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Upper Endoscopy for Gastroesophageal Reflux Disease – ACP Guidelines
Upper Endoscopy for Gastroesophageal Reflux Disease: Best Practice Advice From the Clinical Guidelines Committee of the American College of Physicians (ACP)
Nearly 38% of the upper endoscopies performed in outpatients with gastroesophageal reflux disease and low-risk dyspepsia do not adhere to current best-practice guidelines. The most common inappropriate uses were in patients who received an inadequate course of proton pump inhibitors (PPIs) before upper endoscopy and in those who underwent too-frequent surveillance of Barrett’s esophagus. Inappropriate use of endoscopy generates unnecessary costs and exposes patients to harms without improving outcomes.
Read the full text here and download the paper. http://annals.org/article.aspx?articleid=1470281
Best Practice Advice
- Upper endoscopy is indicated in men and women with heartburn and alarm symptoms (dysphagia, bleeding, anemia, weight loss, and recurrent vomiting).
- Upper endoscopy is indicated in men and women with:
- Typical GERD symptoms that persist despite a therapeutic trial of 4 to 8 weeks of twice-daily proton-pump inhibitor therapy.
- Severe erosive esophagitis after a 2-month course of proton-pump inhibitor therapy to assess healing and rule out Barrett esophagus. Recurrent endoscopy after this follow-up examination is not indicated in the absence of Barrett esophagus.
- History of esophageal stricture who have recurrent symptoms of dysphagia.
- Upper endoscopy may be indicated:
- In men older than 50 years with chronic GERD symptoms (symptoms for more than 5 years) and additional risk factors (nocturnal reflux symptoms, hiatal hernia, elevated body mass index, tobacco use, and intra-abdominal distribution of fat) to detect esophageal adenocarcinoma and Barrett esophagus.
- For surveillance evaluation in men and women with a history of Barrett esophagus. In men and women with Barrett esophagus and no dysplasia, surveillance examinations should occur at intervals no more frequently than 3 to 5 years. More frequent intervals are indicated in patients with Barrett esophagus and dysplasia.
GERD, Barrett Esophagus, and Esophageal Adenocarcinoma
Tissue injury is not necessary to fulfill disease criteria, as 50% to 85% of patients with GERD have nonerosive reflux disease. As many as 40% of U.S. adults report some symptoms of reflux (heartburn and regurgitation), and 10% to 20% have symptoms on a weekly or more frequent basis. Approximately 10% of patients with chronic heartburn symptoms have Barrett esophagus. GERD and Barrett esophagus are associated with an increased risk for esophageal adenocarcinoma. While the absolute risk for adenocarcinoma of the esophagus in the general population remains low (26 cases per 1 million in the U.S. population), its incidence has increased more than 5-fold in the past 40 years. Adenocarcinoma of the esophagus carries a poor prognosis with a 5-year survival rate less than 20%. Given the rising prevalence of chronic GERD, the use of upper endoscopy for GERD indications is rising in an effort to promote early detection and reduce the risk for death from adenocarcinoma of the esophagus. Since 1% to 5% of the U.S. adult population may have Barrett esophagus, the public health and financial implications of endoscopic screening and surveillance programs are substantial.
All 3 major U.S. gastroenterologic professional societies have released guidelines but differ in recommendations.
- The American Society of Gastrointestinal Endoscopy (ASGE) recommends that screening upper endoscopy be considered in selected patients with chronic, longstanding GERD:
- Frequent GERD symptoms (several times per week),
- Chronic GERD symptoms (symptoms for >5 years)
- Age > 50 years
- White race
- Male sex
- Nocturnal reflux symptoms
- The American Gastroenterological Association (AGA) guidelines recommend against screening the general population with GERD for Barrett esophagus and esophageal adenocarcinoma but should be considered in patients with GERD who have several risk factors associated with esophageal adenocarcinoma
- Age 50 years or older
- Male sex
- White race
- Hiatal hernia
- Elevated body mass index
- Intra-abdominal distribution of fat
- The American College of Gastroenterology (ACG) guidelines note that screening for Barrett’s esophagus in the general population cannot be recommended at this time. The use of screening in selective populations at higher risk remains to be established, and therefore should be individualized.
