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Recent Advances in Postoperative Pain Management

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Recent Advances in Postoperative Pain Management View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central YALE JOURNAL OF BIOLOGY AND MEDICINE 83 (2010), pp.11-25. Copyright © 2010. REVIEW Recent Advances in Postoperative Pain Management Nalini Vadivelu, MD a* ; Sukanya Mitra, MD b; and Deepak Narayan, MD c Departments of aAnesthesiology and cSurgery, Yale University School of Medicine, New Haven, Connecticut, and bDepartment of Anaesthesia & Intensive Care, Government Medical College & Hospital, Chandigarh, India Good pain control after surgery is important to prevent negative outcomes such as tachy - cardia, hypertension, myocardial ischemia, decrease in alveolar ventilation, and poor wound healing. Exacerbations of acute pain can lead to neural sensitization and release of medi - ators both peripherally and centrally. Clinical wind up occurs from the processes of N-Methyl D-Aspartate (NMDA†) activation, wind up central sensitization, long-term potentiation of pain (LTP), and transcription-dependent sensitization. Advances in the knowledge of molec - ular mechanisms have led to the development of multimodal analgesia and new pharmaceu - tical products to treat postoperative pain. The new pharmacological products to treat postoperative pain include extended-release epidural morphine and analgesic adjuvants such as capsaicin, ketamine, gabapentin, pregabalin dexmetomidine, and tapentadol. Newer postoperative patient-controlled analgesia (PCA) in modes such as intranasal, regional, transdermal, and pulmonary presents another interesting avenue of development. Proper pain relief is a major concern concerns of the surgeon because of its close and area of focus in the United States today. ties with clinical outcome and acute post - Pre-operatively, one of the most common operative patient well-being. Studies have questions asked by patients pertains to the indicated such negative clinical outcomes amount of pain they will experience after to include decreases in vital capacity and the surgery. Pain is also one of the primary alveolar ventilation, pneumonia, tachycar - *To whom all correspondence should be addressed: Dr Nalini Vadivelu, Department of Anesthesiology and Surgery, Yale University School of Medicine, New Haven, CT 06511; E-mail: [email protected]. †Abbreviations: NMDA, N-Methyl D-Aspartate; LTP, long-term potentiation; PCA, patient- controlled analgesia; BK, bradykinin; 5HT, 5 hydroxytryptamin; CGRP, calcitonin gene-re - lated protein; AMPA, amino-3-hydroxyl-5-methyl-4-proprionic acid; KAR, Kainate; EPSP, excitatory postsynaptic potentials; NO, nitric oxide; SO, superoxides; NK1, neurokinin re - ceptor; COX-2, cycloxygenase 2; EREM, extended-release epidural morphine; fentanyl ITS, fentanyl hydrochloride iontophoretic transdermal system; FDA, U.S. Food and Drug Administration; IV, intravenous; MAOI, monoamine oxidase inhibitors; PCRA, patient-con - trolled regional analgesia; RM, ropivacaine/morphine; RMK, ropivacaine/morphine/ketoro - lac; IN, intranasal; PCINA, patient-controlled intranasal analgesia; NNT, number-needed-to-treat; IA, intraarticular. Keywords: opioids, acute pain, pain mechanisms, postoperative, patient-controlled anal - gesia 11 12 Vadivelu: Advances in postoperative pain management dia, hypertension, myocardial ischemia, my - MOLECULAR MECHANISMS ocardial infarction, transition to chronic pain, poor wound healing, and insomnia It is important to know about the recent [1,2,3]. advances in central sensitization since it Pain has been found to be one of the plays an important role in post surgical and three most common medical causes of de - post traumatic pain [5,6]. Postoperative pain layed discharge after ambulatory surgery, is mostly nociceptive, which is pain percep - the other two being drowsiness and nau - tion following surgical insult. sea/vomiting. Despite this overwhelming However, there can be exacerbation of rationale for effective postoperative pain acute nociceptive pain leading to neural sen - control, the clinical reality is, unfortu - sitization when sensations that are not nor - nately, still far from satisfactory. As a re - mally painful are perceived as painful, as in cent editorial title suggests, we have a long hyperalgesia and allodynia. Mechanical al - way to go to achieve satisfactory postop - lodynia occurs due to the release of several erative pain control [3]. In an often-cited primary and secondary noxious sensitizers study [4] that assessed patients’ postoper - such as PGEs, leukotrienes [7], bradykinin ative pain experience and the status of (BK), histamine, and 5 hydroxytryptamine acute pain management in a random sam - (5HT). These conditions are commonly seen ple, approximately 80 percent of patients