EMERGENCY SEDATION AND PAIN MANAGEMENT - PART 3 doc

NSAIDs inhibit vasodilatory prostaglandins that increase renal flow and glomerular filtration rate and may cause renal ischemia and functional damage in volume-depleted patients. Sodium and water retention, hypertension, hyperkalemia, and acute renal failure may also ensue, especially in patients with congestive heart failure but have otherwise acceptable symptom control. Headache, tinnitus, drowsiness, lightheadedness, and mild dermatologic reactions are among the adverse effects that patients may report. Severe liver problems and bone marrow suppression have been reported, but these occur rarely (Table 8-3). DRUG INTERACTIONS Oral anticoagulants. The antiplatelet effects of NSAIDs added to the anticoagu lant properties of coumadin compound the risk of significant bleeding complica- tions, especially from GI ulcers. Furthermore, NSAIDs displace protein-bound coumadin and cause subsequent increases in prothrombin time at a constant coumadin dose. Avoid adding NSAIDs to patients on warfarin. ACE inhibitors. Concurrent use of NSAIDs with ACE inhibitors may impair renal function and impair the antihypertensive effects of ACE inhibitors. Diuretics. Avoid using NSAIDs in patients who are taking diuretics. They have a greater risk of developing renal failure because of NSAID-mediated, dec reased ren al blood flow. Also, the natriuretic response to diuretics depends in part on prostaglandin-mediated vasodilatation. Glucocorticoids. Patients on corticosteroids will have increased risk of PUD. Addition of NSAIDs should be used cautiously, if at all. Lithium. NSAIDs enhance lithium reabsorption and may directly reduce lithium excretion, leading to increased lithium levels. Central nervous system (CNS) symptoms (drowsiness, confusion, vertigo, convulsions, or t remors), cardiac dysrhythmias, and QRS widening are warnings of lithium toxicity. The lithium dosage should be reduced when adding an NSAID is necessary. Methotrexate. Chronic coadministration of NSAIDs and methotrexate have resulted in prolonged, elevated blood levels of methotrexate, resulting in severe toxicity. A possible mechanism may be the decreased renal perfusion caused by NSAIDs, decreasing the elimination of methotrexate. COMMENTS AND CONTROVERSIES. NSAIDs combine analgesia and anti-inflammatory effects with low abuse potential and much different side effects than the opioids. Oral NSAIDs can be as effective as oral opioids. Parenteral NSAIDs have been shown to be as effective as opioids in some settings. However, parenteral NSAIDs do not appear to work better or faster than oral NSAIDs. Table 8-2. Risk of GI effects of nonselective NSAIDS Lowest risk Ibuprofen 400 mg Intermediate risk Aspirin, indomethacin, naproxen, sulindac, ibuprofen 800 mg High risk Ketorolac, tolmentin, ketoprofen, and piroxicam Table 8-3. Precautions for using nonselective NSAIDS 1. Patients who are dehydrated or hypovolemic are at high risk of acute renal impairment 2. Patients who have impaired renal function, liver disease, or congestive heart failure, in particular, those already taking ACE inhibitors, angiotensin II receptor blockers (ARB), or diuretics 3. Use cautiously in the elderly, who are at greater risk of developing renal toxicity and failure 4. Patients with asthma and known aspirin hypersensitivity are at an increased risk of bronchospasm 5. Third-trimester pregnancy: may prolong gestation or prematurely close the ductus arteriosus (FDA category C) 6. All have the potential for GI side effects 7. They may interfere with the effects of many antihypertensives 8. There is little clinical evidence of individual superiority of any particular NSAID over another 9. The newer agents may cost as much as 50 times more than the older ones Pharmacology of Commonly Utilized Analgesic Agents 47 Different patients respond differently both to the effects and the side effects of different NSAIDs; some experimentation may be necessary to determine the best choice for a particular patient. KETOROLAC TROMETHAMINE (TORADOL). Ketorolac is the first nonopioid analgesic agent available for parenteral use in the United States. For acute musculoskeletal pain, 60 mg ketorolac administered intramuscularly (IM) has been shown to be approximately equivalent in analgesic efficacy to 800 mg of ibuprofen given orally. Because the action of ketorolac is due to the inhibition of prostaglandin synthesis, its onset is no faster than an equivalent agent given orally. Ketorolac is also 10–35 times more expensive than morphine or ibuprofen. COX-2 inhibitors DESCRIPTION. The discovery of two distinct COX iso- enzymes (COX-1 and -2), one (COX-2) associated mostly with pain and inflammation, raised hope that a new class of analgesics could be developed. These would control pain and inflammation with fewer adverse effects (particularly GI mucosal injury) than traditional NSAIDs. Unfortunately, the functional distinction between the nonselective and COX-2 specific NSAIDs has proven to be far less pharmacologically useful than it had seemed at first. In the ED, these agents have a limited role in the initial management of acute pain. However, they have a role in postdischarge use. PHARMACOLOGY Gastrointestinal. Agents that selectively inhibit COX-2 are expected to cause less ulceration and