Thomas J Van de Ven1, Hung-Lun John Hsia. 1. Department of Anesthesiology, Duke University Medical Center/Durham VAMC, Durham, North Carolina, USA. Thomas.vandeven@duke.edu
Abstract
PURPOSE OF REVIEW: Surgical incision invariably causes some measure of nerve damage and inflammatory response that, in most cases, heals quickly without long-term negative consequence. However, a subset of these patients go on to develop lasting neuropathic pain that is difficult to treat and, in many cases, prevents the return to normal activities of life. It remains unknown why two patients with identical surgical interventions may go on to develop completely divergent pain phenotypes or no pain at all. Aggressive, early analgesic therapy has been shown to reduce the incidence of chronic postsurgical pain (CPSP), but no specific regional anesthetic technique or systemic pharmacologic therapy has been shown to prevent CPSP. RECENT FINDINGS: Inflammation and glial cell activation have recently been shown to be just as important in the transition from normal acute pain to pathologic chronic pain as nerve injury itself and that central sensitization may not be solely due to repetitive nociceptive firing at the time of nerve injury. This has opened a number of new therapeutic possibilities for prevention of CPSP. SUMMARY: Here, we discuss the causes of CPSP and current useful preventive strategies in the perioperative period. We also discuss future potential disease-modifying treatments of CPSP.
PURPOSE OF REVIEW: Surgical incision invariably causes some measure of nerve damage and inflammatory response that, in most cases, heals quickly without long-term negative consequence. However, a subset of these patients go on to develop lasting neuropathic pain that is difficult to treat and, in many cases, prevents the return to normal activities of life. It remains unknown why two patients with identical surgical interventions may go on to develop completely divergent pain phenotypes or no pain at all. Aggressive, early analgesic therapy has been shown to reduce the incidence of chronic postsurgical pain (CPSP), but no specific regional anesthetic technique or systemic pharmacologic therapy has been shown to prevent CPSP. RECENT FINDINGS: Inflammation and glial cell activation have recently been shown to be just as important in the transition from normal acute pain to pathologic chronic pain as nerve injury itself and that central sensitization may not be solely due to repetitive nociceptive firing at the time of nerve injury. This has opened a number of new therapeutic possibilities for prevention of CPSP. SUMMARY: Here, we discuss the causes of CPSP and current useful preventive strategies in the perioperative period. We also discuss future potential disease-modifying treatments of CPSP.
Authors: Thomas Buchheit; Thomas Van de Ven; Hung-Lun John Hsia; Mary McDuffie; David B MacLeod; William White; Alexander Chamessian; Francis J Keefe; Chester Trip Buckenmaier; Andrew D Shaw Journal: Pain Med Date: 2016-01 Impact factor: 3.750
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