Deciphering Dysphagia in Clinical Practice:

Alexander T. Reddy, MD

Assistant Professor of Medicine
Division of Gastroenterology
Duke University School of Medicine
Durham, North Carolina

Amit Patel, MD, AGAF, FACG

Professor of Medicine
Division of Gastroenterology
Duke University School of Medicine & Durham Veterans Affairs Medical Center
Durham, North Carolina

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Dysphagia, the sensation of difficulty swallowing, may be experienced by up to 1 in 6 adults in the United States, according to population-based survey data,^1,2 and is frequently encountered in gastroenterology clinical practice. Esophageal dysphagia may stem from various disease states, so discerning among potential etiologies is critical to facilitate effective, patient-tailored management. The initial evaluation of dysphagia should include a careful clinical history and physical exam, followed by consideration of diagnostic investigations, as appropriate.

Clinicians typically should pursue upper endoscopy with consideration of esophageal biopsies as a first step for esophageal-phase dysphagia.³ Additional physiologic testing such as high-resolution esophageal manometry (HRM) with provocative maneuvers,^4,5 functional lumen imaging probe (FLIP) panometry,^6,7 and/or a barium esophagram (typically as a timed upright barium esophagram)⁸ may be used for further assessment based on the clinical context and endoscopic findings. Here, we present 3 hypothetical cases that illustrate practical approaches to clinical presentations of esophageal dysphagia, highlighting the use of modern diagnostic and therapeutic options.

Case 1

A 30-year-old man with a history of asthma was referred for 2 years of intermittent dysphagia to solids. His symptoms occurred several times weekly, particularly with meats, and were localized retrosternally. He had not used any pharmacotherapy to manage his symptoms. His physical exam was unremarkable, and upper endoscopy revealed esophageal edema (decreased vascularity), mild rings, exudates, and longitudinal furrows (Figure 1A; Eosinophilic Esophagitis [EoE] Endoscopic Reference Score [EREFS] of E1R1Ex1F2S0 [edema = 1, rings = 1, exudates = 1, furrows = 2, and strictures = 0]).^9,10 Biopsies from the upper and lower esophagus revealed peak eosinophil counts of 50 and 40 eosinophils per high-power field, respectively.

Diagnosis: EoE

EoE is a chronic allergen-induced, immune- mediated disease of the esophagus resulting in symptoms of esophageal dysfunction, particularly dysphagia in adults.¹¹ The clinicopathologic diagnosis requires compatible esophageal symptoms along with an eosinophil-predominant infiltrate on histologic assessment of endoscopic biopsies, with peak eosinophil counts of at least 15 eosinophils per high-power field.¹¹ Clinicians should exclude alternate etiologies for esophageal eosinophilia (eg, gastroesophageal reflux disease [GERD], medication adverse effects, infection, achalasia, and hypereosinophilic syndrome) before making a diagnosis of EoE.

Scoring tools such as the EREFS at endoscopic evaluation, as above,^9,10 and the Index of Severity for EoE¹² facilitate the standardization and systematic reporting of disease severity. Although the recognition and diagnosis of EoE have increased rapidly in recent decades,¹³ endoscopic findings of EoE may be subtle and/or overlooked, potentially contributing to diagnostic delay.¹⁴ Therefore, at least 2 to 4 esophageal biopsies from at least 2 levels of the esophagus should be pursued in all patents with symptoms suspicious for EoE, including at the time of food impaction.^10,11,15

Management

After a discussion of potential dietary and pharmacologic management options for EoE, the patient opted for 40 mg of omeprazole twice daily. Repeat endoscopy 2 months later demonstrated no improvement either endoscopically (based on EREFS) or histologically (based on peak eosinophil counts on esophageal biopsies).

The patient then opted to switch to swallowed fluticasone (220 mcg at 4 puffs twice daily; total daily dose, 1,760 mcg). Evaluation after 2 months of adherence with fluticasone again demonstrated no significant improvement in his symptoms, EREFS, or peak eosinophil counts on esophageal biopsies. Based on his lack of response with proton pump inhibitor (PPI) and topical corticosteroid therapy, along with shared decision-making regarding his strong preference to avoid dietary elimination approaches, the patient started 300 mg of dupilumab (Dupixent, Regeneron/Sanofi) weekly. When evaluated 3 months after starting dupilumab, the patient reported resolution of dysphagia. His previous endoscopic findings of EoE had normalized, and no eosinophils were present on upper and lower esophageal biopsies (Figure 1B). Given dupilumab’s effectiveness, the patient opted to continue on it as maintenance therapy.