have a lower risk of bleeding. However, COX-2 has been identified in normal gastric mucosa, and its possible role in protection and healing of the gastric mucosa may mean that selective inhibitors may not have any GI-protective advantage. Cardiovascular. COX-2 inhibitors may have prothrombotic effects from greater inhibition of prostacyclin than thromboxane, thus increasing the risk of cardiovascular events. Renal. It had been hoped that COX-2 inhibitors would not decrease renal perfusion as much as traditional NSAIDs. However, COX-2 inhibitors appear to have no advantage, decreasing renin activity and reducing sodium excretion by the same amount (approximately 20%) as do NSAIDs. Selectivity. Selectivity of an agent refers to the extent to which it inhibits COX-2 activity but not COX-1 activity. In vitro, it would appear that there are very significant differences between the different types of agent (COX-1/COX-2 enzyme activity reduction ratio is 0.1 for indomethacin, as compared with 28,000 for valdecoxib). In vivo, however, the selectiv ity does not appear to significantly decrease COX-2 inhibitors’ effects on GI mucosa, renal function, and platelets as compared to COX-1 inhibitors. EFFICACY. No studies on COX-2 inhibitors’ effectiveness in pain relief have been conducted in ED settings. COX- 2 inhibitors are superior to placebo and equivalent to COX-1 inhibitors in acute postoperative dental pain, postoperative orthopedic pain, primary dysmenorrheal, and osteoarthritis. There are no studies comparing COX-2 inhibitors’ efficacy in renal colic, biliary colic, acute gout, headache syndromes, sickle cell crisis, or acute musculoskeletal or soft-tissue injury. At this point, there is no evidence that COX-2 inhibitors are significantly more effective than their COX-1 counterparts for the management of acute pain in the ED. DRUG INTERACTI ONS Nonselective NSAIDs. COX-2 inhibitors should not be combined with NSAIDs because of their similar phar- macological effects. The exception would be ASA for cardioprotection, which is especially important in the context of possible COX-2 inhibitor-associated cardiovascular events. Interactions that are similar to those of nonselective NSAIDs. COX-2 inhibitors have similar interactions as NSAIDs with ACE inhibitors, antihypertensive agents, anticoagulants, and lithium (see above). Antacids. Antacids that contain magnesium or alu- minum reduce COX-2 inhibitor plasma concentrations and may decrease the agent’s clinical effects. Fluconazole. Fluconazole inhibits cytochrome P450- 2C9 isoenzyme and cause increased side effects from COX-2 agents due to decreased metabolism and increased blood levels of these agents. Sulfoamide allergy. Celecoxib has a similar structure to the sulfonamides, and cross-reactive hypersensitivity 48 Analgesia for the Emergency Patient reactions have occurred in sulfa-allergic patients. Other COX-2 agents have not been reported to cause the same problem. SAFETY AND ADVERSE EFFECTS Tolerability. Adverse reactions to COX-2 agents most often occur in the GI tract, but a few patients report vague neurological symptoms such as headache and dizziness. Otherwise, the rate of adverse reactions is not significantly greater than that seen with placebo or traditional NSAIDs. Endoscopic, clinically asymptomatic ulcers, not associated with bleeding, were found in 7–10% of patients taking COX-2 inhibitors as compared with 27–40% of patients taking traditional NSAIDs. Significant GI effects occurred in 1.3% vs 1.8% of patients taking refocoxib vs traditional NSAIDs per year of exposure. The most commonly reported renal events from taking refocoxib were edema (2.1%), hypertension (0.8%), and exacerbation of preexisting hypertension (0.6%). These events were not related to dosage or duration. Serious vascular events. COX-2 agents may have a prothrombotic effect based on their greater inhibition of prostacyclin than of thromboxane. In the VIGOR trial, 1.1% of refocoxib patients suffered serious vascular events, as compared with 0.5% of naproxen patients. In the CLASS study, no clear difference in cardiovascular risk was apparent. Mukherjee et al. suggested that AMI rates in the two studies were higher than the baseline rate in a large meta-analysis and that COX-2 agents, therefore, increased the risk of a cardiovascular event. It is not completely clear that the patient populations were comparable. Although ED physicians are unlikely to prescribe long-term COX-2 inhibitors, they should be aware of the potential increase in risk of cardiovascular events and ensure that patients who are on COX- 2 inhibitors are also taking an appropriate antiplatelet agent, if in- dicated (Table 8-4). SPECIFIC AGENTS. The two COX-2 inhibitors about which we have the most information are celecoxib and refocoxib. Valdecoxib and parecoxib are newer, more highly selective agents that seem to have fewer GI adverse effects but similar efficacy to NSAIDs. Parecoxib is a parenterally administered prodrug that is metabolized to valdecoxib. It is the first IV/IM COX-2 inhibitor available in North America. A 20 mg dose has been shown to provide a similar amount and duration of analgesia to ketorolac (30–60 mg) and lasts longer than IV morphine (4 mg). COMMENTS AND CONTROVERSIES. COX-2 inhibitors have not been studied in the ED for