The perception of acute and post-operative pain is a complex interaction that involves sensory, emotional, and behavioural factors. The role of psychological factors must always be considered to be an important component in the perception and expression of post-operative pain. The biological processes involved in our perception of acute pain are no longer viewed as a simple ''hard-wired'' system with a pure stimulus-response relationship. Trauma to any part of the body, and nerve damage in particular, can lead to changes within other regions of the nervous system, which influence subsequent responses to sensory input. There is increasing recognition that long-term changes occur within the peripheral and central nervous system following noxious input. This plasticity of the nervous system then alters the body's response to further peripheral sensory input. Based on these mechanisms pain relief in postoperative patients represents an important therapeutical aspect, leading to significant physiological benefit. Surgical trauma are associated with an injury response or ''inflammatory response''. Part of the inflammatory response is the release of intracellular contents from damaged cells and inflammatory cells such as macrophages, lymphocytes and mast cells. Nociceptive stimulation also results in a neurogenic inflammatory response with the release of substance P, neurokinin A and calcitonin gene-related peptide (CGRP) from the peripheral terminals of nociceptive afferent fibres. Release of these peptides results in a changed excitability of sensory and sympathetic nerve fibers, vasodilatation, and extravasation of plasma proteins. These interactions result in the release of several inflammatory mediators such as potassium, serotonin, bradykinin, substance P, histamine, cytokines, nitric oxide and products from the cyclooxygenase and lipooxygenase pathways of arach-idonic acid. These chemicals then act to sensitize high-threshold nociceptors which results in the phenomenon of peripheral sensitisation . Following sensitization, low-intensity mechanical and thermal stimuli which would not normally cause pain are now perceived as painful. This zone of ''primary hyperalgesia'' surrounding the site of injury is caused by peripheral changes and is a feature that is commonly observed following surgery and other forms of trauma. Following injury, there is an increased responsiveness to normally innocuous mechanichal stimuli (allodynia) in a zone of ''secondary hyperalgesia'' in uninjured tissue surronding the site of injury. These changes are believed to be a result of processes that occur in the dorsal horn of the spinal cord following injury. This is the phenomenon of central sensitisation . Several changes have been noted to occur in the dorsal horn with central sensitisation. Firstly, there is an expansion in receptive field size so that a spinal neuron will respond to stimuli that would normally be outside the region that respond to nociceptive stimuli. Secondly, there is an increase in the magnitude and duration of the response to stimuli that are above threshold in strength. Lastly, there is a reduction in threshold so that stimuli that are not normally noxious activate neurons that normally transmit nociceptive informations. These changes may be important both in acute pain states such as post-operative pain and in the development of chronic pain syndromes. Transmission of nociceptive information is subject to modulation at several levels of the neuraxis including the dorsal horn. Afferent impulses arriving in the dorsal horn initiate inhibitory mechanisms which limit the effect of subsequent impulses. Inhibition occurs through the effect of local inhibitory interneur-ons and descending pathways from the brain. In the dorsal horn incoming nociceptive messages are modulated by endogenous and exogenous agents that act on opiod, alpha-adreno-, GABA, and glycine receptors located at pre- and post-synaptic sites. Opioids are widely used and generally efficacious in the management of post-operative pain. Opioid receptors are found both pre- and postsynaptically in the dorsal horn, although the majority are located presynaptically. Activation of presynaptic opioid receptors results in a reduction in the release of neurotransmitters from the nociceptive primary afferent. Activation of alpha-adrenoceptors in the spinal cord has an analgesic effect either by endogenous release of nora-drenaline by descending pathways from the brain stem or by exogenous spinal administration of agents such as clonidine. There are a number of alpha-adrenoceptor subtypes and the development of selective alpha-adrenoceptor subtype agonists has the potential to provide effective new analgesic agents with reduced side effects. Both GABA and glycine are involved in inhibition of nociceptive input, and loss of their inhibitory action can result in features of neuropathic pain. Descending inhibition involves the action of endogenous opiod peptides as well as other neuro-transmitters, including serotonin, noradrenaline and GABA. Many of the traditional strategies available in acute and post-operative pain management such as the use of opioids and non-opiod drug administration, such as NSAIDs, act via these inhibitory mechanisms. Opioids have traditionally been viewed as centrally acting drugs. However, there is now evidence for the action of endogenous opioids on peripheral sites following tissue damage. Opioid receptors are transported toward the central terminal in the dorsal horn and toward the periphery. These peripheral receptors then become active following local tissue damage. This occurs with unmasking of opioid receptors and the arrival of immunocompetent cells that possess opioid receptors and have the ability to synthesize opioid peptides. This has led to an interest in the peripheral administration of opioids following surgery or topical administration of morphine. NSAIDs are commonly used for peripheral analgesia and one of their actions is a reduction in the inflammatory response. Agents such as aspirin and other NSAIDs provide their anti-inflammatory action by blocking the cyclooxigenase pathway. Cyclooxigenase exists in two forms, COX1 and COX2. While COX1 is always present in tissues, including the gastric mucosa, COX2 is induced by inflammation. This presents an opportunity for the development of agents that have a selective anti-inflammatory effect without gastric side effects. Selective COX2 inhibitor drugs (e.g. rofecoxib, celecoxib) that may offer analgesia with less gastrointestinal toxicity than NSAIDs have been developed. Besides the peripheral action of NSAIDs, there is increasing evidence that they exert their analgesic effect through central mechanisms . The discovery of the changes associated with the phenomenon of peripheral and central sensitization has led to attempts to prevent these changes occurring. It was hoped that steps which would reduce or abolish noxious imput to the spinal cord during a painful event such as surgery would reduce or minimize spinal cord changes and thereby lead to reduced pain post-operatively. This concept has led to an increasing interest in the use of pre-emptive analgesia. Preemptive analgesia is based on the administration of an analgesic such as opioids and NSAIDs before a painful stimulus generates, so as to prevent the subsequent rebound mechanism . Opioids and NSAIDs have been used alone or in combination and have been administered locally, epidurally, intrathecally or sistemically. Several studies have purported to show that pre-emptive analgesia results in reduced pain, decreased analgesic requirements, improved morbidity and decreased hospital stay [27-30]. However, pre-emptive analgesia may also be important in reducing the incidence and prevention of chronic pain states but further studies are necessary to address this important question. Improvement of post-operative pain control can be achieved by better education for all staff concerned postoperative pain relief and by making the assessment and recording of pain levels part of the routine management of each patient. The best strategy is to reduce or eliminate pain and discomfort with a minimum of side effects. A multidisciplinary acute pain service can ensure an adequate pain assessment and relief using different tools in order to reduce post-operative course with earlier discharge from hospital (Box 4) [31, 32].
Box 4. Organizational aspects of an anaesthesiology-based postoperative pain programme
- Patients and families
2. Areas of regular administrative activity
- Mainteinance of clear lines of communication
- Evaluation of equipment (e.g. pumps)
- Economic issues
- Continuous quality improvement
- Pain management-related research
3. Collaboration with nursing services
- Nursing policies and procedures
- Nurses in-service and continuing education
- Definition of roles in patient care
- Continuous quality improvement
- Research activities
4. Elements of documentation
- Preprinted orders
- Bedside pain management flow sheets
- Daily consultation notes
- Educational packages
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