Chapter 35: Acute Pain Management

Pain is the most common presenting symptom for patients coming to the ED, with 75% to 80% of all patients having pain as their primary complaint.¹ Despite increasing research and information about pain management, oligoanalgesia, or the under treatment of pain, persists.^2,3,4,5 While all patients are susceptible to oligoanalgesia, certain subgroups, such as ethnic minorities, the aged, the very young, and those with diminished cognitive function, are more at risk (Table 35-1).^6,7,8,9 Pain management is further influenced by concerns of prescription opioid misuse, a rising concern in all age groups but most notably in adolescents and young adults. Pain and addiction are not mutually exclusive,¹⁰ and appropriate treatment of acute pain should not be withheld for fear of facilitating drug misuse.

Specific measures to treat pain should occur in addition to, and at the same time as, treatment of the underlying illness or injury. It is not possible to generalize the extent and quality of pain control needed for a specific patient. For example, pain is an indicator of ongoing cardiac ischemia, and the goal should be to eliminate all pain. On the other hand, a patient with a traumatic injury may choose to endure more pain out of personal or cultural beliefs. Physicians may limit analgesics in those with head injuries to perform serial neurologic examinations. Whenever possible, medications that act on specific sites that initiate the pain signal—a mechanistic approach—are preferred to agents such as opioids that mask pain, which is a symptomatic approach. Current migraine treatment is an excellent example of the mechanistic approach; preferred treatment includes a serotonin agonist (triptan)¹¹ or a dopamine antagonist (phenothiazine),¹² rather than opiates.^13,14

Pain is the physiologic response to a noxious stimulus, whereas suffering—the expression of pain—is modified by the complex interaction of cognitive, behavioral, and sociocultural dimensions. Individual pain experience is therefore not static, but varies depending on current and past medical history, physical and emotional maturity, cognitive state, meaning of pain, family attitudes, culture, and environment. Emotions can modify pain either negatively or positively: fear and anxiety may accentuate pain, or pain can be suppressed completely if an essential task must be performed or if there is acute concern about a loved one.

The peripheral nervous system (e.g., nociceptors, C fibers, A-δ fibers, and free nerve endings) initiates the sensation of somatic pain by responding to a noxious stimulus and sending a neuronal discharge to the dorsal horn of the spinal cord.¹⁵ Neurons in the dorsal horn of the spinal cord integrate and modulate input from multiple peripheral nerves and other sensory stimuli. Transmission then proceeds up the spinal cord to the CNS (e.g., hypothalamus, thalamic nuclei, limbic system, and reticular activating system) where further integration and processing generate the perception of pain. Identification and localization of pain, cognitive interpretation, and triggering of emotional and physiologic reactions also occur at these central sites. Unlike somatic pain, which is easily localized, visceral pain pathways are more complex and differ in structure from somatic pain pathways, which may explain the poor localization of visceral pain.

Opioid analgesics work by binding to receptors in the spinal cord and brain. There are four types of opioid receptors: three classic families (delta, kappa, and mu, each with identified subtypes) and nociceptin, a receptor with significant structural homology. These receptors are found in the brain, spinal cord, and GI tract where their physiologic function is to interact with endogenous dynorphins, enkephalins, endomorphins, endorphins, and nociceptin. Opioid analgesics interact with these receptors in varying degrees, accounting for the difference in desired and adverse effects among the drugs in this class. Stimulation of the mu-1 (μ₁) receptor produces supraspinal analgesia. Stimulation of the mu-2 (μ₂) receptor results in euphoria, miosis, respiratory depression, and depressed GI motility. Stimulation of the delta (δ) receptor produces analgesia, but less than the μ₁ receptor, and also exerts an antidepressant effect. Stimulation of the kappa (κ) receptor produces dysphoria, along with dissociation, delirium, and diuresis by inhibiting antidiuretic hormone release.

