surgery (see “Atelectasis,” p. 57).

Nursing Diagnoses and Interventions

Ineffective protection

related to risk for bleeding, obstruction, and perforation secondary to ulcerative process

Desired outcome

Patient is free of signs and symptoms of bleeding, obstruction, perforation, and peritonitis, as evidenced by negative results for occult blood testing, passage of stool and flatus, soft and nondistended abdomen, good appetite, and normothermia.

Nursing Interventions

⧫ Assess for hematemesis and melena, and check any NG aspirate, emesis, and stools for occult blood. These are indicators of bleeding. Report positive findings.

⧫ Monitor results of CBC and coagulation studies. Be alert for hematocrit (Hct) less than 40% (male) or less than 37% (female) and hemoglobin (Hgb) less than 14 g/dL (male) or less than 12 g/dL (female); partial thromboplastin time (PTT) greater than 70 sec or prothrombin time (PT) greater than 12.5 sec.

⧫ If indicated, insert gastric tube. This is to evacuate blood from stomach. Monitor for bleeding, and perform gastric lavage as prescribed. Do not use gastric tubes in patients who have or are suspected of having esophageal varices. This is because the procedure may increase bleeding from the varices.

⧫ If patient is actively bleeding or if Hct is low, administer O₂. Monitor O₂ saturation (SaO₂) via oximetry. This is to evaluate systemic oxygenation status. Report SaO₂ less than 92%.

⧫ Monitor and note abdominal pain, abnormal (increased peristalsis, “rushes,” or “tinkles”) or absent bowel sounds, distention, anorexia, nausea, vomiting, and inability to pass stool or flatus. These are indicators of obstruction. (See “Intestinal Obstructive Processes,” p. 457, for more information.)

⧫ Be alert to sudden or severe abdominal pain, distention and abdominal rigidity, fever, nausea, and vomiting. These are indicators of perforation and peritonitis. Notify health care provider immediately of significant findings. (See “Peritonitis,” p. 461, for more information.)

⧫ Teach signs and symptoms of GI complications and importance of reporting them promptly to staff or health care provider if they occur.

Impaired tissue integrity

related to exposure to chemical irritants (gastric acid, pepsin)

Desired outcomes

Patient verbalizes knowledge of necessary lifestyle alterations within the 24-hr period before hospital discharge and demonstrates compliance with medical recommendations for peptic ulcer throughout the hospital stay. Gastric and duodenal mucosal tissues heal and remain intact as evidenced by reduced or absent pain and absence of bleeding.

Patient-Family Teaching and Discharge Planning

When providing patient-family teaching, include verbal and written information about the following:

⧫ Importance of following prescribed diet to facilitate ulcer healing, prevent exacerbation or recurrence, or control postsurgical dumping syndrome. If appropriate, arrange consultation with dietitian.

⧫ Medications, including drug names, rationale, dosage, schedule, precautions, and potential side effects. Also discuss drug/drug, food/drug, and herb/drug interactions.

⧫ Signs and symptoms of exacerbation and recurrence, as well as potential complications.

⧫ Care of incision line and dressing change technique, as necessary.

⧫ Signs of wound infection, including persistent redness, swelling, purulent drainage, local warmth, fever, and foul odor.

⧫ Role of lifestyle alterations in preventing exacerbation or recurrence of ulcer, including smoking cessation, stress reduction, decreasing or eliminating consumption of alcohol, and avoidance of irritating foods and drugs. Note that histamine H₂-receptor blockers are more effective in individuals who are nonsmokers.

⧫ Referral to health care specialist for assistance with stress reduction as necessary.

⧫ Referrals to local community support groups (e.g., Alcoholics Anonymous [AA]). Additional resources include:

American Gastroenterological Association: www.gastro.org

Alcoholics Anonymous: www.aa.org

Malabsorption/Maldigestion

Overview/Pathophysiology

Malabsorption or maldigestion refers to a condition in which a specific nutrient or variety of nutrients is inadequately digested or absorbed from the gastrointestinal (GI) tract. Although there is a slight distinction between the two terms, malabsorption is used more commonly. Causes of malabsorption are varied and can include the following.

Postsurgical malabsorption

Seen in individuals after subtotal gastrectomy with gastrojejunostomy and gastric bypass surgery because of rapid gastric emptying and decreased intestinal transit time. There is also delayed mixing of biliary and pancreatic secretions with food as a result of altered anatomy.

