Choosing Analgesia to Facilitate Recovery

Abstract

Perioperative Pain and Multimodal AnalgesiaPathophysiology of Surgical Pain S urgical incision and manipulation of tissues lead to cell disruption and activation of humoral and cell-mediated inflammatory responses. A variety of intracellular chemical mediators including potassium, adenosine, prostanoids, bradykinin, nerve growth factors, cytokines, and chemokines are released from the injured tissues, then activate and sensitize peripheral nociceptors such as Aδ and c-fibers to mechanical stimuli (primary hyperalgesia). These pro-inflammatory substances together with the release of substance P and calcitonin gene-related peptide also sensitize silent Aδ nociceptors in the adjacent noninjured tissues (secondary hyperalgesia). Repeated and prolonged stimulation of peripheral nociceptors in the injured area and in the surrounding noninjured tissues leads to an increased firing of neurons at the level of the dorsal horn of the spinal cord, mediated by the activation of N -methyl-D -aspartate (NMDA) receptors (central sensitization). Clinically these pathophysiologic changes manifest with hyperalgesia, allodynia in the area of the surgical incision, with or without late persistent postsurgical pain. Descending sympathetic inhibitory pathways also take an important role at the level of the spinal cord by modulating transmission of noxious inputs. Acute surgical pain can therefore be somatic, visceral, or neuropathic depending on the type of surgery and on the surgical approach. Response to nociception contributes to activate and potentiate the stress response associated with surgery. These stress responses have consequences, such as activation of the hypothalamic-pituitary-adrenal