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Motility disturbances caused by esophagitis
Volume 50, Number 5
November 1965
The Journal of T H O R A C I C A N
CARDIOVASCULAR SURGERY
Motility disturbances caused by esophagitis Arthur M. Olsen, M.D., and Jerry F. Schlegel, B.S. (by invitation), Rochester, Minn.
LOT many years it has been customary at this institution to perform esophagoscopy on all patients who are candidates for repair of esophageal hiatal hernia. Aside from the obvious fact that carcinoma, benign stric ture, or shortening of the esophagus may be present in association with hiatal hernia, the principal purpose of esophagoscopy is to determine the presence or absence of esophagitis. The presence of esophagitis indicates that reflux has occurred and that surgical repair of the hernia is indicated. 1 · 2 Paradoxically, surgeons have recognized that a marked degree of esophagitis may influence adversely the surgical results. When severe esophagitis heals, cicatricial stricture and shortening of the esophagus may occur.3 Even if obvious organic change does not take place, patients with esopha gitis may experience less favorable results than those whose preoperative esophagitis was minimal. For some time, we have From the Section of Medicine, Mayo Clinic and Mayo Foundation (Dr. Olsen). Mr. Schlegel is a technical assistant in the Section of Physiology. Read at the Forty-fifth Annual Meeting of The American Association for Thoracic Surgery, New Orleans, La., March 29-31, 1965.
suspected that esophagitis may cause a disturbance in the normal function of the esophagus. With this in mind, a study of the esophageal motility patterns in patients with an esophagoscopic diagnosis of esophagitis was made. Methods Of 60 patients who had had an esopha goscopic diagnosis of esophagitis, 10 were eliminated from our study because they had clinical, roentgenologic, and manometric evidence of achalasia, diffuse spasm, or scleroderma. The motility records of the remaining 50 patients were evaluated. Based on the description by the esophagoscopist, the cases of esophagitis were classified into three catgories according to the degree of esophagitis. In the 19 cases classified as minimal, there was reddening and thickening of the mucous membrane of the esophagus and the mucosa was readily traumatized as the esophagoscope was passed. Seventeen patients were considered to have moderate esophagitis; in these, there was marked thickening and injection of the mucous membrane, and superficial ulcération often was present. Fourteen 6 0 7
Journal of
608
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
cases were classified as marked esophagitis, characterized by severe ulcération with bleeding. Forty-one of the 50 patients had an esophagoscopic diagnosis of hiatal hernia, and in 4 of these there was shortening of the esophagus with stricture. On review of the roentgenographic findings, 35 of these 50 patients were considered to have hiatal hernia, and 4 of these 35 had shortening of the esophagus with stricture. All of the patients had undergone an esophageal motility examination by manometric techniques. The methods employed and the characteristic motility patterns for such disturbances as achalasia,4 diffuse spasm,5 scleroderma,0 and hiatal hernia 7 ' 8 have been described elsewhere. Particular attention was paid to the resting pressures at the hiatus of the diaphragm and at the lower sphincter and to the responses of the esophagus and the lower sphincter to deglutition. Four detecting units, 5 cm. apart, were employed so that deglutition pressures were recorded simultaneously at various levels in the esophagus. A measure of the transmucosal potential difference (P.D.) was made in all patients.8 Results The resting pressures at the lower sphinc ter were correlated with the degree of esophagitis (Table I). Eight of the patients had normal pressure and P.D. profiles at the gastroesophageal junction (Fig. 1, Table I). In the patients with minimal esophagitis, there were no abnormal findings except for
Table I. Manometric findings on motility at esophagogastric junction in 50 patients with esophagoscopic diagnosis of esophagitis Patients (No.)