For the management of EoE, clinicians should focus on both inflammatory and potential fibrostenotic aspects to improve patient symptoms and minimize complications such as food impaction, stricture formation, and esophageal perforation.¹¹ Anti-inflammatory treatment options include strategic dietary elimination,¹⁶ PPIs, topical steroids (ie, budesonide or fluticasone formulations), and dupilumab.¹⁷

Dupilumab, approved for EoE by the FDA in May 2022, is a monoclonal antibody that blocks the effects of interleukin (IL)-4 and IL-13 involved in the type 2 inflammatory cascade.¹¹ Given limited head-to-head clinical trial data among the anti-inflammatory options, individual disease characteristics and patient preferences via shared decision-making should guide treatment selection.¹⁸

Strategies for optimizing management include counseling on the risks and benefits of treatment options, consultation with gastroenterology-trained nutritionists when pursuing food elimination diets, and structured, timely assessment of response after initiating therapy. A willingness to pursue alternative therapies if indicated, as demonstrated in this case, is crucial. Beyond its use in patients with EoE who are nonresponsive to or intolerant of other therapies, dupilumab can be considered earlier in the management algorithm when a patient has concomitant atopic conditions that also could be treated with dupilumab.¹⁹ Endoscopic dilation as an adjunct to anti-inflammatory approaches can be safely used to treat fibrostenotic features of EoE, including strictures and luminal narrowing. Finally, maintaining effective dietary or pharmacologic therapy can help prevent histologic inflammation and symptom recurrence.¹¹

Case 2

A 55-year-old woman with a history of hypertension was referred for 2 years of progressively worsening dysphagia to solids and liquids, with regurgitation, which now is happening on a daily basis. One year prior, she was evaluated by an outside provider with an unrevealing upper endoscopy and esophageal biopsies. The patient had been taking omeprazole for several months without symptom benefit. Esophageal HRM was discussed and pursued, which revealed 100% failed peristalsis with panesophageal pressurization on single wet swallows and an elevated median integrated relaxation pressure (IRP) of 30 mm Hg in the primary supine position (Figure 2A).

Diagnosis: Type II Achalasia

Achalasia is an esophageal motility disorder characterized by abnormal esophageal peristalsis and incomplete relaxation of the lower esophageal sphincter, classically defined by an abnormally elevated median IRP on esophageal HRM.^4,20 Thresholds for abnormal IRP vary based on patient position and HRM equipment manufacturer. Threshold values are 15 mm Hg in the supine position and 12 mm Hg in the upright position for Medtronic HRM systems, and 22 mm Hg in the supine position and 15 mm Hg in the upright position for the Diversatek and Laborie HRM systems.^4,21

Achalasia is classified into 3 types based on peristaltic patterns at HRM, which can help guide prognosis and therapeutic interventions: Type I achalasia consists of 100% failed peristalsis without evidence of panesophageal pressurization, type II achalasia demonstrates 100% failed peristalsis with panesophageal pressurization in 20% or more of swallows, and type III achalasia is characterized by premature contraction in 20% or more of swallows without evidence of peristalsis.^4,20 Patients who are initially suspected of having GERD but who do not respond to acid-suppressive therapy should be evaluated for achalasia.^20,22

Management

Due to worsening symptoms, the patient underwent upper endoscopy with FLIP, which revealed an American Foregut Society hiatus grade 1 with no mechanical obstruction. FLIP assessment revealed an esophagogastric junction-distensibility index (EGJ-DI) of 0.6 mm²/mm Hg at a 60-mL fill volume and a maximum EGJ diameter of 8 mm at a 70-mL fill volume, consistent with a reduced EGJ opening (REO), and no esophageal body contractile response (Figure 2B).

After discussion of treatment options based on her symptoms and diagnostic findings, the patient opted for per-oral endoscopic myotomy (POEM). At follow-up, she reported resolution of dysphagia and regurgitation symptoms off omeprazole. Surveillance endoscopy with FLIP and wireless pH monitoring 6 months after POEM revealed no reflux esophagitis, an EGJ-DI of 3 mm²/mm Hg with an EGJ diameter of 18 mm, and physiologic esophageal acid exposure times (AETs) less than 4% on all 4 days of the pH study.

In a workup of suspected achalasia, a high-quality endoscopic exam should exclude the presence of pseudoachalasia or other causes of mechanical obstruction. Particularly in the setting of diagnostic uncertainty (eg, manometric EGJ outflow obstruction, borderline IRP, abnormal provocative maneuvers at HRM), evaluation with FLIP and/or a timed upright barium esophagram can be helpful in evaluation, as well as to increase confidence in an actionable diagnosis.^8,20

FLIP is increasingly recognized as a useful tool for esophageal motility evaluation and should be considered if alternate investigations for dysphagia are inconclusive; it may even be considered as part of index endoscopy when the procedure and expertise are readily available.^7,23 As per new consensus and American Gastroenterological Association Clinical Practice Update guidance, an EGJ-DI less than 2.0 mm²/mm Hg and maximum EGJ diameter less than 12 mm on FLIP are classified as REO (as in this case), while a normal EGJ opening (EGJ-DI =2.0 mm²/mm Hg and maximum EGJ diameter =16 mm) has a high negative predictive value for achalasia spectrum disorders on HRM.^6,7

