Perioperative pain control

Perioperative Pain Control: A Strategy for Management
Surgical Clinics of North America - Volume 85, Issue 6 (December 2005)  -  Copyright © 2005 W. B. Saunders Company  -  About This Clinic

Mitchell Jay Cohen, MD
William P. Schecter, MD, FACS ∗[pic]University of California, San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110, USA

|* Correspondingauthor. 1001 Potrero Avenue, Ward 3A33, San |
|Francisco, CA 94110. |

[pic]
|E-mail address:  bschecter@sfghsurg.ucsf.edu |

PII S0039-6109(05)00124-6

A thorough understanding of the anatomy and neurophysiology of the pain response is necessary for the effective treatment of perioperative pain. Pain begins with stimulation ofspecialized nerve endings called nociceptors. Nociceptors exist throughout the body and serve as the proximal end of the sensory nerves. Most prevalent in highly sensate areas, such as the fingertips, extremities, and face, these receptors are most often stimulated directly by injury and surgical incision. In addition to responding to direct stimulation, these receptors also respond to mediators releasedduring surgical trauma, inflammation and stress, leading to impulse formation and pain [1], [2], [3], [4]. These mediators, which include prostaglandins, bradykinins, histamine, and serotonin, act by two mechanisms to cause pain [1], [5], [6]. First, they act on nerve endings to cause pain impulse formation. Second, they amplify other pain signals caused by direct stimulation. These mediators havealso been implicated in prolonged up-regulation of nociceptors, which leads to chronic pain, phantom pain, and hypersensitization [1], [4].
Nociceptor stimulation causes depolarization of the nerve, creating an all-or-nothing response. The nerve impulse travels from the periphery to the dorsal horn of the spinal cord via Lissauer's tract. Myelinated A-δ nerve fibers conduct nerve impulsesrapidly. Relatively slow conduction takes place in unmyelinated C fibers in the viscera, which join autonomic nerves as they travel to join somatic nerves entering the central nervous system. This union of visceral and somatic nerves is responsible for the phenomena of referred pain. Because the visceral nerves enter the cord at the level of the somatic nerves with which they travel, the pain isperceived to be originating from the area innervated by the somatic nerves.
The sensory fiber nerves enter the dorsal horn. Pain and temperature fibers cross the midline and ascend to the brain in the lateral spinothalamic tract. Substance P is the primary neurotransmitter at the synapse between the afferent peripheral and ascending spinothalamic tract nerves. Interestingly, substance P has also beenwell described as a primary mediator in the neuroinflammatory cascade providing a connection between inflammation and chronic pain. The ascending fibers in the spinothalamic tract terminate primarily in the brain stem and thalamus, which then relay the information to the perceptive cerebral cortex. Signal transmission to and within the cerebral cortex causes perception and localization of pain. Othersignals are sent to the limbic system, further processed in the emotional centers, and are thereby responsible for the emotional response to pain.
INFLAMMATION AND PAIN
Inflammation is itself painful. Often this simple fact is not recognized and patients are undertreated. Inflammation causes pain through the up-regulation of stimulated nociceptors and the recruitment of nonstimulated or dormantreceptors [1], [3], [4]. Proinflammatory mediators, including TNF-ɑ, IL-1, IL-6, and the interferons, decrease the threshold for impulse generation, and raise the intensity of the nociceptic impulse. Additionally, the basal rate of discharge of peripheral nociceptors increases in a proinflammatory state [7]. These mechanisms make pain control in the patient with inflammatory conditions both...