As recently as 15 years ago, the approach to pain management was a symptomatic one, whereby the symptom of pain was hidden or minimized with a general analgesic such as an opioid or acetaminophen. Additional pain relief was sought by treating the underlying disease under the assumption that the pain would resolve if you did so.
The symptomatic approach has been almost completely replaced by a mechanistic approach. With this approach, the neurobiological mechanism creating the pain is identified and neutralized with a targeted medication. Although far more applicable in managing chronic pain, the mechanistic approach was first seen in acute pain settings. Witness the change from opioids to dopamine antagonists (eg, chlorpromazine, prochlorperazine, metoclopramide) and serotonin agonists (eg, triptans, ergotamines) for migraine and other vascular headaches. The role of prostaglandins in smooth muscle tension has resulted in the use of nonsteroidal anti-inflammatory drugs (NSAIDs) for renal and biliary colic as well as for severe menstrual cramps. Anticholinergic agents can be effective for both intestinal cramps (hyoscine) and large muscle spasms (benztropine). The indications for the primary use of an opioid in emergency medicine have been refined; there are many fewer indications than before, making their use even more justifiable in these specific instances (eg, extremity fractures, visceral pain, vaso-occlusive crisis).
Pain in the ED
In chronic noncancer pain, specific neurotransmitters and nerve channels have been relatively well-established. In neuropathic pain, either a sodium channel (tricyclic) or a calcium channel (gabapentanoid) blocker serves as first-line therapy, with opioids relegated to third- or fourth-line treatment. In diffuse widespread pain such as fibromyalgia, opioids are not recommended at all, with NSAIDs, tricyclics, or gabapentanoids being the optimal choices.
The indications for the primary use of an opioid in emergency medicine have been refined; there are many fewer indications than before, making their use even more justifiable in these specific instances (eg, extremity fractures, visceral pain, vaso-occlusive crisis).
In managing trauma patients, the last few years have demonstrated that the addition of low-dose (analgesic dose) ketamine serves to decrease the dosing requirements of opioids to control pain. It also serves to block N-methyl-D-aspartate (NMDA) release, thereby decreasing wind-up (pain after discharge and the risk of development of chronic pain). For procedural analgesia, ketamine and nitrous oxide serve as excellent alternatives to opioids. Ketamine, in an analgesic dose (0.2–0.3 mg/kg), seems to lead to less oxygen desaturation and hypoventilation when combined with a sedative than when an opioid, such as fentanyl, is used. The use of “ketofol,” a combination of ketamine and propofol in the same syringe, seems to offer no added value over giving a single dose of ketamine followed by the titration of an ultrashort-acting sedative such as propofol or methohexital.