Outcomes of Treatment for Achalasia Depend on Manometric Subtype

Wout O. Rohof; Renato Salvador; Vito Annese; Stanislas Bruley Des Varannes; Stanislas Chaussade; Mario Costantini; J. Ignasi Elizalde; Marianne Gaudric; André J. Smout; Jan Tack; Olivier R. Busch; Giovanni Zaninotto; Guy E. Boeckxstaens

Disclosures

Gastroenterology. 2013;144(4):718-725. 

In This Article

Results

Patient Characteristics

In the present study, pretreatment manometries of 176 patients were available for analyses. Data from 25 patients (12%) could not be retrieved because of a change of recording system without a back-up (n = 10), inaccessible data files (n = 4), and because 2 centers did not participate in this substudy (n = 11).

Of the 176 patients included, 44 patients (25%) had achalasia type I, 114 patients (65%) had achalasia type II, and 18 patients (10%) had achalasia type III. No statistically significant differences in age and sex were observed between the 3 patient groups. Patients were distributed equally over the 2 treatment protocols (Table 1).

Pretreatment Eckhardt symptom scores were similar for all types, with mean values of 7.3 ± 0.3, 7.1 ± 0.2, and 7.4 ± 0.5 for types I, II, and II, respectively. Type III achalasia patients had a significantly higher median chest pain score of 2 (IQR, 1–2) compared with type I achalasia patients (median, 1; IQR, 1–1; P = .03) and type II achalasia patients (median, 1; IQR, 0–1; P < .01). Other symptoms (dysphagia, regurgitation, and weight loss) were similar in the 3 treatment groups.

Before treatment, LES pressure and the height of the barium column (assessed after 5 minutes) were comparable in the 3 treatment groups (Figure 2). The mean amplitude measured by the pressure sensors in the distal esophagus during wet swallows was higher in type III achalasia, compared with type I (P < .001) and type II (P < .001). Finally, esophageal width was significantly larger in type I patients (4.5 ± 0.23 cm) compared with type II (4.0 ± 0.12 cm; P = .02) and type III patients (3.1 ± 0.30 cm; P < .001).

Figure 2.

(A) Esophageal stasis, (B) LES pressure, and (C) esophageal width are shown for types I, II, and III before and after treatment. Data are presented as mean ± standard error of the mean and tested between the 3 subtypes before and after therapy separately, using a one-way ANOVA with a post hoc Student t test with Bonferroni correction in case of statistically significant differences. *P < .05, **P < .01, and ***P < .001.

Treatment Success

Irrespective of treatment arm, success rate after a mean follow-up period of 43 months (IQR, 29–62 mo) was significantly higher in patients with type II compared with type I (P < .01, log-rank) and type III (P < .001, log-rank) (Figure 3). After 2 years of follow-up evaluation, the success rates were 81%, 96%, and 66% for types I, II, and III, respectively. In comparison with type II, type I (hazard ratio, 4.0; 95% confidence interval, 1.5–11) and type III (hazard ratio, 6.8; 95% confidence interval, 2.3–20) were highly predictive of treatment failure in a Cox regression analysis model.

Figure 3.

Type II achalasia has a higher success rate compared with type I achalasia (P < .01) and type III achalasia (P < .001), as shown in a Kaplan–Meier curve.

Subsequently, we compared treatment success rates of PD with that of LHM for the different manometric subtypes. For type I, no significant difference in success rate between PD (n = 22) and LHM (n = 22) was observed at the end of the entire follow-up period (mean, 43 mo; P = .84, log-rank) or after 2 years (81% vs 85% for LHM and PD, respectively) (Figure 4). In contrast, in type II, the success rate for PD (n = 53) was significantly higher than that of LHM (n = 61) (P = .03, log-rank), with 100% treatment success in the PD group, compared with 93% in the LHM group after 2 years (Figure 4). To achieve this success rate, 7 patients (13%) in the PD group needed redilation. The largest difference in success rates was observed in type III, with success rates of 86% and 40% for LHM (n = 8) and PD (n = 10), respectively (Figure 4). However, because of the low number of patients in this subgroup, this difference was not statistically significant (P = .12, log-rank).

Figure 4.