- GERD symptoms
- Body mass index
Formulation of these guidelines was hampered by the generally poor quality of data about the use of endoscopic screening and surveillance programs. In many cases, expert opinion formed the basis for specific recommendations.
The value of endoscopy is well-substantiated in several clinical settings.
- GERD associated with the alarm symptoms of dysphagia, bleeding, anemia, weight loss, or recurrent vomiting merits investigation with upper endoscopy because of its yield of potentially clinically actionable findings, such as cancer of the esophagus or stomach, bleeding lesions in the foregut, or stenosis of the esophagus or pylorus.
- Patients with a documented history of severe erosive esophagitis (grade B or worse on a validated A-to-D scoring system) treated with PPIs have a substantial rate of incomplete healing with medical therapy and may have Barrett esophagus in the areas of previously denuded esophageal epithelium. For these reasons, follow-up upper endoscopy is recommended after 8 weeks of PPI therapy for severe esophagitis to ensure healing and to rule out Barrett esophagus.
- The use of upper endoscopy in patients with esophageal stricture secondary to GERD is largely symptom-based. Because recurrence of strictures is common, repeated upper endoscopy with dilatation may be required.
- Screening intervals for patients with Barrett esophagus without dysplasia are recommended at 3- to 5-year intervals. More frequent endoscopy is reserved for the subset of patients who develop low- or high-grade dysplasia, as they face a higher risk for progression to cancer.
- In patients with chronic GERD whose initial endoscopic screening results were negative, no additional endoscopic screening is necessary, even if the patient continues medical therapy. Observational data show that the likelihood of development of Barrett esophagus in the 5 years after a negative result in such patients is less than 2%. Therefore, routine serial endoscopy in patients with initially negative results for Barrett esophagus is not recommended. Patient and primary caregiver expectations may promote overuse as patients may anticipate serial cancer screening and may inappropriately view no screening or a once-in-a-lifetime screening upper endoscopy for GERD symptoms as inadequate. Patients who have Barrett esophagus and no dysplasia may be dissatisfied with a 3- to 5-year interval of surveillance examinations, as patients with Barrett esophagus grossly overestimate their risk for esophageal cancer.
Summary of the ACP best practice advice:
The ACP has found evidence that upper endoscopy is indicated in patients with heartburn and alarm symptoms, such as dysphagia, bleeding, anemia, weight loss, and recurrent vomiting. However, upper endoscopy is not an appropriate first step in most patients with GERD symptoms and is indicated only when empirical PPI therapy for 4 to 8 weeks is unsuccessful. Upper endoscopy is not indicated in asymptomatic patients with a history of esophageal stricture but is appropriate in patients with recurrent symptoms of dysphagia. Screening upper endoscopy should not be routinely done in women of any age or in men younger than 50 years regardless of GERD symptoms because the incidence of cancer is very low in these populations. Screening endoscopy may be indicated in men older than 50 years with several risk factors for Barrett esophagus. This screening decision should include an assessment of the patient’s life-limiting comorbid conditions. Risk factors include chronic GERD symptoms (symptoms of >5 years’ duration), nocturnal reflux symptoms, hiatal hernia, elevated body mass index, tobacco use, and intra-abdominal distribution of fat. If an initial screening examination is negative for Barrett esophagus or esophageal adenocarcinoma, recurrent periodic endoscopy is not indicated. Among patients found to have Barrett esophagus on screening upper endoscopy, endoscopic surveillance may be indicated at 3- to 5-year intervals. More frequent endoscopic examinations are reserved for patients with low- or high-grade dysplasia because of their higher risk for progression to cancer.
Unnecessary endoscopy exposes patients to preventable harms, may lead to additional unnecessary interventions, and results in unnecessary costs. Patient education strategies should be used to inform patients about current and effective standards of care.