Document the degree of pain on initial assessment. This process serves to identify patients with severe pain, facilitates treatment, and meets the mandates of regulatory agencies that promote assessing and treating pain. ED pain assessment should determine duration, location, quality, severity, and exacerbating and relieving factors. The patient's subjective reporting of pain, not the physician's impression, is the basis for pain assessment and treatment. There is at best a weak correlation between nonverbal signs, such as tachycardia, tachypnea, and changes in patient expression and movements, and the patient's report of pain, so do not rely on these to determine the severity of a patient's pain^16,17 or response to treatment.¹⁸ Because pain is dynamic and changes with time, periodic pain reassessment is needed.

Although standardized scales for measuring reported pain are commonly used, their impact on effective pain control is uncertain.^19,20 The primary value of pain scales is their essential role in research enabling reproducible comparisons of interventions. Some studies have suggested that the use of pain scales may actually decrease the provision of analgesics. Given the subjectivity both of pain reporting and the provider's interpretation of such reporting, the use of simple descriptors such as "a little" or "an awful lot" is equally valid in the clinical setting. What is important is that the patient's subjective reporting should be the basis for assessment and management. For most, but not all, painful conditions, the goal is to control pain to the level the patient desires. Asking if the patient requires more analgesic may even be simpler and accomplish more than using any standardized pain evaluation tool.^21,22

PAIN SCALES

The purpose of pain scales is to quantitate pain severity, guide the selection and administration of an analgesic agent, and reassess the pain response to determine the need for repeated doses or more effective analgesics. Several self-report instruments are valid in patients with acute pain, and some require only a verbal response (Table 35-2). Each tool has advantages and specific limitations. ED personnel in any one location should use the same tool so information collected is standardized. A value assigned by a patient is not an absolute value but rather a reference point based on past personal experience.²³

PAIN SCALE PERFORMANCE IN SPECIAL PATIENT POPULATIONS

The elderly often report pain differently from younger patients because of physiologic, psychological, and cultural changes associated with aging. Visual, hearing, motor, and cognitive impairments can be barriers to effective pain assessment. Using a numerical pain scale, the elderly may also experience a decrease in the minimum clinically significant noticeable difference in acute pain over time.^24,25 Family members and caregivers are often able to judge nonverbal actions of the patient as representing pain or distress, so they should be used if available to help with pain assessment in the noncommunicating elderly patient.

Trauma patients and those with acute intoxication do not perform as well on pain scales.²⁶ Women are more likely to express pain and to actively seek treatment for pain,^27,28 yet there is a tendency to underestimate and undertreat pain in women. Ethnicity of both the patient and the physician has a bearing on different cultural concepts of pain and on the characteristics of culturally appropriate pain-related behaviors.⁷ Translators and family members should be asked to provide assistance. There is also interplay between the ethnicity of the patient and that of the physician.⁷ When there are language difficulties or cross-cultural differences, the visual analog scale is the preferred pain assessment tool because it is the least affected by these factors.

The administration of pharmacologic agents is the mainstay of acute pain management. The key to effective pharmacologic pain management in the ED is selection of an agent appropriate for the intensity of pain and it's time to onset of analgesic activity, ease of administration, safety, and efficacy.²⁹ Acute pain is usually accompanied by anxiety and feelings of loss of control. If verbal reassurance combined with an analgesic does not suffice, an anxiolytic may be useful.

The "tiered approach" to pain management starts with an agent of low potency regardless of pain intensity, assesses the response after a clinically relevant period, and sequentially changes to agents of higher potency if pain persists. The tiered approach for acute pain management unnecessarily subjects the patient to more prolonged suffering. It is preferable to select initial analgesics that are appropriate to treat the intensity (mild, moderate, or severe) of the patient's pain. Agents such as nonsteroidal anti-inflammatory drugs should be considered for mild to moderate pain, and systemic opioids for moderate to severe pain (Table 35-3). In specific instances such as renal and biliary colic, a parenteral nonsteroidal anti-inflammatory drug may control severe pain, although combination therapy with an opioid is usually superior.