Inadequate presence of digestive substances in the GI tract

Examples are lactase enzyme deficiency, which is characterized by an inability to digest and absorb lactose, a disaccharide found in milk and dairy products; bile deficiency secondary to liver and gallbladder disease and biliary tract obstruction, which is characterized by the inability to digest and absorb fats and fat-soluble vitamins; and pancreatic secretion deficiency secondary to pancreatic insufficiency or obstruction to the flow of pancreatic secretions, as seen with pancreatic disorders or cystic fibrosis.

Inadequate absorptive space in the GI tract

This occurs secondary to GI surgery (especially ileal resection) or trauma and is characterized by general nutrient malabsorption (short bowel syndrome).

Mucosal lesions that impair absorption

Mucosal changes occur secondary to intestinal invasion of microorganisms endemic to tropical islands (tropical sprue) or ingestion of gluten in the diet (celiac disease, nontropical sprue, gluten-induced enteropathy). Grains with gluten include rye, barley, oats, and wheat. With Whipple’s disease, which is a rare disorder, small bowel lipodystrophy occurs, resulting in impaired absorption.

Inflammatory conditions of the GI tract

For example, ulcerative colitis (UC) (see p. 476) and Crohn’s disease (CD) (see p. 484) involve significant diarrhea with malabsorption and deficiencies of various nutrients. Inflammation and mucosal ulceration secondary to chemotherapy also can impair digestion and absorption.

Use of drugs that alter intestinal fluids or mucosa

Includes antacids, mineral oil, broad-spectrum antibiotics, hypocholesterolemic agents, antiinflammatory agents, oral hypoglycemics, and oral KCl, all of which can affect absorption of specific nutrients.

Overgrowth of microbes in the GI tract

Overgrowth is secondary to diverticula (outpouchings) of the small intestine, inadequate gastric acid secretion (e.g., secondary to total or partial gastrectomy or aggressive antisecretory therapy), immunologic defects, gastroenteritis, blind loop syndrome, and intestinal obstruction.

Excessive use of enemas or cathartics

Nutrients pass too rapidly through the intestinal tract to be absorbed. Complications can include specific or generalized malnutrition, fluid and electrolyte imbalances, and acid-base imbalances.

Assessment

Signs and symptoms/physical findings

Vary depending on specific nutrients that are not absorbed. Patient may have unexplained weight loss with muscle atrophy, despite normal or increased appetite; diarrhea; steatorrhea (greasy, pale, foul-smelling stools); bloating; excessive flatus; abdominal cramping; and indicators of specific nutrient deficiencies (e.g., anemia with iron or vitamin B₁₂ deficiency; tetany and paresthesias with calcium (Ca⁺⁺) deficiency; bleeding or easy bruising with vitamin K deficiency).

History and risk factors

GI surgery; excessive use of enemas or cathartics; diseases that cause diarrhea; immunologic defects; diverticulosis; liver, pancreatic, or gallbladder disease; inflammatory/infectious disorders of the intestinal tract; medications that increase GI motility and cause diarrhea; chemotherapy.

Diagnostic Tests

Quantitative stool fat test (72-hr fecal fat)

The gold standard test for fat malabsorption. A high-fat diet is ingested for 2 days and then continued for 3 more days, during which time the 72-hr collection is obtained. Normal fat excretion is less than 7 g/day. A false-negative result occurs if inadequate fat is ingested, and a false-positive result occurs if a mineral oil laxative or suppository is given before stool collection.

Qualitative stool fat test (Sudan stain)

Test requires intake of 100 g fat per day. High sensitivity and specificity is present when fat malabsorption exceeds 10 g/day.

Stool culture

Diagnoses pathogens or bacterial overgrowth.

Schilling’s test

Analysis of a 24-hr urine specimen collected after intramuscular (IM) injection of nonradioactive vitamin B₁₂ followed by ingestion of radioactive vitamin B₁₂ will reveal below-normal levels of B₁₂. Further testing, during which intrinsic factor is administered, will facilitate diagnosis of pernicious anemia from malabsorption or renal disease.

D-Xylose tolerance test

Shows inadequate presence of xylose (an easily absorbed monosaccharide) in a 5-hr collection of urine after oral administration. This test is used to distinguish small intestine mucosal malabsorption from pancreatic insufficiency.

Serum tests

Show depressed levels of carotene, Ca⁺⁺, magnesium, and other electrolytes and minerals, depending on specific malabsorption problem. In addition, serum albumin, total iron-binding capacity, and transferrin may be decreased because of protein depletion.

Hydrogen breath test

For bacterial overgrowth, which causes increased excretion of hydrogen in the breath.