use in acute pain syndromes or acute-on-chronic pain exacerbation. Most of the studies describe adverse events that tend to occur after a much longer duration of therapy than is either used in the ED or prescribed upon discharge home. Though evidence suggests that they are as effective in acute pain as traditional NSAIDs and may be better tolerated, they are generally much more expensive. The risk of serious cardiovascular events constitutes a significant deterrent to their long-term use. Opioids Titrated intravenous opioids are the mainstay of phar- macological management of acute pain. The beneficial effects of opioids have been well documented for cen- turies, as have its toxicity and potential for abuse. Fear of inducing addition has led to underuse of opioids by many physicians. However, many studies have shown that short-term use of opioid analgesics for acute pain syndromes is not associated with future dependence. Pharmacology Opioids bind to several different classes of receptors located throughout the nervous system and suppress neuronal pain transmission peripherally, at the spinal cord, and in the thalamus. They also act to modify the perception of pain at the level of the cortex. There are three main opioid receptors: mu, kappa, and delta. Mu receptors mediate euphoria, sedation, respiratory depression, and nausea. Kappa receptors cause spinal Table 8-4. Precautions for using COX-2 inhibitors 1. Patients with a history of PUD or GI bleeds 2. Elderly or debilitated 3. Volume-depleted patients 4. Patients taking ACE inhibitors or diuretics 5. Patients with renal or hepatic disease 6. Pregnancy (FDA category C) 7. Children under 18 Pharmacology of Commonly Utilized Analgesic Agents 49 analgesia and central sedation; they also produce dys- phoria. Delta receptors inhibit pain transmission and may decrease myocardial and brain oxygen demand. Opioids also suppress the medullary cough center and decrease the hypercarbic drive. They can activate the chemoreceptor trigger zone causing nausea and vomiting. They decrease bowel motility and smooth muscle function, causing urinary retention and constipation (but can be used to slow diarrhea). Opioids cause mast cell destabilization and subsequent histamine release, pro- ducing urticaria, pruritus, and orthostatic hypotension. Because opioids cause euphoria, they are subject to abuse. Patients who use them for prolonged periods will suppress their production of endogenous opioids and develop physiologic dependence and subsequently withdraw if the medication is abruptly stopped. These characteristics make many physicians and patients reluctant to use opioid medica tions, even under appropriate circumstances. Opioids can relieve any level of pain because they lack the ‘‘ceiling’’ effect of many other analgesics. They provide dose-related analgesia with variable sedation and anxiolysis. There is not a standard, fixed, or weight-related dose necessary to produce a given clinical effect: the dose that produces the desired pain relief is the correct dose for that particular patient at that particular time. There is no clinically significant difference between the different mu-receptor agonists; any opioid can relieve severe pain if its side effects can be tolerated when administered in a dose sufficient to relieve the pain. Opioids should be the first-line agents in the management of acute severe pain. Morphine, hydromorphone, hydrocodone, and oxycodone have a short- to-intermediate onset and duration of action. The tim- ing of their clinical effects corresponds with their peak serum levels. Maximal analgesia occurs 60–90 min after oral administrati on, 30 min after IM injection, and 1–6 min after IV administration. Oral doses have significant first-pass metabolism and much higher doses are required for an equivalent effect to a parenterally administered dose. Mixed opioid agonist-antagonist antagonists have a ‘‘ceiling’’ beyond which increasing doses do not afford increasing pain relief. They also have a high rate of side effects and may cause withdrawal symptoms in patients already tolerating large doses of pure agonist opioids. For a given drug and dosing regimen, maximum pain control is achieved when serum levels reach a steady state: requiring five half-lives. Repeating doses at the same period as the half-life after initial titration is an effective way to relieve continuous pain. Prescribing repeat analgesic doses, rather than ‘‘as needed,’’ is the most effective way to accomplish pain relief. The treatment of pain should start by prescribing shorter-acting opioids titrated to pain relief, followed by a longer-acting agent and a planned dosing schedule to maintain relief. The use of long acting, delayed release, or transdermal formulations to begin pain treatment will result in achieving peak serum medication levels long after the initiation of therapy, which may result in the patients receiving too large a dose in an attempt to expeditiously achieve pain relief, or too small a dose in anticipation of subsequently higher levels (see Table 8-5). Specific Agents Morphine Intravenous morphine is the first choice for treatment of acute severe pain in ED patients (Table 8-5). It is typically started at 0.1 mg/kg IV and can be repeated every 5 min at 0.05 mg/kg until pain is relieved. Oral