Plenary Session











Attenzione: apre in una nuova finestra.

Plenary Session 1 Sunday, September 2, 8:00 – 9:45 am
Physiology UES – Body – LES

Chairs:
L.S. Miller (Philadelphia) – K.R. DeVault (Jacksonville)
Discussant:
B.P. McMahon (Dublin)
Secretary: A. Vegesna (Philadelphia)

  • Is there a neurophysiological relationship between the proximal and distal esophagus?
  • What are the differences in esophageal muscle "in vitro" properties between the lower esophageal circular muscle, the clasp muscle, and the sling fibers?  
  • What new modalities (in vivo & in vitro) can be used to evaluate the HPZ of the proximal and distal esophagus (FLIP, MicroCT, EUS)?
  • What is the effect of laryngeal stimulation on the UESP? Is this effect reproducible?
  • To what extent can fluoroscopy and manometry with biomechanics define the various stages of UES opening?
  • Is there a mechanical relationship between anterior hyoid movement, extent of UES opening and aspiration?
  • What is the relationship between pharyngeal contraction, relaxation of upper esophageal sphincter muscle and function in the normal swallow and with dysphagia?
  • What is the function of the muscularis mucosa in the esophagus?
  • What are the differences in esophageal muscle between the striated, transition zone, proximal smooth muscle, distal smooth muscle and LES muscle? How do they affect the "in vivo" compliance and contractility of the esophagus?
  • What is the current understanding of the coordination of contraction passage from proximal to transition to smooth muscle esophageal segments?
  • Which are the most important excitatory and inhibitory neurotransmitters regulating the esophageal striated and smooth muscle esophagus?
  • What non-pharmacological approaches are available that can alter the gastro-esophageal sphincter function?
  • What is the evidence for a physiological sphincter without an anatomical counterpart within the gastro-esophageal segment?
  • Understanding the sphincteric components of the gastro-esophageal segment that are responsible for the generation of the high-pressure zone at the esophago-gastric junction.
  • Do longitudinal muscles of the esophagus contract during various types of LES relaxation and what is its role in LES function?
  • What physiologic abnormalities are present in the muscles of the HPZ in GERD subjects vs normal control subjects (in vitro & in vivo).

Plenary Session 2 Sunday, September 2, 10:15 am- 12:00 pm
UES dysfunction
Diverticula – Globus pharyngeus

Chairs: R.K. Mittal (San Diego) – D. Sifrim (London)
Discussant: E. Rieder (Portland)                 

  • What are the respective advantages of VFSS (video-fluoroscopic swallowing study) and FEES (fiberoptic endoscopic evaluation of swallowing) in the evaluation of UES dysfunction?
  • What is the etiology of Zenker diverticulum?
  • Spectrum dysfunction – From CPM bars to Zenker diverticulum.
  • What is the proper diagnostic algorithm for patients with presumed CP dysfunction?
  • What are the indications of endoscopic methods of treatment?
  • Is myotomy alone reasonable for small diverticula?  
  • How should we treat a diverticulum associated with reflux?              
  • What is the role of CPM dysfunction in globus sensation?
  • What is the mechanism by which reflux contributes to globus pharyngeus?
  • What is the role of reflux in patients with isolated globus?
  • Do we need videofluoroscopy in patients with dysphagia, suspicion of aspiration, or globus?
  • What is the role of endoscopy in the evaluation of globus?
  • What is the role of impedance-manometry and pH testing in globus evaluation?
  • What is the best treatment for globus related to reflux?
  • Of those with impaired UES opening, who are better candidates for surgical intervention?
  • What is the role of psychologic treatment in the globus patient?

