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OESO©2011
 
Volume: The Esophagogastric Junction
Chapter: GER and barrier dysfunction
 

Can any difference in reflux patterns be shown in patients with or without hiatal hernia?

H.R. Koelz (Zurich)

Hiatal hernia is the most important risk factor for gastroesophageal reflux disease (GERD). In prospective endoscopic studies where 17 to 22% of the patients showed axial hiatal hernia, reflux esophagitis was seen in 50 to 58% of the patients, whereas esophagitis in the absence of hiatal hernia occurred in only 16 to 37% [1-3]. This association has been known for many decades, but the mechanism leading to GERD is still not clear.

The question of the mechanism behind the association between hiatal hernia and GERD was addressed again in a few recent studies using ambulatory pH-metry, sometimes combined with manometric and radiological investigations of the gastroesophageal junction. The results of these studies will be summarized below.

Increased total reflux time

An increase in total reflux time was shown in all studies that compared pH-metric results in GERD patients with and without hiatal hernia [4-8]. Since total reflux time closely correlates with the severity of GERD, it is not surprising that patients with hiatal hernia had more severe GERD than those without hernia [6, 8, 9]. This confirms the well-known view that esophageal acid exposure is the most important pathogenic factor in GERD.

Prolonged esophageal clearance time and a lower resting pressure of the lower esophageal sphincter (LES) have been identified as possible mechanisms that could explain the difference in total reflux time.

Prolonged esophageal clearance

Already in 1981, DeMeester et al. reported that radioisotope clearance was prolonged in normal subjects with hiatal hernia and even more in GERD patients with hiatal hernia as compared to persons without hernia, and this was accompanied by a larger number of prolonged reflux episodes lasting >= 5 min. [4]. There was no evidence that delayed clearance was due to an increased number of repetitive reflux episodes or a larger volume of reflux. Furthermore, simple gastropexy (without fundic wrap) according to Hill decreased the average duration of reflux episodes from 18 to 8 min. The authors suggested that longitudinal stretching of the esophagus by surgery improved the propulsive force of the esophageal body. Although there is evidence that the Hill procedure increases resting LES pressure, an improvement of esophageal peristalsis has not been shown directly. In agreement with this, however, Kasapidis demonstrated a reduced peristaltic amplitude of the distal esophagus from 106 ± 41 to 67 ± 33 mmHg in patients with GERD and hiatal hernia compared to those without hernia [6]. In this study, prolonged acid clearance in patients with hiatal hernia explained the increased total reflux time (16 ± 21 vs 4 ± 3 min.) rather than an increased number of reflux episodes, which in fact was somewhat lower (35 ± 15 vs 51 ± 24).

Prolonged clearance time in GERD with hiatal hernia has been confirmed in recent studies [6, 10, 11]. One carefully done combined manometric and videofluoroscopic study by Sloan aimed at identifying the precise mechanism [10]. A summary of the results of this study is provided in Table I. Subjects were divided into three groups:

- subjects with no hernia,

- patients with a "reducing hernia" (visible only during swallows),

- patients with "non reducing" axial hiatal hernia (>= 2 cm long hiatal sac visible also between swallows).
Table I. Summary of data (from [<A HREF=11]). Parameter">

Esophageal emptying was severely impaired in the 12 subjects with non reducing hernias, mainly due to frequent "early retrograde flow" of gastric contents, which occurred immediately after LES relaxation during swallowing. The precise mechanism is not clear, but the authors provided evidence that retrograde flow was probably due to a complete LES relaxation and the LES entirely exposed to the lower intrathoracic pressure, i.e. above the respiratory inversion point. Early retrograde flow was not seen in any of the 24 subjects without non reducing hernia. Instead, these patients showed more frequently "late retrograde flow", defined as reflux after arrival of the stripping wave, i.e. 15 to 20 seconds after initiating swallowing. The explanation of this phenomenon was orad movement of the LES during swallowing, thus forming a transient hernia. In contrast to patients with non reducing hernia, the narrow hiatus in these patients was occluded at least partially by the diaphragmatic crura during inspiration. This allowed an increase in intrahernial pressure during esophageal emptying. After completion of esophageal contraction and restoration of LES pressure, the intrahernial pressure exceeded that of the LES barrier and lead to reflux.

Increased frequency of reflux episodes

Two conflicting sets of results have been published. In the study by Sontag et al. [5], patients with hiatal hernia had significantly more reflux episodes than those without hernia (122 ± 20 vs 59 ± 12). Thus, increased total reflux time in hiatal hernia patients was the result of both frequency and duration of reflux. On the other hand, Kasapidis et al. [6] reported both increased reflux frequency (35 ± 15 vs 51 ± 24) and duration. A difference in the definition of "reflux episode" may account for this discrepancy. Whereas the pH threshold was 4.0 in both investigations, the lower time limit in Sontag's study was 10 as compared to 18 seconds in Kasapidis' study.

Decreased lower esophageal sphincter pressure

The majority of the publications describe an association between hiatal hernia and decreased resting LES pressure [4, 5, 9, 11], but there is at least one exception where no difference in LES pressure was found [6]. A vicious circle between acid reflux or esophagitis leading to a decrease in LES pressure and thus promoting more reflux is unlikely because there is no evidence that motor abnormalities improve after eliminating acid reflux and healing of esophagitis [12, 13]. It appears, therefore, that hiatal hernia impairs LES directly.

