DIAGNOSTIC EVALUATION AND TREATMENT OF GASTROESOPHAGEAL REFLUX DISEASE

By KIMBERLEY TUCKER

A Manuscript submitted in partial fulfillment of The requirements for the degree of MASTER OF NURSING

WASHINGTON STATE UNIVERSITY College of Nursing Intercollegiate Center for Nursing Education July 1999

To the Faculty of Washington State University:

The members of the committee appointed to examine the ICNE Research requirements and manuscript of Kimberley Tucker find it satisfactory and recommend that it be accepted.

ACKNOWLEDGMENTS I would like to extend a very special thank you and acknowledgement to a few special people that have encouraged me and supported me throughout my journey to attain my Masters in Nursing. I would like to thank Dr. Lorna Schumann, my chair and clinical mentor. You have been given a great gift as a mentor to future nurse practitioners. Your passion for your work and clinical expertise, have made you an invaluable asset to students. Thank you for supporting me and challenging me throughout this journey. Thank you Dr. Billie Severtson for your support and time as you served on my manuscript committee. Thanks to Josette Trunnell for serving on my committee as well as for mentoring me in my clinical practice. You are a very gifted practitioner. To Mary Hoerner, thank you for sharing this journey with me. This road has taken us through good times, hard times and funny times.....I'm glad we did it together. Finally, special thanks to my husband Jake. Your patience, love and undying support of me truly made this degree a joint effort. You are wonderful. I love you.

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DIAGNOSTIC EVALUATION AND TREATMENT OF GASTROESOPHAGEAL REFLUX DISEASE By Kimberley Tucker Washington State University July 1999 ABSTRACT Gastroesophageal reflux disease is one of the most common conditions originating from the gastrointestinal tract. Approximately sixty million Americans suffer from heartburn, one of the cardinal symptoms of gastroesophageal reflux disease. This paper reviews the proper diagnostic workup and the wide variety of treatments for gastroesophageal reflux disease, which range from simple lifestyle modifications to surgical repair.

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LIST OF TABLES

Table 1

Factors that decrease LES tone.........................................

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Table 2

Evaluation of diagnostic tests ... ... ... ... ... ... ... ... ...... ... ... ... ...

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Table 3

Four phase "stepped" approach to GERD therapy..................

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Table 4

Non-pharmacologic treatment for GERD

... ... ... ... ... ....

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Table 5

Endoscopic classification of esophagitis

... ... ... .....

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Table 6

Dosing Histamine2-receptor antagonists

... ... ... ... ... ... ... .....

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LIST OF FIGURES

Figure 1

Factors contributing to GERD

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Figure 2

Diagnostic algorithm ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ....

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Figure 3

Endoscopic view of normal esophageal mucosa and Barrett's Esophagus.................................................................

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ABSTRACT

Gastroesophageal reflux disease is one of the most common conditions originating from the gastrointestinal tract. Approximately sixty million Americans suffer from heartburn, one of the cardinal symptoms of gastroesophageal reflux disease. This paper reviews the proper diagnostic workup and the wide variety of treatments for gastroesophageal reflux disease, which range from simple lifestyle modifications to surgical repair.

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INTRODUCTION AND EPIDEMIOLOGY Gastroesophageal Reflux Disease (GERD) is a common disorder that affects the population across the lifespan. GERD, and its major symptom heartburn, is the most frequently occurring disorder of the esophagus and one of the most prevalent conditions originating from the gastrointestinal tract. Some degree of gastroesophageal reflux occurs in the normal population, especially postprandially, and is considered a benign physiologic process that is frequently undetected (Kitchin &Castell, 1991). Gastroesophageal reflux disease; however, is a chronic disease that usually requires lifelong medical management to prevent complications. The term Gastroesophageal Reflux Disease is applied to the symptoms or tissue damage that is caused by the reflux of gastric contents (usually acidic) into the esophagus (Tierney, McPhee, & Papadakis, 1996). The vast majority of patients with GERD have mild symptoms; in fact, many patients with GERD are unaware of the nature of their condition and many do not seek medical attention even with esophageal complications (Reynolds, 1996). This is particularly true in elderly patients who may have decreased acidity of the gastric refluxate or decreased pain perception. Antacids have been the mainstay of "home therapy" for many people with intermittent symptoms. With the FDA approval of over the counter H2 antagonists in 1995, individuals continue to treat their symptoms and do not discuss their complaints with their practitioners. Symptomatic gastroesophageal reflux is one of the most common problems encountered by practitioners of all specialties (Richter, 1986). Sixty million Americans (35-50%) suffer from heartburn at least once a month, while 7-10% of the population experience it daily (Richter, 1995). It has been estimated that approximately 27% of adult Americans take antacids more than twice a month (Kitchin & Castell, 1991).