Consider Food Allergy Testing in Managing Eosinophilic Esophagitis
Food antigens can induce esophageal remodeling with fibrosis, which can resolve with appropriate food antigen elimination. Addressing food allergens in the treatment of eosinophilic esophagitis (EoE) is recommended and although allergy testing is common practice for pediatric gastroenterologists, many adult gastroenterologists are unfamiliar with the practice. A recently (online published) article provides in-depth guidance, including:
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Allergy testing for foods may be more useful in pediatric patients.
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The negative predictive values of tests for identifiable food allergies are generally higher than positive PVs.
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Patients with EoE are often highly atopic and have polysensitization to both food (particularly in children) and aeroallergens (particularly in adults).
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Ample evidence supports use of skin-prick or atopy-patch testing for building an elimination diet in children, but not in adults.
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Do not utilize food-specific panels using serum immunoglobulin E (or other immunoglobulins) in this setting.
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EoE recurs in >90% of pediatric patients after food reintroduction, and only 8% become tolerant of all their food triggers.
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Repeat endoscopic biopsy with histologic evaluation after sequential food reintroduction – do not rely on a positive test for food allergy.
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Consider the possibility of concurrent allergic diatheses in patients with EoE.
Studies recommend that one food or food group be introduced every 4 to 6 weeks with observation of clinical symptoms and a subsequent endoscopy if no change in symptoms occurs. A food trigger is identified based on the recurrence of symptoms and esophageal eosinophilia (≥15 eosinophils/high-power field) after reintroduction of a specific food group. Because patients typically have multiple food triggers, the process should be continued until all foods have been reintroduced into the diet or an acceptable diet is reached. Dieticians can play an important role in identifying possible cross-contamination of specific food items. Clearly, an integrated approach involving allergists, gastroenterologists, and pathologists is warranted in evaluating the possible role of food allergy in eosinophilic esophagitis.
http://www.cghjournal.org/article/S1542-3565(13)01302-5/fulltext
Achalasia
The current guidelines on the diagnosis and treatment of achalasia as published in the American Journal of Gastroenterology by the American College of Gastroenterology are summarized below.
Achalasia is an incurable disease with an incidence of 1/100,000 occurring equally among men and women. Achalasia is characterized by insufficient relaxation of the lower esophageal sphincter and loss of esophageal peristalsis, leading to difficulty in swallowing with dysphagia to solids and liquids, regurgitation, and occasional chest pain with or without weight loss. Achalasia is often misdiagnosed as gastroesophageal reflux disease (GERD). Achalasia must be suspected in those with dysphagia to solids and liquids and in those with regurgitation unresponsive to an adequate trial of proton pump inhibitor (PPI) therapy.
Endoscopic finding of retained saliva with a puckered gastroesophageal junction or a barium swallow showing a dilated esophagus with birds beaking in a symptomatic patient should prompt appropriate diagnostic and therapeutic strategies.
Graded pneumatic dilation or laparoscopic surgical myotomy with a partial fundoplication are recommended as initial therapy for the treatment of achalasia. Surgical myotomy has shown excellent results in most patients and remains the surgery of choice, with more being done laparoscopically. The benefit of adding a fundoplication was demonstrated and a cost–utility analysis found that myotomy plus fundoplication was more cost effective than myotomy alone. Retreatment of patients is likely required within 5 years; retreatment should be individualized based on local expertise.
The guidelines also call for follow-up for symptom relief and esophagus emptying results through use of barium esophagram. Endoscopy surveillance for esophageal cancer is not recommended.
DIAGNOSIS OF ACHALASIA
- All patients with suspected achalasia who do not have evidence of a mechanical obstruction on endoscopy or esophagogram should undergo esophageal motility testing before a diagnosis of achalasia can be confirmed.
- The diagnosis of achalasia is supported by esophagogram findings including dilation of the esophagus, a narrow esophago-gastric junction with “ bird-beak ” appearance, aperistalsis, and poor emptying of barium.
- Barium esophagogram is recommended to assess esophageal emptying and esophago-gastric junction morphology in those with equivocal motility testing.