Severity
of
Total
Normal
Minimal Moderate Severe
19 17 14
Totals
50
2 4 2 8
esophagitis
Hiatal hernia
Feeble sphincter
17 11 9
0 4 5 9*
37*
*Four patients had both feeble sphincter and hiatal hernia.
the signs of hiatal hernia, when it was present. However, among the patients with moderate esophagitis, there were 4 in whom the increase in pressure at the lower sphinc ter was very slight (Fig. 1, lower panel). Hypotensive sphincters were also noted in 5 of the 14 patients who had severe esophagitis. As might be expected, patients with "feeble" sphincters are much more likely to have gastroesophageal reflux than are those with normal pressure at the lower sphincter. Responses to deglutition in these 50 patients were classified into four categories (Table II). Normal responses to deglutition were noted in 14 patients (28 per cent) (Fig. 2, a); however, in 16 (32 per cent) there was evidence of motor incoordination, especially low in the esophagus (Fig. 2, b). The incoordination was evidenced by re petitive contractions in response to swallow ing, and responses were often of greater amplitude than normal. In most instances, the sphincter relaxed in response to swallow ing but excessive contraction of the sphincter often occurred. Very feeble or weak contractions were noted in 16 (32 per cent) of the group (Fig. 2, c ) . It is of special interest that in this group the majority of the contractions were simultaneous and the motility patterns closely resembled the patterns associated with scleroderma or achalasia. However, the sphincter invariably showed some evidence of relaxation after deglutition, and, there fore, the manometric findings were more like those of scleroderma than of achalasia. Finally, 4 patients showed complete motor failure (Fig. 2, d). The pattern resembled that of advanced achalasia or severe sclerodermal involvement of the esophagus. Three of the 4 patients with motor failure had severe esophagitis. Table II correlates the degree of esopha gitis with the type of motility disturbance seen. In the 19 cases of minimal esopha gitis, motility was normal in most cases or, at the most, minor motor incoordination was noted. Only 3 of the patients with minimal esophagitis had weak contractions.
Volume 50 Number 5 November, 1905
Esophagitis
609
P.D = 50 cm. H20
from
0pe
incisors
"-r/p^v~C^ «2
Balloon-Tip Pneumograph-
P. D
-~TVWVY*V*II
. .. .^,c 47
ΑλΛ
ίϊή\ftftyjsw
ΛΑΛ.ΑΜ
VW ΛΑ \Ν M / J V λΛΑ \ΛΛ
\Λ/ M /\Λ W
ί\Λ/ Λ^ hh ΛΛ <\Α vV Λ.
"^wC^tn'i
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ifiTf/VVVW
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46
Fig. 1. Resting pressure and potential difference (P.D.) profiles of the gastroesophageal junction in 2 patients with esophagitis. Each of the arrows indicates a 0.5-cm. cephalad withdrawal of the detecting units from the stomach into the esophagus. The (+) and (-) signs denote the direction of intraluminal pressure swings with inhalation which is represented by an upward deflection on the pneumographic tracing. The pressure and P.D. patterns in the tipper panel are normal. Findings suggestive of hiatal hernia are present in the lower panel. The pressures in the junctional region are low and the change in potential difference is 2 to 3 cm. cephalad to the site of respiratory reversal.
Table II. Manometric findings on esophageal motility responses to deglutition in 50 patients with esophagoscopic diagnosis of esophagitis Patients
(No.)
Motor incoordination
Severity of esophagitis
Total
Minimal Moderate Severe
19 17 14
7 5 2
9 5 2
3 6 7
0 1 3
Totals
50
14
16
lT
4
Normal
In the group of patients with moderate esophagitis, 6 had weak esophageal con tractions and 1 patient had complete motor failure; in the remainder of these patients the motility was either normal or showed motor incoordination. Only 2 of the 14
Weak contractions
Motor failure
patients with severe esophagitis had normal motility. Two others had signs of motor incoordination, while the remainder showed evidence of a serious disturbance with either weak, and usually simultaneous, contractions or complete motor failure.
Journal of
6 10
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
Normal
28 %
Motor
Incoordination
32%
Fig. 2. Patterns of normal and abnormal responses to deglutition in 50 patients with esophagitis. a, Normal, b, Motor incoordination, c, Weak contractions, d, Motor failure.
