MedSurg Digestive System Disorders - PDF

complications to report and assists the patient and family in establishing as normal a common symptom of esophageal disease, may vary from an uncomfortable feeling that a routine as possible. bolus of food is caught in the...

complications to report and assists the patient and family in establishing as normal a common symptom of esophageal disease, may vary from an uncomfortable feeling that a routine as possible. bolus of food is caught in the upper esophagus to acute odynophagia (pain on swallowing). Obstruction of food (solid and soft) and even liquids may occur anywhere Evaluation along the esophagus. Often, the patient can indicate that the problem is located in the Expected patient outcomes may include: upper, middle, or lower third of the esophagus. 1. Achieves nutrition goals a. Attains weight goal b. Tolerates tube feeding prescription without nausea, emesis, cramping, Achalasia abdominal pain, or feelings of early satiety Achalasia is absent or ineffective peristalsis of the distal esophagus accompanied by c. Has acceptable bowel movements without constipation or large-volume liquid stools failure of the esophageal sphincter to relax in response to swallowing. Narrowing of the esophagus just above the stomach results in a gradually increasing dilation of the d. Has normal plasma protein, glucose, vitamin, and mineral levels esophagus in the upper chest. Achalasia is rare, may progress slowly, and occurs most e. Has normal electrolyte values often in people between ages 20 and 40 and ages 60 and 70 years (Swanström, 2019). 2. Is free of infection at enteral access site a. Is afebrile Clinical Manifestations b. Has no induration, redness, pain, or purulent drainage c. Has no scattered papules indicative of a yeast infection The main symptom is dysphagia, with the hallmark being difficulty with solid food. The 3. Has dry, intact skin surrounding enteral access site patient has a sensation of food sticking in the lower portion of the esophagus. As the a. No evidence of excessive drainage or bleeding condition progresses, food is commonly regurgitated either spontaneously or intentionally by the patient to relieve the discomfort produced by prolonged distention of the b. No skin breakdown or hypertrophic tissue growth esophagus by food that will not pass into the stomach. The patient may also report 4. Adjusts to change in body image noncardiac chest or epigastric pain and pyrosis (heartburn) that may or may not be a. Is able to discuss expected changes associated with eating. These symptoms mirror those of GERD, and patients are often b. Verbalizes concerns misdiagnosed and treated for GERD (Swanström, 2019). 5. Demonstrates skill in tube care a. Handles equipment competently Assessment and Diagnostic Findings b. Successfully maintains tube patency c. Keeps an accurate record of intake and output X-ray studies show esophageal dilation above the narrowing at the lower gastroesophageal sphincter, which is called a birds beak deformity. Barium swallow, CT d. Demonstrates how to gently wash tube site daily and keep clean and dry scan of the chest, and endoscopy may be used for diagnosis; however, high-resolution 6. Avoids other complications manometry, a process in which peristalsis, contraction amplitudes, and esophageal a. Exhibits adequate wound healing pressure is measured by a radiologist or gastroenterologist, confirms the diagnosis b. Tube remains intact and is routinely replaced for the duration of therapy (Swanström, 2019). DISORDERS OF THE ESOPHAGUS Management The patient is instructed to eat slowly and to drink fluids with meals. Injection of The esophagus is a mucus-lined, muscular tube that carries food from the mouth to the botulinum toxin into quadrants of the esophagus via endoscopy has been helpful because stomach. It begins at the base of the pharynx and ends about 4 cm below the diaphragm. it inhibits the contraction of smooth muscle. However, because the benefits of these Its ability to transport food and fluid is facilitated by two sphincters. The upper injections fade over time and there is a risk of submucosal fibrosis, botulinum toxin is esophageal sphincter, also called the hypopharyngeal sphincter, is located at the junction only used in patients who cannot receive other definitive treatments (Swanström, 2019). of the pharynx and the esophagus. The lower esophageal sphincter, also called the Achalasia may be treated conservatively by pneumatic dilation to stretch the narrowed gastroesophageal sphincter or cardiac sphincter, is located at the junction of the area of the esophagus (see Fig. 39-9). Pneumatic dilation has a high success rate; esophagus and the stomach. An incompetent lower esophageal sphincter allows reflux however, typically two dilations are required and the long-term results are variable (backward flow) of gastric contents. Because there is no serosal layer of the esophagus, if (Swanström, 2019). Although perforation is a potential complication, its incidence is low surgery is necessary, it is more difficult to perform suturing or anastomosis. (see later discussion). The procedure can be painful; therefore, moderate sedation in the Disorders of the esophagus include motility disorders (achalasia, spasms), hiatal form of an analgesic or tranquilizer, or both, is given for the treatment. hernias, diverticula, perforation, foreign bodies, chemical burns, gastroesophageal reflux disease, Barrett esophagus (BE), benign tumors, and carcinoma. Dysphagia, the most 3403 3404 Achalasia may be treated surgically by esophagomyotomy, called a Heller myotomy, which involves cutting the esophageal muscle fibers. A complete lower esophageal sphincter myotomy is usually performed laparoscopically, with or without a fundoplication (antireflux procedure that minimizes the incidence of GERD). A newer technique, an endoscopic myotomy (per-oral endoscopic myotomy [POEM]) provides an alternative procedure that has been adopted by many high-volume achalasia centers (Swanström, 2019). Esophageal Spasm The three types of esophageal spasm include jackhammer esophagus, diffuse esophageal spasm (DES), and type III (spastic) achalasia. In jackhammer esophagus, referred to as Figure 39-10 A. Sliding esophageal hernia. The upper stomach and hypercontractile esophagus, spasms occur on more than 20% of swallows at a very high gastroesophageal junction have moved upward and slide in and out of the amplitude, duration, and length. In DES, the spasms are normal in amplitude but are thorax. B. Paraesophageal hernia. All or part of the stomach pushes through premature/uncoordinated, move quickly, and occur at various places in the esophagus at the diaphragm next to the gastroesophageal junction. once. Type III achalasia is characterized by lower esophageal sphincter obstruction with esophageal spasms (Clermont & Ahuja, 2018). Clinical Manifestations All three forms of esophageal spasm are characterized by dysphagia, pyrosis, regurgitation, and chest pain similar to that of coronary artery spasm. Assessment and Diagnostic Findings Esophageal manometry, which measures the motility and internal pressure of the esophagus, remains the standard test for irregular and high-amplitude spasms. Management In all three spastic disorders, smooth muscle relaxants such as calcium channel blockers and nitrates may be used to reduce the pressure and amplitude of contractions. Like the treatment for achalasia, botulinum toxin may be used in specific frail patients who cannot tolerate other interventions. Proton pump inhibitors (PPIs) may also be indicated, especially if symptoms of GERD are present (Clermont & Ahuja, 2018). Small, frequent feedings and a soft diet are usually recommended to decrease the esophageal pressure and irritation that lead to spasm. If conservative therapies do not provide relief, Heller myotomy or POEM may be tried (Clermont & Ahuja, 2018). Since many patients also Figure 39-9 Treatment of achalasia by pneumatic dilation. A–C. The dilator experience GERD, surgical procedures that also address GERD may be beneficial (see is