EMERGENCY SEDATION AND PAIN MANAGEMENT - PART 3 doc

COX-2 inhibitors are superior to placebo and equivalent toCOX-1 inhibitors in acute postoperative dental pain,postoperative orthopedic pain, primary dysmenorrheal,and osteoarthritis.. At

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 (Table8-3)

DRUG INTERACTIONS

Oral anticoagulants The antiplatelet effects of NSAIDs

added to the anticoagulant 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 ACEinhibitors may impair renal function and impair theantihypertensive effects of ACE inhibitors

Diuretics Avoid using NSAIDs in patients who aretaking diuretics They have a greater risk of developingrenal failure because of NSAID-mediated, decreased renalblood flow Also, the natriuretic response to diureticsdepends in part on prostaglandin-mediated vasodilatation.Glucocorticoids Patients on corticosteroids will haveincreased risk of PUD Addition of NSAIDs should beused cautiously, if at all

Lithium NSAIDs enhance lithium reabsorption andmay directly reduce lithium excretion, leading toincreased lithium levels Central nervous system (CNS)symptoms (drowsiness, confusion, vertigo, convulsions,

or tremors), cardiac dysrhythmias, and QRS wideningare warnings of lithium toxicity The lithium dosageshould be reduced when adding an NSAID is necessary.Methotrexate Chronic coadministration of NSAIDsand methotrexate have resulted in prolonged, elevatedblood levels of methotrexate, resulting in severe toxicity

A possible mechanism may be the decreased renal fusion caused by NSAIDs, decreasing the elimination ofmethotrexate

per-COMMENTS AND CONTROVERSIES.NSAIDs combine algesia and anti-inflammatory effects with low abusepotential and much different side effects than theopioids Oral NSAIDs can be as effective as oral opioids.Parenteral NSAIDs have been shown to be as effective asopioids in some settings However, parenteral NSAIDs

an-do not appear to work better or faster than oral NSAIDs

Table 8-2 Risk of GI effects of nonselective

NSAIDS

Intermediate risk Aspirin, indomethacin, naproxen,

sulindac, ibuprofen 800 mg

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

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

pro-thrombotic effects from greater inhibition of

prostacy-clin 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

tradi-tional 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 tivity In vitro, it would appear that there are very sig-nificant differences between the different types of agent(COX-1/COX-2 enzyme activity reduction ratio is 0.1for indomethacin, as compared with 28,000 for valde-coxib) In vivo, however, the selectivity does not appear

ac-to significantly decrease COX-2 inhibiac-tors’ effects on GImucosa, renal function, and platelets as compared toCOX-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 toCOX-1 inhibitors in acute postoperative dental pain,postoperative orthopedic pain, primary dysmenorrheal,and osteoarthritis There are no studies comparingCOX-2 inhibitors’ efficacy in renal colic, biliary colic,acute gout, headache syndromes, sickle cell crisis, oracute musculoskeletal or soft-tissue injury At this point,there is no evidence that COX-2 inhibitors are signifi-cantly more effective than their COX-1 counterparts forthe management of acute pain in the ED

DRUG INTERACTIONSNonselective NSAIDs COX-2 inhibitors should not becombined with NSAIDs because of their similar phar-macological effects The exception would be ASA forcardioprotection, which is especially important in thecontext of possible COX-2 inhibitor-associated cardio-vascular events

Interactions that are similar to those of nonselectiveNSAIDs COX-2 inhibitors have similar interactions asNSAIDs with ACE inhibitors, antihypertensive agents,anticoagulants, and lithium (see above)

Antacids Antacids that contain magnesium or minum reduce COX-2 inhibitor plasma concentrationsand may decrease the agent’s clinical effects

alu-Fluconazole Fluconazole inhibits cytochrome 2C9 isoenzyme and cause increased side effects fromCOX-2 agents due to decreased metabolism andincreased blood levels of these agents

P450-Sulfoamide allergy Celecoxib has a similar structure tothe sulfonamides, and cross-reactive hypersensitivity