administration of morphine can be an effective option for moderate or severe outpatient pain, but only 20% of the ingested dose reaches the tissues after first-pass metabolism, and this delayed onset makes titration difficult. A common misperception is that morphine causes more smooth muscle spasm than other narcotics and should be avoided in patients with biliary or renal colic. There is neither any evidence to support this concept nor any that shows superior efficacy of any other narcotic over morphine in these situations. Morphine is chiefly metabolized by conjugation into a three-conjugate and six-conjugate form. The three- conjugate form has no opioid analgesic activity and has been associated with significant CNS side effects (tre- mors, myoclonic jerks, delirium, and seizures) if not cleared by the kidneys; this presents a greater risk in elderly patients and those with renal insufficiency. The six-conjugate form is made in less abundance than the three-conjugate form and has an opioid analgesic potency that is much stronger than that of morphine. It plays an important role in morphine’s efficacy. 50 Analgesia for the Emerg ency Patient Table 8-5. Common opioids and their equipotent doses Generic Oral Intravenous Duration Half-life Comments Precautions Morphine 0.5 mg/kg 40–60 mg 0.1 mg/kg 10 mg 3–4 hr 2–3 hr Standard for comparison Respiratory depression Hypotension Sedation Histamine release Codeine 2.5 mg/kg 200 mg 1.3 mg/kg 130 mg 2–4 hr 2–3 hr Poor analgesic Excellent cough suppressant Constipation, nausea, and vomiting Hydromorphone 0.075 mg/kg 7.5 mg 0.015 mg/kg 1.5 mg 2–4 hr 2–3 hr Inactive metabolites, less accumulation in patients with renal or hepatic disease Hydrocodone 15 mg N/A 3–4 hr 2–3 hr Excellent cough suppressant Fewer side effects than codeine and greater potency Oxycodone 0.125 mg/kg 12.5 mg 0.1 mg/kg 10 mg 3–4 hr 2–3 hr Parenteral form not available in US High bioavailability relative to most opioids Absorbed well in oral form, has been associated with abuse Meperidine (demerol) 3 mg/kg 300 mg 0.75 mg/kg 75 mg 2–3 hr 45–90 min Toxicity from metabolite normeperidine Avoid with MAOI. Caution in renal or hepatic failure Fentanyl 3 lg/kg (transmucosal) 300 lg 1 lg/kg 100 ug 0.5–1.5 hr 0.5 hr No histamine release Transcutaneous and transmucosal absorption For IV administration, push and flush slowly to avoid ‘‘rigid chest’’ syndrome Alfentanil 10 lg/kg 1000 lg 12 min 1.5 hr Duration of action during redistributive phase very short, duration increases with larger doses Muscular rigidity if administered too quickly Oxymorphone 0.1 mg/kg (rectal) 10 mg 0.01 mg/kg 1mg 3–4 hr 2–3 hr Well absorbed rectally Methadone 0.2 mg/kg 20 mg 0.1 mg/kg 10 mg 4–8 hr 15–190 hr Long-acting narcotic used in opioid addiction treatment and for chronic pain Propoxyphene 1 mg/kg 100 mg 0.5 mg/kg 50 mg 2–4 hr 2–3 hr Shown to be inferior to acetaminophen alone in common oral preparations Has little role in the treatment of pain Heroin 0.5 mg/kg 60 mg 0.05 mg/kg 5mg 3–4 hr 0.5 hr Here for illustrative purposes, not used medically, common opioid of abuse Tramadol 50–100 mg Selective mu agonist, not associated with physiologic dependence May precipitate serotonin syndrome in SSRI patients 51 Morphine destabilizes mast cells causing histamine release and can cause pruritus and localized urticaria that can track up the vein after IV administration. This is a common phenomenon and does not constitute an allergic reaction to morphine. Nausea, dizziness, and constipation are other common side effects. When used in combination with acetaminophen, postorthopedic surgery patients used 16% less morphine in their patient-controlled analgesia and reported lower pain scores. A multimodal approach can significantly enhance the delivery of analgesia. Meperidine Meperidine was one of the most commonly used opioids for the treatment of acute pain in the ED. It is metabolized by the cytochrome P-450 system to the metabolite normepridine, which has no analgesic effects but potent CNS excitatory effects. Meperidine blocks muscarinic receptors and has significant anticholinergic effects, causing agitation, delirium, and visual hallucinations. Normeperidine has a half-life of 24–48 hr, as compared to the 2–3 hr half-life of meperidine. Repeated dosing can lead to accumulation of normeperidine and increase the risk of neurotoxicity. Normeperidine also blocks the reuptake of serotonin and norepinephrine and has been associated with serotonin syndrome. Normeperidine is not an opioid and is not reversible with naloxone. These diverse adverse effects related to its principal metabolite make meperedine an inferior choice for pain management compared to most other opioids. It should not be used in the management of acute pain. Hydromorphone Hydromorphone is a semisynthetic derivative of morphine developed in t he 1 920s . I t i s th e p-450 metabolite o f hydrocodone. It is conjugated primarily into several inactive metabolites and is, therefore, better tolerated in elderly patients and those with renal or hepatic impairment than morphine. One of its metabolites has been found to be excitatory in rat models and to accumulate in patients who receive prolonged therapy, but at much lower levels than the e quivalent metabolite in morphine. Hydromorphone is similar to oxycodone and