Achalasia is an infrequent esophageal motility disorder with a prevalence of 10 cases per 100 000 individuals and an annual incidence of 1.6 per 100 000 individuals.^1-3 Its etiology is not fully understood.¹ It has been hypothesized that a neurotropic viral agent is the trigger of inflammation in Auerbach’s plexus. This inflammatory response eventually defeats the infectious agent, but genetically predisposed individuals may develop the disease due to the loss of myenteric plexus neurons.^4-10

Systemic immune response associated with circulating antinuclear antibodies and anti-myenteric autoantibodies (anti-GAD65 and anti-PNMaTa2) have been detected in 56-68% and 80-90% of the patients, respectively.^4,5,11,12

Achalasia’s clinical manifestations include dysphagia, heartburn, chest pain, regurgitation, and weight loss.^13,14

Laparoscopic Heller myotomy and partial fundoplication are preferred treatment options to eliminate the physiologic barrier at the esophagogastric junction (EGJ).^15,16 The disease evolution is relevant for the morphology of the esophagus, which is affected as the condition progresses. Thus, patients without treatment in the advanced stage of the disease are marked by esophageal tortuosity and massive dilation (> 6 cm).^17-19 Changes in the esophageal body (esophageal length, dilation, and tortuosity) could also damage the diaphragmatic hiatus.²⁰ Mittal et al²¹ have described that the esophagus in achalasia patients makes a smaller angle (acute) compared to healthy individuals and observed physical breaks in the left crus of the diaphragm in 50% of the esophagus. Few studies have addressed hiatal hernia (HH) prevalence and incidence in the general population since several patients complain of minimal non-specific symptoms or are asymptomatic.²² Even fewer studies describe the prevalence of HH in patients with achalasia.^23-29

Upper gastrointestinal (UGI) series with a barium swallow is the most sensitive diagnostic test for paraesophageal hernias, but they can also be diagnosed on a UGI endoscopy. Sliding hiatal hernias are detected by esophagogastroduodenoscopy (EGD), UGI, and high-resolution manometry (HRM).^18-29

The shortening of the esophagus and its association with HH has been a subject of interest in esophageal literature.³⁰ However, there is no substantial evidence of the esophagus length in patients with achalasia and even less of its relationship with hiatal hernia.

This study focused on determining (1) the prevalence of HH in patients with achalasia, (2) comparing the esophageal length of the achalasia group with gastroesophageal reflux disease (GERD) and healthy volunteers (HV), (3) measuring the manometric esophageal length to height (MELH) ratio, by dividing the manometric esophageal length (MEL) by the patient’s body height to precisely detect a shortened esophagus, as well as (4) determining if there are differences in symptoms between the achalasia patients with or without HH.

Study Design and Population

This was a cross-sectional study from November 2012 to December 2018 of 87 achalasia and 22 GERD patients and 30 HV (controls) from the Outpatient Clinics of Gastroenterology and Surgery of our hospital, a tertiary-care referral hospital.

The achalasia group (n = 87) belongs to a previously nested cohort.^14,31 Esophagram, HRM (classified based on Chicago version 4.0 [v4.0]), and UGI endoscopy were performed to diagnose achalasia.³² Patients were excluded from the study if they had a history of cancer, genetic disorders, hematologic disease, acute infectious disease, acute inflammatory diseases, Chagas disease, esophageal stricture, eosinophilic esophagitis, scleroderma, or gastric or esophageal cancer.

We retrospectively reviewed the UGI, EGD, and HRM reports in our database and searched for the occurrence of a HH. The esophageal lengths were measured using HRM, UGI, and EGD before any surgical intervention.

The GERD group (n = 22) was retrospectively collected from electronic medical records. Adult patients without laparoscopic anti-reflux surgery and disease diagnosis by EGD, 24-hour pH-impedance monitoring, barium swallow studies, and HRM were enrolled. GERD definition included complaints of heartburn and/or acid regurgitation and patient response to an empiric trial of proton pump inhibitors (PPIs); either with advanced erosive esophagitis (Los Angeles grade A to D), Barrett’s esophagus, or peptic stricture by EGD; or distal esophageal acid exposure time > 6% by pH-impedance monitoring.

