- Email: [email protected]
Editorial comment: The short esophagus: Going, going, gone?
Editorial comment: The short esophagus: Going, going, gone? Steven R. DeMeester, MD and Tom R. DeMeester, MD, Los Angeles, Calif
From the Departments of Cardiothoracic Surgery, and Surgery, the University of Southern California Keck School of Medicine, Los Angeles, Calif
THE TOPIC OF ESOPHAGEAL SHORTENING is one that polarizes surgeons like few others in esophageal surgery. On the one hand are surgeons who have never seen a short esophagus and don’t believe it exists, while on the other there are those that are convinced that foreshortening of the esophagus is a real entity in a subset of patients with reflux disease. Gradually, as experience with antireflux surgery increases, most surgeons are beginning to recognize that in some patients reduction of the gastroesophageal junction below the diaphragmatic hiatus without tension is problematic. In this issue of Surgery (133:358-363), Dr Korn and colleagues have set out to prove that the short esophagus is a myth. To do so they compared esophageal length in 190 control subjects, 77 patients with erosive esophagitis, 74 with Barrett’s, and 29 with complicated Barrett’s (ulcer or stenosis), grouped the patients according to height, and concluded that since the differences they found were not significant, the “so-called short esophagus” does not exist. Before we critically review their methodology and conclusions, perhaps it would be worthwhile to briefly review the history of acquired esophageal shortening. The concern regarding esophageal shortening dates back nearly as far as the history of surgery for hiatal hernia and gastroesophageal reflux disease. Surgeons in the mid-1900s reported having difficulty reducing the gastroesophageal junction Accepted for publication December 13, 2002. Reprint requests: Steven R. DeMeester, MD, Assistant Professor of Cardiothoracic Surgery, Norris Comprehensive Cancer Center, 1441 Eastlake Ave, Ste 7418, Los Angeles, CA 900330804. Surgery 2003;133:364-7. © 2003 Mosby, Inc. All rights reserved. 0039-6060/2003/$30.00 +0 doi:10.1067/msy.2003.116
364 SURGERY
below the diaphragmatic hiatus in patients with advanced reflux disease. Termed “acquired esophageal shortening,” the problem was frequent enough that a variety of surgical options for addressing it were proposed. The most popular solutions included esophageal resection, moving the distal esophagus toward the dome of the diaphragm, stricturoplasty, leaving the fundoplication in an intrathoracic location, and what subsequently has become the most accepted surgical solution, the Collis gastroplasty. It is difficult to believe that all these techniques were developed for a problem that never existed, particularly since most were proposed by insightful and experienced surgeons. Take for example Dr Leigh Collis. He spent many years of his life studying the diaphragm and hiatal hernias and wrote extensively about the anatomy and pathophysiology of this area.1-4 His careful clinical observations established fundamental principles about the pathophysiology of hiatal hernias and reflux disease. In a review of 450 consecutive patients with hiatal hernia, Dr Collis linked anemia with large paraesophageal hiatal hernias, excluded esophagitis as the cause, and proposed the concept of the “riding ulcer” occurring in the portion of the stomach that crosses the crus.5 He applied this same logic and clinicalanatomic knowledge to his surgical solution for acquired esophageal shortening when he proposed the technique of gastroplasty.6 The widespread utilization of his technique, and the acceptance by most of the leading esophageal surgeons during the last 20 years that the entity of acquired esophageal shortening exists, are testimony to the fact that it is a clinical reality. The question arises as to how often is it present, and can it be determined preoperatively? Clearly medical therapy for reflux is far superior today than it was even 20 years ago, and in most patients reflux-induced esophageal injury can be healed
Surgery Volume 133, Number 4
