European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 www.elsevier.com/locate/ejcts

Myenteric plexus abnormalities associated with epiphrenic diverticula§

Thomas W. Rice a,1,*, John R. Goldblum b, Martha M. Yearsley b, Steven S. Shay c, Scott I. Reznik a, Sudish C. Murthy a, David P. Mason a, Eugene H. Blackstone a,d,2

a Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic, Cleveland, OH, USA b Department of Anatomic Pathology, Cleveland Clinic, Cleveland, OH, USA Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021 c Department of , Cleveland Clinic, Cleveland, OH, USA d Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA

Received 5 June 2008; received in revised form 18 August 2008; accepted 8 September 2008; Available online 8 November 2008

Abstract

Objective: To (1) categorize histologic esophageal abnormalities in patients undergoing surgical treatment for epiphrenic diverticulum, and (2) correlate histologic changes with associated esophageal motility disorders and hiatal . Methods: From January 1987 to May 2008, 40 patients had surgery for epiphrenic diverticulum. Esophageal manometry was abnormal in 29 (73%); 23 (58%) had . Esophageal muscle specimens were evaluated for ganglion cell number, myenteric inflammations and myenteric fibrosis. Results: Myenteric plexus abnormalities were present in 31 (78%). Ganglion cells were reduced in 8 (20%) and absent in 13 (33%). Myenteric inflammation was present in 21 (53%) and myenteric fibrosis in 9 (23%). Abnormalities were seen in 10 (83%) with motility disorders only, 5 (83%) with hiatal hernia only, 13 (76%) with both, and 3 (60%) with neither. Abnormalities in diffuse (n = 3) were similar to those of achalasia (n = 14). Ineffective esophageal motility (n = 6) was strongly associated with hiatal hernia, and abnormalities were similar to those of hiatal hernia without motility disorders (n = 6). All patients with nutcracker (n = 3) had hiatal hernia and histologic abnormalities, and two patients with hypertensive lower esophageal sphincter (n = 3, hiatal hernia in 2) had myenteric inflammation. Conclusions: Myenteric plexus abnormalities predominate in epiphrenic diverticulum. Disease-specific patterns exist, but are incomplete. These associations and patterns point to causes of distal obstruction, with some commonality. In the absence of associated disorders, myenteric plexus abnormalities may be the sole finding. Isolated epiphrenic diverticulum is uncommon and may reflect an inability to detect abnormalities by current investigative techniques. # 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

Keywords: Motility disorder; Hiatal hernia; Ganglion cells; Myenteric inflammation; Myenteric fibrosis; Achalasia

1. Introduction (Fig. 2), and study of the esophagus distal to the diverticulum has not been performed. Purposes of this report are to (1) Epiphrenic diverticulum is a false pulsion diverticulum categorize histologic myenteric plexus abnormalities in assumed to result from esophageal obstruction distal to an patients undergoing surgery for epiphrenic diverticulum, area lacking external support of periesophageal tissue or a and (2) correlate these histologic changes with associated point of weakness or absence of the muscularis propria esophageal motility disorders and hiatal hernia. (Fig. 1). We hypothesized that this obstruction may result from or be linked with abnormalities of the myenteric plexus, because the main associated disease, achalasia, has known myenteric plexus abnormalities, including loss of ganglion 2. Patients and methods cells and myenteric inflammation and fibrosis [1,2]. Routine histopathology of the resected diverticulum is unrevealing 2.1. Patients

§ From January 1987 to May 2008, 58 patients with Presented at the 16th European Conference on General Thoracic Surgery, epiphrenic diverticulum underwent surgery at Cleveland Bologna, Italy, June 8—11, 2008. * Corresponding author. Address: Cleveland Clinic, 9500 Euclid Avenue/Mail Clinic. Forty (70%) had a group of preoperative tests, stop J4-1, Cleveland, OH 44195, USA. Tel.: +1 216 444 1921; including esophageal manometry, esophagogastroduodeno- fax: +1 216 445 6876. scopy, and barium esophagram and subsequent postoperative E-mail address: [email protected] (T.W. Rice). 1 assessment of esophageal muscle distal to the diverticulum. Supported in part by the Daniel and Karen Lee Endowed Chair in Thoracic These patients constitute the study group. Surgery. 2 Supported in part by the Kenneth Gee and Paula Shaw, PhD, Chair in Heart Esophageal motility was abnormal in 29 (73%; Table 1), as Research. defined by DeMeester and Costantini [3]. Hiatal hernia was