- Endoscopic assessment of the gastroesophageal junction and gastric cardia is recommended in all patients with achalasia to rule out pseudoachalasia.
TAILORED APPROACH TO TREATING ACHALASIA
- Either graded pneumatic dilation (PD) or laparoscopic surgical myotomy with a partial fundoplication are recommended as initial therapy for the treatment of achalasia in those fit and willing to undergo surgery.
- PD and surgical myotomy should be performed in high-volume centers of excellence.
- The choice of initial therapy should be guided by patients’ age, gender, preference, and local institutional expertise.
- Botulinum toxin therapy is recommended in patients who are not good candidates for more definitive therapy with PD or surgical myotomy.
- Pharmacologic therapy for achalasia is recommended for patients who are unwilling or cannot undergo definitive treatment with either PD or surgical myotomy and have failed botulinum toxin therapy.
PATIENT FOLLOW-UP
- Patient follow-up after therapy may include assessment of both symptom relief and esophageal emptying by barium esophagogram.
- Surveillance endoscopy for esophageal cancer is not recommended.
In summary the new guidelines for diagnosis include:
- Performing an esophageal motility test on all patients suspected of having achalasia (the manometric findings of irregular muscle contractions and incomplete lower esophageal sphincter relaxation without mechanical obstruction establish the diagnosis of achalasia in the appropriate setting);
- Using esophagogram findings to support a diagnosis;
- Using an esophagogram for patients with equivocal motility testing;
- Using endoscopic assessment of the gastroesophageal junction and gastric cardia to rule out pseudoachalasia.
Treatment recommendations offer a tailored approach:
- Initial therapy should be either graded pneumatic dilation (PD) or laparoscopic surgical myotomy with a partial fundoplication in patients fit to undergo surgery;
- Procedures should be performed in high-volume centers of excellence;
- Initial therapy should be based on patient age, sex, preference, and local institutional expertise;
- Botulinum toxin therapy is recommended for patients not suited for PD or surgery;
- Pharmacologic therapy can be used for patients not undergoing PD or myotomy and who have failed botulinum toxin therapy (nitrates and calcium channel blockers are most commonly used).
Eosinophilic Esophagitis
The current clinical guidelines as published by the American College of Gastroenterology (ACG) on the diagnosis and management of Eosinophilic Esophagitis (EoE) are summarized below:
EoE is an increasingly recognized and prevalent condition and important cause of esophageal symptoms. It is presumed to result from eosinophilic activation to dietary antigens, which is limited to the esophagus. Inflammatory strictures, secondary dysmotility and resulting dysphagia are common problems. Current management includes food exclusion diets, swallowed topical steroids and proton pump inhibitors. Strictures may require endoscopic dilatation. Relapse is common and strategies for maintaining remission are being developed.
Definition and Causes of Esophageal Eosinophilia
- Esophageal eosinophilia, the finding of eosinophils in the squamous epithelium of the esophagus, is abnormal and the underlying cause should be identified.
- EoE is clinicopathologic disorder diagnosed by clinicians taking into consideration both clinical and pathologic information without either of these parameters interpreted in isolation, and defined by the following criteria:
- Symptoms related to esophageal dysfunction.
- Eosinophil-predominant inflammation on esophageal biopsy; peak value of ≥15 eosinophils per high-power field (eos/hpf).
- Mucosal eosinophilia is isolated to the esophagus and persists after a PPI trial.
- Secondary causes of esophageal eosinophilia excluded.
- A response to treatment (dietary elimination; topical corticosteroids) supports the diagnosis.
- Esophageal biopsies are required to diagnose EoE. 2-4 biopsies should be obtained from both the proximal and distal esophagus to maximize the likelihood of detecting esophageal eosinophilia in all patients in whom EoE is being considered.
- At the time of initial diagnosis, biopsies should be obtained from the antrum and/or duodenum to rule out other causes of esophageal eosinophilia in all children and in adults with gastric or small intestinal symptoms or endoscopic abnormalities.