with the potent acid-suppression medications currently available. It is likely that these medications are reducing the severity of esophageal injury in many patients and correspondingly the prevalence of esophageal shortening may be decreasing; still, there remain patients with advanced reflux disease who when operated upon are found to have a gastroesophageal junction that will not reduce below the diaphragmatic hiatus without tension. An obvious issue related to the prevalence of a short esophagus is that surgeons have individual interpretations of what constitutes excessive tension. Further, the frequency of encountering a shortened esophagus is related to the types of patients being operated on, with the highest frequency occurring in tertiary referral centers where the most complex patients end up. It also depends on the approach and degree of esophageal mobilization performed prior to length assessment. In spite of these variables, most centers report finding a foreshortened esophagus in 3-14% of patients.7-11 It would be ideal if patients with a short esophagus could be identified before surgery so that the surgeon is prepared to address the problem with extensive esophageal mobilization and if necessary a Collis gastroplasty. With this goal in mind several investigators, including Collis himself, have tried to determine a method to accurately predict esophageal foreshortening prior to surgery. Techniques tried include endoscopic measurements of length, measurements based on the location of the change in electrical potential between the mucosa of the esophagus and stomach, radiographic measurements, external chest measurements, and manometric measurements of length.12-14 None of these methods have proved satisfactory or reliable. Instead, clinical indicators such as a large (5 cm) nonreducing hiatal hernia, long-segment Barrett’s esophagus, severe stricture, intrathoracic stomach, and a failed prior fundoplication all portend the possibility of a foreshortened esophagus.15-17 In this issue of Surgery, Dr Korn and colleagues claim that since they have never seen a short esophagus, the entity doesn’t exist. At the very outset this statement invites concern, since the mere fact that someone hasn’t seen something does not preclude its existence. However, the authors then try to prove that the short esophagus doesn’t exist by comparing the manometrically determined esophageal length in subsets of patients with varying severity of reflux disease. The authors introduce the topic by alluding to Dr Norman Barrett’s misconception about the columnar-lined esophagus being a tubularized stomach in the chest with a
DeMeester and DeMeester 365
congenital short esophagus. Although it is well-recognized now that the condition we call Barrett’s esophagus represents a metaplastic replacement of the squamous esophageal mucosa by columnar mucosa, the fundamental issue of determining precisely where the esophagus ends and the stomach begins in these patients remains problematic. Intraoperatively it is not difficult to confuse a tubularized portion of proximal stomach that has been chronically herniated into the chest with distal esophagus by external appearances only. In fact, it is often beneficial to endoscope these patients intraoperatively to help determine the true location of the gastroesophageal junction. This approach is often not done by surgeons operating on patients with advanced reflux disease and likely was not done by Dr Korn and colleagues. Instead, Dr Korn and colleagues suggest that they have always “found” the gastroesophageal junction (GEJ) at or below the diaphragmatic hiatus. In actuality, it usually needs to be “brought” there by the esophageal surgeon. The real issue is what it takes to bring it there. By pulling hard enough, the GEJ can always be reduced below the crura, but tension on the repair of any hernia increases the likelihood of failure. It is undeniable that the failure rate after antireflux surgery is higher in patients with advanced inflammatory injury associated with strictures and long segments of Barrett’s esophagus. The authors themselves have reported extremely high failure rates after antireflux surgery in patients with Barrett’s esophagus.18 Most patients with strictures or long-segment Barrett’s esophagus have a hiatal hernia; often large, and recurrent hernia is one of the most common forms of failure in these patients. Thus, one has to be cautious about completely dismissing the possibility that esophageal shortening may play a role in failed antireflux procedures. Trying to prove that esophageal shortening does not occur, Dr Korn and colleagues compared esophageal length in 4 groups: controls without reflux symptoms, reflux patients without Barrett’s, uncomplicated long-segment Barrett’s patients, and complicated Barrett’s patients who had a stricture or ulcer in addition to Barrett’s. Within each group, patients and controls were further subdivided based on their height. Esophageal length was calculated by determining the distance between the distal border of the crycopharyngeal sphincter and the distal border of the lower esophageal sphincter (LES) on manometry using a stationary pull-through technique. The authors reported that although the mean esophageal length was 1-2 cm shorter in patients with reflux disease or Barrett’s