morphine in its analgesic effects and adverse effects. Its primary indications are in patients who are allergic to morphine or have renal or hepatic disease. Hydromorphone is available as an injectable solution and its oral tablets come in 1, 2, 4, and 8 mg strengths. There is also a 3 mg rectal suppository. Oral doses are 4–8 mg PO q3–4 hr; IM doses are 1–2 mg q 3–4 hr, IV dosing is 0.015 mg/kg mg every 5 min titrated to pain relief. A sustained release oral hydromorphone formula- tion was recently pulled from the market due to reported overdose potential when combined with alcohol. Fentanyl Fentanyl is a synthetic opioid that is excellent for rapid titration analgesia in acute, severe pain. It is highly li- pophilic and produces analgesia within 1–2 min of IV infusion. It also redistributes rapidly and its duration of action is only 30–60 min. It is metabolized by the p-450 system into inactive metabolites. Drug accumulation and toxicity may occur after tissue saturation following a prolonged infusion, but this is unlikely to happen during acute therapy. Fentanyl releases less histamine than morphine and is associated with fewer peripheral effects. It is more frequently associated with respiratory depression with regular use than morphine, and patients receiving infusions of the drug should be monitored with observation or pulse oximetry. Fentanyl’s short duration of action makes it ideal for use in patients who require serial examinations. Fentanyl is available in IV form, as well as the raspberry- flavored transmucosal lozenges (200, 400, 600, 800, 1,200, and 1,600 mcg). Duragesic Ò patches are used for sustained release of fentanyl in chronic pain patients, but should not be used in the management of acute pain. Oxycodone Oxycodone is a strong opioid agonist. It is widely available in combination with acetaminophen or aspirin as well as by itself. It is also available in long-acting oral formulations. It has a very high bioavailability relative to the other opioids and is quickly and efficiently absorbed. This has led to an association with abuse. Oxycodone is not available in a parenteral form in the United States, although studies have found its IV form to be equia- nalgesic to morphine. 52 Analgesia for the Emergency Patient Similar to the other opioids, the analgesic effects of oxycodone are dose dependent. A 15 mg dose has a similar efficacy to 10 mg of IV morphine. The onset of action of oral oxycodone is 20–30 min. Oxycodone, in combination with acetaminophen, has similar efficacy to a higher dose of oxycodone alone. Oxycodone is available in 5 mg tablets and in a 5 mg/ 5 ml solution. It also comes in 15 and 30 mg tablets and a concentrate of 20 mg/ml. The controlled release forms come in 10, 20, 40, and 80 mg tablets. Hydrocodone Hydrocodone is metabolized in the liver to hydromorphone. It provides greater pain relief when combined with acetaminophen or NSAIDs than either component does alone. Hydrocodone-acetaminophen (5 mg/500 mg) provides comparable analgesia to codeine-acetaminophen (30 mg/500 mg) in patients with acute musculoskeletal pain or who have undergone dental surgery. Hydrocodone causes more drowsiness and dizziness but less nausea or vomiting. Hydrocodone is also used as an antitussive. Hydrocodone-acetaminophen and hydrocodone- ibuprofen combinations are available with 5 or 7.5 mg of hydrocodone per tablet, but the dosing of these combination drugs is limited by the acetaminophen content as well as the combined adverse effects. Hydrocodone itself can be prescribed 5–20 mg PO every 4–6 hr as needed. The combination tablets should be prescribed as 1–2 tablets every 4 hr as needed for pain. Codeine Codeine is the most commonly prescribed opioid, usually in combination with acetaminophen with which it acts synergistically. Codeine is a prodrug with minimal analgesic effect until metabolized in the liver to morphine and other metabolites. Approximately 10% of the population metabolizes codeine poorly and experiences toxicity (nausea, constipation, pruritus) but not pain relief. It is a somewhat effective analgesic against mild to moderate pain but frequently causes GI symptoms (mainly nausea and vomiting) at doses that have limited analgesia or euphoria. The analgesic effect from codeine is dose related, but doses greater than 60 mg cause incrementally more nausea and constipation than pain relief. Codeine is often prescribed for cough suppression. Codeine is available as codeine syrup (5 mg/ml), codeine tablets (15, 30, 60 mg), and as an injection of codeine phosphate (15, 30, and 60 mg/ml). Tylenol with codeine syrup is also available (12.5 mg codeine with 120 mg acetaminophen per 5 ml). Tramadol Tramadol is a synthetic compound that is a selective mu agonist. It is chemically unrelated to the morphine-like opioids. It is metabolized in the liver by the cytochrome P-450 system. One of its metabolites, M1, has an even greater mu-receptor affinity than tramadol and has an elimination half-life of 9 hr. Tramadol also appears to have effects on GABA and serotonin receptors and could theoretically precipitate serotonin syndrome if administered with SSRIs. Tramadol, as a selective mu agonist, should not cause physiologic dependence as the other opioids do. Since its release, however, it has been associated with abuse and