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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
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).
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.
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.
Andrew Leopold was supported by the US National institutes of Health (Grant No. T32 DK067872-19).
None.
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.