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Effective diagnosis and treatment of GERD is complex due to the variability of symptoms.

PATHOPHYSIOLOGY Gastroesophageal reflux historically was thought to be caused primarily by a hiatal hernia, a protrusion of the stomach into the mediastinal cavity through the esophageal hiatus of the diaphragm; and the subsequent irritation of the esophageal mucosa by hydrochloric acid and pepsin. This theory has now been refuted as new evidence suggests that GERD has a multifactorial pathophysiologic basis (Middlemiss, 1997). Currently, four physiologic factors contribute to, either individually or alone, gastroesophageal reflux disease: 1) Incompetent lower esophageal sphincter tone (LES tone) 2) Irritant effects of refluxate 3) Abnormal esophageal clearance and 4) Delayed gastric emptying (Tierney, McPhee, & Papadakis, 1996). Contributions of each of these factors vary from patient to patient necessitating the individuality of treatment. Each of these factors will be explored in the following section. In the majority of patients, reflux occurs when the lower esophageal sphincter pressure falls below intra-abdominal pressure, usually due to intermittent relaxations of the sphincter (Reynolds, 1996). Normally, the LES provides a barrier to acid reflux by active tonic contraction between the stomach and the esophagus. When the LES barrier function is impaired, acid is allowed to reflux into the esophagus. Low resting pressure in the LES is common among patients with severe reflux disease, however; the majority of GERD patients have normal LES pressure, but have abnormal transient lower esophageal sphincter relaxations (Stendal, 1997). Factors that influence the decrease of lower esophageal sphincter pressure are listed in Table 1.

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The physical make-up of gastric contents is key in determining the possibility of esophageal damage. The stomach normally secretes acid at a pH of about 1.5-2.0. The pH in the distal esophagus, by comparison is relatively neutral with a pH of about 6.07.0. Prolonged esophageal mucosal contact with gastric secretions ofa pH less than four is highly associated with severe erosive esophagitis (Middlemiss, 1997). This exposure time correlates well with the severity of injury, but is not suggestive of the severity of symptoms experienced by the patient (Reynolds, 1996). Control of acid exposure and acid neutralization are two of the cornerstones ofGERD therapy. Esophageal clearance of acid reflux is one of the body's normal defense mechanisms against acid reflux disease. "Esophageal clearance is achieved by gravity, saliva, and esophageal contractions....esophageal peristalsis is the primary mechanism by which acid is cleared from the esophagus" (Reynolds, 1996, p. S7). Reflux that occurs nocturnally or in a recumbent position is a common complaint among patients with symptomatic reflux disease. This is due to the fact that gravity is lost and peristalsis slows in the sleeping patient. This leaves the esophagus vulnerable to prolonged periods of acid exposure. Delayed gastric emptying can be caused by abnormalities such as: gastric atony from advanced diabetes, diffuse neuromuscular disorders, vagotomy, idiopathic gastric paresis, pyloric dysfunction and duodenal dysmotility (Stendal, 1997). An increase in gastric volume can lead to transient relaxations of the LES which in turn, lead to acid in the esophagus.

WORK UP FOR GERD Differential diagnosis can be very challenging, because GERD can masquerade as several other diseases and has such a varied clinical presentation. It is very important to

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gather a thorough history and perform a complete physical examination in order to rule out the possible differential diagnoses. Differential diagnoses that should be considered initially include: esophageal carcinoma, peptic ulcer, ischemic heart disease, cholelithiasis, and nonpeptic esophagitis (Stendal, 1997).

