Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

  Browse by Author
  Browse by Movies
OESO©2015
 
Volume: The Esophagogastric Junction
Chapter: GER and barrier dysfunction
 

Hiatal hernia

What are the manometric features of a sliding hiatal hernia? How is the best to reduce false negative lower esophageal sphincter manometries in hiatal hernia?

J.H. Schneider, U. Schott, K.E. Grund, H.D. Becker (Tübingen)

Definition

A hiatal hernia is established when a part of the stomach slips through the diaphragmatic esophageal hiatus into the thorax; but it is still questionable whether this anatomical finding is strictly an esophageal disease or not.

Background

The importance of hiatal hernia in gastroesophageal reflux disease (GERD) was emphased early by Allison [1]. In the mid of the 70th it became clear that the prevalence of a sliding hernia is age-related and can be seen in the youth to 10% over 50 years to 70%, and in 90 years old individuals to 100% [2, 3]. As a result, the importance of a sliding hernia was downplayed for the pathogenesis of GERD [4, 5]. In recent studies in humans and animals new evidence suggests that the extrinsic force of the diaphragmatic crura generates the gastroesophageal junction competence [6, 7]. If it is like this, the damage of the diaphragmatic crus in sliding hernias has to be reevaluated for the importance of the pathogenesis of GERD.

Classification

There are numerous classifications to distinguish sliding hiatal hernias. Rituo determined hernias as congenital or acquired [8]. Richards categorized hernias into true and false hernias, a hernia with a sac is true and without is false [9]. Heitmann classified hypertone, normotone and hypotone lower esophageal sphincter (LES) function [10]. Siewert combined anatomical, manometrical and clinical features to categorize hiatal sliding hernia [2]. Patti used the size of the hernia, the competence of the LES and esophageal acid exposure and mucosal injury [11]. Sloan created a reflux score using a furomanometry technique in patients with sliding hernias [12].

Symptoms

Depending on manometric or endoscopic studies the percentage of patients with symptoms range between 30 to 60% [13]. When symptoms occur, they normally indicate complications of a sliding hernia [14]. Typical symptoms are: dysphagia, substernal burning, nocturnal reflux and heartburn.

The major problem is caused by gastroesophageal reflux. Severe esophagitis is seen uncommonly without a sliding hernia, but the incompetence of the LES is well documented without any evidence of sliding hiatal hernia. There is clinical evidence that the larger the hernia, the more severe is the incompetence of the LES [12].

Bleeding

The occurrence of non-iron deficiency anemia in patients with sliding hernia is controversial. Rüsch and Groitl saw chronic bleedings only in mixed and paraesophageal hernias [15]. Cameron and Kerklin found bleedings also in sliding hernias [16] and its successful surgical repair is well documented [17]. Three locations were found to cause beedings mainly: the esophagus, the gastric pouch and the gastroesophageal junction [18]. Commonly Mallory Weiss lesions are associated with hernias and mucosal intusseption with ortho- or retrograde mucosal prolaps. Concomitant the spontaneous intramural hematoma - a so-called apoplexy of the esophagus - was seen during medical therapy or coagulation deficiency.

Non cardiac chest pain

Sliding hiatal hernias are able to provoke severe chest pain. Similarly to coronary heart disease symptoms may be fugitive and varying in duration, intensity and frequency. The reasons responsible for retrosternal pain attacks are not well understood [19]. Balloon dilation of the distal esophagus produces burning pain, indicating a motor disorder similar to pain sensation after LES dilation in patients with achalasia [20]. The vagal nerve contains efferent and afferent neurons. It might be possible that compression of the vagal nerves or chemical stimulation [21] causes the chest pain.

Own data

Patients and methods

Twenty three symptomatic patients (11 male and 12 females, mean age 53 ± 7.6 years, range 25-73) were referred for evaluation of GERD. Each patient underwent endoscopy, radiographic examination, stationary manometry and 24-hour pH metry. A control group of 32 healthy volunteers (15 male and 17 female, mean age 23 ± 4.8 years, range 19-27) got stationary manometry and 24-hour pH metry.

Symptoms

Each patient was questioned about duration, quality and frequency of dysphagia, substernal burning, nocturnal reflux, heartburn, chest pain and cough (Table I).

Radiographic studies

The results from barium esophagography were reviewed by an experienced radiologist. The axial length and the diameter of the hiatal hernia was measured at mid swallow in prone position when the esophagus reached the maximum of distention with barium. Special provoking maneuvers like Müller maneuver or leg lifts were not performed.

Endoscopy

Endoscopic studies were reviewed and the degree of esophageal injury was graded, according to Savary-Miller classification: grade 1: erythema, grade 2: linear erosions, grade 3: confluent erosions and grade 4: stricture or Barrett's disease.

 

Esophageal manometry

Each symptomatic patient and healthy volunteer underwent a standard stationary esophageal manometry after an overnight fast as described previously [22]. Using the station pull through method the LES pressures were measured, the LES length, the intra-abdominal length of the esophagus and the duration of LES relaxation. Esophageal body motility was measured assessing 10 wet swallows of 5 ml water. Two independent investigators analyzed the contraction amplitude, duration of amplitude and velocity.

24-hour esophageal pH monitoring

Ambulatory 24-hour pH monitoring was performed in each individual. The pH probe was placed 5 cm above the upper border of the manometrically determined LES. The data were analyzed using the DeMeester score.

Results

Symptoms

Preliminary results showed that the occurrence of symptoms increased significantly
(p = 0.05) in patients with GERD and a hiatal hernia larger than 5 cm vs patients with GERD and a smaller hernia (< 3cm). The comparison between controls with negative acid score and hiatal hernia was highly significant.