366 DeMeester and DeMeester
compared to the control group, there was no statistical significance in the data. Interestingly, this 2 cm difference in length is similar to what Collis noted in his 1976 study on esophageal length (controls without hiatal hernia or reflux: 39.2 cm; patients with reflux symptoms: 37.1 cm [lesophagoscopic length]).12 Unfortunately, Dr Korn and colleagues did not report a P value for the results of the analysis of variance testing between all groups in their study and offered no direct comparison between the control group and all patients with reflux or Barrett’s. Additionally, the authors do not provide a power analysis to help determine the likelihood of a type II error in their conclusion that there is no significant difference between groups. The real problem, though, is with the design of the study. First, the authors chose a nonconventional method to determine the length of Barrett’s in patients. Most centers define the length of the columnar-lined esophagus as the difference between the endoscopic location of the squamocolumnar and the gastroesophageal junctions. In contrast, the authors determined the length of Barrett’s changes based on the difference between the endoscopic location of the squamocolumnar junction and the manometric location of the distal extent of the LES. Since the gastric sling-fibers make up a portion of the LES, it is likely that what manometrically they considered to be distal esophagus was in fact proximal stomach, and that they overestimated the length of the Barrett’s segment. While nonconventional, this error has little bearing or significance on the findings and conclusions of their study. The second problem with the design of the study, though, has direct implications on the conclusions reached by Dr Korn and colleagues. Similar to determining the length of the Barrett’s segment, the authors also used the distal extent of the manometrically determined LES in their calculation of esophageal length. While this is readily and reliably determined in control subjects with a normal LES and no or only a small hiatal hernia, it is much more imprecise and error-prone in patients with a low resting pressure in the LES and a hiatal hernia. The mean LES pressure in the group of patients with complicated Barrett’s esophagus was 5.8 mmHg compared to 16.1 mmHg in the control subjects (see Korn et al, Table I). It is well-established that determining the distal extent of the LES in patients with a hiatal hernia and a low-pressure sphincter is difficult since there is often no clear demarcation between the hernia and the distal extent of the sphincter.12 This leads to a tendency to overesti-
Surgery April 2003
mate the length of the sphincter, and with the study design used by Dr. Korn and colleagues, this would result in a tendency to overestimate esophageal length as well. The overestimation would only occur in patients with reflux or Barrett’s esophagus, since few if any controls would have a hiatal hernia and a low-pressure LES. A much more reliable manometric landmark is the upper border of the LES because the point where the pressure drops below esophageal baseline is recognized easily even in patients with a hiatal hernia and a defective LES. Why the authors did not use this as their reference point for measuring esophageal length is unclear. Intriguingly, despite the design flaw in their study which induced a bias to increase length in patients with reflux or Barrett’s esophagus, the authors still found a 1-2 cm difference in esophageal length in favor of the control subjects. In fact, controls had a longer mean esophageal length in every subject height category except in the shortest patients (159 cm). Of course, in the subgroup with the shortest esophagi, a 2-3 cm error in measurement would have the greatest impact, and this may explain why it was only in the subgroup with complicated Barrett’s esophagus and the shortest esophagi that the mean esophageal length was longer than that in the controls (26.4 cm compared to 26.1 cm in controls; see Korn et al, Table II). A further problem with determining esophageal length is how to adjust for the presence and size of a hiatal hernia. Even within an individual patient, the measured esophageal length varies depending on whether the hernia is present or reduced, yet Dr Korn and colleagues did nothing to take this into account. In fact, no information