In: Anesthesia2 Oct 2009
The long list of algogenic substances and complex neu-roanatomical modulating systems indicate that there are diverse therapeutic possibilities for control of the transmission of nociceptive information to the brain. Generally, management of postoperative pain can be accomplished through the following mechanisms:
• preventing nociceptive input at the site of injury;
• blocking the nociceptive impulse along the peripheral nerve;
• prevention of central sensitization;
• multimodal analgesia.
• other behavioral therapy.
Pharmacological. Preventing Nociceptive Input at the Site of Injury. The role of the locally released mediators of pain and inflammation and their actions to sensitize peripheral nerve endings suggests the therapeutic potential of interfering with the release or actions of these mediators and hence preventing transduction in nociception. Because postoperative pain is primarily mediated by trauma-induced release of algogenic substances, a rational approach to treat it may be peripheral inhibition of these algogenic substances. NSAIDs have been proven effective for postoperative dental pain and should be regarded as the basic treatment. Most NSAIDs are thought to act primarily by inhibiting the enzyme COX, thereby preventing local synthesis of prostaglandins from arachidonic acid in the inflamed tissues. It also has been demonstrated in vitro that various NSAIDs are able to block the chemotactic effect of substance P on monocytes and polymorphonuclear cells. This indicates a way of modulating the neurogenic part of the inflammatory process. However, the timing of drug administration is important. Ideally, drugs should be given before the surgical incision and should be timed so that the maximum plasma concentration of the drug is reached at the time of surgical incision. This will, in theory, optimally prevent the release of the inflammatory mediators. This not only has immediate analgesic effects but also blocks the development of hyperalgesia, which can result in exaggerated and prolonged pain. The concept of giving the analgesia before surgical incision is known as preemptive analgesia. However, clinical studies done on preemptive analgesia still show conflicting results. Methodological deficiencies may be the reason that has hindered the interpretation of most of the studies seeking to demonstrate a preemptive analgesic effect. Nonrandomizing of patients, different types of surgery, lack of blinding, inadequacies in control states, lack of sensitivity of the postoperative pain measures used, and other flaws are the usual problems. Because the development of new NSAIDs has not significantly improved the efficacy of postoperative pain control, preemptive analgesia may be the answer to improved pain control with NSAIDs. Save on your pharmacy bills. Buy generic cialis soft tabs online
However, because most NSAIDs inhibit the COXs, they also decrease the production of thromboxane A2, a potent platelet-aggregating agent, thus increasing the risk of postoperative bleeding. Many authors have suggested that NSAIDs be withheld or aspirin therapy stopped preoperatively to prevent excessive postoperative bleeding. But recent studies suggest that this is probably not a problem. The effect of aspirin on post-extraction bleeding has been evaluated in a randomized controlled trial consisting of 39 patients requiring dental extractions who were on long-term prophylactic aspirin.
The authors divided the patients randomly into 2 groups: those who stopped aspirin therapy before extraction and those who continued the aspirin therapy. In both groups a local haemostatic method was sufficient to control postextraction bleeding. The authors concluded that aspirin therapy does not have any significant effect on postextraction bleeding and should not be stopped before the procedure.
There is also evidence that supports the existence of a central action of NSAIDs in humans. It indicates that NSAIDs may inhibit brain prostaglandin synthesis. However, the clinical relevance remains unclear because the pain-related role of prostaglandins in the CNS is not well established. Various mechanisms may be suggested to account for the CNS action of NSAIDs. Interference with the formation of prostaglandins or with transmitters or modulators in the nociceptive system may occur. Alternatively, the CNS action may be mediated in part by endogenous opioid peptides or they may block the release of serotonin by central secretion of bradykinin.
Glucocorticoids represent another potential drug to improve analgesia because they modify several cascade systems involved in the peripheral inflammatory response. By inhibiting COX-2 and phospholipases A2 directly or their synthesis, glucocorticoids reduce prostanoid generation in inflammatory cells, but they have little or no effect on COX-1. The analgesic effects of local glucocorticoid injection in rheumatic disorders are well known, but limited data are available from acute pain studies other than rheumatic disorders. A recent study in a third-molar surgical model indicated that methyl-prednisolone significantly reduces the tissue levels of inflammatory mediators and the pain scores when compared with placebo. But there are other studies showing little or no analgesic benefit in using glucocorticoids in third-molar surgery. Higher-dosing regimens appear to be more successful. The unfortunate lack of systematic studies for determining optimal dosage, timing, and duration of therapy makes any recommendation more or less arbitrary.
