Eleven Common Myths About Pain Control

According to the most recent studies, widely prevalent assumptions with little, if any, basis in fact are leading clinicians to use analgesic drugs ineffectively.

By Robert Dachs, MD

The message is loud and clear: timely and compassionate pain management is expected for all patients with acutely painful conditions. Professional organizations, most notably the American Pain Society, as well as our anesthesiology and nursing colleagues, hospital administrators, regulators, and the public at large have championed this issue and raised it to its current prominence. In an attempt to meet these expectations, a critical look at common myths associated with acute pain care can be enlightening.

MYTH 1

Physicians, nurses, and prehospital care providers do a good job of providing adequate analgesia to patients in pain.

The data are unequivocal: on average, health care providers do a terrible job of managing acute pain. Physicians order inadequate doses of analgesics or no analgesia at all for patients in pain. Nurses, when given a dose range for analgesics, tend to give lower doses or withhold analgesia in PRN cases. Even prehospital care providers with access to analgesics rarely give these drugs to patients with painful conditions such as suspected extremity fractures.

This widespread practice of not providing adequate analgesia has been termed oligoanalgesia, and it has been documented in emergency departments, intensive care units, and medical and surgical wards here in the United States and abroad. Further, certain groups of patients are particularly likely to be on the receiving end of this practice. Both the very young and very old, for example, often receive inadequate analgesia. Dr. Knox Todd and colleagues have demonstrated that Hispanic and African American patients with extremity fractures receive less analgesia than white patients with these same conditions.

A good working knowledge of how to provide appropriate analgesia, together with an honest self-appraisal by all health care providers, is necessary to combat this disservice to our patients.

MYTH 2

Codeine is an effective analgesic and antitussive.

Codeine is a very weak analgesic. In standard doses, codeine produces no more pain relief than NSAIDs or acetaminophen alone. When acetaminophen plus codeine was compared with the NSAID du jour in multiple studies involving postsurgical pain or acute musculoskeletal injuries, the combination was noted to have equivalent analgesic efficacy. Further, when deCrean reviewed 24 trials comparing acetaminophen with codeine to acetaminophen alone, he found only a 5% difference in pain intensity between the agents, as rated by subjects on a 1 to 10 scale (British Medical Journal, vol. 313, p. 321, 1996). This difference is statistically significant, but it has no clinical significance.

Codeine's adverse effects, on the other hand, are legendary. Nausea, vomiting, and constipation are common. Geriatricians often note that codeine produces the "terrible C's"–confusion and constipation–in their patient population.

As for controlling a cough, codeine in standard doses has no more antitussive effect than placebo. The bottom line with this drug is that in the absence of any clear benefit and considering its troublesome side effects, it is difficult to recommend codeine as an analgesic or as an antitussive.

MYTH 3

Propoxyphene is an effective and safe analgesic.

Propoxyphene possesses negligible analgesic effects. When researchers at Texas A&M compared propoxyphene with ibuprofen 400 mg and placebo in patients with acute musculoskeletal trauma, no clinical difference in pain relief was noted between propoxyphene and placebo. Further, a review of 26 trials of propoxyphene with acetaminophen versus acetaminophen alone concluded that there was no evidence to support the use of the combination product.

Propoxyphene and its metabolites have been associated with cardiotoxicity, neurologic sequelae, and death. The major metabolite, norpropoxyphene, has a half life of 30 to 36 hours and produces local anesthetic and antiarrhythmic effects similar to those of lidocaine and quinidine. When it accumulates, either from chronic administration or acute overdose, norpropoxyphene can produce arrhythmias, cardiogenic shock, mental status changes, seizures, coma, and death.

Consensus committees have clearly indicated that propoxyphene should not be given to geriatric patients. In fact, the argument can be made that this drug should not be given to any patient, regardless of age.

Fortunately, there are better choices than codeine and propoxyphene for pain management. Hydrocodone and oxycodone, with and without acetaminophen, are effective analgesics. Oxycodone is available in a long-acting preparation. Transnasal butorphanol is also effective, but it is expensive.

MYTH 4

Morphine 2 mg IV provides adequate analgesia in healthy adults.

The American College of Critical Care Medicine has recognized morphine as the drug of choice in critically ill patients who require analgesia. The dose is a 0.05 to 0.1 mg/kg bolus; it can then be rapidly increased to achieve the desired effect. In many emergency departments, morphine doses of 10, 20, or 30 mg in the first hour are not unusual. Unfortunately, the all-too-common order of 2 mg of morphine will often leave patients in pain.

MYTH 5

"Meperidine 50 mg with hydroxyzine 25 mg IM q4hrs prn" is an appropriate order for hospitalized patients.

This order is so common many physicians can recite it by rote. But how appropriate is it?

Meperidine's clinical effect is very short-lived, often lasting only two or three hours. The need for subsequent repetitive doses can result in deleterious central nervous system side effects. This is because meperidine's inactive metabolite, normeperidine, has a long half-life, and when it accumulates it produces central nervous system excitation and the risk of seizures. That is why many experts recommend avoiding or minimizing meperidine use in hospitalized patients.