1010-7940/$ — see front matter # 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejcts.2008.09.025 T.W. Rice et al. / European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 23

Fig. 1. Radiographic evaluation of epiphrenic diverticulum. (A) Barium esophagram of epiphrenic diverticulum in a patient with achalasia. (B) Barium esophagram of Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021 epiphrenic diverticulum in a patient with hiatal hernia and no motility disorder. (C) Computed tomography of epiphrenic diverticulum (arrow) demonstrating classic position, on the right lateral aspect of the esophagus just above the diaphragm. This is a presumed area of inadequate support or weakness of the esophageal musculature. diagnosed in 23 (58%): by barium esophagram in 7 (30%), features: (1) number of ganglion cells, evaluated in a esophagogastroduodenoscopy in 6 (26%), and both in 10 semiquantitative fashion as normal in number, decreased in (43%). Hiatal hernia and motility disorders coexisted in 17 number, or absent, and (2) presence or absence of myenteric (43%). Diverticulectomy, myotomy, and anterior partial inflammation and fibrosis (Figs. 3—6). The analysis was done fundoplication were performed in 33 (83%) [4], with without knowledge of clinical information or existence of subsequent esophagectomy in 2 (5%). Esophagectomy was motility disorder or hiatal hernia. the first surgery in seven (18%) because their disease was not amenable to primary repair. 2.3.1. Analysis Categorical data are presented as frequencies and percen- 2.2. Tissue procurement tages. These data were approved for use in research by the institutional review board, with patient consent waived. As part of the myotomy performed to relieve distal obstruction, a 2 cm long strip of muscle was removed from the myotomy edge distal to, and 1808 from, the diverticu- 3. Results lectomy site. These strips were subjected to histologic analysis. In esophagectomy patients, a sample of the 3.1. Myenteric plexus abnormalities muscularis propria distal to and opposite the diverticulum was analyzed as part of the pathologic examination of the The myenteric plexus was abnormal in 31 of 40 patients resected specimen. (78%; Table 2). Ganglion cell abnormalities were present in 21 (53%) patients, reduced in number in 8 (20%), and absent in 2.3. Histologic analysis 13 (33%). Myenteric inflammation was present in 21 (53%) patients. Myenteric fibrosis was seen in nine (23%) patients Hematoxylin and eosin stained sections from the esopha- and associated with myenteric inflammation in eight (20%). geal muscle specimens were evaluated for the following Isolated ganglion cell abnormalities were present in nine (23%) patients and isolated myenteric inflammation in eight (20%). Combined abnormalities were present in 14 (35%). Association of these myenteric plexus abnormalities with motility disorders and hiatal hernia is detailed in Table 2.In the text that follows, these associations are amplified.

Table 1 Motility disorders and hiatal hernia in epiphrenic diverticulum.

Motility disorder No. (% of 40) Hiatal hernia

No. %

None 11 (28) 6 54 Achalasia 14 (35) 6 43 DES 3 (8) 1 33 HLES 3 (8) 2 67 Nutcracker 3 (8) 3 100 Fig. 2. Low-magnification appearance of a typical epiphrenic diverticulum. IEM 6 (16) 5 83 The squamous mucosa is hyperplastic and there is moderate degree of chronic Total 40 (100) 23 58 inflammation within the lamina propria and superficial submucosa. The sub- mucosa is fibrotic. Because epiphrenic diverticulum is a false pulsion diverti- Key: DES, ; HLES, hypertensive lower esophageal culum, the muscularis propria and thus the myenteric plexus are absent. sphincter; IEM, ineffective esophageal motility. 24 T.W. Rice et al. / European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021

Fig. 3. Low-magnification view of myenteric plexus from a patient with Fig. 5. Low-magnification view of myenteric plexus from a patient with no epiphrenic diverticulum and achalasia, showing a normal number of ganglion known motility disorder, revealing a reduced number of ganglion cells. Only a cells (yellow arrowheads) with scattered chronic inflammatory cells. single ganglion cell is identified within the myenteric plexus (yellow arrow- head).