When possible, local anesthesia is a useful adjunct (Table 35-4). Peripheral nerve blockade for pain control and for procedures is a useful option, especially if guided by US (see chapter 36, Local and Regional Anesthesia).^30,31

OPIOID ANALGESICS

Opioid analgesics are the cornerstone of pharmacologic management of moderate to severe acute pain (Table 35-5). The term opiate refers to agents that are structurally related to natural alkaloids found in opium, the dried resin of the opium poppy. The term opioid describes any compound with pharmacologic activity similar to an opiate, regardless of chemical structure. Opioid use in the ED is often affected by concern for the precipitation of adverse events, such as respiratory depression or hypotension, or for facilitating drug-seeking behavior. As noted, a greater concern is oligoanalgesia and inadequate dosing of opioids when used. Considerations for use of opioids include (1) desired onset of action, (2) available routes of administration, (3) achievable frequency of administration, (4) concurrent use of nonopioid analgesics and adjunctive agents, (5) possible incidence and severity of side effects, and (6) continuation of the agent in an inpatient or ambulatory setting

Opioids need to be titrated to effect; patients differ greatly in their response to opioid analgesics.^32,33,34 Variation in pain reduction is related to age, initial pain severity, and previous or chronic exposure to opioids, but not body mass^35,36 or gender.³⁷ Relative potency estimates provide a rational basis for selecting the appropriate starting dose to initiate analgesic therapy,³⁸ changing the route of administration (e.g., from parenteral to PO), or switching to another opioid (Table 35-6), but undue reliance on these ratios is an oversimplification with potential for over- or underdosing.³⁹

Opioid hypersensitivity is uncommon, and true allergic reactions are extremely rare. There is minimal evidence of clinical cross-sensitivity within opioid classes, with the possible exception that cross-sensitivity has been suggested among the piperidines (fentanyl, alfentanil, sufentanil, and meperidine). Until more is known, it would be prudent to switch to a drug from a different opioid class if a patient develops a hypersensitivity reaction. When used in equianalgesic doses, there is no compelling evidence to recommend one opioid over another. As much as possible, avoid using multiple agents, and titrate a single drug to the desired effect.

The use of meperidine is discouraged for several reasons: it is often underdosed; meperidine can interact with many drugs to precipitate a serotonin syndrome; and the parent drug is metabolized to normeperidine, which has neuroexcitatory properties and a long elimination half-life (24 to 48 hours).⁴⁰ Normeperidine can accumulate and produce toxicity in the elderly and those with renal failure, although this is a rare event.

Codeine is not a reliable analgesic, and it produces more nausea, vomiting, and dysphoria than other opioids. The analgesic effect of codeine is highly dependent on the metabolic conversion to the active metabolites codeine-6-glucuronide and morphine. Up to 10% of the U.S. population is deficient in the relevant enzymes for this conversion and, therefore, has an inadequate analgesic response to codeine. Conversely, there are case reports of neonatal deaths as a result of breastfeeding from mothers who were hypermetabolizers of codeine. In addition, the standard PO dose of 30 to 60 milligrams produces little analgesic effect above that of acetaminophen or nonsteroidal anti-inflammatory drugs.⁴¹

Tramadol binds to mu-receptors and weakly inhibits the reuptake of norepinephrine and serotonin producing a central opioid analgesic effect. Common side effects include dizziness, nausea, constipation and headache. Tramadol can induce the serotonin syndrome. Severe toxicity can include agitation and seizures. It is one of the many substances that can produce a false-positive result on the urine phencyclidine screen.⁴²

Adverse effects of opioids include nausea, vomiting, constipation, pruritus, urinary retention, confusion, and respiratory depression. Pruritus, urinary retention, confusion, and respiratory depression are more common with IV, transmucosal, and epidural administrations as opposed to PO administration.