about the prevalence or size of a hiatal hernia is provided for either the controls or patients. In summary, although there is continued debate about the existence of acquired esophageal shortening, we believe that most esophageal surgeons recognize the existence of the short esophagus and are incorporating mechanisms in their own practice to handle it when encountered. The emphasis is shifting away from whether it exists and toward how often it is present, how to identify patients with a short esophagus pre-operatively, and how best to manage it when confronted with the problem intraoperatively. It is our opinion that an unrecognized short esophagus contributes significantly to the likelihood of a failed antireflux procedure, and anything that shifts the focus of surgeons away from the possiblity of a shortened esophagus may
DeMeester and DeMeester 367
Surgery Volume 133, Number 4
well end up leading to more failed fundoplications at a time when it is critical that surgeons demonstrate excellent outcomes with the procedure. Consequently, we urge the readers to review carefully the study by Dr Korn and colleagues forewarned about the potentially flawed methodology, and accept the possibility that the study may in fact have flawed conclusions. REFERENCES 1. Collis JL, Kelly TD, Wiley AM. Anatomy of the crura of the diaphragm and the surgery of hiatus hernia. Thorax 1954;9:175. 2. Collis JL. Review of surgical results of hiatus hernia. Thorax 1961;16:114. 3. Collis JL. The diaphragm and hiatus hernia. Proceedings of the Royal Society of Medicine. 1966;59:354-6. 4. Collis JL. Surgical control of reflux in hiatus hernia. American Journal of Surgery. 1968;115:465-71. 5. Windsor CW, Collis JL. Anaemia and hiatus hernia: experience in 450 patients. Thorax. 1967;22:73-8. 6. Collis JL. An operation for haitus hernia with short esophagus. J Thorac Surg 1957;34:768-78. 7. Kauer WK, Peters JH, DeMeester TR, Heimbucher J, Ireland AP, Bremner CG. A tailored approach to antireflux surgery. J Thorac Cardiovasc Surg 1995;110:141-6; discussion 146-7. 8. Ritter MP, Peters JH, DeMeester TR, Gadenstatter M, Oberg S, Fein N, et al. Treatment of advanced gastroesophageal reflux disease with Collis gastroplasty and Belsey partial fundoplication. Archives of Surgery 1998; 133:523-8; discussion 528-9. 9. Johnson AB, Oddsdottir M, Hunter JG. Laparoscopic Collis gastroplasty and Nissen fundoplication. A new technique
10.
11.
12. 13.
14.
15.
16.
17.
18.
for the management of esophageal foreshortening. Surgical Endoscopy 1998;12:1055-60. Horvath KD, Swanstrom LL, Jobe BA. The short esophagus: pathophysiology, incidence, presentation, and treatment in the era of laparoscopic antireflux surgery. Annals of Surgery 2000;232:630-40. Awad ZT, Filipi CJ. The short esophagus: pathogenesis, diagnosis, and current surgical options. Archives of Surgery 2001;136:113-4. Kalloor GJ, Deshpande AH, Collis JL. Observations on oesophageal length. Thorax. 1976;31:284-8. Gozzetti G, Pilotti V, Spangaro M, Bassi F, Grigioni W, Carulli N, et al. Pathophysiology and natural history of acquired short esophagus. Surgery 1987;102:507-14. Mittal SK, Awad ZT, Tasset M, Filipi CJ, Dickason TJ, Shinno Y, et al. The preoperative predictability of the short esophagus in patients with stricture or paraesophageal hernia. Surgical Endoscopy 2000;14:464-8. Gastal OL, Hagen JA, Peters JH, Campos GM, Hashemi M, Theisen J, et al. Short esophagus: analysis of predictors and clinical implications. Archives of Surgery 1999; 34:633-6; discussion 637-8. Horvath KD, Swanstrom LL, Jobe BA. The short esophagus: pathophysiology, incidence, presentation, and treatment in the era of laparoscopic antireflux surgery. Annals of Surgery. 2000;232:630-40. Urbach DR, Khajanchee YS, Glasgow RE, Hansen PD, Swanstrom LL. Preoperative determinants of an esophageal lengthening procedure in laparoscopic antireflux surgery. Surgical Endoscopy. 2001;15:1408-12. Csendes A, Braghetto I, Burdiles P, Puente G, Korn O, Diaz JC, et al. Long-term results of classic antireflux surgery in 152 patients with Barrett’s esophagus: clinical, radiologic, endoscopic, manometric, and acid reflux test analysis before and late after operation. Surgery 1998; 126:645-57.
CORRECTION In the article “Jonathan E. Rhoads, 1907-2002” (Surgery 2003;133:133-4), the authors were listed incorrectly. The sole author is Clyde F. Barker, MD, who is affiliated with the University of Pennsylvania Hospital, 3400 Spruce Street, Philadelphia, Pa. Andrew Warshaw, MD, was incorrectly listed as a coauthor, and his affiliation was incorrectly listed as the affiliation of both authors.