The HV (n = 30) were encouraged to participate in the study. Adult controls had no prior personal or family history of achalasia, GERD symptoms, or any systemic comorbidities at inclusion (eg, diabetes, hypertension, and dyslipidemia). This group was only analyzed using HRM.

Demographic and clinical characteristics were obtained retrospectively for each participant from the hospital’s medical records (Table).

Table. Clinical and Demographic Characteristics of Achalasia Patients and Control Groups

Variables	Healthy volunteers (n = 30)	Achalasia (n = 87)	Type I achalasia (n = 35)	Type II achalasia (n = 52)	P-value HV vs AT HV vs AI HV vs AII	GERD (n = 22)	P-value HV vs GERD GERD vs AT GERD vs AI GERD vs AII
Demographics
Age (yr), Mean ± SD Median Range	39.5 ± 13.0 37 24-84	41.5 ± 14.5 40 18-78	39.5 ± 13.6 38 18-69	42.8 ± 15.1 42 18-78	0.647	46.6 ± 12.8 50 21-69	0.056 0.300
Sex, female (n [%])	19 (63)	54 (62)	17 (49)	37 (71)	> 0.999 0.317 0.471	14 (64)	> 0.999 0.290 0.587
Disease evolution (mo) Mean ± SD Median Range	NA	23.1 ± 24.1 12.5 1-115	21.7 ± 19.5 14.0 1-74	24.1 ± 26.9 12.0 1-115	-	-	-
Clinical variables
Height (cm) Mean ± SD Median Range	163 ± 8.0 163 150-180	161 ± 8.9 161 143-185	162 ± 8.4 162 144-178	160 ± 9.3 160 143-185	0.285	168 ± 9.3 169 149-183	0.089 0.004 0.029 0.003
Weight (kg) Mean ± SD Median Range	67.5 ± 7.8 67.5 56-82	60.2 ± 13.3 59.5 35-92	62.1 ± 11.4 63.0 40-85	58.9 ± 14.4 56.0 35-92	0.008 0.301 0.002	78.9 ± 12.3 81.3 51-100	< 0.001 < 0.001 < 0.001 < 0.001
Body mass index (kg/m2) Mean ± SD Median Range	25.1 ± 2.7 24.8 21.8-34.1	23.7 ± 4.7 23.6 16.5-37.3	24.0 ± 4.4 24.6 17.1-35.2	23.5 ± 5.9 23.0 16.5-37.3	0.259	28.2 ± 4.1 28.2 21.8-36.1	0.008 < 0.001 < 0.001 < 0.001
Overweight (n [%])	10 (33)	23 (26)	12 (34)	3 (6)	0.487 > 0.999 0.003	10 (46)	0.402 0.118 0.418 < 0.001
Obesity (n [%])	2 (7)	8 (9)	3 (9)	5 (10)	> 0.999 > 0.999 > 0.999	6 (27)	0.058 0.035 0.075 0.074
Dysphagia (n [%])	-	87 (100)	35 (100)	52 (100)	1.000 1.000	-	-
Regurgitation (n [%])	-	79 (91)	32 (91)	47 (90)	1.000 1.000	-	-
Heartburn (n [%])	-	55 (63)	22 (69)	33 (63)	1.000 1.000	-	-
Chest pain (n [%])	-	77 (89)	29 (83)	48 (92)	1.000 1.000	-	-
Hiatal hernia (n [%])	-	3 (3)	1 (3)	2 (4)	1.000 1.000	16 (73)	< 0.001 < 0.001 < 0.001
Hiatal hernia (cm) Mean ± SD Median Range	-	2.0 ± 0.0 2.0 2-2	2.0 ± 0.0 2.0 2-2	2.0 ± 0.0 2.0 2-2	1.000 1.000	4.0 ± 1.5 4.0 2-7	0.532 0.532 0.532
Esophageal length
Baseline (cm) Mean ± SD Median Range	22.06 ± 1.52 21.75 19.63-25.77	23.48 ± 2.41 23.47 17.83-29.77	24.10 ± 2.42 24.30 18.27-29.17	23.07 ± 2.33 23.10 17.83-29.77	0.003 < 0.001 0.042	21.64 ± 1.87 21.40 19.00-25.97	0.254 0.002 < 0.001 0.017
Post-swallow (cm) Mean ± SD Median Range	21.97 ± 1.59 21.69 19.97-25.46	23.2 ± 2.21 22.97 18.55-29.17	23.47 ± 2.26 23.34 19.14-29.17	23.01 ± 2.18 22.75 18.55-28.64	0.010 0.005 0.037	21.70 ± 1.65 21.18 19.63-25.78	0.382 0.004 0.003 0.014
MELH ratio
Baseline (cm) Mean ± SD Median Range	0.13 ± 0.01 0.13 0.12-0.16	0.15 ± 0.01 0.15 0.12-0.19	0.15 ± 0.02 0.15 0.12-0.19	0.14 ± 0.01 0.14 0.12-0.17	< 0.001 < 0.001 < 0.001	0.13 ± 0.01 0.13 0.11-0.14	0.025 < 0.001 < 0.001 < 0.001
Post-swallow (cm) Mean ± SD Median Range	0.13 ± 0.01 0.14 0.12-0.16	0.14 ± 0.01 0.14 0.12-0.19	0.14 ± 0.01 0.14 0.12-0.19	0.14 ± 0.01 0.14 0.12-0.17	< 0.001 0.002 < 0.001	0.13 ± 0.01 0.13 0.11-0.15	0.068 < 0.001 < 0.001 < 0.001
Questionnaires
EAT-10 Mean ± SD Median Range	-	28.71 ± 9.42 30.50 4-40	27.88 ± 9.34 29.00 12-40	29.29 ± 9.60 32.00 4-40	-	10.39 ± 9.50 8.00 0-25	< 0.001 < 0.001 < 0.001
Eckardt Mean ± SD Median Range	-	8.91 ± 2.98 9.00 3-26	8.39 ± 2.56 8.00 4-13	9.25 ± 3.23 9.0 3-26	-	-	-
GERD-HRQL Mean ± SD Median Range	-	22.58 ± 12.25 20.50 4-49	23.82 ± 12.27 22.00 5-47	22.04 ± 12.30 20.00 4-49	-	24.94 ± 9.20 24.50 13-45	0.293 0.735 0.194