Fig. 4. Low-magnification view of myenteric plexus from a patient with Fig. 6. Low-magnification view of myenteric plexus from a patient with diffuse epiphrenic diverticulum and achalasia, revealing complete absence of gang- esophageal spasm, revealing complete absence of ganglion cells. There is only lion cells associated with a moderate degree of chronic myenteric inflamma- mild chronic inflammation, but the nerve is extensively fibrotic. tion. Although not easily recognized, the residual nerve is fibrotic (green arrowhead).

3.2. Correlation of myenteric plexus abnormalities with tion only. Six patients (54%) with no motility disorder had motility disorders and hiatal hernia hiatal hernia; five (72%) of these had myenteric plexus abnormalities. Ganglion cell abnormalities were present in Association of motility disorders and hiatal hernia in three (50%) of these patients, reduced in two (20%), and epiphrenic diverticulum is evident from Table 1. Nutcracker absent in one (33%). Myenteric inflammation was present in esophagus or ineffective esophageal motility disorder were three (50%) of these patients and myenteric fibrosis in one strongly associated with hiatal hernia. All patients with (17%). Isolated ganglion cell abnormalities were present in had hiatal hernia, and two (66%) had two (33%) of these patients and isolated myenteric myenteric plexus abnormalities (Table 2). Five patients (83%) inflammation in one (17%). Combined abnormalities were with ineffective motility disorder had hiatal hernia, and four present in two (33%), ganglion cell abnormalities and (66%) of these had myenteric plexus abnormalities (Table 2); myenteric inflammation in one, and myenteric inflammation one patient without hiatal hernia had no myenteric plexus and fibrosis in one. The myenteric plexus was abnormal in abnormalities. three of five patients (60%), with no motility disorder without Patients with hypertensive lower esophageal sphincter or hiatal hernia. Reduced ganglion cells were present in all no motility disorder were as likely to have a hiatal hernia as three patients (60%), an isolated finding in two (40%) and not; two (67%) with hypertensive lower esophageal sphincter combined with myenteric inflammation in one (20%). had hiatal hernia, one with myenteric inflammation only. The Patients with achalasia or diffuse esophageal spasm were one patient without hiatal hernia had myenteric inflamma- unlikely to have hiatal hernia. Of six patients (43%) with T.W. Rice et al. / European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 25

Table 2 Myenteric plexus abnormalities in epiphrenic diverticulum and associated motility disorders and hiatal hernia.

Abnormality Total (n = 40), Motility disorder Hiatal hernia no. (%) None Achalasia DES IEM Nutcracker HLES Present Absent (n = 11) (n = 14) (n =3) (n =6) (n =3) (n =3) (n = 23) (n = 17)

None 9 3 3 0 2 0 1 6 3 Ganglion cells (GC) 21 (53) 6 8 3 2 2 0 8 13 Reduced 8 (20) 5 3 0 0 0 0 1 7 Absent 13 (33) 1 5 3 2 2 0 7 6 Myenteric inflammation (MI) 21 (53) 4 9 1 3 2 2 13 8 Myenteric fibrosis (MF) 9 (23) 1 5 1 1 1 0 4 5 GC only 9 (23) 4 2 2 1 0 0 3 6 MI only 8 (20) 1 3 0 1 1 2 7 1 Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021 MF only 0 (0) 0 0 0 0 0 0 0 0 GC + MI 5 (13) 2 1 0 1 1 0 3 2 GC + MF 1 (3) 0 0 0 0 1 0 1 0 MI + MF 2 (5) 1 0 0 1 0 0 2 0 GC + MI + MF 6 (15) 0 5 1 0 0 0 1 5