From the Departments of Cardiothoracic Surgery, and Surgery, the University of Southern California Keck School of Medicine, Los Angeles, Calif
THE TOPIC OF ESOPHAGEAL SHORTENING is one that polarizes surgeons like few others in esophageal surgery. On the one hand are surgeons who have never seen a short esophagus and don’t believe it exists, while on the other there are those that are convinced that foreshortening of the esophagus is a real entity in a subset of patients with reflux disease. Gradually, as experience with antireflux surgery increases, most surgeons are beginning to recognize that in some patients reduction of the gastroesophageal junction below the diaphragmatic hiatus without tension is problematic. In this issue of Surgery (133:358-363), Dr Korn and colleagues have set out to prove that the short esophagus is a myth. To do so they compared esophageal length in 190 control subjects, 77 patients with erosive esophagitis, 74 with Barrett’s, and 29 with complicated Barrett’s (ulcer or stenosis), grouped the patients according to height, and concluded that since the differences they found were not significant, the “so-called short esophagus” does not exist. Before we critically review their methodology and conclusions, perhaps it would be worthwhile to briefly review the history of acquired esophageal shortening. The concern regarding esophageal shortening dates back nearly as far as the history of surgery for hiatal hernia and gastroesophageal reflux disease. Surgeons in the mid-1900s reported having difficulty reducing the gastroesophageal junction Accepted for publication December 13, 2002. Reprint requests: Steven R. DeMeester, MD, Assistant Professor of Cardiothoracic Surgery, Norris Comprehensive Cancer Center, 1441 Eastlake Ave, Ste 7418, Los Angeles, CA 900330804. Surgery 2003;133:364-7. © 2003 Mosby, Inc. All rights reserved. 0039-6060/2003/$30.00 +0 doi:10.1067/msy.2003.116
364 SURGERY
below the diaphragmatic hiatus in patients with advanced reflux disease. Termed “acquired esophageal shortening,” the problem was frequent enough that a variety of surgical options for addressing it were proposed. The most popular solutions included esophageal resection, moving the distal esophagus toward the dome of the diaphragm, stricturoplasty, leaving the fundoplication in an intrathoracic location, and what subsequently has become the most accepted surgical solution, the Collis gastroplasty. It is difficult to believe that all these techniques were developed for a problem that never existed, particularly since most were proposed by insightful and experienced surgeons. Take for example Dr Leigh Collis. He spent many years of his life studying the diaphragm and hiatal hernias and wrote extensively about the anatomy and pathophysiology of this area.1-4 His careful clinical observations established fundamental principles about the pathophysiology of hiatal hernias and reflux disease. In a review of 450 consecutive patients with hiatal hernia, Dr Collis linked anemia with large paraesophageal hiatal hernias, excluded esophagitis as the cause, and proposed the concept of the “riding ulcer” occurring in the portion of the stomach that crosses the crus.5 He applied this same logic and clinicalanatomic knowledge to his surgical solution for acquired esophageal shortening when he proposed the technique of gastroplasty.6 The widespread utilization of his technique, and the acceptance by most of the leading esophageal surgeons during the last 20 years that the entity of acquired esophageal shortening exists, are testimony to the fact that it is a clinical reality. The question arises as to how often is it present, and can it be determined preoperatively? Clearly medical therapy for reflux is far superior today than it was even 20 years ago, and in most patients reflux-induced esophageal injury can be healed
Surgery Volume 133, Number 4