Barium swallow

Facilitates diagnosis of the specific cause of malabsorption (e.g., diverticula of the small intestine). (For a description, see “Peptic Ulcers,” p. 448.) Small bowel follow-through is accomplished by serial x-ray examinations as the barium progresses through the small intestines.

CT scan of the abdomen

Facilitates diagnosis, especially for pancreatic involvement. Patients are on nothing-by-mouth (NPO) status 3-4 hr before the procedure. If contrast will be used, patients should be assessed in advance for allergy to iodine. Patients may be required to hold several deep breaths during scanning. Oral or IV fluids should be adequate to ensure elimination of the dye via the kidneys after the procedure.

Endoscopy with or without biopsy

Visualization of the small (duodenoscopy) or large (colonoscopy) bowel through a lighted, flexible tube (endoscope) that is inserted through the mouth (duodenoscopy) or anus (colonoscopy). The patient is on NPO status before the procedure. Written consent is required. Sedation is prescribed to relax the patient; atropine may be administered to decrease GI secretions; and glucagon may be administered to facilitate passage of the tube through the pylorus. Tissue samples may be taken for examination, including culture and cytologic evaluation. Hemorrhage and perforation are potential complications, and VS should be monitored closely for 4-8 hr after the procedure.

Endoscopic retrograde cholangiopancreatography (ERCP)

Involves passage of an endoscope into the duodenum to the ampulla of Vater (distal end of the pancreatic and common bile duct drainage system) for visualization. A contrast medium is injected through the scope into the pancreatic ducts or biliary ducts (common bile duct, cystic duct, hepatic ducts), and x-ray images are taken. This test is diagnostic for pancreatic disease and common bile duct pathology (stricture, obstruction, choledocholithiasis). Patient is on NPO status for 8-12 hr before the test and must be assessed for allergies to iodine (and/or to shellfish) before undergoing the test. Written consent is required. Oral or IV fluid should be adequate to ensure elimination of dye via the kidneys after the procedure. A rare but potentially fatal complication of ERCP is acute pancreatitis; monitor for increasing abdominal pain, tachycardia, hypotension, abdominal distention, nausea, and vomiting.

Secretin stimulation test

Gold standard test for pancreatic insufficiency. A collecting tube is passed into the duodenum of the patient who is on NPO status. IV secretin and/or cholecystokinin are given, and the duodenal secretions are collected and analyzed for bicarbonate and trypsin levels, which are decreased with pancreatic insufficiency. Written consent is required.

Collaborative Management

Management varies, depending on specific cause of malabsorption and nutrient deficiencies that are exhibited.

Activity as tolerated

Patient may be fatigued and require limited activity as a consequence of diarrhea, malnutrition, and associated anemia.

Dietary management

A low-residue diet may be useful for controlling diarrhea. For lactase deficiency, a low-lactose diet (avoidance of milk and milk products) is prescribed, and for nontropical sprue, a gluten-free diet is prescribed (BOX 7-1). Until specific problems (e.g., liver or gallbladder disorders) are corrected, dietary intake of fats is avoided. Any specific nutrient deficiencies are corrected. For the seriously malnourished patient, parenteral nutrition may be necessary.

BOX 7-1 GUIDELINES FOR LOW-RESIDUE, HIGH-RESIDUE, AND GLUTEN-FREE DIETS

Low-Residue Diet

Encouraged: Enriched/refined breads and cereals; rice and pasta dishes

To be avoided: Fruits, vegetables, whole-wheat products (cereals and breads)

High-Residue Diet

Encouraged: Fruits, vegetables, large amounts of fluid, whole-grain breads and cereals

To be avoided: Highly refined cereals and pasta (e.g., white rice, white bread, white spaghetti or noodles, ice cream)

Gluten-Free Diet

Encouraged (if allowed): Rice, corn, eggs, potatoes; breads made from rice flour, cornmeal, soybean flour, gluten-free wheat starch, and potato starch; cereals made from corn or rice (grits, cornmeal mush, cooked cream of rice, puffed rice, rice flakes); pasta made from rice or corn flour; homemade ice cream; tapioca pudding

To be avoided if they contain wheat, barley, rye, or oats: Cereals and bakery goods, coffee substitutes, sauces, commercially prepared luncheon meats, gravies, noodles, macaroni, spaghetti, flour tortillas, crackers, cakes, cookies, pastries, puddings, commercial ice cream, alcoholic beverages

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Sep 1, 2016 | Posted by admin in NURSING | Comments Off

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