passed, guided by a previously inserted guide wire. D. When the balloon is in later discussion). proper position, it is distended by pressure sufficient to dilate the narrowed area of the esophagus. Hiatal Hernia In the condition known as hiatal hernia, the opening in the diaphragm through which the esophagus passes becomes enlarged, and part of the upper stomach moves up into the lower portion of the thorax. Hiatal hernia occurs more often in women than in men. There are two main types of hiatal hernias: sliding and paraesophageal. Sliding, or type I, hiatal hernia occurs when the upper stomach and the gastroesophageal junction are displaced upward and slide in and out of the thorax (see Fig. 39-10A). Between 90% and 95% of 3405 3406 patients with esophageal hiatal hernia have a sliding hernia. A paraesophageal hernia Diverticulum occurs when all or part of the stomach pushes through the diaphragm beside the esophagus (see Fig. 39-10B). Paraesophageal hernias are further classified as types II, III, An esophageal diverticulum is an out-pouching of mucosa and submucosa that protrudes or IV, depending on the extent of herniation. Type IV has the greatest herniation, with through a weak portion of the musculature of the esophagus. Diverticula may occur in other intra-abdominal viscera such as the colon, omentum, or small bowel present in the one of the three areas of the esophagus—pharyngoesophageal (upper), midesophageal hernia sac that is displaced through the hiatus along with the stomach (Huerta, Plymale, (middle), or epiphrenic (lower). Barrett, et al., 2019). The most common type of diverticulum is Zenker diverticulum (ZD). Located in the pharyngoesophageal area, ZD is caused by a dysfunctional sphincter that fails to open, which leads to increased pressure that forces the mucosa and submucosa to herniate Clinical Manifestations through the esophageal musculature (called a pulsion diverticulum) (Smith, 2015) (see The patient with a sliding hernia may have pyrosis, regurgitation, and dysphagia, but Fig. 39-11). It is usually seen in people older than 60 years of age. many patients are asymptomatic. The patient may present with vague symptoms of Midesophageal diverticula are uncommon. Symptoms are less acute, and usually the intermittent epigastric pain or fullness after eating. Large hiatal hernias may lead to condition does not require surgery. Epiphrenic diverticula are usually larger diverticula in intolerance to food, nausea, and vomiting. Sliding hiatal hernias are commonly associated the lower esophagus just above the diaphragm. They may be related to the improper with GERD. Hemorrhage, obstruction, volvulus (bowel obstruction caused by a twist in functioning of the lower esophageal sphincter or to motor disorders of the esophagus. the intestines and supporting mesentery), and strangulation can occur with any type of Intramural diverticulosis is the occurrence of numerous small diverticula associated with hernia but are more common with paraesophageal hernia (Huerta et al., 2019). a stricture in the upper esophagus. Assessment and Diagnostic Findings Diagnosis is typically confirmed by x-ray studies; barium swallow; esophagogastroduodenoscopy (EGD), which is the passage of a fiberoptic tube through the mouth and throat into the digestive tract for visualization of the esophagus, stomach, and small intestine; esophageal manometry; or chest CT scan (Kohn, Price, Demeester, et al., 2013). Management Management for a hiatal hernia includes frequent, small feedings that can pass easily through the esophagus. The patient is advised not to recline for 1 hour after eating, to prevent reflux or movement of the hernia, and to elevate the head of the bed on 4- to 8- inch (10- to 20-cm) blocks to prevent the hernia from sliding upward. Surgical hernia repair is indicated in patients who are symptomatic, although the primary reason for the surgery is typically to relieve GERD symptoms and not repair the hernia. Current guidelines recommend a laparoscopic approach (Toupet or Nissen fundoplication procedures) (Huerta et al., 2019), with an open transabdominal or transthoracic approach reserved for patients with complications such as bleeding, dense adhesions, or injury to Figure 39-11 Zenker diverticulum. the spleen. Up to 50% of patients may experience early postoperative dysphagia; therefore, the nurse advances the diet slowly from liquids to solids, while managing nausea and Clinical Manifestations vomiting, tracking nutritional intake, and monitoring weight. The nurse also monitors for Symptoms experienced by the patient with a pharyngoesophageal pulsion diverticulum postoperative belching, vomiting, gagging, abdominal distention, and epigastric chest include dysphagia, fullness in the neck, belching, regurgitation of undigested food, and pain, which may indicate the need for surgical revision; these should be reported gurgling noises after eating. The diverticulum, or pouch, becomes filled with food or immediately to the primary provider. Surgical repair is often reserved for patients with liquid. When the patient assumes a recumbent position, undigested food is regurgitated, more extreme cases that involve gastric outlet obstruction or suspected gastric and coughing may be caused by irritation of the trachea or aspiration. Halitosis (foul odor strangulation, which may result in ischemia, necrosis, or perforation of the stomach from the oral cavity) and a sour taste in the mouth are also common because of the (Kohn et al., 2013). decomposition of food retained in the diverticulum. Although less acute, dysphagia is the primary symptom in the other types of diverticula (Smith, 2015). 3407 3408 Assessment and Diagnostic Findings Management A barium swallow may determine the exact nature and location of a diverticulum. Esophageal perforation requires immediate treatment. Treatment includes having the Manometric studies may be performed for patients with epiphrenic diverticula to rule out patient remain NPO (nil per os; nothing by mouth), beginning IV fluid therapy, a motor disorder. Esophagoscopy usually is contraindicated because of the danger of administering broad-spectrum antibiotics (ampicillin-sulbactam, piperacillin-tazobactam, perforation of the diverticulum, with resulting mediastinitis (inflammation of the organs or a carbapenem [e.g., imipenem]), considering the need for antifungal therapy (if the and tissues that separate the lungs). Blind insertion of an NG tube should be avoided. patient is immunosuppressed, has HIV infection, or shows no improvement with antibiotics), supportive monitoring and care (intensive care unit level-of-care often Management required), and evaluating and preparing the patient for surgery (Raymond, 2020). Surgical repair of the perforation site is performed in most cases, even if the diagnosis is made ZD can be treated by endoscopy (rigid or flexible) or open surgery. Endoscopic after 24 hours. If surgical repair of the perforation is not possible due to the clinical status septotomy effectively treats ZD, with a recurrence rate of 11% to 30% of cases; POEM of the patient, then drainage, diversion, stent placement, or an esophagostomy (removal may be a better option as it is associated with a decreased risk of symptom recurrence of the esophagus) may be performed (Raymond, 2020). (Gutierrez, Ichkhanian, Spadaccini, et al., 2019). If surgery is required, care is taken to Postoperative nutritional status is a major concern. The patient remains NPO for avoid trauma to the common carotid artery and internal jugular veins. In addition to a approximately 7 days, so enteral (e.g., jejunal feeding) or parenteral nutrition is started on diverticulectomy, a myotomy of the cricopharyngeal muscle is often performed to relieve postoperative day 2 or 3 (see Chapter 41 for further discussion of parenteral nutrition). spasticity of the musculature, which seems to contribute to a continuation of symptoms. The nurse uses water to moisten the patient’s mouth for comfort measures only. A repeat An NG tube may be inserted at the time of surgery. Postoperatively, the