with the potent acid-suppression medications currently available. It is likely that these medications are reducing the severity of esophageal injury in many patients and correspondingly the prevalence of esophageal shortening may be decreasing; still, there remain patients with advanced reflux disease who when operated upon are found to have a gastroesophageal junction that will not reduce below the diaphragmatic hiatus without tension. An obvious issue related to the prevalence of a short esophagus is that surgeons have individual interpretations of what constitutes excessive tension. Further, the frequency of encountering a shortened esophagus is related to the types of patients being operated on, with the highest frequency occurring in tertiary referral centers where the most complex patients end up. It also depends on the approach and degree of esophageal mobilization performed prior to length assessment. In spite of these variables, most centers report finding a foreshortened esophagus in 3-14% of patients.7-11 It would be ideal if patients with a short esophagus could be identified before surgery so that the surgeon is prepared to address the problem with extensive esophageal mobilization and if necessary a Collis gastroplasty. With this goal in mind several investigators, including Collis himself, have tried to determine a method to accurately predict esophageal foreshortening prior to surgery. Techniques tried include endoscopic measurements of length, measurements based on the location of the change in electrical potential between the mucosa of the esophagus and stomach, radiographic measurements, external chest measurements, and manometric measurements of length.12-14 None of these methods have proved satisfactory or reliable. Instead, clinical indicators such as a large (5 cm) nonreducing hiatal hernia, long-segment Barrett’s esophagus, severe stricture, intrathoracic stomach, and a failed prior fundoplication all portend the possibility of a foreshortened esophagus.15-17 In this issue of Surgery, Dr Korn and colleagues claim that since they have never seen a short esophagus, the entity doesn’t exist. At the very outset this statement invites concern, since the mere fact that someone hasn’t seen something does not preclude its existence. However, the authors then try to prove that the short esophagus doesn’t exist by comparing the manometrically determined esophageal length in subsets of patients with varying severity of reflux disease. The authors introduce the topic by alluding to Dr Norman Barrett’s misconception about the columnar-lined esophagus being a tubularized stomach in the chest with a
DeMeester and DeMeester 365
congenital short esophagus. Although it is well-recognized now that the condition we call Barrett’s esophagus represents a metaplastic replacement of the squamous esophageal mucosa by columnar mucosa, the fundamental issue of determining precisely where the esophagus ends and the stomach begins in these patients remains problematic. Intraoperatively it is not difficult to confuse a tubularized portion of proximal stomach that has been chronically herniated into the chest with distal esophagus by external appearances only. In fact, it is often beneficial to endoscope these patients intraoperatively to help determine the true location of the gastroesophageal junction. This approach is often not done by surgeons operating on patients with advanced reflux disease and likely was not done by Dr Korn and colleagues. Instead, Dr Korn and colleagues suggest that they have always “found” the gastroesophageal junction (GEJ) at or below the diaphragmatic hiatus. In actuality, it usually needs to be “brought” there by the esophageal surgeon. The real issue is what it takes to bring it there. By pulling hard enough, the GEJ can always be reduced below the crura, but tension on the repair of any hernia increases the likelihood of failure. It is undeniable that the failure rate after antireflux surgery is higher in patients with advanced inflammatory injury associated with strictures and long segments of Barrett’s esophagus. The authors themselves have reported extremely high failure rates after antireflux surgery in patients with Barrett’s esophagus.18 Most patients with strictures or long-segment Barrett’s esophagus have a hiatal hernia; often large, and recurrent hernia is one of the most common forms of failure in these patients. Thus, one has to be cautious about completely dismissing the possibility that esophageal shortening may play a role in failed antireflux procedures. Trying to prove that esophageal shortening does not occur, Dr Korn and colleagues compared esophageal length in 4 groups: controls without reflux symptoms, reflux patients without Barrett’s, uncomplicated long-segment Barrett’s patients, and complicated Barrett’s patients who had a stricture or ulcer in addition to Barrett’s. Within each group, patients and controls were further subdivided based on their height. Esophageal length was calculated by determining the distance between the distal border of the crycopharyngeal sphincter and the distal border of the lower esophageal sphincter (LES) on manometry using a stationary pull-through technique. The authors reported that although the mean esophageal length was 1-2 cm shorter in patients with reflux disease or Barrett’s