HV, healthy volunteers; AT, total achalasia; AI, type I achalasia; AII, type II achalasia; GERD, gastroesophageal reflux disease; MELH ratio, manometric esophageal length to height ratio; EAT-10, Eating Assessment Tool; GERD-HRQL, GERD–health-related quality of life.

P-value was obtained using ANOVA.

High-resolution Manometry Protocol

An esophageal HRM was performed in every patient at baseline and before being referred for surgery. A solid-state HRM probe with 36 circumferential sensors was used (Medtronic, Minneapolis, MN, USA). Having the patient in a sitting position and at 45 degrees, stationary esophageal HRM was performed. After a 12-hour fasting period, the probe was inserted trans-nasally until passing the esophagogastric junction and assessed visually on the computer screen. Ten water swallows of 5 mL separated by 30 seconds were provided. Analyses were performed using Manoview 2.0 (Medtronic). Patients were classified according to the latest Chicago classification v4.0 into 3 groups: (1) type I achalasia (without pressurization within the esophageal body), (2) type II (with > 20% panpressurization), and (3) type III (spastic). Two gastroenterologists (E.C-A. and M.A.V.) specializing in esophageal HRM performed the classification.^14,31 Also, esophagogastric junction was classified accordingly to Chicago classification v4.0 into: Type I, no separation between the lower esophageal sphincter (LES) and crural diaphragm; Type II, minimal separation (> 1 and < 2 cm); Type III, > 2 cm separation.