Key: DES, diffuse esophageal spasm; HLES, hypertensive lower esophageal sphincter; IEM, ineffective esophageal motility. achalasia and hiatal hernia, four had myenteric plexus 4.1.2.1. Myenteric plexus abnormalities and motility dis- abnormalities: classic absence of ganglion cells with orders without hiatal hernia. The histopathology of acha- myenteric inflammation and fibrosis in one, and myenteric lasia without diverticulum centers around the myenteric inflammation alone in the other three. Of the eight patients plexus. Chronic myenteric plexus inflammation has been with achalasia without hiatal hernia, seven had myenteric found in 90% of patients [5].Thisisassociatedwith plexus abnormalities. Ganglion cells were reduced in three decreasing ganglion cell number and, eventually, absence and absent in four, myenteric inflammation was present in of ganglion cells and neural fibrosis [1,2]. A finding of absent five, and fibrosis was present in four. Of the seven, four had ganglion cells in two groups of patients, those with classic ganglion cell abnormalities, myenteric inflammation, myenteric inflammation and those with predominant and fibrosis, and the remaining three had ganglion cell myenteric fibrosis, was proposed by Kilic and colleagues abnormalities, one associated with myenteric inflammation. as evidence for two different disease mechanisms [6]. One patient (33%) with diffuse esophageal spasm and hiatal However, it just as likely represents early versus late hernia had absent ganglion cells. The two without hiatal findings of neural destruction in achalasia. This myenteric hernia also had absent ganglion cells, and one of these had inflammation is predominantly lymphocytic, with ganglion classic achalasia myenteric plexus abnormalities. cell loss a killer T-cell mediated process in the majority of patients [7]. The trigger for this immune-mediated destruction is speculative. 4. Discussion Abnormalities of the muscularis propria are typically less marked and found in later stages of achalasia. Histologic 4.1. Principal findings review of muscularis propria in myotomized patients, presumably early in the course of achalasia, shows mild 4.1.1. Myenteric plexus abnormalities fibrosis (2.1 Æ 0.9 on a scale of 0 [no fibrosis] to 5 [100% The unique findings of this study were that abnormalities fibrosis]) in 30% of patients [8]. In esophagectomy specimens of the distal esophageal myenteric plexus occurred in the of end-stage achalasia patients, fibrosis of the muscularis majority of patients with epiphrenic diverticulum. Approxi- propria was reported in 70% [1]. Histologic assessment of mately half had abnormal ganglion cell number and half muscularis propria hypertrophy is difficult, because there are myenteric inflammation. Fewer, approximately one-fourth, no surrounding normal cells for size comparison. had myenteric fibrosis, which was never seen in isolation. In patients with epiphrenic diverticulum and motility Isolated myenteric plexus abnormalities were slightly more disorder without hiatal hernia, achalasia predominates. common than combined ones. All three abnormalities, Surprisingly, however, two of our patients had normal typical of end-stage achalasia, were seen in only 15% of myenteric plexus examinations, suggesting an alternative, patients. extra-esophageal mechanism for achalasia or sampling error. The remaining achalasia patients had typical findings, with 4.1.2. Correlation of myenteric plexus abnormalities absence of ganglion cells in all and expected combinations of with motility disorders and hiatal hernia the three histologic abnormalities. The three patients with Both motility disorders and hiatal hernia are potential diffuse esophageal spasm had similar findings to those of causes of distal esophageal obstruction that may result in achalasia, supporting the theory that these diseases may be epiphrenic diverticulum. There is a variable association of related [9,10]. However, these findings in diffuse esophageal motility disorders, hiatal hernia, and myenteric plexus spasm are opposite those reported by Champion and abnormalities. colleagues [11], who found normal ganglion cell number 26 T.W. Rice et al. / European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 and no inflammation in the myotomy specimens of two epiphrenic diverticulum were done in only two-thirds of patients with diffuse esophageal spasm. patients with an epiphrenic diverticulum. This highlights the difficulty of preoperative study and need for consistent 4.1.2.2. Myenteric plexus abnormalities and hiatal hernia muscle biopsy protocols. Hiatal hernia itself may be without motility disorder. Although a small group, within this obstructive and the cause of epiphrenic diverticulum. study, the constellation and distribution of myenteric plexus Associated GERD may contribute to this obstruction. Hiatal abnormalities and association with hiatal hernia was strikingly hernia may or may not be a surrogate for GERD, but 24-h pH similar to the pattern seen in patients with ineffective monitoring was not performed. High-resolution esophageal esophageal motility (IEM). This supports the hypothesis that manometry was done in only one patient. It is more accurate hiatal hernia and gastroesophageal reflux disease (GERD) each than standard manometry in detecting esophagogastric can play a role in the genesis of both this motility disorder junction relaxation and segmental hypercontractility [18] [12,13] and epiphrenic diverticulum [4,14,15]. No description because the widely