Discussion Surgeons have long been keenly aware of the frequent association of hiatal hernia and esophagitis.2 Incompetence of the lower esophageal sphincter with gastroesophageal reflux in patients with hiatal hernia often can be demonstrated roentgenographically. 1 · 9 Cineradiographic techniques have been helpful in this regard. Esophagoscopy is essential for the diagnosis of esophagitis. The anatomic and physiologic mecha nisms which prevent the régurgitation of gastric secretions into the esophagus have been reviewed.2-10 Competence of the lower sphincter is certainly the most important factor in prevention of gastroesophageal re
flux.11' 12 Peristaltic activity of the esophagus likewise is a significant factor in the preven tion of reflux, a fact that probably has not received the attention that it deserves. In the absence of peristalsis, regurgitated secretions may remain in the esophagus for considerable periods of time and the pro longed contact of gastric juice with the mucosa hastens the development of esopha gitis. From our studies, it would appear that a significant degree of esophagitis may be responsible for a reduction in the zone of increased pressure at the lower sphincter. This was seen in 9 of our patients, 4 of whom already had roentgenographic evi dence of short esophagus with narrowing
Volume 50
Esophagitis
Number 5
6 11
November, 1965
at the esophagogastric junction. Not only does the feeble sphincter permit reflux but also the resulting inflammatory change in the terminal part of the esophagus may render the lower sphincter more incompetent than ever. Changes in motility of the esophagus itself were more striking than the findings at the sphincter. Only 14 of our patients with esophagitis had normal peristaltic activity. In the remaining 36, there was evidence of motor incoordination, feeble contractions with loss of peristalsis, and, in a few instances, complete motor failure. In several of these cases the changes were so marked that a diagnosis of scleroderma or achalasia was suggested. If at all possible, repair of esophageal hiatal hernia should be undertaken before secondary changes associated with esophagitis have taken place. Hiatal hernia was not demonstrated in 9 of the 50 patients with esophagitis. In most of these cases the esophagitis was caused by vomiting or functional régurgita tion. The motility changes that we have seen with esophagitis are just as likely to occur in this group of patients as in those whose esophagitis appears to be a compli cation of hiatal hernia. Other investigators 13 · 14 have made efforts to correlate reflux of acid with pressure measurements in the lower part of the esophagus. It is possible that the esophagitis was more marked in our patients than in the patients described by Tuttle and Gross man13 and by Besançon and his associates.14 In any case, we found definite derangements of esophageal function in those of our patients who had any marked degree of esophagitis, and some of these patients also had evidence of a weak sphincter. We think that information such as we have obtained should be useful to the surgeon in his eval uation of hiatal hernia. Summary As shown by studies of esophageal motility, esophagitis may have an effect on the function of the esophagus and the lower sphincter. In general, the degree of distur-
bance is proportional to the severity of the esophagitis. The disturbances seen with esophagitis include motor incoordination, feeble and often nonperistaltic contractions, and, in a few instances, complete motor failure. In addition, the lower sphincter may be weak and incompetent. Esophagoscopy is indicated in patients who have symptoms suggestive of esophagitis and in patients who are possible candidates for surgical repair of hiatal hernia. If esophagitis is demonstrated at esophagoscopy, esophageal motility studies are indicated. Such studies are distinctly helpful in determining whether the esophagitis may be associated with a disturbance of motility either in the esopha gus itself or at the lower sphincter. REFERENCES 1 Johnstone, A. S.: Oesophagitis and Peptic Ulcer of the Oesophagus, Brit. J. Radiol. 28: 229, 1955. 2 Allison, P. R.: Reflux Esophagitis, Sliding Hiatal Hernia, and the Anatomy of Repair, Surg., Gynec. & Obst. 92: 419, 1951. 3 Olsen, A. M., and Harrington, S. W.: Esopha geal Hiatal Hernias of Short Esophagus Type: Etiologic and Therapeutic Considerations, J. THORACIC SURG. 17: 189,
1948.