Manometric Esophageal Length and Manometric Esophageal Length to Height Ratio

ManoView Analysis Software 3.0 (Medtronic, Duluth, GA, USA) measured the esophageal lengths with an isobaric contour set at 30 mmHg. Using the smart mouse, we measured the distance from the lower border of the upper esophageal sphincter (UES) to the upper border of the LES. We averaged 3 resting measurements for a baseline length and 10 after each of the swallows for a post-swallow length. The exact process was done for the 3 groups.

The MELH ratio was obtained by dividing the MEL by the patient’s body height to diagnose a shortened esophagus.^33,34

Operational Definitions

Hiatal hernia

HH was defined if the separation among the squamocolumnar junction and the diaphragmatic impression by EGD and the separation of the lower border esophageal sphincter and crural impression in HRM were more extensive than 2 cm in both studies. A morphological assessment of the HH was observed by UGI. All analyses were performed preoperatively. According to previous reports, HRM was considered the most accurate method to assess HH length.^35-37

Hiatal hernia classification³⁷

(1) Type I: Sliding HH. The GEJ migrates into the thorax. (2) Type II: True paraesophageal or rolling hernia. There is a herniation of the gastric fundus into the thorax but the GEJ remains in the normal anatomic location. (3) Type III: Mixed paraesophageal hernia. It has elements of both types I and II hernias. There is a herniation of the GEJ and stomach into the chest. (4) Type IV: There is another intra-abdominal viscera, such as colon, small bowel, omentum, or spleen migrated into the thorax along with the stomach, is associated with a large defect in the phrenoesophageal ligament.

Baseline esophageal length

Metrics were obtained using a smart mouse tool (Manoview), drawing a square from the lower border of the UES to the upper edge of the LES. The final measurement was obtained from the distal square paremeter (red line in Fig. 1). The mean value of 3 measures pre-swallow was considered for analysis.

Figure 1. A representative image of the measure of esophageal length was done from the upper sphincter’s inferior border and the lower sphincter’s superior (lower esophageal sphincter [LES]) border, with the isobaric contour set at 30 mmHg. Delta value from baseline to post-swallow was considered esophageal shortening. (A) LES concords with the diaphragmatic impression (red broken rectangle). (B) LES (red broken rectangle) and separated 2.3 cm from a diaphragmatic impression (blue pointed rectangle, hiatal hernia).

Post-swallow esophageal length

The average of 10 measurements from the inferior UES border to the superior LES border after every 10 swallows.

Manometric esophageal length/patient’s body height

The manometric measure of the distance from the lower border of the UES to the upper border of the LES divided by patient’s body height.

Gastroesophageal reflux disease

Patients of 18 ≥ 65 years old with classic symptoms of GERD and positive response to PPI therapy, either with positive EGD report (Barrett’s esophagus or esophagitis C or D) or 24-hour pH-metry with pathologic acid reflux report. These patients did not receive surgical or endoscopic treatment.

Healthy volunteers

Individuals without known esophageal diseases or symptoms (dysphagia, regurgitation, and retrosternal pain) willingly underwent HRM. Only esophageal lengths were measured. No patient had a HH.

Obesity

Body mass index (BMI) > 30 kg/m².

Overweight

BMI > 25 kg/m² and lower than 30 kg/m².

Symptoms Score Evaluation

At diagnosis, patients completed Eckardt symptom score, Eating Assessment Tool (EAT-10), GERD–health-related quality of life (GERD-HRQL) questionnaires designed to assess the frequency and severity of esophageal symptoms (eg, elevated scores represent higher frequency and severity).¹⁶ Data acquired from the questionnaires and HRM-derived parameters were used as surrogate indicators of disease severity.