nurse observes esophagram is obtained on postoperative day 7 to verify there is no leak or ileus before the incision for evidence of leakage from the esophagus and a developing fistula. Food the NG tube is removed and oral intake is permitted. It is common for broad-spectrum and fluids are withheld until x-ray studies show no leakage at the surgical site. The diet antibiotics to continue for 7 to 10 days postoperatively (Raymond, 2020). begins with liquids and is progressed as tolerated. Surgery is indicated for epiphrenic and midesophageal diverticula only if the symptoms are troublesome and becoming worse. Treatment consists of a Foreign Bodies diverticulectomy and long myotomy. Intramural diverticula usually regress after the esophageal stricture is dilated. Many swallowed foreign bodies pass through the GI tract without the need for medical intervention. However, some swallowed foreign bodies (e.g., dentures, fish bones, pins, small batteries, items containing mercury or lead) may injure the esophagus or obstruct its Perforation lumen and must be removed. Pain and dysphagia may be present, and dyspnea may occur as a result of pressure on the trachea. The foreign body may be identified by x-ray. Esophageal perforation is a surgical emergency. It may result from iatrogenic causes, such Perforation may have occurred (see earlier discussion). as endoscopy or intraoperative injury, or from spontaneous perforation associated with forceful vomiting or severe straining (Boerhaave syndrome), foreign-body ingestion, trauma, and malignancy. Immediate diagnosis and treatment are essential to minimize Quality and Safety Nursing Alert mortality. A delay of more than 24 hours is associated with higher mortality (20%) when The nurse performs an initial and ongoing respiratory (airway-focused) compared to rapid recognition and treatment (7.4%). Perforation can occur at the cervical, assessment of a patient with a foreign body in the esophagus. Intubation may thoracic, or abdominal portion of the esophagus (Olivero, 2019; Raymond, 2020). be required to protect the airway. Clinical Manifestations Glucagon, because of its relaxing effect on the esophageal muscle, may be injected IV The patient has excruciating retrosternal pain followed by dysphagia. Infection, fever, (a 1-mg dose). A flexible endoscope and retrieval devices (e.g., forceps, graspers) may be leukocytosis, and severe hypotension may be noted. In addition, mediastinal sepsis can used to remove the impacted food or object from the esophagus. Foreign bodies such as occur with Boerhaave syndrome, which may be accompanied by pneumothorax and short-blunt objects, long objects, sharp-pointed objects, disc batteries, magnets, coins, or subcutaneous emphysema (see Chapter 19 for discussion of pneumothorax and narcotic packets require special consideration (American Society for Gastrointestinal subcutaneous emphysema). Endoscopy Standards of Practice Committee, 2011; Fung, Sweetser, Wong Kee Song, et al., 2019). Various devices can be used for endoscopic extraction (overtubes, forceps, snares, baskets, etc.) and dilation techniques can be used to facilitate the passage of Assessment and Diagnostic Findings foreign objects to the stomach. Decisions regarding the best course of action consider the X-ray studies, fluoroscopy by either a barium swallow or esophagram (a noninvasive likelihood of the object passing on its own (blunt, nontoxic objects), the patient’s test), or a chest CT scan may be used to identify the site and scope of the injury. condition (airway maintenance), the length of time the obstruction has been present (typical intervention occurs within 24 hours), and the type of foreign object that is 3409 3410 impacted. For example, ingested drug packets are not removed by endoscopy for fear of 2019), BE (see later discussion), peptic ulcer disease, and angina. GERD is associated packet rupture; no intervention or surgical intervention are recommended in these cases. with tobacco use, coffee drinking, alcohol consumption, and gastric infection with The endoscopic procedure usually is performed in the endoscopy suite or clinic by the Helicobacter pylori. gastroenterologist under moderate sedation (Fung et al., 2019). Clinical Manifestations Chemical Burns Pyrosis (heartburn, specifically more commonly described as a burning sensation in the esophagus that is noncardiac in nature) and regurgitation are the hallmark symptoms, but Chemical burns of the esophagus occur most often when a patient, either intentionally patients may also experience dyspepsia (indigestion), dysphagia or odynophagia, (67%; typically adults) or unintentionally (33%; typically children), swallows a strong hypersalivation, and esophagitis. GERD can result in dental erosion, ulcerations in the acid or base, with alkaline agents being the most common (Byard, 2015). The patient is pharynx and esophagus, laryngeal damage, esophageal strictures, adenocarcinoma, and often emotionally distraught as well as in acute physical pain. Chemical burns of the pulmonary complications (Kroch & Madanick, 2017; Patti, 2016). esophagus may also be caused by undissolved medications in the esophagus, or they may occur after swallowing of a battery, which may release a caustic alkaline. The National Capital Poison Center (2018) provides an algorithm for button battery ingestion and Assessment and Diagnostic Findings triage (see Resources section). An acute chemical burn of the esophagus may be The patient’s history aids in obtaining an accurate diagnosis. Diagnostic testing may accompanied by severe burns of the lips, mouth, and pharynx, with pain on swallowing. include ambulatory pH monitoring, which is the gold standard for the diagnosis of Breathing difficulties due to either edema of the throat or a collection of mucus in the GERD, or a PPI trial. Ambulatory pH monitoring involves transnasal catheter placement pharynx may occur. The patient needs to be closely monitored for tracheoesophageal or endoscopic wireless capsule placement for approximately 24 hours. Endoscopy or fistula, perforation of large vessels, mediastinitis, vocal cord paralysis, tracheal stenosis barium swallow is used to evaluate damage to the esophageal mucosa and rule out or tracheomalacia, aspiration pneumonia, empyema, lung abscess, pneumothorax, strictures and hernias (Patti, 2016). spondylodiscitis, and strictures (National Capital Poison Center, 2018). The patient, who may be profoundly toxic, febrile, and in shock, is treated immediately for shock, pain, and respiratory distress. Esophagoscopy and barium Management swallow are performed as soon as possible to determine the extent and severity of Management begins with educating the patient to avoid situations that decrease lower damage. Vomiting and gastric lavage are avoided to prevent further exposure of the esophageal sphincter pressure or cause esophageal irritation. Lifestyle modifications esophagus to the caustic agent. Emergent esophagectomy (a total resection of the include tobacco cessation, limiting alcohol, weight loss, elevating the head of the bed, esophagus) or gastrectomy may be required (Byard, 2015). The patient remains NPO and avoiding eating before bed, and altering the diet (Kroch & Madanick, 2017). See Table IV fluids are given. The use of corticosteroids to reduce inflammation and minimize 39-4 for a list of medications commonly used to manage GERD. subsequent scarring and stricture formation is of questionable value. Antibiotics are If medical management is unsuccessful, surgical intervention may be necessary. prescribed if there is documented infection. Surgical management involves an open or laparoscopic Nissen fundoplication, which After the acute phase has subsided, the patient may need nutritional support via enteral involves wrapping of a portion of the gastric fundus around the sphincter area of the or parenteral feedings. The patient may require further treatment to prevent or manage esophagus (Huerta et al., 2019; Patti, 2016). strictures of the esophagus. Dilation may be sufficient, but may need to be repeated periodically (see previous discussion). For strictures that do not respond to dilation, surgical management may be necessary. Reconstruction may be accomplished by Barrett Esophagus esophagectomy and colon interposition to replace the portion of esophagus removed. This surgery is quite complex and should be considered only when other options have failed. BE is a condition in which the lining of the esophageal mucosa is altered. It occurs predominantly in White men aged 50 or older, and occurs in association with family history of BE or esophageal adenocarcinoma (EAC), GERD, smoking, and obesity. The Gastroesophageal Reflux Disease rate of BE was found to increase by 1.2% for each additional risk factor, indicating the additive effect of risk factors (Qumseya, Bukannan, Gendy, et al., 2019). BE is the only Gastroesophageal reflux disease (GERD) is a fairly common disorder marked by known precursor to EAC, one of the fastest rising cancers in Western populations backflow of gastric or duodenal contents into the esophagus that causes troublesome (Qumseya et al., 2019). The 5-year survival rate for EAC does not exceed 20% (Iyer & symptoms and/or mucosal injury to the esophagus. Excessive reflux may occur because Kaul, 2019; Qumseya et al., 2019). of an incompetent lower esophageal sphincter, pyloric stenosis, hiatal hernia, or a motility disorder. The incidence of GERD seems to increase with aging and is seen in patients with irritable bowel syndrome and obstructive airway disorder exacerbations (e.g., Clinical Manifestations asthma, COPD, cystic fibrosis) (Broers & Tack, 2017; Gabel, Galante, & Freedman, 3411 3412 The patient complains of symptoms of GERD, notably frequent heartburn. The patient describes disorders of the stomach and small intestine, their etiology, may also complain of symptoms related to peptic ulcers or esophageal stricture, or both. pathophysiology, clinical manifestations, management, and related nursing care. Assessment and Diagnostic Findings An EGD provides screening in patients with multiple risk factors. This usually reveals an Gastritis esophageal lining that is pink rather than pale white. Biopsies are performed, and BE is Gastritis (inflammation of the gastric or stomach mucosa) is a common GI problem, diagnosed when the squamous mucosa of the esophagus is replaced by columnar accounting for approximately two million visits to outpatient clinics annually in the epithelium (columnar metaplasia) at least 1 cm above the gastric folds, and that area United States, with increasing prevalence occurring in adults older than 60 years of resembles that of the stomach or intestines (intestinal metaplasia) as evidenced by the age (Wehbi, Dacha, Sarver, et al., 2019). It affects women and men about equally. presence of goblet cells (Iyer & Kaul, 2019). Gastritis may be acute, lasting several hours to a few days, or chronic, resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis. Management Acute gastritis may be classified as erosive or nonerosive, based on pathologic manifestations present in the gastric mucosa (Wehbi et al., 2019). The erosive form of Monitoring varies depending on the extent of cell changes. When BE is caught and acute gastritis is most often caused by local irritants such as aspirin and other treated early, endoscopic ablation techniques have been shown to eliminate BE in up to nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., ibuprofen); corticosteroids; 80% of patients, thereby preventing progression to dysplasia, the bizarre cell growth alcohol consumption; and gastric radiation therapy (National Institute of Diabetes and resulting in cells that differ in size, shape, or arrangement from other cells of the same tissue type. Such dysplasia is indicative of early EAC. Follow-up biopsies are Digestive and Kidney Diseases [NIDDK], 2020a; Norris, 2019; Wehbi et al., 2019). recommended no sooner than 3 to 5 years after a biopsy shows no evidence of dysplasia The nonerosive form of acute gastritis is most often caused by an infection with a (Iyer & Kaul, 2019; Sharma, Katzka, Gupta, et al., 2015). Treatment is individualized for spiral-shaped gram-negative bacterium, Helicobacter pylori (H. pylori) (Wehbi et al., each patient. Recommendations include surveillance with biopsies, the use of PPIs (see 2019). It is estimated that 50% of individuals globally are infected with H. pylori Table 39-4) to control reflux symptoms, followed by endoscopic resection and/or (Santacroce & Bhutani, 2019). radiofrequency ablation (high-frequency heat/cold energy that kills surrounding cells and A more severe form of acute gastritis is caused by the ingestion of strong acid or tissues) for progression of dysplasia (Iyer & Kaul, 2019; Sharma et al., 2015). alkali, which may cause the mucosa to become gangrenous or to perforate (see Chapter 67). Scarring can occur, resulting in pyloric stenosis (narrowing or tightening) or obstruction. Acute gastritis also may develop in acute illnesses, Benign Tumors of the Esophagus especially when the patient has had major traumatic injuries, burns, severe infection, lack of perfusion to the stomach lining, or major surgery. This type of acute gastritis is Benign tumors are rare, but can arise anywhere along the esophagus. The most common often referred to as stress-related gastritis or ulcer (Clarke, Ferraro, Gbadehan, et al., lesion is a leiomyoma (tumor of the smooth muscle), which can occlude the lumen of the 2020; Norris, 2019). esophagus and cause dysphagia, pain, and pyrosis. Half of patients with benign tumors Chronic gastritis is often classified according to the underlying causative are asymptomatic and the other half present with multiple symptoms that have been mechanism, which most often includes an infection with H. pylori. Chronic H. pylori present for a long period of time. The diagnosis may be made incidentally and is gastritis is implicated in the development of peptic ulcers, gastric adenocarcinoma confirmed by endoscopy and needle biopsy. Due to the slow growth of most of these (cancer), and gastric mucosa–associated lymphoid tissue lymphoma (Akiva & tumors, monitoring and minimally invasive techniques (endoscopic, thoracic, or Greenwald, 2019; Lloyd & Leiman, 2019). Chronic gastritis may also be caused by a laparoscopic resections) tend to be indicated rather than surgical resection (Ha, Regan, chemical gastric injury (gastropathy) as the result of long-term drug therapy (e.g., Cetindag, et al., 2015). aspirin and other NSAIDs) or reflux of duodenal contents into the stomach, which most often occurs after gastric surgery (e.g., gastrojejunostomy, gastroduodenostomy). Autoimmune disorders such as Hashimoto thyroiditis, Addison disease, and Graves disease are also associated with the development of chronic gastritis (see Chapter 45) (Akiva & Greenwald, 2019; Norris, 2019). Pathophysiology Gastritis is characterized by a disruption of the mucosal barrier that normally protects the stomach tissue from digestive juices (e.g., hydrochloric acid [HCl] and pepsin). The impaired mucosal barrier allows corrosive HCl, pepsin, and other irritating agents 3413 3434 (e.g., alcohol, NSAIDs, H. pylori) to come in contact with the gastric mucosa, & Piper, 2018). Some patients with chronic gastritis have no symptoms (Marcus & resulting in inflammation. In acute gastritis, this inflammation is usually transient and Greenwald, 2019) (Table 40-1). self-limiting in nature. Inflammation causes the gastric mucosa to become edematous and hyperemic (congested with fluid and blood) and to undergo superficial erosion Assessment and Diagnostic Findings (Fig. 40-1). Superficial ulceration may occur as a result of erosive disease and may lead to hemorrhage. In chronic gastritis, persistent or repeated insults lead to chronic The definitive diagnosis of gastritis is determined by an endoscopy and histologic inflammatory changes, and eventually atrophy (or thinning) of the gastric tissue examination of a tissue specimen obtained by biopsy (Akiva & Greenwald, 2019; (Norris, 2019). Wehbi et al., 2019). A complete blood count (CBC) may be