Adjuncts are sometimes used to enhance the analgesic effect, reduce the amount of opioid required, and prevent side effects (Table 35-7). Depending on the agent, amount, route, and setting, a beneficial effect can be seen. However, appropriate titration with opioids in the ED is highly effective, and there are few data to support the routine use of adjuncts with opioids in the ED.⁴³ Pretreatment with antiemetics is not necessary given the low risk of emesis,⁴⁴ but symptom-targeted therapy is sometimes necessary.

Transdermal formulations are not useful for acute pain treatment because of delayed onset and prolonged duration of action. Transdermal fentanyl and transdermal buprenorphine preparations are used for chronic pain, particularly in cancer patients. When such patients are treated for acute pain in the ED, it is best to remove the delayed-release transdermal opioid patches to better titrate the acute opioid dose and to minimize adverse reactions from the combination of agents.

OPIOID AGONISTS-ANTAGONISTS

Opioid agonists-antagonists are used to minimize some of the adverse effects of pure opioid agonists (Table 35-8). The major benefit claimed is a ceiling on respiratory depression (no further reduction in respiration with increasing doses past a set amount). It is not clear if there is a ceiling effect for analgesia. The variability in efficacy relates to each particular agent's affinity for the various central opioid receptors. Because of the antagonistic effects, these agents should be used with extreme caution in patients with opioid addiction as they may precipitate withdrawal symptoms.

NONOPIOID AGENTS

Acetaminophen (paracetamol) is an effective analgesic for mild to moderate pain (Table 35-9).⁴⁵ Acetaminophen does not affect platelet aggregation and does not have anti-inflammatory properties. No change is required for renal or mild hepatic impairment (see chapter 190, Acetaminophen).

Aspirin and the nonsteroidal anti-inflammatory drugs are both anti-inflammatory agents and analgesics. As anti-inflammatory agents, aspirin and nonsteroidal anti-inflammatory drugs decrease the production of prostanoids and arachidonic acid–mediated inflammatory peptides generated at the site of tissue injury, diminishing the inflammatory response seen with some noxious stimuli. As analgesics, inhibition of the cyclooxygenase-2 enzyme in the spinal cord decreases the excitability of dorsal horn neurons that produce hyperalgesia and allodynia. These agents do not cause sedation or respiratory depression or interfere with bowel or bladder function. Nonsteroidal anti-inflammatory drugs have significant opioid dose-sparing effects.

Adverse effects of nonsteroidal anti-inflammatory drugs include platelet dysfunction, GI irritation and mucosal bleeding, nephropathy, headaches, and dizziness. All nonsteroidal anti-inflammatory drugs increase the risk of cardiac death in patients with ischemic heart disease,^46,47 although the cyclooxygenase-2–specific agents appear to carry higher risk than the nonselective agents.^48,49 Nonsteroidal anti-inflammatory drug–induced acute renal failure is more common in elderly patients and in those who are volume depleted, have preexisting renal or cardiac disease, or are taking loop diuretics.

OTHER PHARMACOLOGIC AGENTS

Ketamine

A phencyclidine derivative, ketamine produces analgesia and/or dissociative anesthesia with the advantage of causing minimal respiratory depression with usual doses (see chapter 37, Procedural Sedation). Low-dose (subdissociative) infusions of ketamine are effective in combination with opioids for patients in severe pain.^50,51,52 Ketamine dosing for analgesia is typically a loading dose of 0.15 to 0.4 milligrams/kg IV over 10 minutes followed by an infusion if desired. Ketamine can be used in trauma patients, resulting in a lower opioid requirement for pain control, and is also effective in controlling acute flare-ups of neuropathic pain. Ketamine is also useful as an SC infusion in palliative care patients. Adverse effects include hypersalivation and reemergence phenomena (disagreeable dreams or hallucinations upon awakening), especially when larger induction doses are used (1.5 milligrams/kg IV).