Ethical Considerations

The institutional review board authorized this study (Reference No. 1522). It was performed in compliance with the Declaration of Helsinki, the Good Clinical Practice guidelines, and local regulatory requirements. All individuals gave written informed consent.

Statistical Methods

A descriptive analysis was performed. The normality test for distribution was made with Shapiro-Wilk test. If the distribution was normal, the t student test (unpaired) or ANOVA (unpaired) was used. One-way ANOVA with Dunn’s posthoc test was performed to compare demographic, clinical characteristics, and esophageal lengths/ratios between groups. To compare the HH and non-HH subgroups, the Mann-Whitney U test or Kruskal-Wallis was performed. All the statistical tests were performed 2-sided, and P-values less than 0.05 were considered statistically significant. The Prism 6 GraphPad program (GraphPad Software, San Diego, CA, USA) was used to perform the statistical analyses. Data were represented as the mean ± SD.

Clinical and Demographic Characteristics

A total of 87 patients with achalasia were included in the study. The mean age was 41.5 ± 14.5 years; 54 patients (62%) were females. The mean disease duration was 23.1 ± 24.1 months, the mean height was 161 ± 8.9 cm, the mean BMI was 23.7 ± 4.7 kg/m², and the mean weight was 60.2 ± 13.3 kg. The most frequent type of achalasia was type II (n = 52 [60%]). Twenty-six and nine percent of the achalasia patients were overweight or obese, respectively. Of the 87 patients, all complained of dysphagia, 79 of regurgitation (91%), 55 of heartburn (63%), and 48 (92%) of chest pain (Table and Fig. 2).

Figure 2. Morphometric measures. (A) Height, (B) Weight, and (C) Body mass index (BMI). Data are expressed as mean ± SD. HV, healthy volunteers; GERD, gastroesophageal reflux disease.

In the GERD group, 22 patients were enrolled, of whom 14 (64%) were women, with a mean age of 46.6 ± 12.8 years, mean BMI of 28.2 ± 4.1 kg/m², mean weight of 78.9 ± 12.3 kg, and mean height was 168 ± 9.3 cm. The prevalence of overweight was 46%, and obesity of 23% (Table and Fig. 2). Thirteen patients (59%) had esophagitis (grade A, n = 5; grade B, n = 6 and grade C, n = 2 patients).

The HV group included 30 patients; 19 (63%) were females, the mean age was 39.5 ± 13.0 years, the mean BMI was 25.1 ± 2.7 kg/m², and the mean height was 163 ± 8.0 cm. Thirty-three percent were overweight, and 7% were obese (Table and Fig. 2).

Esophageal Length

There was no intragroup difference between the baseline and post-swallow manometric measurements in achalasia (23.48 ± 2.41 cm vs 23.20 ± 2.21 cm, P = 0.425); in GERD (21.64 ± 1.87 cm vs 21.70 ± 1.65 cm, P = 0.814) nor HV group (22.06 ± 1.52 cm vs 21.97 ± 1.59 cm, P = 0.652).

The patients with achalasia had a longer esophagus at baseline (23.48 ± 2.41 cm) compared to the GERD group (21.64 ± 1.87 cm; P = 0.002) and the HV group (22.06 ± 1.52 cm; P = 0.003; Table and Fig. 3A). No statistically significant differences were found between GERD and HV group (P = 0.254).

Figure 3. Esophageal length and manometric esophageal length to height (MELH) ratio. (A) Esophageal lengths at baseline, (B) Esophageal length post-swallow, (C) MELH ratio at baseline, and (D) MELH ratio post-swallow. Data are expressed as mean ± SD. HV, healthy volunteers; GERD, gastroesophageal reflux disease.

