Antonio Montes1, Gisela Roca, Sergi Sabate, Jose Ignacio Lao, Arcadi Navarro, Jordi Cantillo, Jaume Canet. 1. From the Department of Anesthesiology, Parc de Salut MAR, Institut Municipal d'Investigació Mèdica, Universitat Autònoma de Barcelona, Barcelona, Spain (A.M., J. Cantillo); Department of Anesthesiology, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain (G.R., J. Canet); Department of Anesthesiology, Fundació Puigvert, Barcelona, Spain (S.S.); Genomic Genetics International, Barcelona, Spain (J.I.L.); and Department of Experimental and Health Sciences (Universitat Pompeu Fabra) and Institute of Evolutionary Biology (Universitat Pompeu Fabra-CSIC), Centre de Regulació Genòmica, National Institute for Bioinformatics, Institució Catalana de Recerca I Estudis Avançats, Barcelona, Spain (A.N.).
Abstract
BACKGROUND: Chronic postsurgical pain (CPSP) has been linked to many surgical settings. The authors aimed to analyze functional genetic polymorphisms and clinical factors that might identify CPSP risk after inguinal hernia repair, hysterectomy, and thoracotomy. METHODS: This prospective multicenter cohort study enrolled 2,929 patients scheduled for inguinal hernia repair, hysterectomy (vaginal or abdominal), or thoracotomy. The main outcome was the incidence of CPSP confirmed by physical examination 4 months after surgery. The secondary outcome was CPSP incidences at 12 and 24 months. The authors also tested the associations between CPSP and 90 genetic markers plus a series of clinical factors and built a CPSP risk model. RESULTS: Within a median of 4.4 months, CPSP had developed in 527 patients (18.0%), in 13.6% after hernia repair, 11.8% after vaginal hysterectomy, 25.1% after abdominal hysterectomy, and 37.6% after thoracotomy. CPSP persisted after a median of 14.6 months and 26.3 months in 6.2% and 4.1%, respectively, after hernia repair, 4.1% and 2.2% after vaginal hysterectomy, 9.9% and 6.7% after abdominal hysterectomy, and 19.1% and 13.2% after thoracotomy. No significant genetic differences between cases and controls were identified. The risk model included six clinical predictors: (1) surgical procedure, (2) age, (3) physical health (Short Form Health Survey-12), (4) mental health (Short Form Health Survey-12), (5) preoperative pain in the surgical field, and (6) preoperative pain in another area. Discrimination was moderate (c-statistic, 0.731; 95% CI, 0.705 to 0.755). CONCLUSIONS: Until unequivocal genetic predictors of CPSP are understood, the authors encourage systematic use of clinical factors for predicting and managing CPSP risk.
BACKGROUND: Chronic postsurgical pain (CPSP) has been linked to many surgical settings. The authors aimed to analyze functional genetic polymorphisms and clinical factors that might identify CPSP risk after inguinal hernia repair, hysterectomy, and thoracotomy. METHODS: This prospective multicenter cohort study enrolled 2,929 patients scheduled for inguinal hernia repair, hysterectomy (vaginal or abdominal), or thoracotomy. The main outcome was the incidence of CPSP confirmed by physical examination 4 months after surgery. The secondary outcome was CPSP incidences at 12 and 24 months. The authors also tested the associations between CPSP and 90 genetic markers plus a series of clinical factors and built a CPSP risk model. RESULTS: Within a median of 4.4 months, CPSP had developed in 527 patients (18.0%), in 13.6% after hernia repair, 11.8% after vaginal hysterectomy, 25.1% after abdominal hysterectomy, and 37.6% after thoracotomy. CPSP persisted after a median of 14.6 months and 26.3 months in 6.2% and 4.1%, respectively, after hernia repair, 4.1% and 2.2% after vaginal hysterectomy, 9.9% and 6.7% after abdominal hysterectomy, and 19.1% and 13.2% after thoracotomy. No significant genetic differences between cases and controls were identified. The risk model included six clinical predictors: (1) surgical procedure, (2) age, (3) physical health (Short Form Health Survey-12), (4) mental health (Short Form Health Survey-12), (5) preoperative pain in the surgical field, and (6) preoperative pain in another area. Discrimination was moderate (c-statistic, 0.731; 95% CI, 0.705 to 0.755). CONCLUSIONS: Until unequivocal genetic predictors of CPSP are understood, the authors encourage systematic use of clinical factors for predicting and managing CPSP risk.
Authors: David Borsook; Andrew M Youssef; Nadia Barakat; Christine B Sieberg; Igor Elman Journal: Neurosci Biobehav Rev Date: 2018-02-21 Impact factor: 8.989