4 Butin, J. W., Olsen, A. M., Moersch, H. J., and Code, C. F.: Study of Esophageal Pres sures in Normal Persons and Patients With Cardiospasm, Gastroenterology 23: 278, 1953. 5 Creamer, B., Donoghue, E., and Code, C. F.: Pattern of Esophageal Motility in Diffuse Spasm, Gastroenterology 34: 782, 1958. 6 Creamer, B., Andersen, H. A., and Code, C. F.: Esophageal Motility in Patients With Scleroderma and Related Diseases, Gastroenterologia 86: 763, 1956. 7 Code, C. F., Kelley, M. L., Jr., Schlegel, J. F., and Olsen, A. M.: Detection of Hiatal Herhia During Esophageal Motility Tests, Gastro enterology 43: 521, 1962. 8 Helm, W. J., Schlegel, J. F., Code, C. F., and Summerskill, W. H. J.: Identification of the Gastroesophageal Mucosal Junction by Transmucosal Potential in Healthy Subjects and Pa tients With Hiatal Hernia, Gastroenterology 48: 25, 1965. 9 Vandervelde, G. M., and Carlson, H. C : Esophageal Reflux, Am. J. Roentgenol. 92: 989, 1964. 10 Lyons, W. S., Ellis, F. H., Jr., and Olsen, A. M.: The Gastroesophageal "Sphincter"
Journal of
6 12
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
Mechanism: A Review, Proc. Staff Meet., Mayo Clin. 31: 605, 1956. 11 Fyke, F. E., Jr., Code, C. F., and Schlegel, J. F.: The Gastroesophageal Sphincter in Healthy Human Beings, Gastroenterologia 86: 135, 1956. 12 Meiss, J. H., Grindlay, J. H., and Ellis, F. H., Jr.: The Gastroesophageal Sphincter Mecha nism. II. Further Experimental Studies in the Dog,
J. THORACIC SURG. 36: 156,
1958.
13 Tuttle, S. G., and Grossman, M. I.: Detection of Gastroesophageal Reflux by Simultaneous Measurement of Intraluminal Pressure and pH, Proc. Soc. Exper. Biol. & Med. 98: 225, 1958. 14 Besançon, F., Baujat, J.-P., and Debray, C : Le reflux gastro-œsophagien: étude pH-graphique et électromanographique, Semaine hôp. Paris 38: 1569, 1962. (For Discussion, see page 631)
November 1965
The Journal of T H O R A C I C A N
CARDIOVASCULAR SURGERY
Motility disturbances caused by esophagitis Arthur M. Olsen, M.D., and Jerry F. Schlegel, B.S. (by invitation), Rochester, Minn.
LOT many years it has been customary at this institution to perform esophagoscopy on all patients who are candidates for repair of esophageal hiatal hernia. Aside from the obvious fact that carcinoma, benign stric ture, or shortening of the esophagus may be present in association with hiatal hernia, the principal purpose of esophagoscopy is to determine the presence or absence of esophagitis. The presence of esophagitis indicates that reflux has occurred and that surgical repair of the hernia is indicated. 1 · 2 Paradoxically, surgeons have recognized that a marked degree of esophagitis may influence adversely the surgical results. When severe esophagitis heals, cicatricial stricture and shortening of the esophagus may occur.3 Even if obvious organic change does not take place, patients with esopha gitis may experience less favorable results than those whose preoperative esophagitis was minimal. For some time, we have From the Section of Medicine, Mayo Clinic and Mayo Foundation (Dr. Olsen). Mr. Schlegel is a technical assistant in the Section of Physiology. Read at the Forty-fifth Annual Meeting of The American Association for Thoracic Surgery, New Orleans, La., March 29-31, 1965.