withdrawal similar to that of other opioids, but at low enough rate that, after a review in 1998, its status as an unscheduled drug was maintained. Tramadol has been found to be an efficacious pain medication at low doses. At increasing doses, it is associated with nausea and vomiting, limiting its use to low doses. Tramadol 37.5 mg combined with acetaminophen 325 mg was found to have similar efficacy to hydrocodone 5 mg combined with acetaminophen 325 mg. Side effects include nausea, vomiting, and dizziness. In combination with SSRIs or tricyclic antidepressants, tramadol may lower the seizure threshold in patients with epilepsy. Tramadol is available in oral tablets of 50 mg, recommended dose is 50–100 mg every 4 hr. It is also available in combination with acetaminophen, 37.5 mg/ 325 mg. FOLLOW-UP/CONSULTATION CONSIDERATIONS A patient who has received opioid medications for acute pain syndromes should be discharged in the company of a responsible, competent adult who will provide and Pharmacology of Commonly Utilized Analgesic Agents 53 supervise transportation home and ensure that there is someone who will monitor the patient overnight. Close follow-up with a primary care provider is essential for ongoing pain management. Discharge prescriptions should provide sufficient amounts of medication to adequately treat the patient through the expected course of the injury or until follow- up. Patients receiving courses of narcotics that are expected to last longer than 5–7 days should be warned about the likelihood of tolerance to the medication and the possible need for tapering of the medication as the treatment concludes, and should have close follow-up with a primary care provider to oversee the management of this. SUMMARY There is no ‘‘one-size-fits-all’’ approach to managing acute or acute-on-chronic pain. If nonpharmacologic adjuncts are available, such as environmental effects (e.g., dimming the lights), psychological distraction, and physical modalities (positioning, ice), then these should be used. Physicians should know the expected effects of analgesic therapy and monitor patients for side effects from different analgesic agents. Patient responses to the effects or side effects of an analgesic can vary considerably. BIBLIOGRAPHY 1. Schug SA, Sidebotham DA, McGuinnety M, et al. Acetaminophen as an adjunct to morphine by patient- controlled analgesia in the management of acute postoperative pain. Anesth Analg 1998;87:368–372. 2. Barkin R. Acetaminophen, aspirin or ibuprofen in combination analgesic products. Am J Ther 2001;8:433–442. 3. McEvoy GK. American hospital formulary service. Bethesda, MD: American Society of Health System Pharmacists, 2000. 4. Hylek EM, Heiman H, Skates SJ, et al. Acetaminophen and other risk factors for excessive warfarin anticoagulation. JAMA 1998;279:657–662. 5. Lipsky PE, Brooks P, Cro fford LJ, et al. Unresolved issues in the role of cyclooxygenase–2 in normal physiologic processes and disease. Arch Intern Med 2000;160: 913–920. 6. Turturro MA, Paris PM, Seaberg DC. Intramuscular ketorolac versus oral ibuprofen in acute musculoskeletal pain. Ann Emerg Med 1995;26:117–120. 7. Loewen PS. Review of the selective COX-2 inhibitors celecoxib and refocoxib: Focus on clinical aspects. Can J Emerg Med 2002;4:268–275. 8. Mukherjee D, Nissen SE, Topol E. Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMA 2001;286:954–959. 9. Joranson DE, Ryan KM, Gilson AM, et al. Trends in medical use and abuse of opioid analgesics. JAMA 2000:283(13): 1710–1714. 10. Jovey RD. Opioid analgesics. In Managing pain, ed. RD Jovey. Toronto, Canada: Healthcare and Financial Pub- lishing, for the Canadian Pain Society, 2002, pp. 47–61. 11. Latta K, Ginsberg B, Barkin RL. Meperidine: A critical review. Am J Ther 2002;9:53–68. 12. Weiner AL. Meperidine as a potential cause of serotonin syndrome in the emergency department. Acad Emerg Med 1999;6:156–158. 13. Quigley C. Hydromorphone for acute and chronic pain. Cochrane Database Syst Rev 2002;1:CD003447. 14. Edwards JE, Moore RA, McQuay JH. Single dose oxycodone and oxycodone plus acetaminophen for acute postoperative pain. Cochrane Database Syst Rev 2000;4: CD002763. 15. Turturro MA, Paris PM, Yealy DM, et al. Hydrocodone vs codeine in acute musculoskeletal pain. Ann Emerg Med 1991;20:1100–1103. 16. Silverstein F, Fai ch G, Goldstein J, et al. Gastrointestinal toxicity with celecoxib versus non-steroidal anti- inflammatory drugs for osteoarthritis and rheumatoid arthritis JAMA 2000;234:1247–12 55. 54 Analgesia for the Emergency Patient 9 Patient Assessment: Pain Scales and Observation in Clinical Practice Tania D. Strout and Dawn B. Kendrick SCOPE OF THE PROBLEM CLINICAL ASSESSMENT MEASUREMENT CONCEPTS Reliability Validity Clinical Significance vs Statistical Significance Unidimensional vs Multidimensional Scales PAIN SCALES Unidimensional Pain Scales NRS VAS Verbal descriptor scale (VDS) The Wong-Baker FACES Pain Scale The FACES Pain Scale Multidimensional Pain Scales The Preverbal, Early Verbal Pediatric Pain Scale The CRIES scale MPQ – Short Form (SF-MPQ) Memorial Pain Assessment Card (MPAC) Brief Pain Inventory – Short Form (BPI-SF) SUMMARY BIBLIOGRAPHY SCOPE OF THE PROBLEM The measurement of a patient’s pain intensity is inher- ently complex. The pain experience is unique to each