Plenary Session 3 Sunday, September 2, 2:30 – 4:15 pm
Achalasia

Chairs:
C.A. Pellegrini (Seattle) – R. Dantas (Ribeirao Preto)
Discussant: R. Penagini (Milan)
Secretary: E.B. Wassenaar (Seattle)

  • Should achalasia be considered as a strictly Primary myopathy?
  • How has HRM (and stationary impedance) redefined the diagnosis of non-achalasia spastic disorders of the esophagus?
  • Can cases where relaxation is preserved considered as initial stages?
  • How is the LESP function in Chagas’ disease?
  • Is the mega-esophagus of Chagas’ disease physiologically comparable to that of idiopathic achalasia?
  • Does failure of balloon dilation foretell a poor result from surgery?
  • In what circumstances should surgical treatment be considered from the outset?
  • Are sensory neural pathways impaired in achalasia?
  • Based on manometry, what are different subtypes of achalasia, and how does longitudinal muscle contraction pattern differ among them?
  • When should esophagectomy be considered for the treatment of achalasia?
  • What are the technical components of surgery for achalasia that are important to success?
  • When esophagectomy is required, what is the best substitute?
  • How do you approach someone with recurrent dysphagia after Heller myotomy?
  • Which components of the lower esophageal high pressure zone are abnormal in achalasia?
    (lower esophageal circular muscle, clasp muscle, sling muscle, or a combination of these muscles)
  • Is a totally endoscopic approach to esophageal myotomy a better option?

Plenary Session 4 Sunday, September 2, 4:30 - 6:15 pm
Primary disorders / Esophageal body
Diffuse Esophageal Spasms – Nutcracker esophagus – Intermediate forms

Chairs: Castell (Charleston)
Discussant: R. Tutuian (Bern)

General Concepts

  • How does circular and longitudinal muscle contraction coordinate during normal peristalsis and discoordinate in spastic   
    motor disorders?                                                                                                  
  • How and why is the latency of distal esophageal contraction affected in diffuse esophageal spasm?            
  • How has HRM (and stationary impedance?) redefined the diagnosis of disorders with impaired peristalsis in the esophagus? What is the value of the latency point?                   
  • Is there a relationship among physiology/pathophysiology, function/dysfunction and biomechanics of longitudinal muscle in the esophagus?
  • What is the evidence that DES, nutcracker esophagus, and achalasia represent a spectrum of diseases?

DES

  • What is the role of nitric oxide in pathophysiology of DES?                                                         
  • Does the absence of neural abnormalities in DES exclude a neurogenic origin?                              
  • What are the different clinical features of DES?  Can DES be asymptomatic?                                            
  • What is the importance of associated hiatal hernia or GER in DES?                                                       
  • Is the LES always normal in DES?  Is it easy to differentiate from achalasia?                                              
  • Is there an effective therapy for DES?                       
  • What is the success rate of surgical treatment?

Nutcraker Esophagus

  • Is the natural history of nutcracker esophagus known?                                                      
  • What criteria allow for differentiation of this syndrome from that of DES?                                              
  • Is esophageal clearance always normal?

Plenary Session 5 Monday, September 3, 8:15 - 10:00 am
LES dysfunction
Chairs: J.E. Richter (Tampa) – P. Bechi (Florence)
Discussant: K.K. Wang (Rochester, MN)

  • What is the value of the meticulous endoscopic and histological assessment of the gastric cardia?
  • Is functional heartburn different from NERD?
    – Which are the mechanisms of symptoms in functional heartburn?
  • What are the phreno-esophageal ligaments and what role do they play in the pathogenesis of 
hiatus hernia?                      
  • Which pharmacologic agents can alter the frequency of transient LES relaxation and why are they still not in clinical practice? 
  • Is reflux possible in the presence of tone in the muscles within the gastro-esophageal sphincter?
  • Is the definition of TLESR mechanical or physiological, and what is the evidence that TLESR is the cause 
  of GERD?            
  • Can distensibility testing help identify EGJ sub-components and their function in health and disease?
  • Is the relationship between hiatal hernia and reflux mechanical or physiological?
  • What is the status of fundic relaxation and accommodation in GE Reflux?
  • What is the role of the acid pocket in clinical reflux disease?
  • What is the role of the crico-pharyngeus muscle in reflux disease?
  • How do endoscopic GERD treatments improve LES dysfunction?
  • How does anti-reflux surgery correct LES dysfunction?

