Many patients report inadequate pain management shortly after surgery. Adverse reactions to analgesic drugs remains a problem.
For instance, between 1980 and 1999 the incidence of respiratory depression during analgesia has declined slightly, but the incidence of hypotension has not changed. Acute pain can lead to chronic pain and associated morbidity. Current and future acute pain management options are outlined in this review.Non-pharmacological intervention is sometimes ignored, but it is often an effective strategy for the management of acute pain. One example of the influence psychological state has on pain is the higher reports of pain among athletes catastrophizing about an injury and surgery. Health care information concerning the surgery and recovery and social support among other psychoeducational care interventions can improve recovery and reduce pain sensitivity following surgery. This intervention along with other non-pharmacological treatments such as acupuncture are promising avenues of future research.Oral or injectable opioids, the standard pharmacological treatment of pain, prevent neurotransmission by inhibiting high voltage calcium channels, tetrodotoxin-sensitive sodium channels and other non-selective cation channels. Their use is hampered by respiratory depression, sedation, constipation and other serious adverse reactions. The narcotics also have abuse potential. These unwanted effects could be avoided by developing opioid drugs that target peripheral rather than central nerves. This strategy attacks pain at the source. Opioid receptors are expressed in the periphery and inflammatory responses in the periphery recruit cells carrying opioid peptides such as the endorphins. Thus, rationale exists for the targeting of peripheral opioid neurotransmission in acute pain management.There remains much work on the clinical effectiveness of peripheral opioid targeting. Tetrapeptide agonists that do not cross the blood-brain barrier readily are effective analgesic and anti-inflammatory agents in animal models. Clinical data show that morphine applied to the site of injury provides analgesia only when inflammation is present. Adverse events also restrict the benefits of cyclooxygenase (COX) inhibition to pain management despite development of selective COX-2
inhibitors. All COX inhibitors prevent arachodonic acid synthesis. The selectivity of COX-2 inhibitors lies in their ability to bind to a side pocket within the catalytic channel of the enzyme. This site is not available in COX-1. Of these non-steroidal anti-inflammatory drugs (NSAIDs), only acetylsalicylic acid irreversibly acetylates COX.Expression of the COX-1 enzyme dominates under unstressed physiological conditions. Growth factors and other stress-related molecules upregulate COX-2 dramatically resulting in pain and inflammation. Unselective COX inhibitors have unwanted effects in tissues because of its constitutive and widespread expression.Selective and unselective COX inhibitors are equally effective for control of moderate to severe acute pain, but because of their selectivity the use of COX-2 inhibitors is associated with fewer gastric ulcerations. However, there is still concern over the use of COX-2 inhibitors in patients at risk for ulceration such as the elderly, those receiving corticosteroids, or those who have a history of ulcers.Platelet aggregation is not affected by COX-2 inhibitors, but a prothrombotic response was suggested for one of these drugs. A clinical trial showed that rofecoxib increased the incidence of myocardial infarction relative to naproxen. Because of the controversial nature of the data, COX-2 inhibitors should be used with caution in patients who are at risk.The COX-2 enzyme is constitutively expressed in the kidney, so the effects of selective and unselective COX inhibition on renal function are similar. In contrast, selective and unselective COX inhibitors may have different influences on respiration. Some data suggestthat COX-2 inhibitors do not cause bronchospasm in patients with acetylsalicylic acid-induced asthma.Single-dose intravenous
paracetamol is another effective post-operative analgesic. Intravenous administration is preferable to oral administration especially in patients at risk of developing adverse events because it produces more predictable blood levels. The mechanism of action is unclear but may involve inactivation of a putative central nervous system COX-3 or inhibition of serotonergic neurotransmission.A nitric oxide-releasing form of paracetamol, Nitroxyparacetamol, has been developed with both analgesic and anti-inflammatory properties. It is more potent than paracetamol in animal models and may be less hepatotoxic.Early diagnosis of acute neuropathic pain after surgery can help prevent progression to a chronic condition. Neuropathic pain presents as burning, stinging, or shooting pain. It continues despite gtissue healing and doesn’t respond to typical post-operative opioid doses. Severe acute neuropathic pain can be controlled quickly by lidocaine or ketamine whereas long-term treatment should include anticonvulsants and tricyclic antidepressants.While non-pharmacologic and pharmacologic management of pain is effective, the serious adverse events associated with pharmacologic interventions limits their usefulness. Current research is addressing this problem with promising results. The quality of pain management will improve significantly as this research progresses.