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Chapter 72 - Acute Postoperative Pain

Christopher L. Wu

FUNDAMENTAL CONSIDERATIONS

A revolution in the management of acute postoperative pain has occurred during the past 2 decades. Widespread recognition of the undertreatment of acute pain by clinicians, economists, and health policy experts has led to the development of a national clinical practice guideline for acute pain management by the Agency for Healthcare Quality and Research (formerly the Agency for Health Care Policy and Research) of the U.S. Department of Health and Human Services.^[1] This landmark document includes acknowledgment of the historic inadequacies in perioperative pain management, importance of good pain control, need for accountability for adequate provision of perioperative analgesia by health care institutions, and a statement on the need for involvement of specialists in appropriate cases. Several professional societies have also developed clinical practice guidelines for acute pain management. ^{[2] [3]} In 2000, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) unveiled new pain management standards.^[4]

With their knowledge of and familiarity with pharmacology, various regional techniques, and the neurobiology of nociception, anesthesiologists are continually in the forefront of clinical and research advances in acute postoperative pain management. Anesthesiologists are leaders in the development of acute postoperative pain services, ^[5] application of evidence-based practice to acute postoperative pain, and creation of innovative approaches to acute pain management, ^{[6] [7] [8]} all of which are a natural part of the anesthesiologist in becoming the "perioperative physician," a consultant and therapist throughout an institution, and a highly skilled expert in the operating room. Provision of effective analgesia for surgical and other patients is an important component of this vision.

Pain Pathways and the Neurobiology of Nociception

Surgery produces tissue injury with consequent release of histamine and inflammatory mediators, such as peptides (e.g., bradykinin), lipids (e.g., prostaglandins), neurotransmitters (e.g., serotonin), and neurotrophins (e.g., nerve growth factor) ^[9] (see Chapter 73 ). The release of inflammatory mediators activates peripheral nociceptors, which initiate transduction and transmission of the nociceptive information to the central nervous system (CNS) and the process of neurogenic inflammation in which release of neurotransmitters (i.e., substance P and calcitonin gene-related peptide) in the periphery induces vasodilatation and plasma extravasation.^[9] Noxious stimuli are transduced by the peripheral nociceptors and transmitted by Aδ and C nerve fibers from peripheral visceral and somatic sites to the dorsal horn of the spinal cord, where integration of peripheral nociceptive and descending modulatory input (i.e., serotonin, noradrenaline, and enkephalin) occurs. Further transmission of nociceptive information is determined by complex modulating influences in the

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Continuous release of inflammatory mediators in the periphery sensitizes functional nociceptors and activates dormant ones.^[10] Sensitization of peripheral nociceptors may occur and is marked by a decreased threshold for activation, increased discharge rate with activation, and increased rate of basal (spontaneous) discharge.^[10] Intense noxious input from the periphery may also result in central sensitization ("persistent postinjury changes in the CNS that result in pain hypersensitivity"^[11] ) and hyperexcitability ("exaggerated and prolonged responsiveness of neurons to normal afferent input after tissue damage"^[11] ). Such noxious input may lead to functional changes in the dorsal horn of the spinal cord and other consequences that may later cause postoperative pain to be perceived as more painful than it would otherwise have been. The neural circuitry in the dorsal horn is extremely complex, and we are just beginning to elucidate the specific role of the various neurotransmitters and receptors in the process of nociception.^{[9] [12]} However, it seems that certain receptors (e.g., N-methyl-D-aspartate [NMDA]) may be especially important for the development of chronic pain after an acute injury^[6] although others (e.g., substance P, protein kinase C-γ) may also play important roles in spinal cord sensitization and chronic pain.^{[6] [13]} Our understanding of the neurobiology of nociception has progressed from the hard-wired system proposed by Descartes in the 17th century to the current view of neuroplasticity in which there is dynamic integration and modulation of nociceptive transmission at several levels. There still are many gaps in our knowledge of the specific roles of various receptors, neurotransmitters, and molecular structures in the process of nociception.

An understanding of the neurobiology of nociception is important for appreciating the transition from acute to chronic pain. The traditional dichotomy between acute and chronic pain is arbitrary, because animal and clinical studies demonstrate that acute pain may quickly transition into chronic pain.^[10] Experimental studies show that noxious stimuli can produce expression of new genes (which are the basis for neuronal sensitization^[10] ) in the dorsal horn of the spinal cord within 1 hour and that these changes are sufficient to alter behavior within the same time frame.^[12] Clinical studies also suggest that the intensity of acute postoperative pain is a significant predictor of chronic postoperative pain.^{[14] [15] [16] [17]} Control of acute postoperative pain and the timing, duration (e.g., preemptive analgesia), and fashion in which it is implemented (e.g., multimodal perioperative management) may be important in facilitating short- and long-term patient convalescence after surgery.