Kaplan–Meier curves comparing PD and LHM are shown for the 3 subtypes for up to 60 months after treatment. Success rates are comparable in type I achalasia (P = .84). Pneumodilation has a significantly higher success rate in type II achalasia (P = .03). Success rates, however, are high for both treatments. In type III patients the largest difference is observed, which, however, is not statistically significant (P = .12).

Symptom Control and Esophageal Function After Treatment

To identify the symptoms contributing to the differences in success rate, we compared individual symptom scores during the follow-up period. The dysphagia score of type I and III patients was significantly higher compared with type II patients (P = .03 and P = .001, respectively) (Table 2). Yet, dysphagia was the main symptom in all 3 subgroups. In contrast, chest pain and regurgitation scores in type III patients were higher compared with type I and II patients (chest pain: P < .01 and P < .001; regurgitation; P < .05 and P < .01). Weight loss was uncommon in all subtypes after therapy and therefore no differences were observed between the 3 types. These data indicate that the main persisting symptom in all 3 subtypes was dysphagia, whereas mainly chest pain and regurgitation were reported more frequently by type III patients.

Assuming that symptoms are generated by impaired emptying and/or dilation of the esophagus, we anticipated that the height and/width of the contrast column on timed barium esophagogram would be higher in type III patients. Surprisingly, esophageal stasis and width in type III patients were comparable with those in type II patients. In contrast, barium height was highest in type I achalasia (6.2 ± 0.74 cm) and significantly higher compared with type II (3.1 ± 0.33; P < .001) and type III (4.0 ± 1.1; P < .05). In addition, type I patients had a significantly wider esophagus compared with patients with type II (3.6 ± 0.21 cm vs 2.8 ± 0.10 cm; P < .001) (Figure 2). No differences were observed between the subgroups with respect to LES pressure after treatment.

Comparing PD with LHM, we found that type III patients treated by PD did have significantly more esophageal stasis compared with type III patients treated by LHM (6.2 ± 2.1 cm vs 1.1 ± 1.1 cm; P < .05) (Figure 5). Moreover, there is a trend for a larger esophageal width (3.1 ± 0.54 cm vs 1.9 ± 0.20 cm; P = .06) and a higher LES pressure (17 ± 4.1 mm Hg vs 9.0 ± 3.2 mm Hg; P = .12) in patients treated with PD compared with patients treated by LHM. In line with this, patients who underwent PD had a significantly higher dysphagia score (1.6 ± 0.3 vs 0.7 ± 0.4; P < .05) whereas the regurgitation score (0.7 ± 0.3 vs 0.1 ± 0.1; P = .07) tended to be higher compared with patients after LHM. Chest pain was similar after PD and LHM (1.1 ± 0.3 vs 0.6 ± 0.2; P = .20).

Figure 5.

Esophageal stasis and LES pressure are shown for PD and LHM in the 3 subtypes for 3 months, 1 year, and 2 years after treatment. Data are tested using a 2-way ANOVA. Patients with type III achalasia treated by PD have significantly more stasis compared with patients with type II achalasia during 2 years of follow-up evaluation.

Evolution of Subtypes After Treatment

It is hypothesized that the 3 types of achalasia represent a different stage of achalasia.[9,15] To define the course of the subtypes after treatment, we collected 397 post-treatment manometries from 107 patients (median, 2 post-treatment manometries; range, 1–8 post-treatment manometries). During the follow-up period, the mean contraction amplitude remained the lowest in type I patients (type I, 17 ± 0.9 mm Hg; type II, 37 ± 1.5 mm Hg; and type III, 78 ± 7.6 mm Hg; P < .0001, 1-way ANOVA). After therapy, most patients with type I achalasia were classified as having absent peristalsis (n = 16; 89%), whereas simultaneous contractions (with an amplitude of >30 mm Hg) were observed in 11% of patients (n = 2), classified as having esophageal spasm in the context of treated achalasia. In contrast, in patients with type II achalasia, only 7% of patients were classified as having absent peristalsis. In these patients this pattern was observed starting after a mean of 2.6 years after treatment. Spastic or simultaneous contractions were observed in follow-up manometries in 83% of type II patients, and weak peristalsis was observed in follow-up manometries in 10% of patients. All type III patients were classified as having esophageal spasms during the entire follow-up period.

Comments

3090D553-9492-4563-8681-AD288FA52ACE

processing....