The post-swallow esophageal length was also higher in patients with achalasia (23.20 ± 2.21 cm) compared to the GERD group (21.70 ± 1.65 cm; P = 0.004) and the HV group (21.97 ± 1.59 cm; P = 0.010; Table and Fig. 3B). No statistically significant differences were found between GERD and HV groups (P = 0.382).

We also did not find statistically significant differences in esophageal length at baseline or post-swallow between the achalasia subtypes (Table; Fig. 3A and 3B).

Esophageal Length in Patients With Hiatal Hernia

The patients with achalasia and HH had a longer esophagus at baseline (24.06 ± 1.91 cm) compared to the GERD and HH group (21.23 ± 1.72 cm; Fig. 4A). Likewise, the achalasia patients without HH had a longer esophagus at baseline (22.75 ± 1.97 cm) compared to the GERD patients without HH (23.46 ± 2.43 cm; Fig. 4A).

Figure 4. Esophageal length and manometric esophageal length to height (MELH) ratio in patients with or without hiatal hernia (HH). (A) Esophageal lengths at baseline, (B) esophageal length post-swallow, (C) MELH ratio at baseline; and (D) MELH ratio post-swallow. Data are expressed as mean ± SD. GERD, gastroesophageal reflux.

The post-swallow esophageal length was also higher in achalasia patients and HH (24.17 ± 1.93 cm) compared to the GERD and HH group (21.35 ± 1.51 cm; P = 0.025; Fig. 4B).

The patients with achalasia without HH had a longer esophagus (23.16 ± 2.23 cm) than the GERD patients without HH (22.65 ± 1.76 cm; Fig. 4B).

Importantly, GERD patients with HH had significantly shorter esophageal lengths than GERD patients without HH (21.35 ± 1.51 cm vs 22.65 ± 1.76 cm, P = 0.050; Fig. 4B).

Manometric Esophageal Length to Height Ratio

The MELH ratio is an objective predictor of a shortened esophagus preoperatively. A lower MELH ratio is a strong predictor of HH. It should be noted that at baseline, patients with achalasia had the highest MELH ratio (0.15) than GERD patients (0.13) and HV (0.13; P < 0.001; Table and Fig. 3C).

Post-swallow, the MELH ratio in achalasia patients (0.14) was the highest compared to GERD patients (0.13) and HV (0.13; P < 0.001; Table and Fig. 3D).

Manometric Esophageal Length to Height Ratio in Patients With Hiatal Hernia

The achalasia patients with HH had a higher MELH ratio at baseline (0.150 ± 0.000) compared to the GERD and HH group (0.128 ± 0.010; Fig. 4C). Likewise, the achalasia patients without HH had a higher MELH ratio (0.146 ± 0.013) compared to the GERD patients without HH (0.133 ± 0.010; Fig. 4C).

The post-swallow MELH ratio was also higher in achalasia patients and HH (0.147 ± 0.006) compared to the GERD and HH group (0.128 ± 0.009; P = 0.011; Fig. 4D). The achalasia patients without HH had a higher MELH ratio (0.144 ± 0.013) than the GERD patients without HH (0.133 ± 0.008; P = 0.050; Fig. 4D).

Hiatal Hernia Prevalence

Only 3 (3%) HHs were found in the achalasia patient group. One HH was diagnosed in type I and 2 in type II achalasia patients. In contrast, we found a HH prevalence of 73% in the GERD group (P < 0.001); the most common type of hernia, according to Hill’s classification, was type I (68.2%), followed by type III (4.5%). The median size of hernia in the achalasia group was 2.0 ± 0.0 cm, and in the GERD group, 4.0 ± 1.5 cm. All HH (n = 16) were diagnosed by endoscopy; out of the total hernias, 9 were diagnosed by UGI and 3 by HRM in the GERD group. Although there is a tendency, we did not find differences in the size of hernias between GERD and achalasia (Table).

Symptom Scores

Regarding the GERD-HRQL score, the achalasia group did not significantly differ compared with GERD patients (Fig. 5A). There were also no differences in GERD-HRQL scores between achalasia or GERD patients with or without HH (Fig. 5C).

