Recent Advances in Postoperative Pain Management. Yale J Biol Med. 2. Mar; 8. 3(1): 1. 1–2. Published online 2. Mar. Exacerbations of acute pain can lead to neural sensitization and release of mediators 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 molecular mechanisms have led to the development of multimodal analgesia and new pharmaceutical 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. Keywords: opioids, acute pain, pain mechanisms, postoperative, patient- controlled analgesia. 339-355, 1993 Printed in Great Britain 0()16-7185/93 $6.00+0.00 1993 Pergamon Press Ltd Interviewing Business Owners and Managers: a Review of Methods and Techniques MICHAEL J.
Breathing Techniques, Practices, Exercises, Theory, Lore In Yoga, T'ai Chi Ch'uan, Qigong, Meditation, Fitness Research by Michael P. Garofalo Links Bibliography Quotations Exercises Cloud Hands Blog Relaxation. Proper pain relief is a major concern and area of focus in the United States today. Pre- operatively, one of the most common questions asked by patients pertains to the amount of pain they will experience after the surgery. Pain is also one of the primary concerns of the surgeon because of its close ties with clinical outcome and acute postoperative patient well- being. Studies have indicated such negative clinical outcomes to include decreases in vital capacity and alveolar ventilation, pneumonia, tachycardia, hypertension, myocardial ischemia, myocardial infarction, transition to chronic pain, poor wound healing, and insomnia . Despite this overwhelming rationale for effective postoperative pain control, the clinical reality is, unfortunately, still far from satisfactory. As a recent editorial title suggests, we have a long way to go to achieve satisfactory postoperative pain control . In an often- cited study . Nine Yin Manual Techniques To DrainThe authors concluded that despite an increased focus on pain management programs and the development of new standards for pain management, many patients continue to experience intense pain after surgery. During the last couple of decades and especially the last few years, major technological breakthroughs that have the potential to significantly advance the field of postoperative analgesia have occurred and are still underway. This article discusses some of the more important of these recent advances. We focus on the developments particularly over the last five years. There are several strands of development that overlap, and it is difficult to do justice to this burgeoning area within the scope and limits of this article. This review will outline the main directions of this development and dwell upon a few selected recent ones in some detail. The recent advances in postoperative pain management can be loosely grouped in the following areas: Molecular Mechanisms. Pharmaceutical products. Routes and modes of delivery. Other modes of analgesia. Organizational and procedural aspects. Molecular mechanisms. It is important to know about the recent advances in central sensitization since it plays an important role in post surgical and post traumatic pain . Postoperative pain is mostly nociceptive, which is pain perception following surgical insult. However, there can be exacerbation of acute nociceptive pain leading to neural sensitization when sensations that are not normally painful are perceived as painful, as in hyperalgesia and allodynia. Mechanical allodynia occurs due to the release of several primary and secondary noxious sensitizers such as PGEs, leukotrienes . These conditions are commonly seen in those patients developing neuropathic pain. Primary hyperalgesia occurs when there is sensitization of peripheral nociceptors, while secondary hyperalgesia is associated with the sensitization of the spinal cord and the central nervous system. In peripheral sensitization, there is a release of primary mediators such as prostaglandins, 5 hydroxytryptamine, leukotrienes, and bradykinins. These primary mediators stimulate the release of peptides such as calcitonin gene- related protein (CGRP) . Histamine- induced vasodilatation, nerve growth factor release, and reflex sympathetic efferent release of norepinephrine are other processes related with peripheral sensitization. Impulses from the peripheral nociceptors travel via A delta and C fibers to synapse in the lamina II and lamina V of the spinal cord. C fibers also synapse in the lamina I of the spinal cord. The second order neurons of the spinal cord are of two types: the first, in lamina I, responds to impulses from the C fibers; the second is the wide dynamic range neuron located in lamina V that responds to both noxious and non noxious stimuli. Neurotransmitters such as glutamate and aspartate present in lamina V produce fast synaptic transmission. They do so by binding and activating amino- 3- hydroxyl- 5- methyl- 4- proprionic acid (AMPA) and Kainate (KAR) receptors that