drawn to assess for anemia as a result of hemorrhage or pernicious anemia. Diagnostic measures for detecting H. pylori infection may be used and are discussed later in this chapter in the Peptic Ulcer Disease section. TABLE 40-1 Clinical Manifestations of Acute and Chronic Gastritis Acute Gastritis Chronic Gastritis Gastrointestinal Anorexia Belching Manifestations Epigastric pain Early satiety (rapid onset) Intolerance of spicy or fatty Hematemesis foods Hiccups Nausea and vomiting Melena or Pyrosis hematochezia Sour taste in mouth Nausea and Vague epigastric discomfort Figure 40-1 Endoscopic view of erosive gastritis (left). Damage from vomiting relieved by eating irritants (right) results in increased intracellular pH, impaired enzyme function, disrupted cellular structures, ischemia, vascular stasis, and tissue Systemic death. Image at left reproduced with permission from Strayer, D. S., Saffitz, Possible signs of Anemia Manifestations shock J. E., & Rubin, E. (2015). Rubin’s pathology: Mechanisms of human Fatigue disease (8th ed., Fig. 19-15). Philadelphia, PA: Lippincott Williams & Wilkins. Adapted from Marcus, A. J., & Greenwald, D. (2019). Chronic gastritis. Medscape. Retrieved on 2/25/2020 at: www.emedicine.medscape.com/article/176156; Wehbi, M., Dacha, S., Sarver, G., et al. (2019). Acute gastritis. Medscape. Retrieved on 2/25/2020 at: Clinical Manifestations www.emedicine.medscape.com/article/175909 The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia (indigestion; upper abdominal discomfort Medical Management associated with eating), anorexia, hiccups, or nausea and vomiting, which can last The gastric mucosa is capable of repairing itself after an episode of acute gastritis. As from a few hours to a few days. Erosive gastritis may cause bleeding, which may a rule, the patient recovers in about 1 day, although the patient’s appetite may be manifest as blood in vomit or as melena (black, tarry stools; indicative of occult diminished for an additional 2 or 3 days. Acute gastritis is also managed by blood in stools) or hematochezia (bright red, bloody stools) (Wehbi et al., 2019). instructing the patient to refrain from alcohol and food until symptoms subside. When The patient with chronic gastritis may complain of fatigue, pyrosis (a burning the patient can take nourishment by mouth, a nonirritating diet is recommended. If the sensation in the stomach and esophagus that moves up to the mouth; heartburn) after symptoms persist, intravenous (IV) fluids may need to be given. If bleeding is eating, belching, a sour taste in the mouth, halitosis, early satiety, anorexia, or nausea present, management is similar to the procedures used to control upper GI tract and vomiting. Some patients may have only mild epigastric discomfort or report hemorrhage discussed later in this chapter. intolerance to spicy or fatty foods or slight pain that is relieved by eating (Akiva & Therapy is supportive and may include nasogastric (NG) intubation, antacids, Greenwald, 2019). Patients with chronic gastritis may not be able to absorb vitamin histamine-2 receptor antagonists (H2 blockers) (e.g., famotidine, cimetidine), proton B12 because of diminished production of intrinsic factor by the stomach’s parietal pump inhibitors (e.g., omeprazole, lansoprazole), and IV fluids (Wehbi et al., 2019). cells due to atrophy, which may lead to pernicious anemia (see Chapter 29) (Zayouna Fiberoptic endoscopy may be necessary. In extreme cases, emergency surgery may be required to remove gangrenous or perforated tissue. A gastric resection or a 3435 3436 gastrojejunostomy (anastomosis of jejunum to stomach to detour around the pylorus) Pharmacologic Major Action Key Nursing Considerations may be necessary to treat gastric outlet obstruction, also called pyloric obstruction, Agent a narrowing of the pyloric orifice, which cannot be relieved by medical management. Antibiotics Chronic gastritis is managed by modifying the patient’s diet, promoting rest, Amoxicillin A bactericidal antibiotic that reducing stress, recommending avoidance of alcohol and NSAIDs, and initiating May cause abdominal pain assists with eradicating H. medications that may include antacids, H2 blockers, or proton pump inhibitors (Akiva and diarrhea pylori bacteria in the gastric mucosa Should not be used in patients & Greenwald, 2019). H. pylori may be treated with select drug combinations which allergic to penicillin typically include a proton pump inhibitor, antibiotics, and sometimes bismuth salts (Table 40-2). Clarithromycin Exerts bactericidal effects to May cause GI upset, eradicate H. pylori bacteria in headache, altered taste the gastric mucosa Nursing Management Many drug–drug interactions (e.g., colchicine, lovastatin, Reducing Anxiety warfarin); interacts with If the patient has ingested acids or alkalis, emergency measures may be necessary (see grapefruit juice Chapter 67). The nurse offers supportive therapy to the patient and family during Metronidazole A synthetic antibacterial and treatment and after the ingested acid or alkali has been neutralized or diluted. In some Should be given with meals to antiprotozoal agent that cases, the nurse may need to prepare the patient for additional diagnostic studies decrease GI upset; may cause assists with eradicating H. (endoscopies) or surgery. The patient may be anxious because of pain and planned pylori bacteria in the gastric anorexia and metallic taste treatment modalities. The nurse uses a calm approach to assess the patient and to mucosa when given with Patient should avoid alcohol; answer all questions as completely as possible. other antibiotics and proton increases blood-thinning pump inhibitors effects of warfarin Promoting Optimal Nutrition Tetracycline Exerts bacteriostatic effects to May cause photosensitivity For acute gastritis, the nurse provides physical and emotional support and helps the eradicate H. pylori bacteria in reaction; advise patient to use patient manage the symptoms, which may include nausea, vomiting, and pyrosis. The the gastric mucosa sunscreen patient should take no foods or fluids by mouth—possibly for a few days—until the May cause GI upset acute symptoms subside, thus allowing the gastric mucosa to heal. If IV therapy is Must be used with caution in necessary, fluid intake and output are monitored, along with serum electrolyte values. patients with renal or hepatic After the symptoms subside, the nurse may offer the patient ice chips followed by impairment clear liquids. Introducing solid food as soon as possible may provide adequate oral Milk or dairy products may nutrition, decrease the need for IV therapy, and minimize irritation to the gastric reduce effectiveness mucosa. As food is introduced, the nurse evaluates and reports any symptoms that suggest a repeat episode of gastritis. Antidiarrheal The nurse discourages the intake of caffeinated beverages, because caffeine is a Bismuth Suppresses H. pylori bacteria in Given concurrently with central nervous system stimulant that increases gastric activity and pepsin secretion. subsalicylate the gastric mucosa and assists antibiotics to eradicate H. The nurse also discourages alcohol use. Discouraging cigarette smoking is important. with healing of mucosal ulcers pylori infection The level of nicotine measured in gastric acid can be 10 times greater than arterial Should be taken on empty blood and 80 times greater than venous blood. Nicotine will increase secretion of stomach gastric acid and will also interfere with the mucosal barrier in the GI tract (Berkowitz, May darken the bowel Schultz, Salazar, et al., 2018). When appropriate, the nurse initiates and refers the movements patient for alcohol counseling and smoking cessation programs. H2 Receptor Antagonists Cimetidine Decreases amount of HCl Least expensive of H2 receptor produced by stomach by blocking action of histamine antagonists on histamine receptors of May cause confusion, parietal cells in the stomach agitation, or coma in older 3437 3439  adults or those with renal or Pantoprazole Same as for esomeprazole hepatic insufficiency