Diagnostic Challenges: PPI-responsive esophageal eosinophilia and GERD
- Proton-pump inhibitor esophageal eosinophilia (PPI-REE) should be diagnosed when patients have esophageal symptoms and histologic findings of esophageal eosinophilia, but demonstrate symptomatic and histologic response to proton-pump inhibition.
- At this time, the entity is considered distinct from EoE, but not necessarily a manifestation of GERD.
- To exclude PPI-REE, patients with suspected EoE should be given a 2-month course of a PPI followed by endoscopy with biopsies.
- A clinical, endoscopic and/or histologic response to a PPI does not establish gastroesophageal reflux as the cause of esophageal eosinophilia. To determine whether reflux is contributing to esophageal eosinophilia, additional evaluation for GERD, as per standard clinical practice, is recommended. This may include ambulatory pH testing in selected cases.
Pharmacologic Treatments
- Topical steroids (i.e., fluticasone or budesonide, swallowed rather than inhaled, for an initial duration of 8 weeks) are a first-line pharmacologic therapy for treatment of EoE.
- Prednisone may be useful to treat EoE if topical steroids are not effective or in patients who require rapid improvement in symptoms. Patients without symptomatic and histologic improvement after topical steroids might benefit from a longer course of topical steroids, higher doses of topical steroids, systemic steroids, elimination diet, or esophageal dilation.
- There are few data to support the use of mast cell stabilizers or leukotriene inhibitors, and biologic therapies remain experimental at this time.
Fluticasone
- Children b 88 – 440 mcg / day in a divided dose
- Adults 880 – 1760 mcg / day in a divided dose
Budesonide
- Children 1 mg/day
- Adults 2 mg day, typically in a divided dose
Dietary Treatments
- Dietary elimination can be considered as an initial therapy in the treatment of EoE in both children and adults.
- The decision to use a specific dietary approach (elemental, empiric, or targeted elimination diet) should be tailored to individual patient needs and available resources.
- Clinical improvement and endoscopy with esophageal biopsy should be used to assess response to dietary treatment when food antigens are either being withdrawn from or reintroduced to the patient.
- Gastroenterologists should consider consultation with an allergist to identify and treat extraesophageal atopic conditions, assist with treatment of EoE, and to help guide elemental and elimination diets.
Strategies for Dietary Elimination
- Total elimination of all food allergens with elemental or amino-acid-based formula.
- Targeted elimination diet guided by allergy testing, typically skin prick testing or patch testing.
- Empiric six-food elimination diet: soy, egg, milk, wheat, nuts, and seafood.
- The duration of the treatment is usually 4-8 weeks, followed by a reintroduction period once remission has been achieved. One food or food group can be introduced every 2-4-6 weeks with observation of clinical symptoms and a subsequent endoscopy if no change in symptoms occur. A food trigger is identified based on the recurrence of symptoms and esophageal eosinophilia. Because patients typically have more than one food trigger, the process is continued until all foods have been added or an acceptable diet is reached. Patients who are treated with an elemental formula undergo a substantially longer reintroduction process. Once food triggers are identified, patients are advised to eliminate these agents from their diet completely.
Endoscopic Treatment
- Esophageal dilation may be used as an effective therapy in symptomatic patients with strictures that persist in spite of medical or dietary therapy. Patients should be well informed of the risks of esophageal dilation in EoE including post-dilation chest pain (up to 75% of patients), bleeding, and esophageal perforation.
Maintenance Therapy
- While knowledge of the natural history of EoE is limited, patients should be counseled about the high likelihood of symptom recurrence after discontinuing treatment due to the chronic nature of this disease.
- The overall goal of maintenance therapy is to minimize symptoms and prevent complications of EoE, preserve quality of life, with minimal long-term adverse effects of treatments.
- Maintenance therapy with topical steroids and/or dietary restriction should be considered for all patients, but particularly in those with severe dysphagia or food impaction, high-grade esophageal stricture and rapid symptomatic/histologic relapse following initial therapy.