spaced pressure sensors in standard of myenteric plexus abnormalities in patients with either manometry catheters misinterpret vertical esophagogastric hiatal hernia or GERD could be found in the literature. junction displacement as relaxation and miss segmental Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021 abnormalities. However, because of its recent introduction, 4.1.2.3. Myenteric plexus abnormalities and motility dis- high-resolution manometry was not available in the majority orders with hiatal hernia. Some patients in this study had of patients. Prolonged manometry was not performed, but as both a motility disorder and a hiatal hernia. In achalasia previously described, may increase the detection of subtle patients, there was a predominance of inflammation and few motility disorders [19]. The myenteric plexus abnormalities ganglion cell abnormalities. This could be explained by may be cause or effect; our evaluation was not designed to different disease mechanisms or a variable tempo of determine which. As with any negative finding, possibility of myenteric plexus change in patients with epiphrenic diverti- a false-negative result exists. This is an observational study, culum and associated achalasia with hiatal hernia. Diffuse and analysis is limited to pattern recognition. esophageal spasm with or without hiatal hernia had myenteric plexus abnormalities similar to those seen with achalasia. All patients with nutcracker esophagus had both hiatal hernia and 5. Conclusions myenteric plexus abnormalities. Nutcracker esophagus has been reported to have similar clinical, radiographic, and Myenteric plexus abnormalities in epiphrenic diverticulum manometric findings, whether or not it is associated with predominate, and disease-specific patterns, although incom- GERD [16]. Evaluation of the myenteric plexus in additional plete, are present. The role these associations play is only patients with nutcracker esophagus and no diverticulum may speculative. In the absence of motility disorders or hiatal improve our understanding of this motility disorder. However, hernia, myenteric plexus abnormalities may be an isolated the reported findings are in contrast to those of Champion and finding. Isolated epiphrenic diverticulum is uncommon and colleagues [11], who found neither ganglion cell abnormalities may reflect an inability of present investigative techniques to nor inflammation in myotomy specimens from four patients detect abnormalities. In patients with epiphrenic diverticu- with nutcracker esophagus and no epiphrenic diverticulum. lum, addition of a muscle biopsy during myotomy and Hypertensive lower esophageal sphincter is an uncommon histologic review of the myenteric plexus in esophagectomy spastic motility disorder that has been reported both in specimens are encouraged to increase our understanding of isolation and with GERD [17]. Although we had only three these diseases to improve the care of these patients. such patients, this dual etiology is consistent with our findings. Myenteric inflammation was the only myenteric plexus abnormality seen in hypertensive lower esophageal References sphincter. In contrast, Champion and colleagues [11] found no ganglion cells or myenteric inflammation in three patients [1] Goldblum JR, Whyte RI, Orringer MB, Appelman HD. Achalasia. A morpho- with hypertensive lower esophageal sphincter. logic study of 42 resected specimens. Am J Surg Pathol 1994;18:327—37. [2] Goldblum JR, Rice TW, Richter JE. Histopathologic features in esopha- gomyotomy specimens from patients with achalasia. Gastroenterology 4.1.2.4. Myenteric plexus abnormalities and neither moti- 1996;111:648—54. lity disorders nor hiatal hernia. In the absence of associated [3] DeMeester TR, Costantini M. Function tests. In: Patterson GA, Cooper JD, esophageal disorders, myenteric plexus abnormalities were Deslauriers J, Lerut A, Luketich JD, Rice TW, editors. Pearson’s thoracic & the sole finding in more than half this small group. This could esophageal surgery. Philadelphia: Churchill Livingstone/Elsevier; 2008. [4] Reznik SI, Rice TW, Murthy SC, Mason DP, Apperson-Hansen C, Blackstone be explained by the existence of other esophageal disorders EH. Assessment of a pathophysiology-directed treatment for sympto- that were not appropriately studied and therefore not matic epiphrenic diverticulum. Dis Esophagus 2007;20:320—7. detected. However, two patients had an isolated epiphrenic [5] Raymond L, Lach B, Shamji FM. Inflammatory aetiology of primary diverticulum, suggesting that either abnormalities of distal oesophageal achalasia: an immunohistochemical and ultrastructural study of Auerbach’s plexus. Histopathology 1999;35:445—53. obstruction were subclinical, or epiphrenic diverticulum may [6] Kilic A, Krasinskas AM, Owens SR, Luketich JD, Landreneau RJ, Schuchert rarely occur as an isolated finding. MJ. Variations in inflammation and nerve fiber loss reflect different subsets of achalasia patients. J Surg Res 2007;143:177—82. 4.2. Limitations [7] Clark SB, Rice TW, Tubbs RR, Richter JE, Goldblum JR. The nature of the myenteric infiltrate in achalasia: an immunohistochemical analysis. Am J Surg Pathol 2000;24:1153—8. The group of preoperative tests for motility disorders and [8] Bloomston M, Fraiji E, Boyce Jr HW, Gonzalvo A, Johnson M, Rosemurgy histologic examination of the esophagus distal to the AS. Preoperative intervention does not affect esophageal muscle histol- T.W. Rice et al. / European Journal of Cardio-thoracic Surgery 35 (2009) 22—27 27