For the management of achalasia, definitive therapies with well-established clinical benefit include pneumatic dilation, surgical laparoscopic Heller myotomy (LHM) accompanied by partial fundoplication to help prevent GERD, and POEM. All 3 approaches are comparable and may be considered reasonable options for types I and II achalasia, with selection guided by individual patient characteristics, local expertise, discussions of potential risks and outcomes (eg, POEM may be associated with GERD), and shared decision-making.^20,24 POEM is the preferred treatment for type III achalasia, given the potential to tailor the myotomy to the spastic segment of the esophageal body.^20,25,26 A botulinum toxin injection typically should be reserved for patients who are not candidates for the more definitive therapies described above.²⁰ When available, intra-procedural FLIP during myotomy, whether POEM or LHM, may be helpful in tailoring or guiding the adequacy of disruption to the lower esophageal sphincter.²⁶ Finally, patients who undergo POEM should be monitored for GERD, with treatment offered as appropriate.²⁶

Case 3

A 50-year-old man with a history of obesity and diabetes mellitus was referred for endoscopy after experiencing 3 months of dysphagia to solids. He reported long-standing heartburn and regurgitation, for which he took over-the-counter antacids on an as-needed basis. Upper endoscopy revealed Los Angeles Grade D esophagitis with luminal narrowing at the EGJ (Figure 3A). He was started on 40 mg of omeprazole twice daily with plans for repeat upper endoscopy.

Diagnosis: Erosive Esophagitis (EE) And Peptic Stenosis

GERD is a common condition in which refluxate of acidic contents from the stomach into the esophagus results in bothersome symptoms (commonly heartburn, regurgitation, and noncardiac chest pain). While these typical symptoms in the absence of alarm symptoms can prompt a 4- to 8-week trial of PPI therapy with assessment of response,²⁷ GERD can lead to the formation of peptic strictures, mechanical narrowing that can cause dysphagia. Per the updated Lyon Consensus, the presence of LA Grades B/C/D EE, peptic stricture, and/or biopsy-proven Barrett’s esophagus represent conclusive evidence for a diagnosis of GERD (as in this case).²⁸

If these findings are not present on endoscopy, a diagnosis of GERD may be established with ambulatory reflux monitoring, with distal esophageal AETs more than 6% indicating the presence of pathologic GERD.^27,28 If ambulatory reflux monitoring is inconclusive based on AET, then adjunctive evidence such as numbers of reflux episodes, reflux symptom association, and mean nocturnal baseline impedance may support a diagnosis of GERD.^29-31 A personalized approach to management is warranted, with further evaluation and/or escalation of anti-reflux therapy, including invasive anti-reflux interventions, pursued thoughtfully with shared decision-making.^27,32,33

Management

The patient returned for follow-up endoscopy 2 months later on 40 mg of omeprazole twice daily. Although he reported partial improvement in his dysphagia, upper endoscopy demonstrated LA Grade C esophagitis and ongoing luminal narrowing at the EGJ. Given persistent and severe EE and stricture despite adherence with a high dose of omeprazole, the patient was switched to 20 mg of vonoprazan (Voquezna, Phathom) daily. After 1 month of vonoprazan therapy, upper endoscopy revealed resolution of his reflux esophagitis (Figure 3B).

Across 2 endoscopies, the patient’s peptic stricture was successfully dilated to a diameter of 18 mm using through-the-scope balloon dilators (Figure 3C). He reported resolution of his dysphagia and reflux symptoms at follow-up.

In the setting of EE, optimized antisecretory therapy facilitates healing and can be followed by repeat upper endoscopy to document healing and exclude the presence of Barrett’s esophagus.³⁴ High-dose PPIs are most commonly used as first-line therapy for the healing of EE given their effectiveness, accessibility, safety profile, and cost.²⁷ However, potassium-competitive acid blockers (P-CABs) such as vonoprazan, which received FDA approval for EE in November 2023, are a newer class of antisecretory medications that can provide more potent acid inhibition than PPI formulations, with faster onset of action and longer duration of effect and without premeal dosing requirements.^35,36

Although P-CABs currently are less accessible and more costly than PPIs in the United States, they may be superior to PPIs for the healing and maintenance of healing of more severe (LA Grades C/D) EE and may be associated with more rapid healing.^36,37 Beyond representing an effective therapeutic option for patients with more severe EE and those with documented reflux who fail twice-daily PPI therapy (as in this case), the rapid onset of acid inhibition of P-CABs raises their potential utility as on-demand therapy for reflux-related symptoms.^36,38

For peptic strictures, endoscopic dilation, whether employing balloon or bougie techniques, is safe and effective.^39,40

Conclusion

Through these representative hypothetical cases, we have outlined practical approaches to the evaluation of esophageal dysphagia and the basic management of EoE, achalasia, and reflux esophagitis with peptic stenosis, incorporating clinical pearls and more recent esophageal diagnostic and therapeutic advances, such as dupilumab, FLIP, POEM, and vonoprazan. As demonstrated through these cases, we are fortunate as gastroenterology providers to be able to thoughtfully evaluate our patients with dysphagia with the assistance of insightful diagnostic modalities and also, when indicated, treat our patients with a growing arsenal of effective, patient-tailored management options.

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