- The endpoints of therapy of EoE include improvements in clinical symptoms and esophageal eosinophilic inflammation. While complete resolution of symptoms and pathology is an ideal endpoint, acceptance of a range of reductions in symptoms and histology is a more realistic and practical goal in clinical practice. Symptoms are an important parameter of response in EoE, but cannot be used alone as a reliable determinant of disease activity and response to therapy, given that compensatory dietary and lifestyle factors can mask symptoms.
Diseases Associated with Esophageal Eosinophilia
- Eosinophilic gastrointestinal diseases
- PPI-responsive esophageal eosinophilia
- Celiac disease
- Crohn’s disease
- Infection
- Hypereosinophilic syndrome
- Achalasia
- Drug hypersensitivity
- Vasculitis
- Pemphigus
- Connective tissue diseases
- Graft vs. host disease
- PPI, proton-pump inhibitor.
Proposed Classification/Grading System for the Endoscopic Assessment of Esophageal Features of EoE
Major features
Edema (decreased vascular markings, mucosal pallor)
- Grade 0: Absent. Distinct vascularity present
- Grade 1: Loss of clarity or absence of vascular markings
Fixed rings (concentric rings, corrugated esophagus, corrugated rings, ringed esophagus, trachealization)
- Grade 0: None
- Grade 1: Mild-subtle circumferential ridges
- Grade 2: Moderate-distinct rings that do not impair passage of a standard diagnostic adult endoscope (outer diameter 8 – 9.5 mm)
- Grade 3: Severe-distinct rings that do not permit passage of a diagnostic endoscope
Exudates (white spots, plaques)
- Grade 0: None
- Grade 1: Mild-lesions involving less than 10 % of the esophageal
- surface area
- Grade 2: Severe-lesions involving greater than 10 % of the esophagealsurface area
Furrows (vertical lines, longitudinal furrows)
- Grade 0: Absent
- Grade 1: Vertical lines present
Stricture
- Grade 0: Absent
- Grade 1: Present (specify estimated luminal diameter)
Minor features
Crepe paper esophagus (mucosal fragility or laceration upon passage of endoscope, not after esophageal dilation)
- Grade 0: Absent
- Grade 1: Present
Narrow-caliber esophagus (reduced luminal diameter of the majority of the tubular esophagus)
- Grade 0: Absent
- Grade 1: Present
Diagnosis And Management Of Gastroesophageal Reflux Disease
The current GERD diagnosis and treatment guidelines as published by the American College of Gastroenterology provide an overview of GERD, its presentation, and recommendations for the diagnosis and management of this important disease.
Diagnosis:
- Typical symptoms (i.e. heartburn, regurgitation) establish a diagnosis of GERD. Therefore empiric PPI therapy is reasonable.
- The diagnosis of non-cardiac chest pain (due to reflux) requires the exclusion of cardiac causes.
- Routine EGDs are not needed in classic GERD patients to establish a diagnosis of reflux, but are advised if alarm symptoms are reported (i.e. hematemesis, dysphagia, weight-loss, anemia etc.).
- Routine follow-up EGDs are not needed in patients without Barrett’s or new symptoms.
- pH- and/or impedance-monitoring are indicated before endoscopic or surgical therapy in NERD (non-erosive reflux) patients and those patients who fail conventional therapy.
Medical Treatment:
To help reduce reflux symptoms and treat the acid injury, several treatment strategies can be used:
- Weight loss, elevation of the head of bed, and avoidance of meals before bedtime are recommended.
- The routine recommendations of avoidance of trigger foods (i.e. chocolate, caffeine, alcohol, acidic or spicy foods) are no longer strongly supported.
- PPIs (proton-pump inhibitors) should be used for 8 weeks. PPIs (i.e. omeprazole (Prilosec or Zegerid), pantoprazole (Protonix), lanzoprazole (Prevacid), esomeprazole (Nexium), dexlansoprazole (Kapidex), rabeprazole (Aciphex) are all similar in effect. PPIs should be given 30-60 min before a meal, staring at a once a day morning dose; dose and timing adjustment are reasonable (i.e. increasing the dose, switching to another PPI) if poor response to daily dosing is noted.