ogy or patient outcomes in patients undergoing laparoscopic Heller for 3 cm. I then construct a very modified two-stitch, one-layer Belsey. We myotomy. J Gastrointest Surg 2003;7:181—8. discussion 188—90. have published this in Diseases of the Esophagus. [9] Millan MS, Bourdages R, Beck IT, DaCosta LR. Transition from diffuse Dr J. Duffy (Nottingham, UK): Can I just ask, if you do preoperative esophageal spasm to achalasia. J Clin Gastroenterol 1979;1:107—17. manometry on these patients and you find it is normal, do you still do the [10] Khatami SS, Khandwala F, Shay SS, Vaezi MF. Does diffuse esophageal myotomy? spasm progress to achalasia? A prospective cohort study. Dig Dis Sci Dr Rice: Yes. 2005;50:1605—10. Dr Mattioli: We have one minute for speculation, because I am very [11] Champion JK, Delise N, Hunt T. Myenteric plexus in spastic motility interested in this. What do you think, what do you speculate on the disorders. J Gastrointest Surg 2001;5:514—6. pathogenesis of this funny disease? We have seen a hundred achalasias without [12] Ho SC, Chang CS, Wu CY, Chen GH. Ineffective esophageal motility is a diverticulum. Why do we see in some diverticulum? primary motility disorder in gastroesophageal reflux disease. Dig Dis Sci Dr Rice: Epiphrenic diverticulum is the result of a disease; usually you 2002;47:652—6. don’t find it in isolation. In only 2 of our 40 patients, we did not find an [13] Fornari F, Callegari-Jacques SM, Scussel PJ, Madalosso LF, Barros EF, associated abnormality. It is the result of distal obstruction, be it temporary or Barros SG. Is ineffective oesophageal motility associated with reflux permanent, from achalasia or not. The motility disorder may be subtle. Our oesophagitis? Eur J Gastroenterol Hepatol 2007;19:783—7. findings suggest that there may be a couple of types of achalasia, not always [14] Debas HT, Payne WS, Cameron AJ, Carlson HC. Physiopathology of lower