Figure 5. Symptom scores. (A) Gastroesophageal reflux disease–health-related quality of life (GERD-HRQL) score, (B) Eating Assessment Tool (EAT-10) score; (C) GERD-HRQL score between patients with and without hiatal hernia (HH), (D) EAT-10 score between patients with and without HH, and (E) Eckardt score between patients with and without HH. Data are expressed as mean ± SD. HV, healthy volunteers; GERD, gastroesophageal reflux.

The EAT-10 score was significantly higher in the achalasia than GERD group (P < 0.001, Fig. 4B). Moreover, the achalasia patients without HH had higher EAT-10 than those with achalasia with HH and GERD (P = 0.044, Fig. 5D).

The Eckardt score was higher in achalasia patients without HH than in patients with HH (P = 0.044, Fig. 5E).

Achalasia occasionally coexists with HH, but the incidence, demographics, and the presence or absence of reflux symptoms, are not fully identified and much less described.²⁴

Thus, this study focused on determining the prevalence of HH and measuring the esophageal length, MELH ratio, and symptom severity in 2 surgical pathologies of the esophagus, achalasia and GERD, and their comparison with HV. The prevalence of HH in the general population has been determined between 10 and 17%.²²

Bivariate analyses have shown that HH prevalence in the general population increased with age, from 2.4% in the sixth decade of life to 7.0% in the seventh, 14.0% in the eighth, and 16.6% in the ninth decade. The individuals with HH were considerably older than those without HH (P < 0.001). Furthermore, HH occurrence was higher in adult females (12.7%) than in males (7.0%) (prevalence ratio = 1.8 [95% CI, 1.5 to 2.3]). Besides, its prevalence varied by race/ethnicity (non-Hispanic whites [12.1%], African/Americans [9.4%], Hispanic/Latinos [11.0%], and Asian/Americans [2.9%]; P < 0.001). Likewise, other associations were found for indicators related to obesity (central obesity, hip circumference, waist circumference, and BMI), height, PPI use, current smoking status, and educational attainment.²²

In our study, we found a HH prevalence of 73% (n = 16) in GERD patients and 3% (n = 3) in achalasia patients (overweight and older than 62 years), as previously reported.^20,22-29

This may be associated with the fact that, regardless of the achalasia subtype, the esophageal lengths and MELH ratios were significantly higher in achalasia than in HV and patients with GERD.³³ Moreover, our results also show that achalasia patients with HH have a higher esophageal length and MELH ratio than those without hernia and GERD patients without or with HH.

The data obtained from our study suggests that the pathophysiology of HH in achalasia differs from that in GERD. This could be associated with the esophageal length and the morphological changes of the esophagus (tortuosity and dilation) in patients with achalasia.^19,20 For example, the 3D-pressure profile of the EGJ at end-expiration and forced inspiration has revealed that the lower esophageal sphincter turns to the left as it enters from the chest into the abdomen, forming an angle between the spine and lower esophageal sphincter. It is smaller in achalasia patients (104°) than in healthy individuals (124°). This is related to physical breaks in the left crus of the diaphragm in 50% of the achalasia patients.^20,21

It is interesting to note that patients with GERD are taller than patients with achalasia (168 cm vs 161 cm, P = 0.004), have more weight (78.9 kg vs 60.2 kg, P < 0.001), have a shorter esophagus (21.64 cm vs 23.48 cm, P = 0.002), a lower MELH ratio (0.13 vs 0.15, P < 0.001), and a higher prevalence of HH (73% vs 3%).

In GERD patients, lesions caused by acid reflux in the esophagus may increase esophageal mucosal permeability, edema, inflammatory cell infiltration, and subsequent transmural fibrosis. As a result of fibrosis, the longitudinal shrinkage of connective tissue can shorten the esophagus, resulting in traction of the EGJ and the consequent gastric herniation.³⁵ This phenomenon has been observed in neonates and infants with severe reflux that presents a shorter esophagus.^35,36 These data are also relevant to explain why the association of achalasia with HH is so low, in contrast to GERD patients.