- Long-term therapy is warranted in patients with recurrent symptoms after PPIs were discontinued, and with complicated disease i.e. erosive esophagitis, Barrett’s. Long-term therapy should be offered at the lowest possible dose.
- Nighttime H2 blockers can be used in patients with break through symptoms. H2 blockers may offer an effective alternative to PPIs in patients without erosive disease. But are usually not as effective.
- Therapy for GERD other than acid suppression, including prokinetic therapy and/or baclofen, should not be used without prior diagnostic evaluation.
- There is no role for sucralfate (Carafate) in the non-pregnant GERD patient. PPIs are safe in pregnant patients if clinically indicated (UGs personal comment: omeprazole is a category C drug and should be avoided).
Surgical Options:
For those who fail medical therapy and life style modifications, surgery (a Nissen fundoplication) may be a viable option but should be discussed with the treating physician.
- Surgical therapy is generally not recommended in patients who do not respond to PPI therapy (UGs personal comment: possible exceptions to this rule must be carefully reviewed with the treating physician).
- Preoperative ambulatory pH monitoring is mandatory in patients without evidence of erosive esophagitis.
- All patients should undergo preoperative manometry to rule out achalasia or scleroderma-like esophagus.
- Surgical therapy equally effective when compared to medical therapy in patients with chronic GERD when performed by an experienced surgeon.
- Obese patients contemplating surgical therapy for GERD should be considered for bariatric surgery. Gastric bypass would be the preferred operation in these patients.
- Currently the usage of current endoscopic therapy or transoral incisionless fundoplication cannot be recommended as an alternative to medical or traditional surgical therapy.
Potential Risks of PPIs:
- Patients with known osteoporosis can remain on PPI therapy. Concern for hip fractures and osteoporosis should not affect the decision to use PPI long-term except in patients with other risk factors for hip fracture.
- PPI therapy can be a risk factor for Clostridium difficile infection; use with care in patients at risk.
- Short-term PPI usage may increase the risk of community-acquired pneumonia. The risk does not appear elevated in long-term users.
- PPI therapy does not need stopped in clopidogrel (Plavx) users as there does not appear to be an increased risk for adverse cardiovascular events.
Atypical Reflux Presentations:
While GERD can be a potential factor in patients with asthma, chronic cough, or laryngitis, careful evaluation for non-GERD causes should be undertaken.
A diagnosis of reflux laryngitis should not be made based upon laryngoscopy findings. (… as often suggested by ENT physicians – UG personal comment).
- A PPI trial is recommended to treat extraesophageal symptoms in patients who also have typical symptoms of GERD.
- Upper endoscopy is not recommended as a means to establish a diagnosis of GERD-related asthma, chronic cough, or laryngitis. (UG personal comment: … unless other reasons warrant an EGD or a BRAVO pH monitoring system is placed).
- Reflux monitoring should be considered before a PPI trial in patients with extraesophageal symptoms who do not have typical symptoms of GERD.
- Non-responders to a PPI trial should be considered for further diagnostic testing and are addressed in the refractory GERD section below.
- Surgery should generally not be performed to treat extraesophageal symptoms of GERD in patients who do not respond to acid suppression with a PPI.
Refractory GERD:
The first step in management of refractory GERD is optimization of PPI therapy. Upper endoscopy should be performed in refractory patients with typical or dyspeptic symptoms .
- In patients in whom extraesophageal symptoms of GERD persist despite PPI optimization, assessment for other etiologies should be pursued through concomitant evaluation by ENT, pulmonary, and allergy specialists.
- Patients with refractory GERD and negative evaluation by endoscopy (typical symptoms) or evaluation by ENT, pulmonary, and allergy specialists (extraesophageal symptoms), should undergo ambulatory reflux monitoring.
- Reflux monitoring off medication can be performed by any available modality (pH or impedance-pH). Testing on medication should be performed with impedance-pH monitoring in order to enable measurement of nonacid reflux.
- Refractory patients with objective evidence of ongoing reflux as the cause of symptoms should be considered for additional antireflux therapies, which may include surgery. Patients with negative testing are unlikely to have GERD and PPI therapy should be discontinued.
