Acute pain resolves within the expected period of healing and is self-limited. Common examples include pain from dental caries, kidney stones, surgery, or trauma. Management of acute pain depends on comprehending the type of pain (somatic, visceral, or neuropathic) and on understanding the risks and benefits of potential therapies. At times, treating the underlying cause of the pain (eg, dental caries) may be all that is needed, and pharmacologic therapies may not be required for additional analgesia. On the other hand, not relieving acute pain can have consequences beyond the immediate suffering. Inadequately treated acute pain can develop into chronic pain in some patients. This transition from acute to chronic pain (so-called “chronification” of pain) depends on the pain’s cause, type, and severity and on the patient’s age, psychological status, and genetics, among other factors. This transition is an area of increasing study because chronic pain leads to significant societal costs beyond the individual’s experiences of suffering, helplessness, and depression. Emerging studies have shown that increased intensity and duration of acute pain may be correlated with a higher incidence of chronic pain, and regional anesthesia, ketamine, gabapentinoids, and cyclooxygenase (COX) inhibitors may be helpful for prevention of chronic postsurgical pain. These approaches are particularly important given concerns that exposure to opioids in the perioperative period can lead to chronic opioid dependence beyond the immediate postoperative period.
The Oxford League Table of Analgesics is a useful guide; for example, it lists the number-needed-to-treat for specific doses of various medications to relieve acute pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) or COX inhibitors are at the top of the list, with the lowest number-needed-to-treat. These medications can be delivered via oral, intramuscular, intravenous, intranasal, rectal, and other routes of administration. They generally work by inhibiting COX-1 and -2 and therefore reduce the levels of prostaglandins involved in inflammatory nociception (eg, PGI2 and PGE2). These oxygenase enzymes also determine levels of other breakdown products such as other prostaglandins, thromboxane, and prostacyclins that play a role in renal, gastrointestinal, and cardiovascular homeostasis. For this reason, the primary limitation of the COX inhibitors is their side effect profile of gastritis, kidney dysfunction, bleeding, hypertension, and cardiovascular adverse events such as myocardial infarction or stroke. Ketorolac is primarily a COX-1 inhibitor that has an analgesic effect as potent as morphine at the appropriate dosage. Like most pharmacologic therapies, the limitation of COX inhibitors is that they have a “ceiling” effect, meaning that beyond a certain dose, there is no additional benefit.
Acetaminophen (paracetamol) is effective as a sole agent, or in combination with a COX inhibitor or an opioid in acute pain. Its mechanism of action remains undetermined but is thought to act centrally through mechanisms such as the prostaglandin, serotonergic, and opioid pathways. It is one of the most widely used and best tolerated analgesics; its primary limitation is hepatoxicity when given in high doses or to patients with underlying impaired liver function.
Postoperatively, patient-controlled ...