366 DeMeester and DeMeester
compared to the control group, there was no statistical significance in the data. Interestingly, this 2 cm difference in length is similar to what Collis noted in his 1976 study on esophageal length (controls without hiatal hernia or reflux: 39.2 cm; patients with reflux symptoms: 37.1 cm [lesophagoscopic length]).12 Unfortunately, Dr Korn and colleagues did not report a P value for the results of the analysis of variance testing between all groups in their study and offered no direct comparison between the control group and all patients with reflux or Barrett’s. Additionally, the authors do not provide a power analysis to help determine the likelihood of a type II error in their conclusion that there is no significant difference between groups. The real problem, though, is with the design of the study. First, the authors chose a nonconventional method to determine the length of Barrett’s in patients. Most centers define the length of the columnar-lined esophagus as the difference between the endoscopic location of the squamocolumnar and the gastroesophageal junctions. In contrast, the authors determined the length of Barrett’s changes based on the difference between the endoscopic location of the squamocolumnar junction and the manometric location of the distal extent of the LES. Since the gastric sling-fibers make up a portion of the LES, it is likely that what manometrically they considered to be distal esophagus was in fact proximal stomach, and that they overestimated the length of the Barrett’s segment. While nonconventional, this error has little bearing or significance on the findings and conclusions of their study. The second problem with the design of the study, though, has direct implications on the conclusions reached by Dr Korn and colleagues. Similar to determining the length of the Barrett’s segment, the authors also used the distal extent of the manometrically determined LES in their calculation of esophageal length. While this is readily and reliably determined in control subjects with a normal LES and no or only a small hiatal hernia, it is much more imprecise and error-prone in patients with a low resting pressure in the LES and a hiatal hernia. The mean LES pressure in the group of patients with complicated Barrett’s esophagus was 5.8 mmHg compared to 16.1 mmHg in the control subjects (see Korn et al, Table I). It is well-established that determining the distal extent of the LES in patients with a hiatal hernia and a low-pressure sphincter is difficult since there is often no clear demarcation between the hernia and the distal extent of the sphincter.12 This leads to a tendency to overesti-
Surgery April 2003
mate the length of the sphincter, and with the study design used by Dr. Korn and colleagues, this would result in a tendency to overestimate esophageal length as well. The overestimation would only occur in patients with reflux or Barrett’s esophagus, since few if any controls would have a hiatal hernia and a low-pressure LES. A much more reliable manometric landmark is the upper border of the LES because the point where the pressure drops below esophageal baseline is recognized easily even in patients with a hiatal hernia and a defective LES. Why the authors did not use this as their reference point for measuring esophageal length is unclear. Intriguingly, despite the design flaw in their study which induced a bias to increase length in patients with reflux or Barrett’s esophagus, the authors still found a 1-2 cm difference in esophageal length in favor of the control subjects. In fact, controls had a longer mean esophageal length in every subject height category except in the shortest patients (159 cm). Of course, in the subgroup with the shortest esophagi, a 2-3 cm error in measurement would have the greatest impact, and this may explain why it was only in the subgroup with complicated Barrett’s esophagus and the shortest esophagi that the mean esophageal length was longer than that in the controls (26.4 cm compared to 26.1 cm in controls; see Korn et al, Table II). A further problem with determining esophageal length is how to adjust for the presence and size of a hiatal hernia. Even within an individual patient, the measured esophageal length varies depending on whether the hernia is present or reduced, yet Dr Korn and colleagues did nothing to take this into account. In fact, no information about the prevalence or size of a hiatal hernia is