Sloan et al. tested several different reflux-provoking maneuvers (coughing, Müller maneuver, Valsalva maneuver, leg-lifting, and inflation of an abdominal cuff) during videofluoroscopic and manometric monitoring of the LES in control subjects and patients with various degrees of hiatal hernia [8]. Resting LES pressure was markedly decreased in patients with hernias (5.3 ± 4.3 vs controls 12.9 ± 7.1 mmHg). A stepwise regression analysis revealed that axial length of hernia as measured between swallows was the most important factor. The correlation could be significantly improved by a second variable, resting LES pressure. Interestingly, there was a close direct correlation between these two factors, so a combined factor (hernia size x LES pressure) was entered into the equation and proved to further improve the correlation. The authors concluded that both hiatal hernia and LES pressure contribute to reflux during abrupt increases in intraabdominal pressure.

Reflux pattern in patients with and without hiatal hernia

A detailed analysis on reflux patterns as measured by 24-hour pH-monitoring in patients with and without hiatal hernia has not been published. As mentioned above, patients with hiatal hernia have an increased total acid reflux score and frequent prolonged reflux episodes due to both more frequent reflux episodes and slow acid clearance. They may show an increased incidence of short reflux episodes immediately following deglutition as well as episodes of stress reflux induced by intraabdominal pressure rises. In order to identify these mechanisms, combined 24-hour monitoring of pH and pressure is required. Unlike current devices equipped with the pH electrode located at the tip of the catheter and positioned a few centimeters above the LES, additional pressure sensors would be required more distally in the hiatal hernia and in the main stomach. Such investigations do not lead to immediate therapeutic consequences, but they might improve our understanding of the respective contributions of hiatal hernia and LES to GERD as well as to the understanding of the pathogenesis of GERD in general. An attempt in this direction was made by Sontag et al. [5]. A new statistical modeling called "structural analysis" of pH-metric, manometric and endoscopic data led to the conclusion that the presence of a hiatal hernia, not the pressure of the LES, is the most important predictor of reflux frequency, acid contact time, and esophagitis.

References

1. Wright RA, Hurwitz AL. Relationship of hiatal hernia to endoscopically proved reflux esophagitis. Dig Dis Sci 1979;24:311-313.

2. Stene-Larsen G, Weberg R, Frøyshov Larsen I, Bjørtuft Ø, Hoel B, Berstad A. Relationship of overweight to hiatus hernia and reflux esophagitis. Scand J Gastroenterol 1988;23:427-432.

3. Berstad A, Weberg R, Larsen IF, Hoel B, Hauerjensen M. Relationship of hiatus hernia to reflux esophagitis. A prospective study of coincidence, using endoscopy. Scand J Gastroenterol 1986;21:55-58.

4. DeMeester TR, Lafontaine E, Joelsson BE, Skinner DB, Ryan JW, O'Sullivan GC, Brunsden BS, Johnson LF. J Thorac Cardiovasc Surg 1981;82:547-558.

5. Sontag SJ, Schnell TG, Miller TQ, Nemchausky B, Serlovsky R, O'Connell S, Chejfec G, Seidel UJ. The importance of hiatal hernia in reflux esophagitis compared with lower esophageal sphincter pressure of smoking. J Clin Gastroenterol 1991;13:628-643.

6. Kasapidis P, Vassilakis JS, Tzovaras G, Chrysos E, Xynos E. Effect of hiatal hernia on esophageal manometry and pH-metry in gastroesophageal reflux disease. Dig Dis Sci 1995;40:2724-2730.

7. Ott DJ, Glauser SJ, Ledbetter MS, Chen MY, Koufman JA. Association of hiatal hernia and gastroesophageal reflux: correlation between presence and size of hiatal hernia and 24-hour pH monitoring of the esophagus. AJR Am J Roentgenol 1995;165:557-559.

8. Schindlbeck NE, Klauser AG, Voderholzer W, Müller-Lissner SA. Frequency and importance of axial hiatus hernia in gastro-oesophageal reflux disease. 4th European Gastroenterology Week, Berlin, 17-21 Sept. 1995; Abstract #428.

9. Sloan S, Rademaker AW, Kahrilas PJ. Determinants of gastroesophageal junction incompetence: hiatal hernia, lower esophageal sphincter, or both? Ann Intern Med 1992;117:977-982.

10. Mittal RK, Lange RC, McCallum RW. Identification and mechanism of delayed esophageal acid clearance in subjects with hiatus hernia. Gastroenterology 1987;92:130-135.

11. Sloan S, Kahrilas PJ. Impairment of esophageal emptying with hiatal hernia. Gastroenterology 1991;100:596-605.

12. Sonnenberg A, Lepsien G, Müller-Lissner SA, Koelz HR, Siewert JR, Blum AL. When is esophagitis healed? Esophageal endoscopy, histology and function before and after cimetidine treatment. Dig Dis Sci 1982;27:297-302

13. Eckardt VF. Does healing of esophagitis improve esophageal motor function? Dig Dis Sci 1988;33:161.


Publication date: May 1998 OESO©2011