Plenary Session 6 Monday, September 3, 10:15 am - 12:00 pm
Functional testing

Chairs:
R. Penagini (Milan) – C.P. Gyawali (St Louis)
Discussant: B.P. McMahon (Dublin)
Secretary: I. Bravi (Milan)

  • What are the current irrefutable indications for pH monitoring?
  • What criteria define abnormal pH measurements above the UES?
  • Is there a role for single site pharyngeal pH monitoring using the ResTech device?
  • When does wireless pH monitoring need to be extended beyond 48 hours?
  • Should gastric pH be recorded as part of ambulatory pH monitoring?
  • What has combined pH-impedance monitoring contributed to the understanding of GERD pathophysiology?
  • Is pH-impedance monitoring useful in differentiating NERD from functional heartburn?
  • Are inter- and intra-observer agreement acceptable in pH and Impedance analysis?
  • Can events associated with TLESR be accurately described using the Endoflip distensibility testing?
  • What does Endoflip add to assessment of reflux disease?
  • Does ambulatory high-resolution manometry (HRM) with or without impedance have a role in clinical esophagology?
  • Is HRIM the new gold standard in evaluating esophageal motility?
  • What is the current value of 3D HRM?
  • Will HRM replace sleeve measurements in evaluating tLESRs?
  • Do bread swallows improve the diagnostic yield of routine clinical HRM/HRIM studies?

Plenary Session 7 Monday, September 3, 2:30 – 4:15 pm
Barrett's esophagus
Endoscopic - Surgical treatments

Chairs:
A.Repici (Milan) – B.D. Greenwald (Baltimore)
Discussant: J. Abrams (New York)
Secretary: A.K. Roorda (Morgantown)

  • What is the effect of endoscopic therapy on the BE genotype?
  • Should patients with non-dysplastic BE offered ablative therapy?
  • Should patients with non-dysplastic BE not offered ablative therapy?
  • Should patients with low-grade dysplastic BE offered ablative therapy?
  • Should patients with low-grade dysplastic BE not offered ablative therapy?
  • EMR or ablation or both for HGD?
  • How is cryotherapy comparing to radiofrequency for BE ablation?
  • How to endoscopically select ablation or EMR for dysplastic BE?
  • What is the value of trans-nasal endoscopy for BE screening?
  • Is ESD preferable to EMR for nodular lesions in Barrett’s esophagus?
  • What is the current role of confocal endomicroscopy in Barrett's surveillance?
  • How to approach proximal BE following esophago-gastric anastomosis?
  • Are GERD and BE more prevalent in gastroparesis?
  • Esophagectomy or endoscopic resection for HGD and early cancer?
  • What is the role of fundoplication in BE?

Plenary Session 8 Monday, September 3, 4:30 – 6:15 pm
Barrett's esophagus and cancer

Chairs:
L. Bonavina (Milan ) –  S.J. Spechler (Dallas)
Discussant:
R.C. Fitzgerald (Cambridge)
Secretary: G. Saino (Milan)

  • Which molecular changes (amplification/deletion/mutation) are associated with progression from Barrett’s to adenocarcinoma?
  • What is the status of predictive biomarkers based on identified molecular genetic changes?
  • Which molecular changes (amplification/deletion/mutation) are associated with EAC?
  • Which molecular alterations in EAC represent potential targets for therapy?
  • What is the role of implication of the genes encoding interleukin (IL-1b) and Tumor Necrosis Factor (TNFa)?
  • Does the Shh/Bmp4/Sox9 pathway have a role in the development of Barrett's oesophagus?
  • Bile acids and nuclear receptors in esophageal carcinogenesis.
  • What is the “intrinsic” inflammatory pathway and how does it contribute to carcinogenesis in Barrett’s esophagus?
  • What is the role of Cox-1 and Cox-2 in progression of non-dysplastic BE to adenocarcinoma?
  • Is limited surgical resection an adequate procedure for submucosal adenocarcinoma of the esophagogastric junction ?
  • Can sentinel node technology secure limited surgical resections for adenocarcinoma of the esophagogastric junction?
  • What is the current evidence for various types of resection for adenocarcinoma of the  esophago-gastric junction based on Siewert’s classification?
  • Is extended mediastinal lymphadenectomy (2-field-LAD) the gold standard for surgical resection of esophageal adenocarcinoma?
  • What is the influence of prior EMR on complications and outcomes following RFA in BE?