individual, influenced by many factors such as medical condition, developmental level, emotional and cognitive state, culture, the hospital environment, family issues and attitudes, language barriers, and levels of fear and anxiety. The often chaotic, loud, and hurried emergency department (ED) environment only serves to compound these difficulties. It is well documented in scientific literature that oligoanalgesia is a significant issue within emergency medicine. In order to appropriately manage patients’ pain, we must attempt to accurately assess their pain. CLINICAL ASSESSMENT There are multiple barriers to the clinical assessment of pain, including, but not limited to, provider biases, patient anxiety, family attitudes, cultural beliefs, and provider suspicion of ‘‘drug-seeking’’ behavior. The National Institutes of Health has stated that patient self- report is the most reliable indicator of the existence and intensity of pain. Barriers to pain assessment are greatest for those patient populations who cannot self-report their pain experience. Pediatric patients and those with impaired cognition communicate and display pain in very different ways. Infants and young children often cry or whimper when 55 they are in pain. They often cannot localize or describe their pain and, therefore, it may be difficult to assess and quantify. This may be similar in the elderly patient with dementia or other cognitive and communicative impairments. In thes e patients or those with or inability to characterize their pain owing to endotracheal intu- bation, it is often useful to observe and assess for changes in behavior, body language, vocalizations, per- formance of activities of daily living, and physiologic parameters. Providers of emergency care must be aware of these limitations and use available tools and direct observation to ensure the best possible outcomes for their patients. Despite these and other barriers to pain measurement, a vast literature describing a great number of pain measurement instruments and their properties exists today. The utilization of such measurement instruments provides emergency clinicians a common language with which to communicate assessment finding s in a consistent manner. For patients, these instruments can be a tool that assists them in better communicating the subjective pain experience to their clinicians. However, all scales are not appropriate for all patient populations, and the appropriate instrument should be chosen. Specifically, a patient’s age, cognit ive and developmental abilities, and preferences need to be addressed when choosing the appropriate tool. MEASUREMENT CONCEPTS Understanding several concepts central to scale devel- opment is useful in assisting clinicians when choosing a scale to use with their particular population. Knowledge of reliability, validity, and the differences between unidimensional and multidimensional scales can be helpful in ensuring that an appropriate tool is utilized. Reliability Reliability addresses the consistency of a given measure over time. When evaluating pain measurement instruments, two types of reliability are of particular interest. The first type is termed stability, or test-retest reliability. Here, the clinician is concerned with the consistency of the scale over time. Ideally, a pain scale should give the same rating at time a and at time b if the patient’s pain intensity has not changed. Interrater reliability, or equivalence, is the second type of reliability that clinicians should consider when choosing a pain rating tool. This refe rs to the ability of two independent observers to use the same scale at the same time to observe the same patient and obtain the same result. Validity Validity is concerned with the extent to which a too l actually measures what it is intended to measure. Three primary types of validity are described in the literature: content validity, construct validity, and predictive validity. Evide nce of content validity examines the extent to which the tool includes the major elements rel- evant to what is being measured. Construct validity is concerned with the degree of agreement between a particular measure and other measures that evaluate the same concept, for example, the degree of agreement between two separate pain scales. Predictive validity addresses the ability to predict future outcome on the basis of the score provided the given instrument. Here, we would expect that a score would indicate lower pain intensity after a patient receives pain medication. Figure 9-1 depicts the relationship between validity and reliability. The image in quadrant A represents a situation where the measure is both reliable and valid, meaning that the results are consistent and that it measures what it is intended to measure. Quadrant B illustrates a situation of high reliability without validity; the measure is consistently not measuring what it is intended to measure. High validity with low reliability is displayed in Quadrant C, where this measure would provide a valid, but inconsistent, group estimate. Finally, in Quadrant D there is a situation of both low reliabi lity and validity, meaning that the measure is not consistent and does not measure what it should. Clinical Significance vs Statistical Significance Recent contributions to the emergency medicine literature discuss clinically significant changes in scores obtained with the numerical rating (NRS) and visual analog scales (VAS). When evaluating pain, it is important to consider the difference between clinical and statistical significance in pain score changes. Clinicians should keep in mind that clinically significant changes are those experienced by the patient. A statistically significant change in pain score does not necessarily 56 Analgesia for the Emerg ency Patient [...]