HISTORY TAKING The cardinal symptoms of GERD are heartburn and regurgitation. Many patients describe their heartburn as a "retrosternal burning pain that may be noted in the epigastrium, neck, throat, and occasionally in the back" (Nord, 1994, p.3). Complaints of heartburn or regurgitation of acidic fluids into the esophagus and mouth that occur after the ingestion of a large or fatty meal and upon reclining or bending, are typical. The use of over-the-counter medications such as antacids or baking soda, with some degree of relief of symptoms is classic. Patients with a straightforward clinical presentation can usually be diagnosed without further workup with a high degree of reliability. Empiric acid suppression is usually started. Empiric therapy; however, "with the possible advantages of cost and convenience to patients and physicians must be weighed against the possible risk of misdiagnosis and inadequate therapy of more severe conditions" (DeVault & Castell, 1995, p.2167). Symptoms suggestive of severe disease or extraesophageal symptoms always warrant further diagnostic investigation. These include: atypical (non-cardiac) chest pain, chronic hoarseness, chronic cough, wheezing, recurrent pneumonia, dysphagia or odynophagia, or patients who are not responding to empiric medical therapy or whose symptoms are worsening.

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PHYSICAL EXAMINATION It is important to keep in mind that history alone can dictate therapy; however, a focused exam is essential. First, determine if the patient is overweight. If the patient is obese (more than 30% above ideal body weight), he or she should be counseled to lose weight; even a 10 pound weight loss can decrease symptoms (Uphold & Graham, 1994). Palpate the abdomen for masses or tenderness to rule out an acute abdomen or malignancy. Check the stool for occult blood. With asymptomatic disease, dental erosions may also be evident. "Physical exam and laboratory studies are normal in uncomplicated disease" (Tierney, McPhee, & Papadakis,1996, p. 514). Patients with atypical symptoms or more severe disease are generally referred for diagnostic workup. "The practitioner can obtain a complete blood count, and biochemical screen to assess for anemia, blood glucose level, liver function, and any therapeutic drug ranges that may be applicable" (Middlemiss, 1997, p.52). Referral to gastroenterology for diagnostic studies is appropriate at this point. DIAGNOSTIC TESTS The choice of diagnostic tests depends on the clinical question being asked; and history and physical examination should guide the appropriate diagnostic workup. (Fennerty, Castell, Fendrick, Halpern, Johnson, Kahrilas, Lieberman, Richter, & Sampliner, 1996). Table 2 compares the most commonly performed diagnostic tests for the work-up ofGERD. It provides an analysis of the sensitivity and specificity, the time to results, cost and patient preparation for each of the tests. Patients with complicated or recurrent disease symptoms should have an evaluation of the esophageal mucosa for injury. Diagnostic test choices include aircontrast barium esophagram, and upper gastrointestinal endoscopy (DeVault & Castell,

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1995). The endoscopy procedure is up to three times the expense of the barium series; however, it has a much higher sensitivity and allows for direct visualization of the mucosa with the ability to biopsy at the site for histological changes. "Up to 40% of patients may have histologic changes alone and can be diagnosed only with endoscopic biopsy" (DeVault & Castell, 1995, p.2167). The barium swallow is the most sensitive test for the detection of esophageal strictures. It can also provide information about esophageal motor function and can detect hiatal hernia. It is less expensive than endoscopy in most situations (Fennerty, et aI., 1996). Ambulatory pH monitoring provides important information about pathological esophageal reflux. A number of parameters can be examined: a quantitative measure of reflux duration, information on reflux frequency, information on when reflux occurs, symptoms-reflux correlation, and information on the esophageal clearance of refluxed acid (Stendal, 1997). Generally, it is useful for patients suspected of having atypical symptoms such as: atypical chest pain, hoarseness, or other pulmonary type manifestations to help clarify symptoms. The vast majority of patients with typical GERD symptoms benefit little from this test (DeVault & Castell, 1994). An additional use of this test, as outlined by the algorithm in Figure 1, is for patients who continue to have symptoms while they are on acid suppression therapy and have already undergone endoscopy. Esophageal manometry is usually performed on patients who are going to undergo a surgical procedure for their reflux disease. It is used to evaluate esophageal peristalsis and function of the LES. The findings help indicate the appropriate surgical procedure (Fennerty, et aI., 1996). This test, itself: is not diagnostic ofGERD.