Nitrous Oxide

Nitrous oxide is a fast-onset, short-acting analgesic and sedative inhalational agent useful for brief, minor procedures (see chapter 37) and for prehospital analgesia.⁵³ The primary adverse effects are nausea and vomiting. Nitrous oxide is usually supplied as a preblended 50% mixture with oxygen and administered to the patient by face mask, but if available, the 70/30 nitrous oxide/oxygen mixture is more effective. Barriers to ED use of nitrous oxide include the need for patient cooperation and an effective scavenging system. In addition, nitrous oxide is contraindicated in patients with altered mental status, head injury, suspected pneumothorax, or perforated abdominal viscus. Severe pulmonary disease also may alter the respiratory elimination of nitrous oxide.

Cyclic Antidepressants and Anticonvulsants

Patients with acute-onset neuropathic pain, such as postherpetic or trigeminal neuralgia, are difficult to treat with short-acting opioid analgesics. It may be difficult to identify neuropathic causes of pain in ED patients, but if suspected, more specific therapy and follow-up instructions are needed. Long-acting opioids, cyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and anticonvulsants are effective for neuropathic pain (Table 35-10). When initiating an agent for patients with new-onset neuropathic pain, close follow-up with the primary care physician is important so that titration to effect may continue.^54,55 Patients already taking one of these agents for chronic neuropathic pain may require either titration upward of their medication or addition of a second agent; this should be discussed with the patient's regular physician.

Topical Medications

Topical administration of medications at the site of injury or inflammation can provide pain relief with reduced systemic drug absorption and a lower risk of adverse drug reactions (Table 35-11).⁵⁶ This approach differs from the transdermal drug administration to achieve systemic effects, typically with opioids (see Route of Administration). Topical nonsteroidal anti-inflammatory drugs are effective for treating acute soft tissue injuries such as sprains and strains and also for chronic joint pain from osteoarthritis. Topical lidocaine therapy is effective for patients with postherpetic neuralgia and diabetic neuropathy. Topical capsaicin has produced variable results depending on the treatment population and dose applied; regular use appears necessary for prolonged pain relief. A single 60-minute application of a high-dose preparation (8% capsaicin topical patch) is effective for postherpetic neuralgia but requires professional application and removal to minimize side effects.

The primary adverse reaction of topical medications is local burning, particularly seen with capsaicin, which is derived from chili peppers. Rare cases of localized burns have been reported with topical muscle and joint pain relievers.⁵⁷ Most of the serious burns were associated with agents containing menthol (>3% concentration) and/or methyl salicylate (>10% concentration).

ROUTE OF ADMINISTRATION

Systemic pain medications can be given by multiple routes (Table 35-12). Oral administration is convenient, inexpensive, and appropriate once the patient can tolerate oral intake; it is a mainstay of pain management in the ambulatory ED population.

IV opioids are suitable for bolus administration or continuous infusion and are preferred to intermittent IM injections. IM injections are painful, do not allow for easy titration, and have no clinically relevant advantage over PO medications. Absorption can be variable, especially in sickle cell patients (due to scarring) and hypotensive or volume-depleted patients. Patient-controlled IV analgesic systems are particularly effective for ED patients with acute abdominal pain and in addicts with pain when compared with the usual approach of intermittent nurse-administered parenteral medications.^58,59,60 Intra-articular analgesia using opioids or bupivacaine can provide sustained relief during the immediate postoperative period following hip and knee surgery.^61,62,63 Nasal and buccal preparations of fentanyl are available primarily for breakthrough pain in opioid-tolerant cancer patients, and these routes may have a role in prehospital and ED acute pain management.⁶⁴ Sublingual buprenorphine is described as effective for ED management of acute pain from fractures.⁶⁵

DOSAGE AND PRECAUTIONS

Safe and effective use of opioids is facilitated by choosing an appropriate initial dose⁶⁶ and subsequently titrating additional doses toward the desired effect, thus avoiding overmedication and minimizing unwanted effects. In unmonitored opioid-naïve patients, excessive doses of opioids can result in respiratory depression and decreased levels of consciousness. Hypotension is infrequent, is almost always due to histamine release with the first dose of medication, and is usually of short duration. With comorbidities, such as altered mental status, hemodynamic instability, respiratory dysfunction, or multisystem trauma, initial dosing should be decreased, and dose titration is important for achieving satisfactory pain relief.