in those patients developing neuropathic said they experienced acute pain after sur - pain. Primary hyperalgesia occurs when gery. The authors concluded that despite an there is sensitization of peripheral nocicep - increased focus on pain management pro - tors, while secondary hyperalgesia is asso - grams and the development of new stan - ciated with the sensitization of the spinal dards for pain management, many patients cord and the central nervous system. continue to experience intense pain after In peripheral sensitization, there is a re - surgery. lease of primary mediators such as During the last couple of decades and prostaglandins, 5 hydroxytryptamine, especially the last few years, major techno - leukotrienes, and bradykinins. These pri - logical breakthroughs that have the potential mary mediators stimulate the release of pep - to significantly advance the field of postop - tides such as calcitonin gene-related protein erative analgesia have occurred and are still (CGRP) [8], substance P [9], and cholecy - underway. This article discusses some of the tokinin [10] at the site of injury. Histamine- more important of these recent advances. We induced vasodilatation, nerve growth factor focus on the developments particularly over release, and reflex sympathetic efferent re - the last five years. lease of norepinephrine are other processes There are several strands of develop - related with peripheral sensitization. ment that overlap, and it is difficult to do Impulses from the peripheral nocicep - justice to this burgeoning area within the tors travel via A delta and C fibers to scope and limits of this article. This review synapse in the lamina II and lamina V of the will outline the main directions of this de - spinal cord. C fibers also synapse in the lam - velopment and dwell upon a few selected re - ina I of the spinal cord. cent ones in some detail. The second order neurons of the spinal The recent advances in postoperative cord are of two types: the first, in lamina I, re - pain management can be loosely grouped in sponds to impulses from the C fibers; the sec - the following areas: ond is the wide dynamic range neuron located in lamina V that responds to both noxious and • Molecular Mechanisms non noxious stimuli. Neurotransmitters such • Pharmaceutical products as glutamate and aspartate present in lamina V • Routes and modes of delivery produce fast synaptic transmission. They do so • Other modes of analgesia by binding and activating amino-3-hydroxyl- • Organizational and procedural aspects 5-methyl-4-proprionic acid (AMPA) and Vadivelu: Advances in postoperative pain management 13 Kainate (KAR) receptors that regulate Na+ scription independent in the induction phase. and K+ ion influx. AMPA and KAR are almost Long-term potentiation of pain increases the impervious to Ca++ ions. Once the AMPA and excitatory postsynaptic potentials (EPSP) in - KAR receptors are activated, they start the volved in chronic pain. priming of NMDA, which is voltage mediated [11]. Transcription-independent and transcription-dependent central NMDA receptor and central sensitization sensitization NMDA is a membrane protein that reg - Central sensitization can be transcrip - ulates the flow of Na+ and Ca++ into the tion dependent and transcription independ - cell and the outflow of K+ outside the cell ent. Both activation of NMDA wind up and by an ion channel present intrinsically. The early LTP of pain are transcription-indepen - NMDA receptor is made up of four subunits: dent processes. There is increasing pain with two NR1, one NR2A, and one NR2B. Each each repetitive stimulation [15]. The tran - of these has a cytoplasmic portion outside scription-independent process is heterosy - the cytoplasm that can be allosterically mod - naptic central sensitization, in which low ified by zinc ions. threshold A Beta input elicit responses after NMDA receptors require ligand binding C fiber conditioning. Wind up and early LTP with glutamate and aspartate and AMPA-in - are reversible processes. duced membrane depolarization and a posi - Transcription-dependent sensitization tive change in the voltage inside the cell. occurs in prolonged noxious facilitation This makes NMDA receptors ligand de - leading to the activation of genes, mRNA pendent and voltage gated. Activated AMPA transcription, and subsequent translation receptors produce a depolarization that dis - into modified proteins. Excitotoxicity occurs lodges a magnesium plug from the ion chan - from increased influx of Ca++ with resultant nel of the NMDA receptor. The removal of increase in prostaglandins PGE, nitric oxide the magnesium plug initiates the entry of (NO), and superoxides (SO). Transcription- calcium ions into the neuronal. Direct action dependent sensitization affects the spinal of glutamate at the glutamate
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