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Several tests previously used to evaluate symptoms of GERD are rarely used today because of the better sensitivity and specificity of alternative tests, eg, ambulatory pH monitoring, and endoscopy. These include the esophageal acid infusion test, the water siphon test during barium swallow, scintigraphy, and the standard acid reflux test (Fennerty, et aI., 1996). The algorithm in Figure 2, by the American College of Gastroenterology, is a helpful guide in determining a diagnostic workup based on symptoms.

TREATMENT The goals of treatment for the patient with GERD are four-fold: to eliminate symptoms, to heal esophageal injury, to manage and prevent complications, and to prevent relapse. The appropriate medical therapy for the symptomatic patient should focus on the degree of esophagitis and the presence of acid-reflux complications (Fass, Hixson, Ciccolo, Gordon, Hunter, & Rappaport, 1997). It is essential to individualize treatment due to the variability of symptoms. Long-term drug maintenance is the key to this chronic, relapsing disease. For most patients, treatment involves a progressive "stepped" approach. Table 3 outlines the four phases of "stepped" treatment for GERD. Many patients seeking a practitioner have tried over-the-counter antacids and histamine H2 antagonists and perhaps some degree of lifestyle modification. The foundation of initial therapy, or "phase one," involves lifestyle modification and usually an alginic acid-antacid, namely Gaviscon. Antacids work by increasing the pH of the gastric contents, and also deactivate pepsin. They may also increase LES pressure and decrease the amount of reflux from the stomach (DeVault & Castell, 1994). For patients with nocturnal reflux, antacids have no effect. Over-the-counter histamine H2 antagonists

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are a recent addition to phase one therapy (Fass, et aI., 1997). Non-pharmacological treatment and lifestyle modification education information are listed in Table 4. Failure to respond to phase one therapy requires phase two intervention. This step involves a further investigation of the reflux symptoms, and the addition of histamine H2 antagonists with or without prokinetic medications. Non-pharmacological interventions should continue throughout all phases of therapy. Endoscopy would be warranted at this step to assess the degree of esophageal damage. Therapeutic response to therapy depends on the degree of esophageal damage and duration oftherapy. Table 5 describes the endoscopic classification of esophagitis. Histamine H 2 antagonists decrease esophageal exposure to acid by reducing gastric acid secretion and volume. Single agent therapy with histamine H 2 antagonists may be best for treating patients with milder grades of endoscopic esophagitis. Grades I and II heal in about 75-90% of patients and grades III and IV heal in only about 40-50% of patients (Nord, 1994). Healing rates improve when the therapy is extended from 4 weeks to 8 or 12 weeks and with the use of high doses of histamine H2 antagonists (Brady and Ogorek, 1996). Table 6 gives dosage information for histamine H2 antagonists. Prokinetic agents are useful in reducing reflux by two mechanisms: increasing LES pressure and accelerating gastric emptying (Fass, et aI., 1997). Agents that are currently available include: bethanechol (Urecholine), metoclopramide (Reglan), and cisapride (Propulsid). "The clinical efficacy of bethanechoI and metoclopramide in the treatment of gastroesophageal reflux disease has not been consistently confirmed" (Fass, et aI., 1997, p.207). Both drugs also carry a considerable risk of toxicity and metoclopramide can cause extrapyramidal reactions. The efficacy of cisapride is

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comparable to low dose histamine H2 antagonists, but has no advantage over them and is more expensive than the generic version (Fennerty, et aI., 1996). If symptoms of reflux remain refractory after four weeks of therapy in phase two, it is advisable to move to phase three. In this phase, the histamine H2 antagonist is replaced with a proton pump inhibitor and sulcrafate (Carafate) is added for esophagitis (Middlemiss, 1997). Proton Pump Inhibitors (PPI's), such as omeprazole (Prilosec) and lansoprazole (Prevacid), are potent and long-acting inhibitors of gastric acid secretion. They are the most effective agents to treat esophagitis (Reynolds, 1996). PPI's are superior to histamine H2 antagonists in their symptom relief and healing. "In a dose of 40 mg / day, omeprazole achieves complete healing in 80-97% of patients with esophagitis who were refractory to H 2 receptor antagonists" (Reynolds, 1996, p.S9). Once healing is achieved with the PPI, patients can often be cycled offthe histamine H 2 antagonist and continue phase one interventions. Sulcrafate (Carafate) produces a physical barrier against gastric acid by adhering to the esophageal and gastric mucosa. It provides short-term healing rates in mild and moderate esophagitis that are comparable to conventional doses of histamine H 2 antagonists (Fass, et aI., 1997). For patients with severe or refractory GERD, a step up to phase four may be necessary. In this phase, the PPI is maintained and a prokinetic drug such as cisapride (Propulsid) may be added. For patients with resistant disease, the combination of omeprazole (Prilosec) and cisapride (Propulsid) is more effective than ranitidine (Zantac) plus cisapride (Propulsid) (Reynolds, 1996). Surgical intervention is considered the most aggressive treatment for GERD and is reserved for special cases. "Surgery at present is limited to patients who are resistant