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

tra-ditional NSAIDs

Endoscopic, clinically asymptomatic ulcers, not

as-sociated 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

metabo-lized to valdecoxib It is the first IV/IM COX-2 inhibitor

available in North America A 20 mg dose has beenshown to provide a similar amount and duration ofanalgesia to ketorolac (30–60 mg) and lasts longer than

IV morphine (4 mg)

COMMENTS AND CONTROVERSIES.COX-2 inhibitors havenot been studied in the ED for use in acute pain syn-dromes or acute-on-chronic pain exacerbation Most ofthe studies describe adverse events that tend to occurafter a much longer duration of therapy than is eitherused in the ED or prescribed upon discharge home.Though evidence suggests that they are as effective inacute pain as traditional NSAIDs and may be bettertolerated, they are generally much more expensive.The risk of serious cardiovascular events constitutes asignificant deterrent to their long-term use

OpioidsTitrated intravenous opioids are the mainstay of phar-macological management of acute pain The beneficialeffects of opioids have been well documented for cen-turies, as have its toxicity and potential for abuse Fear ofinducing addition has led to underuse of opioids bymany physicians However, many studies have shownthat short-term use of opioid analgesics for acute painsyndromes is not associated with future dependence

PharmacologyOpioids bind to several different classes of receptorslocated throughout the nervous system and suppressneuronal pain transmission peripherally, at the spinalcord, and in the thalamus They also act to modify theperception of pain at the level of the cortex There arethree main opioid receptors: mu, kappa, and delta Mureceptors mediate euphoria, sedation, respiratorydepression, 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

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

func-tion, 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 medications, even under

ap-propriate 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

par-ticular 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

man-agement of acute severe pain Morphine,

hydro-morphone, 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 administration, 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

ad-ministered 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 paincontrol is achieved when serum levels reach a steadystate: requiring five half-lives Repeating doses at thesame period as the half-life after initial titration is aneffective way to relieve continuous pain Prescribingrepeat analgesic doses, rather than ‘‘as needed,’’ is themost effective way to accomplish pain relief

The treatment of pain should start by prescribingshorter-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, delayedrelease, or transdermal formulations to begin paintreatment will result in achieving peak serum medica-tion levels long after the initiation of therapy, whichmay result in the patients receiving too large a dose in

an attempt to expeditiously achieve pain relief, or toosmall a dose in anticipation of subsequently higherlevels (see Table8-5)

Specific AgentsMorphineIntravenous morphine is the first choice for treatment

of acute severe pain in ED patients (Table 8-5) It istypically started at 0.1 mg/kg IV and can be repeatedevery 5 min at 0.05 mg/kg until pain is relieved Oraladministration of morphine can be an effective option formoderate or severe outpatient pain, but only 20% of theingested dose reaches the tissues after first-pass metabo-lism, and this delayed onset makes titration difficult

A common misperception is that morphine causesmore smooth muscle spasm than other narcotics andshould be avoided in patients with biliary or renal colic.There is neither any evidence to support this conceptnor any that shows superior efficacy of any other nar-cotic over morphine in these situations

Morphine is chiefly metabolized by conjugation into athree-conjugate and six-conjugate form The three-conjugate form has no opioid analgesic activity and hasbeen associated with significant CNS side effects (tre-mors, myoclonic jerks, delirium, and seizures) if notcleared by the kidneys; this presents a greater risk inelderly patients and those with renal insufficiency Thesix-conjugate form is made in less abundance than thethree-conjugate form and has an opioid analgesicpotency that is much stronger than that of morphine Itplays an important role in morphine’s efficacy

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

metab-olized 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

com-pared 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 the 1920s It is the p-450 metabolite of

hydrocodone It is conjugated primarily into several

inac-tive 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 equivalent metabolite in morphine

Hydromorphone is similar to oxycodone and

mor-phine in its analgesic effects and adverse effects Its

primary indications are in patients who are allergic tomorphine or have renal or hepatic disease

Hydromorphone is available as an injectable solutionand its oral tablets come in 1, 2, 4, and 8 mg strengths.There is also a 3 mg rectal suppository Oral doses are4–8 mg PO q3–4 hr; IM doses are 1–2 mg q 3–4 hr, IVdosing is 0.015 mg/kg mg every 5 min titrated to painrelief A sustained release oral hydromorphone formula-tion was recently pulled from the market due to reportedoverdose potential when combined with alcohol