suspected that esophagitis may cause a disturbance in the normal function of the esophagus. With this in mind, a study of the esophageal motility patterns in patients with an esophagoscopic diagnosis of esophagitis was made. Methods Of 60 patients who had had an esopha goscopic diagnosis of esophagitis, 10 were eliminated from our study because they had clinical, roentgenologic, and manometric evidence of achalasia, diffuse spasm, or scleroderma. The motility records of the remaining 50 patients were evaluated. Based on the description by the esophagoscopist, the cases of esophagitis were classified into three catgories according to the degree of esophagitis. In the 19 cases classified as minimal, there was reddening and thickening of the mucous membrane of the esophagus and the mucosa was readily traumatized as the esophagoscope was passed. Seventeen patients were considered to have moderate esophagitis; in these, there was marked thickening and injection of the mucous membrane, and superficial ulcération often was present. Fourteen 6 0 7
Journal of
608
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
cases were classified as marked esophagitis, characterized by severe ulcération with bleeding. Forty-one of the 50 patients had an esophagoscopic diagnosis of hiatal hernia, and in 4 of these there was shortening of the esophagus with stricture. On review of the roentgenographic findings, 35 of these 50 patients were considered to have hiatal hernia, and 4 of these 35 had shortening of the esophagus with stricture. All of the patients had undergone an esophageal motility examination by manometric techniques. The methods employed and the characteristic motility patterns for such disturbances as achalasia,4 diffuse spasm,5 scleroderma,0 and hiatal hernia 7 ' 8 have been described elsewhere. Particular attention was paid to the resting pressures at the hiatus of the diaphragm and at the lower sphincter and to the responses of the esophagus and the lower sphincter to deglutition. Four detecting units, 5 cm. apart, were employed so that deglutition pressures were recorded simultaneously at various levels in the esophagus. A measure of the transmucosal potential difference (P.D.) was made in all patients.8 Results The resting pressures at the lower sphinc ter were correlated with the degree of esophagitis (Table I). Eight of the patients had normal pressure and P.D. profiles at the gastroesophageal junction (Fig. 1, Table I). In the patients with minimal esophagitis, there were no abnormal findings except for
Table I. Manometric findings on motility at esophagogastric junction in 50 patients with esophagoscopic diagnosis of esophagitis Patients (No.)
Severity
of
Total
Normal
Minimal Moderate Severe
19 17 14
Totals
50
2 4 2 8
esophagitis
Hiatal hernia
Feeble sphincter
17 11 9
0 4 5 9*
37*
*Four patients had both feeble sphincter and hiatal hernia.
the signs of hiatal hernia, when it was present. However, among the patients with moderate esophagitis, there were 4 in whom the increase in pressure at the lower sphinc ter was very slight (Fig. 1, lower panel). Hypotensive sphincters were also noted in 5 of the 14 patients who had severe esophagitis. As might be expected, patients with "feeble" sphincters are much more likely to have gastroesophageal reflux than are those with normal pressure at the lower sphincter. Responses to deglutition in these 50 patients were classified into four categories (Table II). Normal responses to deglutition were noted in 14 patients (28 per cent) (Fig. 2, a); however, in 16 (32 per cent) there was evidence of motor incoordination, especially low in the esophagus (Fig. 2, b). The incoordination was evidenced by re petitive contractions in response to swallow ing, and responses were often of greater amplitude than normal. In most instances, the sphincter relaxed in response to swallow ing but excessive contraction of the sphincter often occurred. Very feeble or weak contractions were noted in 16 (32 per cent) of the group (Fig. 2, c ) . It is of special interest that in this group the majority of the contractions were simultaneous and the motility patterns closely resembled the patterns associated with scleroderma or achalasia. However, the sphincter invariably showed some evidence of relaxation after deglutition, and, there fore, the manometric findings were more like those of scleroderma than of achalasia. Finally, 4 patients showed complete motor failure (Fig. 2, d). The pattern resembled that of advanced achalasia or severe sclerodermal involvement of the esophagus. Three of the 4 patients with motor failure had severe esophagitis. Table II correlates the degree of esopha gitis with the type of motility disturbance seen. In the 19 cases of minimal esopha gitis, motility was normal in most cases or, at the most, minor motor incoordination was noted. Only 3 of the patients with minimal esophagitis had weak contractions.
Volume 50 Number 5 November, 1905
Esophagitis
609
P.D = 50 cm. H20
from
0pe
incisors
"-r/p^v~C^ «2
Balloon-Tip Pneumograph-
P. D
-~TVWVY*V*II
. .. .^,c 47
ΑλΛ
ίϊή\ftftyjsw
ΛΑΛ.ΑΜ
VW ΛΑ \Ν M / J V λΛΑ \ΛΛ
\Λ/ M /\Λ W
ί\Λ/ Λ^ hh ΛΛ <\Α vV Λ.