If meperidine is necessary, the addition of an antiemetic (traditionally, hydroxyzine) will not potentiate the effect of the narcotic, as is widely believed. While an antiemetic may make the patient drowsy and decrease nausea, the clinician should not lower the dose of the analgesic if an antiemetic is added. And hydroxyzine should never be chosen as the antiemetic. The drug can only be given intramuscularly and is extraordinarily painful and irritating to soft tissue.

Again, better choices exist. Adequate doses of morphine would be the first-line choice. Fentanyl is an excellent alternative in hemodynamically unstable patients or those with exaggerated histamine response to morphine. Hydromorphone is another excellent alternative.

MYTH 6

Use of narcotic analgesic agents will result in chronic opioid dependence.

Avoiding the use of appropriate narcotic analgesia out of fear of inducing chronic opioid dependence and drug-seeking behavior is completely unfounded. Researchers at Boston University reviewed the records of 11,882 patients given narcotics during a hospital stay and found only four patients who later developed an opioid dependence.

When a clinician subscribes to this myth and avoids using these drugs, he or she may actually help perpetuate a course of chronic pain and unwittingly create a reliance on analgesics in patients. With undertreatment of acute pain, recruitment of increasing numbers of nerve fibers occurs. The ensuing windup of the sensory nervous system can result in long-standing modification in pain sensation. Consequently, early and aggressive use of analgesics followed by a rapid tapering of the dose is encouraged in patients with acute pain.

MYTH 7

Injectable ketorolac is more effective and has less gastrointestinal toxicity than oral NSAIDs.

Many clinicians mistakenly believe that ketorolac possesses some magical analgesic property because it can be administered intramuscularly or intravenously. Study after study, however, has refuted this theory. Also, regardless of the route of administration, ketorolac's ability to inhibit prostaglandin synthesis can disrupt the stomach's mucosal barrier. Therefore, even though the drug is not taken orally, gastrointestinal toxicity is still possible.

MYTH 8

NSAIDs have more analgesic effect than acetaminophen.

In a landmark study, Bradley and colleagues randomly assigned patients with osteoarthritis of the knee to receive either 4000 mg acetaminophen, 1200 mg ibuprofen, or 2400 mg ibuprofen per day. The result: acetaminophen was just as effective as either dose of ibuprofen (New England Journal of Medicine, vol. 325, p. 87, 1991).

It seems reasonable that 4000 mg acetaminophen and 1200 mg ibuprofen per day would produce similar results. But why doesn't the 2400-mg/day dose of ibuprofen produce additional analgesic effect? Because increased doses of NSAIDs further inhibit prostaglandin synthesis. This is useful in managing patients with prostaglandin-mediated diseases such as rheumatoid arthritis. However, when it comes to analgesia, NSAIDs have a ceiling effect–that is, no further analgesic effect will occur with increased doses. Therefore, 2400 mg/day of ibuprofen in non-prostaglandin-mediated diseases such as osteoarthritis and soft tissue injury will produce no additional analgesia.

MYTH 9

NSAIDs should be first-line agents in soft-tissue injuries such as ankle sprains.

NSAIDs do have a role in the care of patients with acutely painful conditions that involve a prostaglandin-mediated process. Examples of such conditions include renal colic, biliary colic, dysmenorrhea, and gout. Soft-tissue injuries, however, are not primarily prostaglandin-mediated events, and there are no data to support NSAID use for such injuries.

In addition, when treating patients with non-life-threatening conditions such as sprains and strains, the clinician must seriously consider the dangers associated with NSAIDs. Wolfe and colleagues documented that the mortality rate associated with NSAID use in 1997 was equivalent to the mortality rate from AIDS in the United States that same year (New England Journal of Medicine, vol. 340, p.1888, 1999). Cautious use of these agents is clearly warranted.

MYTH 10

COX-2 inhibitors are more effective than traditional NSAIDs in controlling pain.

When it comes to analgesic efficacy, the newer COX-2 inhibitors, celecoxib and rofecoxib, are no more potent than their traditional counterparts. Even the question of whether these newer agents produce fewer gastrointestinal complications than NSAIDs is up for debate. Two recent high-profile studies found a 50% decrease in the rate of gastrointestinal complications with COX-2 inhibitors. However, both studies were manufacturer-supported trials with design flaws that may invalidate the findings. Further, the CLASS trial noted that no decrease in the rate of gastrointestinal complications was associated with celecoxib use in patients taking just one aspirin a day.

MYTH 11

Tramadol is an effective analgesic.

In separate studies, pain relief with tramadol has been shown to be inferior to hydrocodone with acetaminophen and codeine with acetaminophen and no more effective than placebo. This lack of analgesic effect was noted with both the 50- and 100-mg doses. Tramadol is simply not an effective analgesic.

ELIMINATING OLIGOANALGESIA

The goal of eliminating the practice of oligoanalgesia should be at the top of every primary care provider's agenda. Being aware of common myths associated with pain management is a key step in moving toward this goal.