FentanylFentanyl is a synthetic opioid that is excellent for rapidtitration analgesia in acute, severe pain It is highly li-pophilic and produces analgesia within 1–2 min of IVinfusion It also redistributes rapidly and its duration ofaction is only 30–60 min It is metabolized by the p-450system into inactive metabolites Drug accumulationand toxicity may occur after tissue saturation following aprolonged infusion, but this is unlikely to happen dur-ing acute therapy

Fentanyl releases less histamine than morphine and

is associated with fewer peripheral effects It is morefrequently associated with respiratory depression withregular use than morphine, and patients receivinginfusions of the drug should be monitored with obser-vation or pulse oximetry Fentanyl’s short duration ofaction makes it ideal for use in patients who requireserial examinations

Fentanyl is available in IV form, as well as the flavored transmucosal lozenges (200, 400, 600, 800, 1,200,and 1,600 mcg) Duragesic patches are used forsustained release of fentanyl in chronic pain patients, butshould not be used in the management of acute pain

raspberry-OxycodoneOxycodone is a strong opioid agonist It is widelyavailable in combination with acetaminophen or aspirin

as well as by itself It is also available in long-acting oralformulations It has a very high bioavailability relative tothe other opioids and is quickly and efficiently absorbed.This has led to an association with abuse Oxycodone isnot available in a parenteral form in the United States,although studies have found its IV form to be equia-nalgesic to morphine

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

hydro-morphone It provides greater pain relief when

com-bined 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

mor-phine and other metabolites

Approximately 10% of the population metabolizes

codeine poorly and experiences toxicity (nausea,

consti-pation, 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 isoften prescribed for cough suppression

Codeine is available as codeine syrup (5 mg/ml),codeine tablets (15, 30, 60 mg), and as an injection ofcodeine phosphate (15, 30, and 60 mg/ml) Tylenol withcodeine syrup is also available (12.5 mg codeine with

120 mg acetaminophen per 5 ml)

TramadolTramadol is a synthetic compound that is a selective muagonist It is chemically unrelated to the morphine-likeopioids It is metabolized in the liver by the cytochromeP-450 system One of its metabolites, M1, has an evengreater mu-receptor affinity than tramadol and has anelimination half-life of 9 hr Tramadol also appears tohave effects on GABA and serotonin receptors and couldtheoretically precipitate serotonin syndrome if admin-istered with SSRIs

Tramadol, as a selective mu agonist, should not causephysiologic dependence as the other opioids do Since itsrelease, however, it has been associated with abuse andwithdrawal similar to that of other opioids, but at lowenough rate that, after a review in 1998, its status as anunscheduled drug was maintained

Tramadol has been found to be an efficacious painmedication at low doses At increasing doses, it isassociated with nausea and vomiting, limiting its use tolow doses Tramadol 37.5 mg combined with acet-aminophen 325 mg was found to have similar efficacy tohydrocodone 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 patientswith epilepsy

Tramadol is available in oral tablets of 50 mg,recommended dose is 50–100 mg every 4 hr It is alsoavailable in combination with acetaminophen, 37.5 mg/

325 mg

FOLLOW-UP/CONSULTATIONCONSIDERATIONS

A patient who has received opioid medications for acutepain syndromes should be discharged in the company of

a responsible, competent adult who will provide and

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

treat-ment 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

anal-gesic 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

post-operative 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 andother risk factors for excessive warfarin anticoagulation.JAMA 1998;279:657–662

5 Lipsky PE, Brooks P, Crofford LJ, et al Unresolved issues

in the role of cyclooxygenase–2 in normal physiologicprocesses and disease Arch Intern Med 2000;160:913–920

6 Turturro MA, Paris PM, Seaberg DC Intramuscularketorolac versus oral ibuprofen in acute musculoskeletalpain Ann Emerg Med 1995;26:117–120

7 Loewen PS Review of the selective COX-2 inhibitorscelecoxib and refocoxib: Focus on clinical aspects Can JEmerg Med 2002;4:268–275