regulate Na+ and K+ ion influx. AMPA and KAR are almost impervious to Ca++ ions. Once the AMPA and KAR receptors are activated, they start the priming of NMDA, which is voltage mediated . The NMDA receptor is made up of four subunits: two NR1, one NR2. A, and one NR2. B. Each of these has a cytoplasmic portion outside the cytoplasm that can be allosterically modified by zinc ions. NMDA receptors require ligand binding with glutamate and aspartate and AMPA- induced membrane depolarization and a positive change in the voltage inside the cell. This makes NMDA receptors ligand dependent and voltage gated. Activated AMPA receptors produce a depolarization that dislodges a magnesium plug from the ion channel of the NMDA receptor. The removal of the magnesium plug initiates the entry of calcium ions into the neuronal. Direct action of glutamate at the glutamate binding site further sensitizes the channel . This process is termed as “wind up,” which is the excitation of the dorsal horn neurons not dependent on transcription of specific genes. Long- term potentiation of pain. Clinical hyperalgesia occurs from the processes of NMDA activation, wind up, and central sensitization . Central sensitization can occur in the spinal cord as well as in the supraspinal regions of the central nervous system, such as anterior cingulate gyrus, amygdale, and rostroventral medulla. Activation of the NMDA in the spinal cord and the supraspinal areas and increased neuronal calcium ion (Ca++) influx lead to wind up and early LTP . Long- term potentiation of pain increases the excitatory postsynaptic potentials (EPSP) involved in chronic pain. Transcription- independent and transcription- dependent central sensitization. Central sensitization can be transcription dependent and transcription independent. Both activation of NMDA wind up and early LTP of pain are transcription- independent processes. There is increasing pain with each repetitive stimulation . The transcription- independent process is heterosynaptic central sensitization, in which low threshold A Beta input elicit responses after C fiber conditioning. Wind up and early LTP are reversible processes. Transcription- dependent sensitization occurs in prolonged noxious facilitation leading to the activation of genes, m. RNA transcription, and subsequent translation into modified proteins. Excitotoxicity occurs from increased influx of Ca++ with resultant increase in prostaglandins PGE, nitric oxide (NO), and superoxides (SO). Transcription- dependent sensitization affects the spinal cord and other areas within the central nervous system. It is now thought that transcription- dependent sensitization is mediated by inflammation and related alterations in the dorsal root ganglion, the dorsal horn, and irreversible structural modifications in the central nervous system . Transcription- dependent sensitization can take two forms: activity independent localized form, which includes the late phase of LTP, and the activity independent widespread form. Late phase LTP has been studied mainly in the hippocampus and other cortical areas . The genes for Dynorphin and NK1 have been seen to be upregulated in the spinal cord, and widespread COX- 2 has been seen to be upregulated in many areas of the central nervous system by pain facilitation . However, NK1 and COX2, which are involved in central sensitization, are not involved in hippocampal LTP. It is also known that NMDA receptors, essential for activity dependent central sensitization, also are necessary for the initiation of LTP, which has a role in the consolidation of memory. The common mechanisms in hippocampal early phase LTP and central sensitization are phosphorylation of synaptic receptors and the insertion of AMPA receptors into the post- synaptic membrane. There is only synaptic strengthening in hippocampal LTP, while central sensitization also can cause neuronal network changes and other cellular mechanisms. It is necessary then to avoid the interruption of memory formation and cortical function while treating central sensitization since the process of LTP is present in central sensitization as well as in memory mechanisms in the cortex . We will highlight the important recent advances in pharmaceutical products and the routes through which they can be given, as well as important non- pharmacological advances in pain control that are useful for health care personnel treating postoperative pain. Non- pharmacological advances in analgesia are exemplified by application of acupuncture, and related therapies for postoperative pain control will be discussed. In addition, drug tolerance in patients with illicit drug use or a history of taking high doses of pain prescription medications prior to admission are making postoperative pain management a challenge and warrants discussion as well. Advances in pharmaceutical products.
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