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to or intolerant of medical therapy, who have complications of GERD such as recurrent aspiration or esophageal stricture formation, or who are young and face lifelong medical treatment" (Brady & Ogorek, 1996, p.86). The most popular surgical option at this time is the Nissen fundoplication, which can be performed laparoscopically. Careful esophageal assessment with manometry and pH testing prior to surgery are warranted. "Up to 80-900A» of patients have satisfactory long-term outcome" (Nord, 1994, p 6).

COMPLICATIONS Patients with longstanding GERD can experience severe complications. Peptic stricture results from chronic scarring by acid exposure in the esophagus. Patients may present with complaints of difficulty swallowing and food sticking in the esophagus. Acid reflux symptoms may lessen as the esophageal opening narrows. Barrett's esophagus is the most serious complication ofGERD. In this condition, the normal squamous epithelium of the distal esophagus becomes replaced by metaplastic columnar epithelium in order to become more resistant to acid injury. Barrett's esophagus is a pathologic condition that does not present with its own symptoms. Patients with Barrett's esophagus have approximately a 30-fold increased risk of developing esophageal cancer. These patients should be followed by endoscopy and a gastroenterologist. (www.phanninfo.com/disease/gerd/gerdfagI3.html. 1998) Figure 3 shows normal esophageal

mucosa and Barrett's epithelium as seen with endoscopy.

CONCLUSION Gastroesophageal Reflux Disease is a common, treatable disease. An understanding of the pathophysiology, common presenting symptoms, as well as atypical presentations are crucial to successful diagnosis, treatment or possible referral by the practitioner. A patient with mild symptoms or a typical presentation ofGERD, can be

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easily managed by the practitioner with conservative treatment. However, knowing when to refer for further diagnostic workup with gastroenterology or cardiology is equally important.

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BffiLIOGRAPHY Blair, D., Kaplan, B., Spiegler, MS. (1997). Patient characteristics and lifestyle recommendations in the treatment of gastroesophageal reflux disease. The Journal of Family Practice, 44(3), 266-272. Brady, W., Ogorek, C. (1996). Gastroesophageal reflux disease: the long and short of therapeutic options. Postgraduate Medicine, 100(5),76-89. DeVault, K., Castell, D. (1994). Current diagnosis and treatment of gastroesophageal reflux disease. Mayo Clin Proc, 69, 867-876. DeVault, K., Castell, D. (1995). Guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Archives of Internal Medicine, 155(13),2165-2173. Fass, R., Hixson, L., Ciccolo, M., Gordon, P., Hunter, G., Rappaport, W. (1997). Contemporary medical therapy for gastroesophageal reflux disease. American Family Physician, 55(1), 205-212. Fennerty, M.B., Castell, D., Fendrick, A.M., Halpern, M., Johnson, D., Kahrilas, P., Lieberman, D., Richter, J., Sampliner, R. (1996). The diagnosis and treatment of gastroesophageal reflux disease in a managed care environment. Archives of Internal Medicine, 156, 477-484. Fuchs, K., DeMeester, T., Albertucci, M. (1987). Specificity and sensitivity of objective diagnosis of gastoresophageal reflux disease. Surgery, 102(4), 575-580. Hixson, L., Kelley, C., Jones, W., Tuohy, C. (1992). Current trends in the pharmacotherapy for gastroesophageal reflux disease. Archives of Internal Medicine, 152,717-723.