provided for either the controls or patients. In summary, although there is continued debate about the existence of acquired esophageal shortening, we believe that most esophageal surgeons recognize the existence of the short esophagus and are incorporating mechanisms in their own practice to handle it when encountered. The emphasis is shifting away from whether it exists and toward how often it is present, how to identify patients with a short esophagus pre-operatively, and how best to manage it when confronted with the problem intraoperatively. It is our opinion that an unrecognized short esophagus contributes significantly to the likelihood of a failed antireflux procedure, and anything that shifts the focus of surgeons away from the possiblity of a shortened esophagus may
DeMeester and DeMeester 367
Surgery Volume 133, Number 4
well end up leading to more failed fundoplications at a time when it is critical that surgeons demonstrate excellent outcomes with the procedure. Consequently, we urge the readers to review carefully the study by Dr Korn and colleagues forewarned about the potentially flawed methodology, and accept the possibility that the study may in fact have flawed conclusions. REFERENCES 1. Collis JL, Kelly TD, Wiley AM. Anatomy of the crura of the diaphragm and the surgery of hiatus hernia. Thorax 1954;9:175. 2. Collis JL. Review of surgical results of hiatus hernia. Thorax 1961;16:114. 3. Collis JL. The diaphragm and hiatus hernia. Proceedings of the Royal Society of Medicine. 1966;59:354-6. 4. Collis JL. Surgical control of reflux in hiatus hernia. American Journal of Surgery. 1968;115:465-71. 5. Windsor CW, Collis JL. Anaemia and hiatus hernia: experience in 450 patients. Thorax. 1967;22:73-8. 6. Collis JL. An operation for haitus hernia with short esophagus. J Thorac Surg 1957;34:768-78. 7. Kauer WK, Peters JH, DeMeester TR, Heimbucher J, Ireland AP, Bremner CG. A tailored approach to antireflux surgery. J Thorac Cardiovasc Surg 1995;110:141-6; discussion 146-7. 8. Ritter MP, Peters JH, DeMeester TR, Gadenstatter M, Oberg S, Fein N, et al. Treatment of advanced gastroesophageal reflux disease with Collis gastroplasty and Belsey partial fundoplication. Archives of Surgery 1998; 133:523-8; discussion 528-9. 9. Johnson AB, Oddsdottir M, Hunter JG. Laparoscopic Collis gastroplasty and Nissen fundoplication. A new technique
10.
11.
12. 13.
14.
15.
16.
17.
18.
for the management of esophageal foreshortening. Surgical Endoscopy 1998;12:1055-60. Horvath KD, Swanstrom LL, Jobe BA. The short esophagus: pathophysiology, incidence, presentation, and treatment in the era of laparoscopic antireflux surgery. Annals of Surgery 2000;232:630-40. Awad ZT, Filipi CJ. The short esophagus: pathogenesis, diagnosis, and current surgical options. Archives of Surgery 2001;136:113-4. Kalloor GJ, Deshpande AH, Collis JL. Observations on oesophageal length. Thorax. 1976;31:284-8. Gozzetti G, Pilotti V, Spangaro M, Bassi F, Grigioni W, Carulli N, et al. Pathophysiology and natural history of acquired short esophagus. Surgery 1987;102:507-14. Mittal SK, Awad ZT, Tasset M, Filipi CJ, Dickason TJ, Shinno Y, et al. The preoperative predictability of the short esophagus in patients with stricture or paraesophageal hernia. Surgical Endoscopy 2000;14:464-8. Gastal OL, Hagen JA, Peters JH, Campos GM, Hashemi M, Theisen J, et al. Short esophagus: analysis of predictors and clinical implications. Archives of Surgery 1999; 34:633-6; discussion 637-8. Horvath KD, Swanstrom LL, Jobe BA. The short esophagus: pathophysiology, incidence, presentation, and treatment in the era of laparoscopic antireflux surgery. Annals of Surgery. 2000;232:630-40. Urbach DR, Khajanchee YS, Glasgow RE, Hansen PD, Swanstrom LL. Preoperative determinants of an esophageal lengthening procedure in laparoscopic antireflux surgery. Surgical Endoscopy. 2001;15:1408-12. Csendes A, Braghetto I, Burdiles P, Puente G, Korn O, Diaz JC, et al. Long-term results of classic antireflux surgery in 152 patients with Barrett’s esophagus: clinical, radiologic, endoscopic, manometric, and acid reflux test analysis before and late after operation. Surgery 1998; 126:645-57.
CORRECTION In the article “Jonathan E. Rhoads, 1907-2002” (Surgery 2003;133:133-4), the authors were listed incorrectly. The sole author is Clyde F. Barker, MD, who is affiliated with the University of Pennsylvania Hospital, 3400 Spruce Street, Philadelphia, Pa. Andrew Warshaw, MD, was incorrectly listed as a coauthor, and his affiliation was incorrectly listed as the affiliation of both authors.