Esophageal manometry

Tables II and III summarize the results of esophageal motility. The LES pressure was significantly decreased in larger hernias when compared to healthy individuals. The duration of LES relaxation during swallowing was prolonged in larger hernia.
Table II. Esophageal motility and lower esophage
Table III. Esophageal motility, esophageal contr

The proximal esophageal body motility showed no significant difference between healthy volunteers and patients with hiatal hernia and positive acid score. In the distal esophageal body, the contraction amplitude and velocity were significantly decreased
(p = 0.05).

Esophageal acid exposure

Data of 24-hour pH monitoring are summarized in Table IV. Hernias > 5 cm vs 3 cm induced more gastroesophageal acid reflux. The difference was not significant, but compared to the control group, highly significant.
Table IV. The gastroesophageal reflux was in bot

Conclusion

The difficulty to get the right diagnosis in patients with diaphragmatic hiatal esophageal hernia starts with the definifion. In radiographic examinations it is well established that the gastroesophageal junction normally slips during swallowing and respiratory movements through the diaphragmatic hiatus into the thoracic cavity [23]. Due to the tension of the longitudinal muscle layer, the tubular esophagus becomes shorter and the high pressure zone of the gastroesophageal junction becomes, for some seconds, detectable above the diaphragm [24]. To distinguish a physiological from a pathological situation, the persistence of a sliding hiatal hernia should be diagnosed in recumbent position, out of a swallowing event. In some cases, it might be helpful to increase the abdominal pressure by using the Müller maneuver, or to lift the legs. Our data confirm, as in recent studies, that esophageal manometry is only helpful to evaluate motility abnormalities in patients with gastroesophageal reflux, although the majority of diaphragmatic esophageal hernias persist without gastroesophageal reflux and detectable injuries of the esophageal mucosa.

References

1. Allison PR. Reflux esophagitis, sliding hiatal hernia and anatomy of repair. Surg Gynecol Obstet 1951;92:419-431.

2. Blum AL, Siewert JR. Pathogenese, Diagnostik und konservative Therapie der Refluxkrankheit. In: Siewert JR, Blum AL, Waldeck F, eds. Funktionsstörungen der Speiseöhre. Berlin, Heidelberg, New York: Springer.

3. Dodds WJ, Dent J, Hogan WJ. Mechanism of gastroesophageal reflux esophagitis. NEJM 1982;307:1547-1552.

4. Zaninotto G, DeMeester TR, Schwizer W. The lower esophageal sphincter in health and disease. Am J Surg 1988;155:104-111.

5. DeMeester TR, Lafontaine E, Joelsson BE. Relationship of a hiatal hernia to the function of the body of the esophagus and gastroesophageal junction. J Thorac Cardiovasc Surg 1981;82:547-558.

6. Mittal RK, Rochester DF, McCallum RW. Electrical and mechanical activity in the human lower esophageal sphincter during diaphragmatic contraction. J Clin Invest 1988;81:1182-1189.

7. Mittal RK, Rochester DF, McCallum RW. Sphincteric action of the diaphragm during relaxed lower esophageal sphincter in humans. Am J Physiol 1989;256:G139-G144.

8. Rituo M. Diaphragmatic hernia. JAMA 1930;94:15.

9. Richards LG. Non traumatic hernia of the diaphragm. An embryological viewpoint. Ann Otol Rhinol Laryngol 1923;32:1146.

10. Heitmann P. Der gastroosophageale Verschlussmechanismus bei Hiatusgleithernien. Interist 1969;10:249.

11. Patti MG, Goldberg HJ, Arcerto M, et al. Hiatal hernia size affects lower esophageal sphincter function esophageal acid exposure and degree of mucosal injury. Am J Surg 1996;171:182-186.

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

13. Stilson WL, et al. Hiatal hernia and gastroesophageal reflux. A clinical analysis of more than 1000 cases. Radiology 1969;93:1323.

14. Kerr RM. Hiatal hernia and mucosal prolaps. In: Castell DO, ed. The esophagus. Boston, Toronto, London: Little, Brown and Company, 1992:759-780.

15. Groitl H. Hat der gastroösophageale Prolaps eine klinische Bedeutung? 14. Kurs für prakt. Gastroenterologaen, Erlangen 1979.

16. Cameron AJ. Incidence of iron deficiency anemia in patients with large diaphragmatic hernia. A controlled study. Mayo Clin Proc 1976;51:767.

17. McCormath RJM, Walbaum PR. Hiatus hernia and anemia. J R Coll Surg Edinb 1968;13:150.

18. Holt J, et al. Iron absorption and blood loss in patients with hiatal hernia. Br Med J 1968;3:22.

19. Kemp HG, Vokonas PS, Cohn PF. The anginal syndrom associated with normal coronary arteriograms. Am J Med 1973;54:735-742.

20. Kramer P, Hollander W. Comparision of experimental esophageal pain with clinical pain of angina pectoris an esophageal disease. Gastroenterology 1955;29:719-743.

21. Christensen J. Origin and sensation in the esophagus. Am J Physiol 1984;246:221-225.

22. Schneider JH, Incarbone R, Rauch TH, Becker HD, Bremner CG, DeMeester TR. The contribution of the circular muscle of Willis to the lower esophageal sphincter. Gastroenterology 1994;106:564.

23. Dodds WJ, Stewart ET, et al. Movement of the feline esophagus associated with respiration and peristalsis. J Clin Invest 1973;52:1-13.

24. Winans CS. Alteration of lower esophageal sphincter characteristics with respiration. Gastroenterology 1972;62 380-382.


Publication date: May 1998 OESO©2015