... (5): 431 – 438 Seguin D A nurse-initiated pain management advanced triage protocol for ED patients with an extremity injury at a level I trauma center J Emerg Nurs 2004 ;30 (4): 33 0 33 5 Meunier-Sham J, Ryan K Reducing pediatric pain during ED procedures with a nurse-driven protocol: An urban pediatric emergency department’s experience J Emerg Nurs 20 03; 29(2):127– 132 Kelly AM A process approach to improving pain. .. Statistics, vol 37 2, ed U.S Department of Health and Human Services, 2006 2 Tanabe P, Buschmann M A prospective study of ED pain management practices and the patient’s perspective J Emerg Nurs 1999;25 (3) : 171–177 3 Coman M, Kelly A Safety of a nurse-managed, titrated analgesia protocol for the management of severe pain 8 9 10 11 12 13 14 15 in the emergency department Emerg Med 1999;11 (3) : 128– 132 Hwang U,... Acad Emerg Med 20 03; 10(4) :39 0 39 2 5 Berthier F, Potel G, Leconte P, Touze MD, Baron D Comparative study of methods of measuring acute pain intensity in an ED Am J Emerg Med 1998;16(2): 132 – 136 6 Kendrick DB, Strout TD The minimum clinically significant difference in patient-assigned numeric scores for pain Am J Emerg Med 2005; 23( 7):828– 832 7 Acute Pain Management Guideline Panel Acute pain management: Operative... ASSESSMENT PAIN /SEDATION CONSIDERATIONS PAIN /SEDATION MANAGEMENT FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY SCOPE OF THE PPROBLEM The concepts of patient expectation and desired outcomes for patients with acute pain in the emergency department (ED) are surprisingly simple Most patients present to the ED with pain Patients with pain expect pain relief The obvious desired outcome is relief of pain. .. reliable and valid pain measurement instruments emergency clinicians should be familiar with the concepts of reliability and validity in relation to pain scales and should be familiar with the properties of commonly utilized scales (Table 9-2 ) BIBLIOGRAPHY 1 Summers S Evidence-based practice part 2: Reliability and validity of selected acute pain instruments J Perianesth Nurs 2001;16(1) :35 –40 2 Todd KH Pain. .. patient and is thus limited to those who are literate, physically able to use pen and paper, and without Moderate Mood scale Strong Just noticeable Worst mood Best mood Mild Excruciating No pain Severe Weak 2 4 Relief scale Pain scale Least possible pain 1 Worst possible pain No relief of pain Complete relief of pain 3 Figure 9-1 0 MPAC (From Fishman B, Pasternak S, Wallenstein SL, et al The Memorial Pain. .. cancer pain Cancer 1987;60(5):1151–1158 22 Erdek MA, Pronovost PJ Improving assessment and treatment of pain in the critically ill Int J Qual Health Care 2004;16(1):59–64 23 Labus JS, Keefe FJ, Jensen MP Self-reports of pain intensity and direct observations of pain behavior: When are they correlated? Pain 20 03; 102(1–2):109–124 24 Gordon DB, Dahl JL Editorial quality improvement challenges in pain management. .. last 24 hours 0 No Pain 1 2 3 4 5 6 7 8 9 10 Pain As Bad As You Can Imagine 5 Please rate your pain by marking the box beside the number that best describes your pain on the average 0 No Pain 1 2 3 4 5 6 7 8 9 10 Pain As Bad As You Can Imagine 6 Please rate your pain by marking the box beside the number that tolls how much pain you have right now 0 No Pain 1 2 3 4 5 6 7 8 9 10 Pain As Bad As You Can Imagine... assessment and management of pain by triage nurses in Greater London A&E departments Emerg Nurs 2000;8(2):18–24 Boyd R, Stuart P The efficacy of structured assessment and analgesia provision in the paediatric emergency department Emerg Med J 2005;22 :30 32 Campbell P, Dennie M Dougherty K et al Implementation of an ED protocol for pain management at triage at a busy Level I trauma center J Emerg Nurs 2004 ;30 ... treatment of pain has been characterized as a major health problem the joint commission on accreditation of healthcare organizations now mandates assessment and documentation of pain in all patients it has been demonstrated that improved pain assessment and documentation leads to improved pain management for patients Central to the accurate assessment and planning of interventions around pain treatment . Please rate your pain by marking the box beside the number that tolls how much pain you have No Pain No Pain No Pain No Pain 01 234 5678910 01 234 5678910 01 234 5678910 01 234 5678910 Pain As Bad As You. represents your pain. No pain Worst possible pain Figure 9 -3 . VAS. Table 9-1 . Dimensions of pain Pain dimension Description Example of measures Sensory-discriminative dimension Pain location,. distinct COX iso- enzymes (COX-1 and -2 ), one (COX-2) associated mostly with pain and inflammation, raised hope that a new class of analgesics could be developed. These would control pain and inflammation

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