A delayed-release tablet that is to be swallowed whole and Long-term use may cause taken before meals diarrhea, dizziness, and gynecomastia May cause diarrhea and hyperglycemia, headache, Many drug–drug interactions abdominal pain, and abnormal (e.g., amiodarone, liver function tests amitriptyline, benzodiazepines, metoprolol, nifedipine, Rabeprazole Same as for esomeprazole phenytoin, warfarin) A delayed-release tablet that is to be swallowed whole and Famotidine Same as for cimetidine taken without regard to meals; Best choice for patient who is however, if used for duodenal critically ill because it is known ulcers give after meals and to have the least risk of drug– when used for H. pylori drug interactions; does not treatment, give with food. alter liver metabolism May cause abdominal pain, Prolonged half-life in patients diarrhea, nausea, and with renal insufficiency headache Short-term relief for GERD Drug–drug interactions with Nizatidine Same as for cimetidine digoxin, iron, and warfarin Used for treatment of ulcers and GERD Prostaglandin E1 Analogue Prolonged half-life in patients Misoprostol Synthetic prostaglandin; Used to prevent ulceration in with renal insufficiency protects the gastric mucosa May cause headache, patients using NSAIDs from agents that cause ulcers; dizziness, diarrhea, also increases mucus Administer with food nausea/vomiting, GI upset, production and bicarbonate May cause diarrhea and and urticaria levels cramping (including uterine cramping) Proton Pump Inhibitors of Gastric Acid Used mainly for the treatment Esomeprazole Decreases gastric acid secretion of duodenal ulcers Used mainly for treatment of by slowing the H+,K+-ATPase Pregnancy category X (i.e., duodenal ulcer disease and H. pump on the surface of the should not be taken by a parietal cells of the stomach pylori infection A delayed-release capsule that pregnant woman as it can is to be swallowed whole and soften the cervix and result in taken before meals miscarriage or premature labor.) Lansoprazole Same as for esomeprazole A delayed-release capsule that Sucralfate Creates a viscous substance in Should be taken without food is to be swallowed whole and the presence of gastric acid taken before meals but with water 1 h prior to that forms a protective Omeprazole Same as for esomeprazole barrier, binding to the surface meals A delayed-release capsule that Other medications should be of the ulcer, and prevents is to be swallowed whole and digestion by pepsin taken 2 h before or after this taken before meals medication May cause diarrhea, nausea, Many drug–drug interactions constipation, abdominal pain, (e.g., digoxin, phenytoin, vomiting, headache, or warfarin) dizziness 3440 3441 May cause constipation or patient’s condition warrants. Guidelines for managing upper GI tract bleeding are nausea discussed later in this chapter. CNS, central nervous system; GERD, gastroesophageal reflux disease; GI, gastrointestinal; H2, Relieving Pain histamine-2; HCl, hydrochloric acid; H+,K+-ATPase, hydrogen–potassium adenosine triphosphatase; NSAIDs, nonsteroidal anti-inflammatory drugs. Measures to help relieve pain include instructing the patient to avoid foods and Adapted from Karch, A. M. (2018). Lippincott nursing drug guide. Philadelphia, PA: Lippincott beverages that may irritate the gastric mucosa as well as the correct use of Williams & Wilkins. medications to relieve chronic gastritis. The nurse must regularly assess the patient’s level of pain and the extent of comfort achieved through the use of medications and avoidance of irritating substances. Chart 40-1 HOME CARE CHECKLIST Promoting Home, Community-Based, and Transitional Care The Patient with Gastritis Educating Patients About Self-Care At the completion of education, the patient and/or caregiver will be able to: The nurse evaluates the patient’s knowledge about gastritis and develops an State the impact of gastritis on physiologic functioning, ADLs, IADLs, roles, individualized education plan that includes information about stress management, relationships, and spirituality. diet, and medications (see Table 40-2). Dietary instructions take into account the State the need for vitamin B12 injections if patient has pernicious anemia. patient’s daily caloric needs as well as cultural aspects of food preferences and Explain the importance of and necessity for adherence with prescribed patterns of eating. The nurse and patient review foods and other substances to be medication regimen. avoided (e.g., spicy, irritating, or highly seasoned foods; caffeine; nicotine; alcohol). Demonstrate methods of keeping track of the medication regimen and Consultation with a dietitian may be recommended (Chart 40-1). storage of the prescribed medications and use reminders such as beepers Providing information about prescribed medications, which may include antacids, and/or pillboxes. H2 blockers, or proton pump inhibitors, may help the patient to better understand why State the name, dose, side effects, frequency, and schedule for all medications. these medications assist in recovery and prevent recurrence. The importance of Identify foods and other substances that may cause gastritis (e.g., spicy, completing the medication regimen as prescribed to eradicate H. pylori infection must highly seasoned foods, caffeine, nicotine, alcohol). be reinforced to the patient and caregiver (see later discussion). Identify side effects and complications (e.g., increased or return of abdominal discomfort, inability to ingest adequate solids and liquids) that should be Continuing and Transitional Care reported to primary provider. The nurse reinforces previous education and conducts ongoing assessment of the State how to reach primary provider with questions or complications. patient’s symptoms and progress. Patients with malabsorption of vitamin B12 need State time and date of follow-up appointments and testing. information about lifelong vitamin B12 injections; the nurse may instruct a family ADLs, activities of daily living; IADLs, instrumental activities of daily living. member or caregiver how to administer the injections or make arrangements for the patient to receive the injections from the primary provider. Finally, the nurse emphasizes the importance of keeping follow-up appointments with the primary Promoting Fluid Balance provider. Daily fluid intake and output are monitored to detect early signs of dehydration (minimal fluid intake of 1.5 L/day, urine output of less than 1 mL/kg/h). If food and oral fluids are withheld, IV fluids (3 L/day) usually are prescribed and a record of Peptic Ulcer Disease fluid intake plus caloric value (1 L of 5% dextrose in water = 170 calories of carbohydrate) needs to be maintained. Electrolyte values (sodium, potassium, Peptic ulcer disease affects approximately 4.6 million Americans annually, with the chloride) are assessed every 24 hours to detect any imbalance (see Chapter 10). peak onset between 30 and 60 years of age (Anand, 2020; Norris, 2019). A peptic The nurse must always be alert to any indicators of hemorrhagic gastritis, which ulcer may be referred to as a gastric, duodenal, or esophageal ulcer, depending on its include hematemesis (vomiting of blood), tachycardia, and hypotension. All stools location. A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosa should be examined for the presence of frank or occult bleeding. If these occur, the of the stomach, in the pylorus (the opening between the stomach and duodenum), in primary provider should be notified, and the patient’s vital signs are monitored as the the duodenum (the first portion of the small intestine, between the stomach and the jejunum), or in the esophagus. Erosion of a circumscribed area of mucosa is the cause 3442 3443 (Fig. 40-2). This erosion may extend as deeply as the muscle layers or through the The use of NSAIDs, such as ibuprofen and aspirin, represents a major risk factor muscle to the peritoneum (thin membrane that lines the inside of the wall of the for peptic ulcers. Studies report that both NSAIDs and H. pylori impair the protective