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Kitchin, L., Castell, D. (1991). Rationale and efficacy of conservative therapy for gastroesophageal reflux disease. Archives of Internal Medicine, 151, 448-454. McQuaid, K. (1996). Symptoms and signs of gastrointestinal disease. In L.M. Tierney, Jr., S, J. McPhee, & M.A. Papadakis (Eds.), Current Medical Diagnosis and Treatment (35 th ed., pp. 514-517). Stamford, CT: Appleton & Lange.Middlemiss, C., (1997). Gastroesophageal Reflux Disease: A common condition in the elderly. The Nurse Practitioner, 22(11), 51-59. Nord, H.J. (1994). Gastroesophageal reflux disease. The American Society for Gastrointestinal Endoscopy website, (www.asge.org). Reynolds, J. (1996). Influence of pathophysiology, severity, and cost on the medical management of gastroesophageal reflux disease. American Journal of HealthSystemPham., 53(15), S5-S12. Richter, J. (1986). A critical review of current medical therapy for gastroesophageal reflux disease. Journal of Gastroenterology, 8 (Supp. 1), 72-80 Richter, J. (1995). Long-term management of gastroesophageal reflux disease and its complications. The American Journal of Gastroenterology, 92(4), 30S-35S. Robinson, M. (1995). Prokinetic therapy for gastroesophageal reflux disease. American Family Physician, 52(3), 957-962. Sandmark, S., Carlsson R., Fausa 0., Lundell L. (1988). Omeprazole or ranitidine in the treatment of reflux esophagitis: results of a double-blind, randomized, scandinavian multicenter study. Scandinavian Journal of Gastroenterology, 23, 625-632. Sellar, R.J., Caestecker, DE, Heading, R.C. (1987). Barium radiology: a sensitive test for gastro-esophageal reflux. Clinical Radiology, 38, 303-307.

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Stendal, C. (1997). Practical Guide to Gastrointestinal Function Testing. Massachusetts: Blackwell Science Ltd. Timmer, R., Breumelho( R., Nadorp, J., Smout, A., (1993). Esophageal motility in low-grade reflux esophagitis, evaluated by stationary and 24 -hour ambulatory manometry. The American Journal of Gastroenterology, 88, 837-841. The American College of Gastroenterology. (1998). Ignoring persistent heartburn symptoms can lead to severe consequences. The American College of Gastroenterology website. (www.pharminfo.com!disease/gerd/gerdfaq 14. html) Uphold, C.R., & Graham, M.V. (1994). Clinical Guidelines in Family Practice

(2od ed.), Gainesville, FL: Baramarrae, pp. 515-517.

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FIGURE 1 FACTORS CONTRIBUTING TO GERD

Impaired esophageal clearance Incompetent LES tone Irritant effects of refluxate Delayed gastric emptying

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TABLE 1 FACTORS THAT DECREASE LOWER ESOPHAGEAL SPHINCTER TONE Hormones-Estrogens, progesterone, glucagon, secretin and cholecystokinin Smoking Drugs--Anticholinergic Calcium channel blocking agents Dopamine Diazepam Meperidine Morphine Theophylline Foods-Chocolate Peppermint Alcohol High fat foods

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FIGURE 2 BERD Symptoms

AWBULATORY pH~NnoR

ACID

CONSIDER OTHER DIAGNOSIS

SUPPRESSION THERAPY

STOP

MEDICATION AFTER 11-8 WKS

ENDOSCOPY

PAN THERAPY

AMBULATORY pH MONITOR

NO

MAX. .IZE MEDICAL

THERAPY

Reprinted with permission from the American College of Gastroenterology, website, ~~!!~.&_Q!g, 1996.

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TABLE 2 EVALUATION OF DIAGNOSTIC TESTS TEST

SENSITIVITY / SPECIFICITY

TIME TO RESULTS

COST ANALYSIS

PATIENT TEACHING / PREPARATION

Ambulatory pH Monitoring

Sensitivity 85% Specificity 95%

Generally done over a 24 hour period.

