ORIGINAL ARTICLE High-resolution manometry combined with impedance measurements discriminates the cause of dysphagia in children Nathalie Rommel 1,2,3 & Taher I. Omari 3,4,5 & Margot Selleslagh 1,3 & Stamatiki Kritas 3 & Charles Cock 4,6 & Rachel Rosan 7,8 & Leonel Rodriguez 7,8 & Samuel Nurko 7,8 Received: 14 January 2015 /Revised: 7 June 2015 /Accepted: 12 June 2015 # Springer-Verlag Berlin Heidelberg 2015 Abstract Pressure-flow analysis allows assessing esopha- geal bolus transport in relation to esophageal pressures. This study aimed to characterize pressure-flow metrics in relation to dysphagia in paediatric patients. We analysed esophageal pressure-impedance recordings of 5 ml liquid and viscous swallows from 35 children (17 M, mean 10.5±0.8 years). Primary indication for referral was gastroesophageal reflux disease (GERD) (9), post- fundoplication dysphagia (5), idiopathic dysphagia (16), trachea-esophageal fistula (2) and other (3). Peristaltic function was assessed using the 20 mmHg iso-contour defect and the timing between bolus pressure and flow was assessed using the Pressure Flow Index, a metric elevated in relation to dysphagia. Patients were stratified in relation to dysphagia and to peristaltic defect size. Dysphagia was characterized by a weaker peristalsis for liquids and higher Pressure Flow Index for viscous. When patients were stratified based on weak or normal peristal- sis, dysphagia with weak peristalsis related to a larger iso- contour defect size and dysphagia with normal peristalsis related to higher Pressure Flow Index. Conclusion: Pressure-flow analysis enables differentia- tion of patients with dysphagia due to weak peristalsis (poor bolus clearance) from abnormal bolus flow resis- tance (esophageal outflow obstruction). This new dichot- omous categorization of esophageal function may help guide the selection of optimal treatment such as pharma- cological or endoscopic therapy. Communicated by Peter de Winter * Nathalie Rommel nathalie.rommel@med.kuleuven.be Taher I. Omari taher.omari@flinders.edu.au Margot Selleslagh margot.selleslagh@med.kuleuven.be Stamatiki Kritas stamatiki.kritas@med.kuleuven.be Charles Cock charles.Cock@health.sa.gov.au Rachel Rosan rachel.rosen@childrens.harvard.edu Leonel Rodriguez leonel.Rodriguez@childrens.harvard.edu Samuel Nurko sam.nurko@childrens.harvard.edu 1 Neurosciences, ExpORL, University of Leuven, Leuven, Belgium 2 Neurogastroenterology & Motility, Gastroenterology, University Hospital Leuven, Leuven, Belgium 3 Translational Research Center for Gastrointestinal Diseases (TARGID), University of Leuven, Leuven, Belgium 4 School of Medicine, Flinders University, Bedford Park, South Australia, Australia 5 The Robinson Institute, University of Adelaide, Adelaide, South Australia, Australia 6 Investigation and Procedures Unit, Repatriation General Hospital, Daw Park, South Australia, Australia 7 Harvard Medical School, Boston, MA, USA 8 Centre for Motility and Functional GI Disorders, Boston Children’ s Hospital , Boston, MA, USA Eur J Pediatr DOI 10.1007/s00431-015-2582-9