J Neurogastroenterol Motil 2024; 30(4): 517-519  https://doi.org/10.5056/jnm24088
Opioid-induced Esophageal Dysfunction Masquerading as Type I Achalasia
Andrew Leopold,1* Nicol Tugarinov,2 and Guofeng Xie1,3
1Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; 2Department of Internal Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; and 3Division of Gastroenterology and Hepatology, VA Maryland Healthcare System, Baltimore, MD, USA
Published online: October 30, 2024
© The Korean Society of Neurogastroenterology and Motility. All rights reserved.

cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background

Opioid induced esophageal dysfunction (OIED) is an esophageal motility disorder defined by symptoms of dysphagia or chest pain with abnormal manometric testing in the setting of at least 3 months of daily opioid use.1,2 Findings of distal esophageal spasm, type III achalasia, esophagogastric junction (EGJ) outflow obstruction, and hypercontractile esophagus on high-resolution esophageal manometry (HREM) are required to diagnose OIED. The mechanism of OIED is elusive, but thought to be through the nitric oxide pathway, which inhibits lower esophageal sphincter (LES) relaxation.3 A prior study suggested that patients with achalasia and chronic opioid use respond less reliably to endoscopic treatment, but patients with type I achalasia (T1A) were not identified.4 The consensus approach to OIED is opiate cessation, repeat symptom evaluation, and repeat HREM, but it is recognized that opiate cessation may be challenging.5

Case Report

A 49-year-old male with a history of opioid use disorder in remission on buprenorphine presented with solid and liquid dysphagia. His Eckardt Score (ES) was 6. Esophagogastric duodenoscopy was normal. Barium esophagram (BE) showed EGJ narrowing with contrast stasis (Fig. 1A). HREM (Diversatek, Milwaukee, WI, USA) suggested T1A, with a high integrated relaxation pressure and absent peristalsis (Fig. 1B). Integrated relaxation pressure could not be quantified because the catheter could not traverse the LES. Endoluminal functional lumen imaging probe (EndoFLIP) (Medtronic, Minneapolis, MN, USA) was consistent with T1A; findings were reduced EGJ opening with a weak contractile response. (Fig. 1C).

Figure 1. Barium esophagram, high-resolution esophageal manometry (HREM), and endoluminal functional lumen imaging probe (EndoFLIP) prior to buprenorphine cessation. (A) The barium esophagram shows a narrowing at the gastroesophageal junction with delayed contrast emptying of the esophagus. (B) HREM shows absent esophageal body peristalsis, and a suggestion of elevated integrated relaxation pressure, which could not be quantified due to the inability of the HREM catheter to traverse the lower esophageal sphincter (LES). (C) EndoFLIP demonstrates a low median distensibility index of 0.83 at a maximum diameter of 5.7, with a classification of reduced esophagogastric junction (EGJ) opening and weak contractile response.8,9

Buprenorphine tapering was recommended. Three months after initial presentation, his buprenorphine dose was 4 mg daily, and his Eckardt score improved to 3. He underwent an esophagogastric duodenoscopy with LES botulinum toxin (Botox) injection, with no clinical response by ES 1 month post-operatively.

The patient stopped buprenorphine use 6 months after initial presentation, resulting in symptom resolution (ES of 0). Repeat BE demonstrated prompt esophageal barium passage (Fig. 2A). Repeat HREM (Diversatek) was normal (Fig. 2B). He remains asymptomatic 2 years later.

Figure 2. Barium esophagram and high-resolution esophageal manometry (HREM) 1 year after cessation of buprenorphine. (A) The barium esophagram demonstrated normal contrast emptying. (B) The HREM was normal, with integrated relaxation pressure of 15 mmHg (normal ≤ 20 with Diversatek’s ZVU). UES, upper esophageal sphincter; LES, lower esophageal sphincter; EGJ, esophagogastric junction.
Discussion

OIED is characterized by dysphagia or chest pain, accompanied by specific, but heterogeneous manometric findings, in the setting of more than 3 months of daily opioid use.1,2,5 We describe, for the first time, a case of a patient with OIED masquerading as T1A in the setting of chronic opioid use, successfully managed with opioid medication cessation.

This patient did not have a definitive manometric diagnosis of T1A, as the HREM catheter could not traverse the LES. The association of achalasia and LES traversal failure has been previously described.6,7 T1A suspicion was confirmed on EndoFLIP showing reduced EGJ opening with weak contractile response, and contrast stasis on BE.8-10 The mechanism of a T1A pattern resulting from OIED is unclear, but may result from the use of buprenorphine, which has a high potency at a 30:1 morphine milliequivalent ratio. This patient’s buprenorphine dose was 240 morphine milliequivalents daily.

LES Botox injection was attempted to determine the patient’s myotomy candidacy. Despite decrementing buprenorphine doses yielding symptomatic improvement, there was doubt that this was OIED, as T1A patterns in OIED had not yet been described. A study evaluating patients with achalasia and chronic opiate use found chronic opiate use was a predictor of failed treatment response to LES Botox injection.4 This patient’s LES Botox injection failure, evaluated after 30 days, supported OIED diagnosis, leading to management concordant with that of OIED. He was successfully treated with complete buprenorphine tapering.

We describe a case of OIED disguised as T1A, refractory to Botox injection, whose symptoms and manometric findings normalized after cessation of chronic opioid medication. Our case report adds T1A to the heterogenous motility disorders associated with OIED that should be treated with chronic opioid medication cessation.

Financial support

Andrew Leopold was supported by the US National institutes of Health (Grant No. T32 DK067872-19).

Conflicts of interest

None.

Author contributions

Andrew Leopold: designed the study, reviewed the case, interpreted the case, drafted the manuscript, revised the manuscript critically for important intellectual content, approved the final version of the manuscript, and agrees to be accountable for all aspects of the work; Nicol Turginov: reviewed the case, interpreted the case, drafted the manuscript, revised the manuscript critically for important intellectual content, approved the final version of the manuscript, and agrees to be accountable for all aspects of the work; and Guofeng Xie: designed the study, reviewed the case, interpreted the case, revised the manuscript critically for important intellectual content, approved the final version of the manuscript, and agrees to be accountable for all aspects of the work.

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