$300-350

48 hours prior to the study the patient should stop taking medications such as: nitrates, calcium channel blockers, promotility agents, sedatives, analgesics, antidepressants, H 2 blockers, anticholenergics. Antacids should be stopped 24 hours before the study. Proton pump inhibitors should be stopped 7 days before the study.

Information from the ambulatory recorder is uploaded on to the labs computer immediately following the test for interpretation of results.

The patient comes to the GI laboratory after an overnight fast. (at least 6 hours) Normal activity No showers or baths with the equipment in place Regular diet-·all meals need to be eaten at one sitting within 30 minutes, 4 hours apart. No chewing gum or carbonated beverages, tea, coffee, alcohol, fruit juice, tomatoes, or candy Teaching about the "event" buttons on the monitor device and how to operate during the test. Instruct patient to keep a diary of meals, sleep, and symptoms and the times they occur.

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Endoscopy with biopsy

High Sensitivity

Immediate visualization of tissue. Histological samples are read by a pathologist

EGD $550-600 Biopsy $150

No restriction on meds prior to the test. NPO for a minimum of 6 hours prior to study. Patient will be given conscious sedation. (usually Demerol and Versed) No restrictions after the test.

Double Contrast Sensitivity 74% Barium Study Specificity 86% with measurement of the internal diameter of the cardiac oesophagus

Immediate visualization of esophageal motility disorders. Does not gIve information about tissue damage.

$375-400

NPO for a minimum of 8 hours.

Esophageal Manometry

Result in approx.45 minutes.

$400

NPO for a minimum of 4 hours prior to study. No restriction on meds prior to test. Usually have to do an EGD prior to the study to confirm placement ofthe catheter.

Low sensitivity (58%) for abnormal acid exposure Low specificity (84%) for abnormal acid exposure

Table 2 provides an evaluation of the most common diagnostic tests performed in the diagnosis and treatment ofGERD.

Sources: Stendal, 1997, The American Society for Gastrointestinal Endoscopy www.asge.org, 1998, DeVault & Castell, 1995, Seller, R.J., Caestecker, J.S., Heading, R.C., 1987. Cost Analysis based on figures from Our Lady of Lourdes Health Center~ Pasco, Washington 1998

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TABLE 3 FOUR PHASE "STEPPED" APPROACH TO GERD MANAGEMENT Patient education on the pathophysiology of GERD and lifestyle Phase One modification measures Antacids after meals and at bedtime Over-the-counter H2 antagonists

Phase Two

PhaseThree

Phase Four

**failure to respond to phase one therapy, move to phase two** Continue phase one interventions Further history and physical evaluation including endoscopy Addition of histamine H 2 antagonist with or without prokinetic agent **ifsymptoms remain refractory after 4 weeks of phase two therapy, move to phase three** Continue phase one interventions Replace histamine H2 antagonist with a proton pump inhibitor and add sulcrafate for esophagitis **for severe or refractory GERD, move to phase four** Continue phase one interventions Maintain the proton pump inhibitor Addition of a prokinetic drug before meals and at bedtime Referral to gastroenterologist Surgery

Adapted from: Middlemiss, 1997

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TABLE 4 NON-PHARMACOLOGIC TREATMENT FOR GERD Dietary-Avoidance of large meals, fatty foods, and foods that decrease LES pressure Consumption of last meal of the day at least three hours before bedtime Avoidance of exercise after meals Avoid lying down after meals Elevation of the head of the bed 6 inches on blocks Weight loss Avoidance of drugs that decrease LES pressure Avoid positions that increase intra-abdominal pressure such as lifting and bending Avoidance of smoking and alcohol Avoidance of tight fitting garments

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TABLES ENDOSCOPIC CLASSIFICATION OF ESOPHAGITIS Grade 0 1 2 3 4

Description Normal esophageal mucosa Erythema and lor edema Isolated erosions Circumferential, confluent erosions or ulceration Circumferential erosions plus deep ulceration, stricture, and I or Barrett's esophagus

Source: Sandmark, et.aI. (1988) in Hixson, et aI., (1992)

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FIGURE 3 ENDOSCOPIC VIEW OF NORMAL ESOPHAGEAL MUCOSA AND BARRETT'S ESOPHAGUS

Barrett's Esophagus as seen with endoscopy

~onnalesophagealrnucosa

as seen with endoscopy