abdomen) (Norris, 2019). gastric mucosa, and the failure of the GI tract to repair the mucosa may result in Peptic ulcers are more likely to occur in the duodenum than in the stomach. As a ulceration (Anand, 2020; Norris, 2019). It is believed that smoking and alcohol rule, they occur alone but they may occur in multiples. Chronic gastric ulcers tend to consumption may be risks, although the evidence is inconclusive (Anand, 2020; occur in the lesser curvature of the stomach, near the pylorus. Esophageal ulcers occur NIDDK, 2020c). as a result of the backward flow of HCl from the stomach into the esophagus Familial tendency also may be a significant predisposing factor. People with blood (gastroesophageal reflux disease [GERD]). type O are more susceptible to the development of peptic ulcers than are those with blood type A, B, or AB. There also is an association between peptic ulcer disease and chronic obstructive pulmonary disease, cirrhosis of the liver, chronic kidney disease, and autoimmune disorders (Anand, 2020). Peptic ulcer disease is also associated with Zollinger-Ellison syndrome (ZES). ZES is a rare condition in which benign or malignant tumors form in the pancreas and duodenum that secrete excessive amounts of the hormone gastrin (NIDDK, 2020d; Roy, 2019). The excessive amount of gastrin results in extreme gastric hyperacidity and severe peptic ulcer disease. While the exact cause of ZES is unknown, 25% to 30% of cases are linked to an inherited, genetic condition called multiple endocrine neoplasia, type 1 (MEN-1) (NIDDK, 2020b; Norris, 2019). Pathophysiology Peptic ulcers occur mainly in the gastroduodenal mucosa because this tissue cannot withstand the digestive action of gastric acid (HCl) and pepsin. The erosion is caused by the increased concentration or activity of acid–pepsin or by decreased resistance of the normally protective mucosal barrier. A damaged mucosa cannot secrete enough Figure 40-2 Deep peptic ulcer. Reprinted with permission from Strayer, mucus to act as a barrier against normal digestive juices. Exposure of the mucosa to D. S., Saffitz, J. E., & Rubin, E. (2015). Rubin’s pathology: Mechanisms of gastric acid (HCl), pepsin, and other irritating agents (e.g., NSAIDs or H. pylori) human disease (8th ed., Fig. 19-23). Philadelphia, PA: Lippincott Williams & Wilkins. leads to inflammation, injury, and subsequent erosion of the mucosa. Patients with duodenal ulcers secrete more acid than normal, whereas patients with gastric ulcers tend to secrete normal or decreased levels of acid. When the mucosal barrier is Women have 8% to 11% and men have an 11% to 14% lifetime risk of developing impaired, even normal or decreased levels of HCl may result in the formation of peptic ulcers (Anand, 2020). The rates of peptic ulcer disease among middle-age men peptic ulcers. have diminished over the past several decades, whereas the rates among older adults The use of NSAIDs inhibits prostaglandin synthesis, which is associated with a have increased, particularly among women (Anand, 2020). Those who are 65 years disruption of the normally protective mucosal barrier. Damage to the mucosal barrier and older present to both outpatient and inpatient settings for treatment of peptic also results in decreased resistance to bacteria, and thus infection from H. pylori ulcers more than any other age group. This trend may be explained, at least in part, by bacteria may occur (Anand, 2020; Norris, 2019). higher rates of NSAID use and H. pylori infections in older adult populations (Anand, ZES is suspected when a patient has several peptic ulcers or an ulcer that is 2020). resistant to standard medical therapy. It is identified by the following: hypersecretion In the past, stress and anxiety were thought to be causes of peptic ulcers, but of gastrin, duodenal ulcers, and gastrinomas (islet cell tumors) in the pancreas or research has documented that most peptic ulcers result from infection with H. pylori, duodenum. More than 80% of gastrinomas are found in the “gastric triangle,” which which may be acquired through ingestion of food and water. Person-to-person encompasses the cystic and common bile ducts, the second and third portions of the transmission of the bacteria also occurs through close contact and exposure to emesis. duodenum, and the junction of the head and body of the pancreas. Most gastrinomas Although H. pylori infection is common in the United States, most infected people do tend to grow slowly; however, more than 50% of these tumors are malignant not develop ulcers. It is not known why H. pylori infection does not cause ulcers in all (Bonheur & Nachimuthu, 2019). The patient with ZES may experience epigastric people, but most likely the predisposition to ulcer formation depends on certain pain, pyrosis, diarrhea, and steatorrhea (fatty stools). Patients with ZES associated factors, such as the type of H. pylori and other as yet unknown factors (Anand, 2020; with MEN-1 syndrome may have coexisting pituitary or parathyroid tumors. ZES- Norris, 2019; Santacroce & Bhutani, 2019). associated MEN-1 syndrome is diagnosed with hyperparathyroidism; therefore, 3444 3445 patients may exhibit signs of hypercalcemia for several years before MEN-1 is Although vomiting is rare in an uncomplicated peptic ulcer, it may be a symptom diagnosed (NIDDK, 2020b). of a complication of an ulcer. It results from gastric outlet obstruction, caused by Stress ulcer is the term given to the acute mucosal ulceration of the duodenal or either muscular spasm of the pylorus or mechanical obstruction from scarring or acute gastric area that occurs after physiologically stressful events, such as burns, shock, swelling of the inflamed mucous membrane adjacent to the ulcer. Vomiting may or sepsis, and multiple organ dysfunction syndrome (Clarke et al., 2020). Stress ulcers, may not be preceded by nausea; usually, it follows a bout of severe pain and bloating, which are clinically different from peptic ulcers, are most common in patients which is relieved by vomiting. Emesis may contain undigested food eaten many hours following significant burn injuries, traumatic brain injury, or who require mechanical earlier. Constipation or diarrhea may occur, probably as a result of diet and ventilation. Stress ulcers are believed to be a result of ischemia to gastric mucosa and medications. alterations in the mucosa barrier (Clarke et al., 2020; Norris, 2019). When the patient The patient with bleeding peptic ulcers may present with evidence of GI bleeding, recovers, the lesions are reversed. This pattern is typical of stress ulceration. such as hematemesis or the passage of melena (Anand, 2020). Approximately 20% of Differences of opinion exist as to the actual cause of mucosal ulceration in stress patients with bleeding peptic ulcers do not experience abdominal pain at the time of ulcers. Usually, the ulceration results from a disruption of the normally protective diagnosis (Norris, 2019). Peptic ulcer perforation results in the sudden onset of signs mucosal barrier and decreased mucosal blood flow (ischemia). Mucosal ischemia and symptoms. The patient often reports severe, sharp upper abdominal pain, which results in the reflux of duodenal contents into the stomach, which increases exposure may be referred to the shoulder; extreme abdominal tenderness; and nausea or of the unprotected gastric mucosa to the digestive effects of gastric acid (HCl) and vomiting. Hypotension and tachycardia may occur, indicating the onset of shock pepsin (Anand, 2020; Clarke et al., 2020; Norris, 2019). The combination of mucosal (Azer, 2018). ischemia and increased gastric acid and pepsin exposure creates an ideal climate for ulceration. Assessment and Diagnostic Findings Specific types of ulcers that result from stressful conditions include Curling ulcers and Cushing ulcers. Curling ulcer is frequently observed after extensive burn injuries A physical examination may reveal pain, epigastric tenderness, or abdominal and often involves the antrum of the stomach or the duodenum (Anand, 2020). distention. Upper endoscopy is the