Complications Associated with GERD:
Complications of GERD include esophageal strictures, Barrett’s metaplasia, or bleeding. The Los Angeles (LA) classification system should be used when describing the endoscopic appearance of erosive esophagitis.
- Grade A: One (or more) mucosal break no longer than 5 mm, that does not extend between the tops of two mucosal folds (a mucosal break being defined as an area of slough or erythema with discrete demarcation from the adjacent mucosa).
- Grade B: One (or more) mucosal break more than 5 mm long that does not extend between the tops of two mucosal folds.
- Grade C: One (or more) mucosal break that is continuous between the tops of two or more mucosal folds but which involves less than 75% of the circumference.
- Grade D: One (or more) mucosal break which involves at least 75% of the esophageal circumference.
Patients with LA Grade A esophagitis should undergo further testing to confirm the presence of GERD. If severe reflux injury is encountered during an EGD, a repeat endoscopy should be performed e after a course of therapy to exclude underlying Barrett’s esophagus. Continuous PPI therapy is recommended following peptic stricture dilation to improve dysphagia and reduce the need for repeated dilations. Injection of intra-lesional corticosteroids can be used in refractory, complex strictures due to GERD. Treatment with a PPI is suggested following dilation in patients with lower esophageal (Schatzki) rings. Screening for Barrett’s esophagus should be considered in patients with GERD at high risk based on epidemiologic profile (See the UG Barrett’s article).
Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol 2013; 108:308–328
Gastro-Esophageal Reflux Disease (GERD)
GERD, more commonly referred to as heartburn, occurs when acidic contents in the stomach flow back into the food pipe (esophagus). This phenomenon occurs because the valve between the stomach and the esophagus (the lower esophageal sphincter) inappropriately relaxes, allowing acid to travel back into the esophagus.
What are symptoms of GERD?
Heartburn and acid indigestion are the most common symptoms. However, when acid bathes the esophagus, the problem can manifest as other less-classic symptoms. These can include a sour or bitter taste in the mouth, involuntary regurgitation of food or fluid into the mouth, hoarseness, sore throat or the need to clear the throat, dental erosions, wheezing, dental erosions, or unexplained cough.
What causes GERD?
Temporary relaxation of the lower esophageal sphincter, which allows the backflow of stomach acid into the esophagus, is influenced by a variety of conditions. Large meals as well as certain foods contribute to these episodic relaxations. Obesity, tight clothing around the waist and pregnancy can also contribute by increasing pressure in the abdomen, which can allow acid to overcome the barrier between the stomach and the esophagus. Smoking, excessive alcohol use, and hiatal hernias can also induce GERD.
What harm can occur?
The stomach has a tough lining that is made to resist acid, but the esophagus does not. Thus, the most common complication of heartburn is esophagitis, or inflammation of the esophagus, which can cause ulcers or bleeding. Sometimes the inflammation can lead to scarring or narrowing of the esophagus. Pre-malignant changes, which can progress to cancer, can occur due to changes in the cells that line the esophagus. This is commonly referred to as Barrett’s esophagus and should be followed closely to ensure cancer does not develop.
How do you treat GERD?
The first step in treating GERD is dietary and lifestyle modification. Avoid fatty or spicy foods, tomato-based products, citrus drinks, chocolate, coffee, and peppermint. It is also recommended to eat smaller meals, lose weight, stop smoking, and abstain from alcohol. Nighttime symptoms can be improved by not eating within three hours of sleeping, or propping up the head of the bed. If symptoms persist, then over-the-counter antacids can help for a short period of time. More potent prescription medications can also be used under the direction of your doctor. Surgery is an option for patients who don’t respond fully to medical therapy or for those with severe GERD.
When should I see a doctor about GERD?
See a doctor if your classic symptoms are not controlled with dietary and lifestyle modifications or if you are using over-the-counter medications more than twice a week. You should seek immediate medical attention if you have chest pain, unexplained weight loss, food that sticks in your chest after swallowing, bloody vomit, or black, tarry bowel movements.
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