Plenary Session 9 Tuesday, September 4, 7:30 - 9:45 am
New therapeutic strategies for squamous cell cancer and adenocarcinoma
Chairs: Daniela Kandioler (Vienna) – D.H. Ilson New York
Discussant: M. Krasna (Neptune)

Topic A: Targeted agents and biomarkers in esophageal squamous cell and adenocarcinoma

  1. Trastuzumab: is there a role for distal esophageal adenocarcinoma, or any potential for treatment for esophageal dysplasia/intra-epithelial neoplasia?
  2. Are there SNP’s that are potentially prognostic or predictive of therapy outcome in squamous cancers or adenocarcinoma, and are there such biomarkers in potentially high risk populations?
  3. What is the role of phenotype and genotype in selecting patients for targeted therapy for esophageal cancer?
  4. Are there any promising new targets for new drug development, what targeted agents are in phase II and III trials?
  5. What is the current role of FDG PET scan in staging, response assessment, and therapy decision making in esophageal squamous cell and adenocarcinoma

Topic B: What is the current role of different surgical approaches and what is the impact of surgical complications?

  1. Does neo-adjuvant treatment increase peri-operative morbidity and/or mortality rates after esophagectomy?
  2. Do complications really influence long term prognosis? Does it depend on the severity?
  3. Is there a place for trans-hiatal esophagectomy in treatment of the esophageal cancer?
  4. Does the level of the intra-thoracic esophago-gastrostomy matter with respect to outcome?

Topic C: Combined modality therapy as preoperative or definitive therapy

  1. How do we treat patients with significant residual disease (N+) after preoperative chemotherapy, and is postoperative chemotherapy justified?
    a.    Yes  
    b.    No
  2. Are there indications for neo-adjuvant chemo-radiation in early stage esophageal cancer?
  3. What is the current role of salvage esophagectomy following local failure of definitive chemo-radiation without prior surgery?
  4. Does surgery play a role for stage III squamous cancer after chemoradiotherapy?  
    a.     Yes  
    b.     No
  5. The optimal preoperative treatment prior to surgery is:
    a.    Chemotherapy
    b.    Chemoradiotherapy

Topic D: What is the best palliative approach to dysphagia?

  1. In what circumstances is surgical palliation better than a self-expansible prosthesis in the treatment of advanced esophageal cancer?
  2. Palliation of malignant dysphagia: stent, brachy-therapy, both, or chemo-radiation?
    a.    Chemoradiation or stent  
    b.    Chemotherapy
  3. Are there advantages in using radioactive or drug eluting stents?

Plenary Session 10 Tuesday, September 4, 10:00 - 11:45 am
Esophageal cancer
Chairs: P.M. Schneider (Zurich) – J.M. Collard (Brussels)
Discussant: S. Law (Hong Kong)  

  • What testing should be made for targeted therapy in esophageal cancers?
  • Does the level of the intra-thoracic esophago-gastrostomy matter with respect to lymphadenectomy and outcome?                                                                                                                                    
  • Is minimally-invasive esophagectomy as good as open surgery?                                                   
  • Is there still a role for surgical resection of cervical esophageal squamous cell cancer?      
  • Are pure surgical arms still justified in future randomized trials evaluating multimodality treatment regimens?            
  • Does neo-adjuvant treatment in past randomized trials compensate for low quality surgery or is it truly beneficial?
  • Should early FDG-PET response monitoring be performed in neo-adjuvant treatment strategies?
  • What is the current impact of molecular response evaluation in neo-adjuvant treatment strategies?
  • What is the short and long term toxicity of definitive chemo-radiation and should we follow our patients?                   
  • What type of anastomosis should be performed after subtotal esophagectomy?               
  • Should para-aortic lymph node dissection be performed in E-G junction tumors?           
  • What is the best strategy for T2 esophageal cancer?                                                                   
  • Do m3- sm1 cancers need radical esophagectomy after endoscopic resection for staging?
  • Does EUS provide additional useful information to PET-CT regarding lymph node metastases?