"^wC^tn'i
Open-Tip
+++++ + ""4/
Pneumograph
ifiTf/VVVW
W^.rvWW^Wl „■ ,,( VWWWW<
46
Fig. 1. Resting pressure and potential difference (P.D.) profiles of the gastroesophageal junction in 2 patients with esophagitis. Each of the arrows indicates a 0.5-cm. cephalad withdrawal of the detecting units from the stomach into the esophagus. The (+) and (-) signs denote the direction of intraluminal pressure swings with inhalation which is represented by an upward deflection on the pneumographic tracing. The pressure and P.D. patterns in the tipper panel are normal. Findings suggestive of hiatal hernia are present in the lower panel. The pressures in the junctional region are low and the change in potential difference is 2 to 3 cm. cephalad to the site of respiratory reversal.
Table II. Manometric findings on esophageal motility responses to deglutition in 50 patients with esophagoscopic diagnosis of esophagitis Patients
(No.)
Motor incoordination
Severity of esophagitis
Total
Minimal Moderate Severe
19 17 14
7 5 2
9 5 2
3 6 7
0 1 3
Totals
50
14
16
lT
4
Normal
In the group of patients with moderate esophagitis, 6 had weak esophageal con tractions and 1 patient had complete motor failure; in the remainder of these patients the motility was either normal or showed motor incoordination. Only 2 of the 14
Weak contractions
Motor failure
patients with severe esophagitis had normal motility. Two others had signs of motor incoordination, while the remainder showed evidence of a serious disturbance with either weak, and usually simultaneous, contractions or complete motor failure.
Journal of
6 10
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
Normal
28 %
Motor
Incoordination
32%
Fig. 2. Patterns of normal and abnormal responses to deglutition in 50 patients with esophagitis. a, Normal, b, Motor incoordination, c, Weak contractions, d, Motor failure.
Discussion Surgeons have long been keenly aware of the frequent association of hiatal hernia and esophagitis.2 Incompetence of the lower esophageal sphincter with gastroesophageal reflux in patients with hiatal hernia often can be demonstrated roentgenographically. 1 · 9 Cineradiographic techniques have been helpful in this regard. Esophagoscopy is essential for the diagnosis of esophagitis. The anatomic and physiologic mecha nisms which prevent the régurgitation of gastric secretions into the esophagus have been reviewed.2-10 Competence of the lower sphincter is certainly the most important factor in prevention of gastroesophageal re
flux.11' 12 Peristaltic activity of the esophagus likewise is a significant factor in the preven tion of reflux, a fact that probably has not received the attention that it deserves. In the absence of peristalsis, regurgitated secretions may remain in the esophagus for considerable periods of time and the pro longed contact of gastric juice with the mucosa hastens the development of esopha gitis. From our studies, it would appear that a significant degree of esophagitis may be responsible for a reduction in the zone of increased pressure at the lower sphincter. This was seen in 9 of our patients, 4 of whom already had roentgenographic evi dence of short esophagus with narrowing
Volume 50
Esophagitis
Number 5
6 11
November, 1965
at the esophagogastric junction. Not only does the feeble sphincter permit reflux but also the resulting inflammatory change in the terminal part of the esophagus may render the lower sphincter more incompetent than ever. Changes in motility of the esophagus itself were more striking than the findings at the sphincter. Only 14 of our patients with esophagitis had normal peristaltic activity. In the remaining 36, there was evidence of motor incoordination, feeble contractions with loss of peristalsis, and, in a few instances, complete motor failure. In several of these cases the changes were so marked that a diagnosis of scleroderma or achalasia was suggested. If at all possible, repair of esophageal hiatal hernia should be undertaken before secondary changes associated with esophagitis have taken place. Hiatal hernia was not demonstrated in 9 