preferred diagnostic procedure because it allows Cushing ulcer is common in patients with a traumatic head injury, stroke, brain tumor, direct visualization of inflammatory changes, ulcers, and lesions. Through endoscopy, or following intracranial surgery. Cushing ulcer is thought to be caused by increased a biopsy of the gastric mucosa and any suspicious lesions can be obtained. Endoscopy intracranial pressure, which results in overstimulation of the vagal nerve and an may reveal lesions that, because of their size or location, are not evident on x-ray increased secretion of gastric acid (HCl) (Norris, 2019). Cushing ulcers are typically studies. H. pylori infection may be determined by endoscopy and histologic deep, single ulcerations and have increased risk of perforation (Anand, 2020). examination of a tissue specimen obtained by biopsy, or a rapid urease test of the biopsy specimen. Other less invasive diagnostic measures for detecting H. pylori Clinical Manifestations include serologic testing for antibodies against the H. pylori antigen, stool antigen test, and urea breath test (Anand, 2020). Symptoms of peptic ulcer disease may last for a few days, weeks, or months and may The patient who has a bleeding peptic ulcer may require periodic CBCs to disappear only to reappear, often without an identifiable cause. Many patients with determine the extent of blood loss and whether or not blood transfusions are advisable peptic ulcers have no signs or symptoms. These silent peptic ulcers most commonly (see Chapter 28). Stools may be tested periodically until they are negative for occult occur in older adults and those taking aspirin and other NSAIDs (Anand, 2020). blood. Gastric secretory studies are of value in diagnosing ZES and achlorhydria As a rule, the patient with an ulcer complains of dull, gnawing pain or a burning (lack of HCl), hypochlorhydria (low levels of HCl), or hyperchlorhydria (high levels sensation in the mid epigastrium or the back. There are few clinical manifestations of HCl). that differentiate gastric ulcers from duodenal ulcers; however, classically, the pain associated with gastric ulcers most commonly occurs immediately after eating, Medical Management whereas the pain associated with duodenal ulcers most commonly occurs 2 to 3 hours after meals. In addition, approximately 50% to 80% of patients with duodenal ulcers Once the diagnosis is established, the patient is informed that the condition can be awake with pain during the night, whereas 30% to 40% of patients with gastric ulcers managed. Recurrence may develop; however, peptic ulcers treated with antibiotics to voice this type of complaint. Patients with duodenal ulcers are more likely to express eradicate H. pylori have a lower recurrence rate than those not treated with antibiotics. relief of pain after eating or after taking an antacid than patients with gastric ulcers The goals are to eradicate H. pylori as indicated and to manage gastric acidity. (Anand, 2020). Methods used include medications, lifestyle changes, and surgical intervention. Other nonspecific symptoms of either gastric ulcers or duodenal ulcers may include pyrosis, vomiting, constipation or diarrhea, and bleeding. These symptoms are Pharmacologic Therapy often accompanied by sour eructation (burping), which is common when the patient’s Currently, the most commonly used therapy for peptic ulcers is a combination of stomach is empty. antibiotics, proton pump inhibitors, and sometimes bismuth salts that suppress or 3446 3447 eradicate H. pylori. Recommended combination drug therapy is typically prescribed The patient is advised to adhere to and complete the medication regimen to ensure for 10 to 14 days and may include triple therapy with two antibiotics (e.g., complete healing of the ulcer. The patient also is advised to avoid the use of NSAIDs. metronidazole or amoxicillin and clarithromycin) plus a proton pump inhibitor (e.g., Because most patients become symptom free within a week, the nurse stresses to the lansoprazole, omeprazole, or rabeprazole), or quadruple therapy with two antibiotics patient the importance of following the prescribed regimen so that the healing process (metronidazole and tetracycline) plus a proton pump inhibitor and bismuth salts can continue uninterrupted and the return of chronic ulcer symptoms can be (Anand, 2020; Marcus & Greenwald, 2019). Research is currently being conducted to prevented. Maintenance dosages of H2 blockers are usually recommended for 1 year. develop a vaccine against H. pylori (Liu, Zhong, Chen, et al., 2020). For patients with ZES, hypersecretion of gastrin stimulates the release of gastric H2 blockers and proton pump inhibitors that reduce gastric acid secretion are used acid (HCl), which may be controlled with proton pump inhibitors. Octreotide, a to treat ulcers not associated with H. pylori infection. Table 40-3 provides information medication that suppresses gastrin levels, also may be prescribed (Daniels, Khalili, about the medication regimens for peptic ulcer disease. Morano, et al., 2019). Patients with ZES will require periodic endoscopy to evaluate the effectiveness of medication therapy. TABLE 40-3 Drug Regimens for Peptic Ulcer Disease Patients at high risk for stress ulcers (e.g., patients who are mechanically ventilated for more than 48 hours) may be treated prophylactically with either H2 blockers or Indications Drug Regimen Nursing Considerations proton pump inhibitors, and cytoprotective agents (e.g., misoprostol, sucralfate) Ulcer healing H2 receptor antagonist Should be used for 6–8 wks for because of the increased risk of upper GI tract hemorrhage (Clarke et al., 2020; Cimetidine 400 mg bid or 800 mg at complete peptic ulcer healing; Young, Bagshaw, Forbes, et al., 2020). bedtime patients who are at high risk require Famotidine 20 mg bid or 40 mg at a maintenance dose for 1 yr bedtime Nizatidine 150 mg bid or 300 mg at Quality and Safety Nursing Alert bedtime Misoprostol should not be taken by a pregnant woman as it can soften the PPIs: Should be used for 4–8 wks for cervix and result in miscarriage or premature labor. The nurse should be Esomeprazole 40 mg daily complete peptic ulcer healing; aware of this risk when caring for women of childbearing age. Lansoprazole 30 mg daily patients who are at high risk require Omeprazole 20 mg daily a maintenance dose for 1 yr Pantoprazole 40 mg daily Smoking Cessation Rabeprazole 20 mg daily Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, H. pylori Quadruple therapy with bismuth Efficacy of therapy is approximately resulting in increased acidity of the duodenum. Continued smoking is also associated infection subsalicylate 525 mg qid, plus 85% qid dosing may decrease tetracycline 500 mg qid, plus adherence to the regimen with delayed healing of peptic ulcers (Berkowitz et al., 2018; Kennedy & Winter, metronidazole 500 mg bid, plus a PPI 2017). Therefore, the patient is encouraged to stop smoking. Refer to Chapter 23 for daily for 10–14 days information on how the nurse may promote cessation of tobacco use. Alternate therapy with clarithromycin 500 mg bid, amoxicillin 1 g bid, Dietary Modification metronidazole 500 mg bid, plus PPI for 10–14 days The intent of dietary modification for patients with peptic ulcers is to avoid oversecretion of acid and hypermotility in the GI tract. These can be minimized by Prophylactic Peptic ulcer healing doses of PPIs Prevents recurrent ulceration in therapy for (above) approximately 80–90% of patients; avoiding extremes of temperature in food and beverages and overstimulation from the NSAID Misoprostol 100–200 mcg qid qid dosing may decrease adherence consumption of alcohol, coffee (including decaffeinated coffee, which also stimulates ulcers to the regimen acid secretion), and other caffeinated beverages. In addition, an effort is made to Pregnancy category X (i.e., should not neutralize acid by eating three regular meals a day. Small, frequent feedings are not be taken by a pregnant woman as it necessary as long as an antacid or an H2 blocker is taken. Diet compatibility becomes