The Elderly

Acute pain management for the elderly can be a challenge; these patients may have more than one source of pain and/or multiple comorbidities and are at increased risk for drug–drug and drug–disease interactions.⁶⁷ Opioid-naïve elderly patients are more sensitive to the analgesic effects of opioid drugs, because they experience a higher peak and longer duration of pain relief. Moreover, they are more sensitive to sedation, respiratory depression, and cognitive and neuropsychiatric dysfunction. Initial IV opioid doses in the elderly are typically half those used in younger adults (e.g., morphine 0.05 milligram/kg and hydromorphone 0.0075 milligram/kg), although single doses may not achieve adequate pain control for elderly patients with acute severe pain.⁶⁸

Addiction and Dependence

Addiction is the misuse of a medication or drug to the detriment of the patient's well-being. Dependence infers that abrupt cessation of a medication will result in acute withdrawal symptoms. Dependence on opioids requires regular daily usage for 4 to 6 weeks in most patients, whereas addiction may occur after one use of heroin. Care should be taken to assess a patient's risk for addiction or diversion of prescription medications, but when uncertainty exists, the general approach is to err on the side of acute pain control, although management in opioid-tolerant patients can be a challenge.⁶⁹ Contemporary and rigorous evidence is that dependence and addiction occur in up to one-third of patients on chronic opioid therapy,⁷⁰ but there is little knowledge regarding the risk of short-term (<2 weeks) opioid therapy following an ED visit for an acute injury or temporary illness. Although EDs are not where most cases of opioid abuse originate, they are perceived as a potential perpetuator of misuse.⁷¹ Distinguishing patient requests for medications because of oligoanalgesia from addiction often requires multiple patient assessments over time; subjective assessment in the ED during a single visit is usually inaccurate for identifying addiction versus aberrant behavior due to oligoanalgesia.⁷² Use of an assessment tool such as the Drug Abuse Screening Test may provide a more objective means of screening for addiction.⁷³

Renal and Hepatic Dysfunction

Because most analgesics are metabolized by the liver or kidney, take care when using opioids in patients with impaired hepatic or renal function. Renal excretion is a major route of elimination for such pharmacologically active opioid metabolites such as norpropoxyphene, normeperidine, morphine-6-glucuronide, and dihydrocodeine. Mild renal failure can impede excretion of the metabolites of many opioids, resulting in clinically significant narcosis and respiratory depression. In patients with renal failure, hydromorphone and fentanyl are the preferred opioids. Mild hepatic dysfunction has little effect on opioid metabolism. In patients with severe hepatic dysfunction, titration with low doses of analgesics will minimize the risk of overdose.

Respiratory Insufficiency

Patients with respiratory insufficiency and those with chronic obstructive pulmonary disease, cystic fibrosis, and neuromuscular disorders affecting respiratory effort (e.g., muscular dystrophy and myasthenia gravis) are particularly vulnerable to the respiratory depressant effects of opioids and nitrous oxide. Careful dose titration and monitoring of oxygenation and ventilation are necessary. Ketamine may be a useful alternative agent in such cases.

Drug Interactions

Opioids may have adverse synergistic sedative effects in patients with psychiatric illnesses taking anxiolytics or other psychoactive drugs. The use of monoamine oxidase inhibitors with meperidine is associated with severe adverse reactions, including death as the result of precipitating a serotonin syndrome (see chapter 178, Atypical and Serotonergic Antidepressants). The cyclic antidepressants clomipramine and amitriptyline may increase morphine levels and potentiate the opioid effects.

