Alterations of the upper esophageal sphincter (UES) are frequently reported in patients with esophageal achalasia and appear to relate to the degree of esophageal pressurization and impaired bolus transit. Several retrospective and short-term series suggest that POEM, while targeted to the lower esophageal sphincter (LES), may also change proximal esophageal motility and reduce UES resting and residual pressures with symptom improvement.  

The aim of the study was to prospectively quantify UES structural/functional abnormalities in treatment-naïve achalasia patients, and to determine the long-term effects of POEM on UES metrics, proximal esophageal motility, and relevant clinical outcomes (dysphagia, regurgitation, cough, aspiration risk).

Study design: single-center prospective observational cohort.

Population: consecutive adult patients with manometrically confirmed achalasia (Chicago Classification v4.0) scheduled for primary POEM.

Assessments and timing: High-resolution manometry (HRM) with standardized UES protocol (resting pressure, residual pressure during wet swallows), at baseline and 12 months post-POEM. 

Symptom scores: Eckardt score at baseline and 12 months after POEM

Primary endpoint: change in UES basal and residual pressure (pre- to 12 month post-POEM) 1) evaluation of changes in UES pressures before and after POEM; 2) correlation between Eckradt score and changes in UES pressures.

Secondary endpoints: try to obtain a cut-off value of UES change and symptom improvement (Eckardt score) after POEM; define risk factors to residual UES dysfunction.

Out of 179 patients from 2019 to 2024, 27 were selected for the present study. 152 have missing data needed to obtain primary and secondary outcomes or were affected by other esophageal motility disorders. Three patients had achalasia type I with mean UES basal pressure 51,5 mmHg with mean residual pressure 9,3 mmHg.  After POEM, these patients had mean UES basal pressure 86,7 mmHg and UES residual pressure 10,7 mmHg.

Eckardt score generally decreased in these patients with a mean 7 before and a mean 2 after POEM.

22 patients had type II achalasia with mean UES basal pressure 75,1 mmHg and residual pressure 17,7 mmHg. After POEM, mean UES basal pressure became 66,9 mmHg and residual pressure 9,5 mmHg. Eckardt score generally decreased also in this group with a mean value of 8 before and a mean value of 1 after POEM.

The remaining two patients had type III achalasia with a mean UES basal pressure 45,8 mmHg and residual pressure 6,4 mmHg. After POEM, mean UES basal pressure and residual pressure were reported respectively 52,6 mmHg and 2,8 mmHg.

Eckardt score decreased in both cases from a mean of 8,5 to a mean of 1 after POEM.

Although in type I and III significant correlations cannot be found due to the small number of patients, in type II patients>65 years tend to have lesser post-POEM UES pressures decrease (mean pre-POEM UES basal 45,5 mmHg residual 15,3 mmHg vs post-POEM UES basal 42,2 mmHg residual 10,3 mmHg).

Furthermore, higher post-POEM UES residual pressure >12 mmHg was related to higher Eckardt score that points to a role of UES pressure on dysphagic symptoms (mean post-POEM Eckardt score 3 vs mean post-POEM Eckardt score 1,2).

Our prospective, standardized evaluation of UES metrics before and after POEM evidenced the prevalence and mechanisms of proximal sphincter dysfunction in achalasia, define the UES recovery after LES myotomy especially in achalasia type II, and identify older age and post-POEM UES residual pressure>12mmHg as risks for persistent symptoms.