of the 50 patients with esophagitis. In most of these cases the esophagitis was caused by vomiting or functional régurgita tion. The motility changes that we have seen with esophagitis are just as likely to occur in this group of patients as in those whose esophagitis appears to be a compli cation of hiatal hernia. Other investigators 13 · 14 have made efforts to correlate reflux of acid with pressure measurements in the lower part of the esophagus. It is possible that the esophagitis was more marked in our patients than in the patients described by Tuttle and Gross man13 and by Besançon and his associates.14 In any case, we found definite derangements of esophageal function in those of our patients who had any marked degree of esophagitis, and some of these patients also had evidence of a weak sphincter. We think that information such as we have obtained should be useful to the surgeon in his eval uation of hiatal hernia. Summary As shown by studies of esophageal motility, esophagitis may have an effect on the function of the esophagus and the lower sphincter. In general, the degree of distur-
bance is proportional to the severity of the esophagitis. The disturbances seen with esophagitis include motor incoordination, feeble and often nonperistaltic contractions, and, in a few instances, complete motor failure. In addition, the lower sphincter may be weak and incompetent. Esophagoscopy is indicated in patients who have symptoms suggestive of esophagitis and in patients who are possible candidates for surgical repair of hiatal hernia. If esophagitis is demonstrated at esophagoscopy, esophageal motility studies are indicated. Such studies are distinctly helpful in determining whether the esophagitis may be associated with a disturbance of motility either in the esopha gus itself or at the lower sphincter. REFERENCES 1 Johnstone, A. S.: Oesophagitis and Peptic Ulcer of the Oesophagus, Brit. J. Radiol. 28: 229, 1955. 2 Allison, P. R.: Reflux Esophagitis, Sliding Hiatal Hernia, and the Anatomy of Repair, Surg., Gynec. & Obst. 92: 419, 1951. 3 Olsen, A. M., and Harrington, S. W.: Esopha geal Hiatal Hernias of Short Esophagus Type: Etiologic and Therapeutic Considerations, J. THORACIC SURG. 17: 189,
1948.
4 Butin, J. W., Olsen, A. M., Moersch, H. J., and Code, C. F.: Study of Esophageal Pres sures in Normal Persons and Patients With Cardiospasm, Gastroenterology 23: 278, 1953. 5 Creamer, B., Donoghue, E., and Code, C. F.: Pattern of Esophageal Motility in Diffuse Spasm, Gastroenterology 34: 782, 1958. 6 Creamer, B., Andersen, H. A., and Code, C. F.: Esophageal Motility in Patients With Scleroderma and Related Diseases, Gastroenterologia 86: 763, 1956. 7 Code, C. F., Kelley, M. L., Jr., Schlegel, J. F., and Olsen, A. M.: Detection of Hiatal Herhia During Esophageal Motility Tests, Gastro enterology 43: 521, 1962. 8 Helm, W. J., Schlegel, J. F., Code, C. F., and Summerskill, W. H. J.: Identification of the Gastroesophageal Mucosal Junction by Transmucosal Potential in Healthy Subjects and Pa tients With Hiatal Hernia, Gastroenterology 48: 25, 1965. 9 Vandervelde, G. M., and Carlson, H. C : Esophageal Reflux, Am. J. Roentgenol. 92: 989, 1964. 10 Lyons, W. S., Ellis, F. H., Jr., and Olsen, A. M.: The Gastroesophageal "Sphincter"
Journal of
6 12
Olsen and Schlegel
Thoracic and Cardiovascular Surgery
Mechanism: A Review, Proc. Staff Meet., Mayo Clin. 31: 605, 1956. 11 Fyke, F. E., Jr., Code, C. F., and Schlegel, J. F.: The Gastroesophageal Sphincter in Healthy Human Beings, Gastroenterologia 86: 135, 1956. 12 Meiss, J. H., Grindlay, J. H., and Ellis, F. H., Jr.: The Gastroesophageal Sphincter Mecha nism. II. Further Experimental Studies in the Dog,
J. THORACIC SURG. 36: 156,
1958.
13 Tuttle, S. G., and Grossman, M. I.: Detection of Gastroesophageal Reflux by Simultaneous Measurement of Intraluminal Pressure and pH, Proc. Soc. Exper. Biol. & Med. 98: 225, 1958. 14 Besançon, F., Baujat, J.-P., and Debray, C : Le reflux gastro-œsophagien: étude pH-graphique et électromanographique, Semaine hôp. Paris 38: 1569, 1962. (For Discussion, see page 631)