Lal et al³³ have determined that the MELH ratio is an objective predictor of a shortener esophagus. Those patients with a MELH ratio of 0.12 or lower have a dramatically increased rate of hiatus hernia.³³ Thus, it is unsurprising that patients with GERD (MELH ratio: 0.13) have a higher HH prevalence than achalasia patients (MELH ratio: 0.15).

Regarding symptoms in patients with or without HH, the GERD-HRQL and EAT-10 questionnaires did not show significant differences. While in the achalasia patients, the Eckardt questionnaire score was higher and statistically significant in patients without HH.

This study is clinically relevant because the difference in preoperative symptoms between achalasia patients with or without a HH is imperceptible. Thus, reflux symptoms related to sliding hernia could be masked and confused with dysphagia (the clinically most predominant symptom in achalasia). Due to the rarity in the coexistence of achalasia and HH, the masking of symptoms, and the lack of a detailed intraoperative evaluation of the esophageal hiatus, the presence of a HH could miss.

For this reason, the surgeon should be advised not to rule out a HH. Although the probability of the coexistence of both pathologies is low, the surgeon should encourage to perform a systematic review of the esophageal hiatus during laparoscopy since if this condition is not identified and corrected, the risk of postoperative reflux may increase.

The present study has some limitations, such as bias since all patients belong to the same hospital and the retrospective nature limits it. Besides, the prevalence of HH in healthy individuals was not evaluated. Also, we must accept that there is no perfect instrument to measure the esophageal length with high fidelity. This is due to the esophageal shape that makes it difficult to measure the length, as the probe can bend as it passes throughout the esophageal body. Also, using an esophagram, there is a similar issue due to the sigmoid form of the esophagus in this patient and the difficulty of measuring it in an anteroposterior projection captured during the study.

Among the study’s strengths are the not negligible number of patients with achalasia included in the analysis and the comparison groups (healthy individuals and GERD), which have never been reported. This study is the first to analyze the esophageal length of patients with achalasia, compare it with healthy individuals and patients with GERD, and provide a possible biomechanical mechanism that relates the length of the esophagus with the presence of hiatus hernias.

In conclusion, patients with achalasia have a longer esophagus, higher MELH ratio, and lower prevalence of HH than GERD patients and healthy subjects. Thus, the esophageal length of achalasia patients could explain the lower prevalence of HH. Even though the probability of the coexistence of achalasia and HH is low, the surgeon should encourage to review of the esophageal hiatus during laparoscopy since if this condition is not identified and corrected, the risk of postoperative reflux may increase, and with it esophagitis, peptic strictures, Barrett’s esophagus, and even esophageal carcinoma.

We thank all patients involved in the study.

None.

None.

Enrique Coss-Adame, Janette Furuzawa-Carballeda, Andric C Perez-Ortiz, Ana López-Ruiz, and Gonzalo Torres-Villalobos: wrote the manuscript; Ana López-Ruiz, José Peralta-Figueroa, Héctor Olvera-Prado, Sofía Narváez-Chávez, and Fidel López-Verdugo, Óscar Santés-Jasso and Diana Aguilar-León: collected the data from the clinical files, conducted and programmed the preoperative studies, and created the database; Janette Furuzawa-Carballeda, Ana López-Ruiz, Josué Sánchez-Gómez, and Gonzalo Torres-Villalobos: performed the analysis and interpretation; Gonzalo Torres-Villalobos, Enrique Coss-Adame, Janette Furuzawa-Carballeda, and Miguel A Valdovinos: performed a critical revision of the manuscript for important intellectual content; and Gonzalo Torres-Villalobos, Enrique Coss-Adame, and Janette Furuzawa-Carballeda: were responsible for the study conception and design.