Traditionally, nonpharmacologic techniques of pain management in the ED have been limited to application of heat or cold and immobilization and elevation of injured extremities. Other techniques may be useful in the ED and after discharge. Cognitive-behavioral techniques can be effective in reducing pain and anxiety, may control mild pain when used alone, and can enhance patient satisfaction. Such techniques include reassurance, explanation, relaxation, music, psychoprophylaxis, biofeedback, guided imagery, hypnosis, and distraction. They are a useful adjunct to pharmacologic management of moderate to severe pain. Successful application of these therapies requires a cognitively intact patient and skilled personnel, but many of the techniques require only a few minutes to teach the patient.

Physical nonpharmacologic agents are becoming increasingly relevant to acute pain management. In addition to the traditional techniques noted above, less commonly used physical modalities, such as transcutaneous electrical nerve stimulation and acupuncture, may have some potential role in the ED. Although specific technical skills and equipment are required, there is no need for IV access, and there is no systemic effect such as respiratory depression or altered mental status.

ABDOMINAL PAIN

Early administration of IV opioids is safe for the treatment of acute abdominal pain in the ED and does not affect the accuracy of the evaluation, diagnosis, or management.^74,75,76,77 The dogma against the use of opioids for patients with acute abdominal pain stated in previous editions of Cope's Early Diagnosis of the Acute Abdomen was revised in 2000.⁷⁸ The one valid concern regarding analgesia and abdominal pain is that reduction in pain does not indicate improvement in pathophysiology. Analgesia without proper evaluation is as inappropriate as proper evaluation without analgesia.

MIGRAINE

There is no one, consistent, best analgesic agent for the management of a patient with migraine headache in the ED.^11,12,14 Opioid use for acute migraine treatment has lost favor due to poor performance in clinical trials, but can be considered if other agents have been ineffective.¹⁴ The high success rates with promethazine, chlorpromazine, and prochlorperazine are tempered by the extrapyramidal side effects, seen in as many as 45% of patients, and occasional intense dysphoria (see chapter 165, Headache).¹³

TRAUMA

Patients in shock and those with trauma, burns, and hemodynamic or respiratory instability need judicious use of opioids.² Fentanyl, first as a bolus and then as an infusion, may be the opioid of choice due to its lesser impact on hemodynamic function. Use of regional analgesia is encouraged.²⁹ Nonsteroidal anti-inflammatory drugs should not be given to patients with major trauma due to the risks of excessive bleeding from platelet dysfunction and gastric stress ulcers and the potential for acute renal failure in a volume-depleted patient.

Although rare, intractable acute pain can be a primary reason for hospital admission. Otherwise, most patients may be safely discharged with a plan for pain management that includes instructions for use of short-acting analgesics (i.e., those with a duration of action of up to 6 hours). Persistent pain after ED discharge is common.^79,80,81 Prescriptions for long-acting agents (e.g., methadone, controlled-release preparations of morphine or oxycodone) are generally avoided upon ED discharge but are sometimes used for special patients, such as those with cancer in whom short-acting agents are no longer effective (see chapter 38, Chronic Pain).

Patients should be counseled to take subsequent doses on a regular basis or when their pain begins to return, rather than when it approaches its peak. Patients with recurrence of severe pain or changes in the quality of pain should be told to return to the ED for reassessment. It is best to prescribe only a few days' worth of analgesics, because conditions with a longer duration of pain require follow-up with the primary care physician. If opioids are prescribed to the elderly or those naïve to narcotics, home observation by a responsible adult is recommended so that adverse effects can be quickly recognized. Discharge instructions for those given opioids should include instructions to avoid making important decisions while medicated and to avoid driving, operating machinery, climbing or working from heights, and so on, and should also include instructions for treatment of constipation. Education about securing opioid prescriptions is important because up to 85% of prescription opioids misused by adolescents come from their parents' medication cabinet.