the classic findings. They may represent a special form of achalasia or a special Downloaded from https://academic.oup.com/ejcts/article/35/1/22/357545 by guest on 24 September 2021 esophageal diverticulum and its implications for treatment. Surg Gynecol way the patient decompresses his esophagus. They certainly are a peculiar and Obstet 1980;151:593—600. different group. Not surprisingly, you may have a patient with epiphrenic [15] Castrucci G, Porziella V, Granone PL, Picciocchi A. Tailored surgery for diverticulum and achalasia who does just fine and may not require treatment. esophageal body diverticula. Eur J Cardiothorac Surg 1998;14:380—7. It is an amazing disease. It serves as a decompressive outlet for the obstructed [16] Silva LF, de Oliveira Lemme EM. Are there any differences between esophagus and may mask symptoms. nutcracker esophagus with and without reflux? 2007;22: Dr G.A. Patterson (St. Louis, MO): Can I just make a comment. I am 245—50. somewhat fearful of standing up and making a remark for fear somebody will [17] Tamhankar AP, Almogy G, Arain MA, Portale G, Hagen JA, Peters JH, mistake me for an expert in , but I think what you just said a Crookes PF, Sillin LF, DeMeester SR, Bremner CG, DeMeester TR. Surgical moment ago is a very important point, and that is, do what is right for the management of hypertensive lower esophageal sphincter with dysphagia patient and what is wrong with them rather than put the incisions in small or . J Gastrointest Surg 2003;7:990—6. discussion 996. number in a place that provides poor access. I have seen a number of videos of [18] Pandolfino JE, Ghosh SK, Rice J, Clarke JO, Kwiatek MA, Kahrilas PJ. laparoscopic epiphrenic diverticula repair or myotomy and diverticulectomy, Classifying esophageal motility by pressure topography characteristics: a and I have to say that that, in my mind, is really stretching the application of study of 400 patients and 75 controls. Am J Gastroenterol 2008;103:27—37. laparoscopic surgery. I believe that a laparoscopic fundoplication is basically [19] Nehra D, Lord RV, DeMeester TR, Theisen J, Peters JH, Crookes PF, the same operation, but I do not believe that a laparoscopic epiphrenic Bremner CG. Physiologic basis for the treatment of epiphrenic diverti- diverticular repair is the same operation. Do you want to comment on that? culum. Ann Surg 2002;235:346—54. Dr Rice: I think you did it eloquently, and I can’t improve upon it. Dr T. Lerut (Leuven, Belgium): I couldn’t agree more with what you said. A. Conference discussion But just following, the theory that it is the obstructive phenomenon that is playing a key role in the onset of the diverticulum compared to your classic Dr S. Mattioli (Bologna, Italy): Can you specify the type of manometric achalasia series. In your series of epiphrenic diverticula are you measuring a patterns you have registered in these patients, and, second question not mean of LES pressure that is higher versus the LES pressures you measure in strictly related to your paper, what do you do surgically? your series of the achalasia patients? That is what one might expect. Dr Rice: I am a firm believer that the quality or result should not be Dr Rice: No. The LES resting pressure has the same frequency and/or same measured by the length and number of incisions but by managing the patient distribution in epiphrenic diverticula patients. About two-thirds of patients properly and avoiding a leak, which can be a fatal complication in these had a normal value of resting pressure, and one-third elevated. It is not a patients. To laparoscopically approach an epiphrenic diverticulum, you may difference in LESP. not mobilize it completely, and it is resected with a scissors-like stapler.I fear a Dr Lerut: So then we are back to Sandro’s question on the pathogenesis. leak. So, I use a small left thoracotomy and perform an epiphrenic Dr Mattioli: At any rate, many are not epiphrenic. They are 5 cm above the diverticulectomy, and on the wall opposite, I do a myotomy, starting at the GE junction, which makes it different. I agree that is difficult and risky to try to base of the diverticulum, about 1808 opposite, and carry it onto the stomach finish this operation. We agree.