Blocking the Nociceptive Impulse Along the Peripheral Nerve. Nociceptive transmission along the trigeminal nerve pathways is routinely blocked during third-molar surgery by local anesthetic. The effect of the local anesthetic agent such as lidocaine usually extends for only 1-2 hours postoperatively. The offset of the local anesthetic coincides with the peak release of major pain mediators such as prostaglandins and bradykinin. If not treated, this is accompanied by intense pain because these mediators maximize nociceptive input from direct effects on nerve endings and by magnifying the effects of other mediators through development of peripheral hyperalgesia. generic avodart
The use of a long-acting local anesthetic such as bu-pivacaine provides a method for blocking postoperative pain for hours after surgery. This could delay the onset of sensation until the peak levels of inflammatory mediators have subsided. There are studies that support this technique of reducing pain in third-molar surgery. However, there are concerns about the slight increase in morbidity and discomfort associated with the use of these long-acting local anesthetics. One recent development is the incorporation of local anesthetics in polymer microspheres, which can provide anesthesia for up to several days.
Prevention of Central Sensitization. The CNS reacts to nociceptive input with changes that lead to the development of central sensitization and to hyperalgesia, which can last for days and results in increased pain from peripheral input that otherwise might not be painful. Prevention of the development of central sensitization can potentially reduce postoperative pain. There are 2 approaches to overcome the effect of central sensitization. The first approach is to use NMDA receptor antagonists as a means of suppressing the pain amplification related to central sensitization, thus preventing or relieving allodynia and hyperalgesia. Ketamine and dextromethorphan, for example, are both currently available. Ketamine is very effective but has intolerable side effects. Dextromethorphan is less effective but better tolerated. Opioids administered parenterally, epidurally, or intrathecally before injury can also prevent or attenuate NMDA receptor activation. Unfortunately, once windup occurs, clonidine, an alpha-2 receptor agonist administered intrathecally, is better at reducing allodynia and hyperalgesia than are opioids. It has been proposed that combining agents such as opioids and agents of other classes, eg, NMDA antagonists, may produce synergy and a greater suppression of central sensitization than the use of each agent alone. The second approach is to avoid the effects of central sensitization by preventing its induction through blocking the arrival of nociceptive input to the spinal cord. Again, this uses the concept of preemptive analgesia to preempt the initiation of central sensitization. This can be accomplished by using regional or systemic analgesic, eg, NSAIDs given before surgical incision. rimonabant online
Multimodal Analgesia. Multimodal analgesia refers to a combination of various analgesic modalities in postoperative pain management, resulting in better analge¬sia, with a concomitant reduction in total doses of analgesics and reduced adverse effects. The effectiveness of an individual analgesic may be enhanced by the additive or synergistic effects of multiple analgesic drugs that have different mechanisms of analgesia. This is logical because we can see from the review on the pathogenesis of postoperative pain that the numbers of pain mediators involved are many and complex. For example, the combination of an opioid with an NSAID may be an ideal analgesic regimen because opioids provide superior pain relief in the early recovery period, whereas NSAIDS provide superior pain relief in the late recovery period because of their longer half-life. An example of this multimodal analgesia for oral surgery would be intravenous fentanyl for intraoperative analgesia followed by oral Rofecoxib during the recovery period for long postoperative analgesia.
Theoretically, a drug that consists of a combination of an NSAID and an opioid, eg, ibuprofen and codeine/ hydrocodone, should give a better analgesic effect than does ibuprofen or codeine/hydrocordone used alone. However, many studies of third-molar surgical pain have not been able to show that the combination of NSAIDs and opioid is better than NSAIDs used alone. There has been 1 study showing that the ibuprofen-codeine combination has a better analgesic effect than does ibuprofen alone, but with a higher incidence of side effects due to the opioid. Although many studies show that single-entity NSAIDs demonstrate anagelsic superiority when compared with opioid combinations, the combination is still very popular among clinicians and patients. A plausible explanation is that opioids have the potential not only to act antinociceptively but also to reduce the affective component of pain.
Psychological and Physical Therapy. Psychological factors can produce exaggerated pain complaints or suppress pain report when it should be present. Because emotion is an integral part of the pain experience, it has to be managed effectively for good postoperative pain management. There is evidence that preoperative anxiety may affect postoperative pain perception, and control of this anxiety decreases postoperative pain experience. Psychological techniques like hypnosis, relaxation, and biofeedback have been used effectively for controlling acute pain. orlistat 120 mg
Although, there is evidence for the efficacy of acupuncture and TENS for postoperative pain, their use remains experimental and is not widespread. The reason may be that many physicians are not familiar with these alternative modalities. In addition, there are also other contrasting studies that show that these alternative therapies are ineffective for pain control.
Blog invites submissions of review articles, reports on clinical techniques, case reports, conference summaries, and articles of opinion pertinent to the control of pain and anxiety in dentistry.