8 Mukherjee D, Nissen SE, Topol E Risk of cardiovascularevents associated with selective COX-2 inhibitors JAMA2001;286:954–959

9 Joranson DE, Ryan KM, Gilson AM, et al Trends inmedical use and abuse of opioid analgesics JAMA2000:283(13): 1710–1714

10 Jovey RD Opioid analgesics In Managing pain, ed RDJovey 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 criticalreview Am J Ther 2002;9:53–68

12 Weiner AL Meperidine as a potential cause of serotoninsyndrome in the emergency department Acad Emerg Med1999;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 doseoxycodone and oxycodone plus acetaminophen for acutepostoperative pain Cochrane Database Syst Rev2000;4: CD002763

15 Turturro MA, Paris PM, Yealy DM, et al Hydrocodone vscodeine in acute musculoskeletal pain Ann Emerg Med1991;20:1100–1103

16 Silverstein F, Faich G, Goldstein J, et al Gastrointestinaltoxicity with celecoxib versus non-steroidal anti-inflammatory drugs for osteoarthritis and rheumatoidarthritis JAMA 2000;234:1247–1255

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

ReliabilityValidityClinical Significance vs Statistical SignificanceUnidimensional vs Multidimensional ScalesPAIN SCALES

Unidimensional Pain ScalesNRS

VASVerbal descriptor scale (VDS)The Wong-Baker FACES Pain ScaleThe FACES Pain Scale

Multidimensional Pain ScalesThe Preverbal, Early Verbal Pediatric Pain ScaleThe 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

depart-ment (ED) environdepart-ment 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 ASSESSMENTThere are multiple barriers to the clinical assessment ofpain, including, but not limited to, provider biases,patient anxiety, family attitudes, cultural beliefs, andprovider suspicion of ‘‘drug-seeking’’ behavior TheNational Institutes of Health has stated that patient self-report is the most reliable indicator of the existence andintensity of pain Barriers to pain assessment are greatestfor those patient populations who cannot self-reporttheir pain experience

Pediatric patients and those with impaired cognitioncommunicate 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 these 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 findings in a

con-sistent 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, cognitive 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

uni-dimensional and multiuni-dimensional 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

instru-ments, 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 thatclinicians should consider when choosing a pain ratingtool This refers to the ability of two independentobservers to use the same scale at the same time toobserve the same patient and obtain the same result

ValidityValidity is concerned with the extent to which a toolactually measures what it is intended to measure Threeprimary types of validity are described in the literature:content validity, construct validity, and predictivevalidity Evidence of content validity examines the ex-tent to which the tool includes the major elements rel-evant to what is being measured Construct validity isconcerned with the degree of agreement between aparticular measure and other measures that evaluate thesame concept, for example, the degree of agreementbetween two separate pain scales Predictive validityaddresses the ability to predict future outcome on thebasis of the score provided the given instrument Here,

we would expect that a score would indicate lower painintensity after a patient receives pain medication.Figure 9-1 depicts the relationship between validityand reliability The image in quadrant A represents asituation where the measure is both reliable and valid,meaning that the results are consistent and that itmeasures what it is intended to measure Quadrant Billustrates a situation of high reliability without validity;the measure is consistently not measuring what it isintended to measure High validity with low reliability isdisplayed in Quadrant C, where this measure wouldprovide a valid, but inconsistent, group estimate Finally,

in Quadrant D there is a situation of both low reliabilityand validity, meaning that the measure is not consistentand does not measure what it should

Clinical Significance vs Statistical SignificanceRecent contributions to the emergency medicine litera-ture discuss clinically significant changes in scoresobtained with the numerical rating (NRS) and visualanalog scales (VAS) When evaluating pain, it is im-portant to consider the difference between clinical andstatistical significance in pain score changes Cliniciansshould keep in mind that clinically significant changesare those experienced by the patient A statisticallysignificant change in pain score does not necessarily

indicate a change that is meaningful in the life of a

patient Additional research in this area is needed to

further elucidate the relevance of pain score changes

during clinical management

Unidimensional vs Multidimensional Scales

Melzack and Casey have proposed that there are three

distinct dimensions of the pain experience that are

assessable: the sensory-discriminative dimension, the

affective-motivational dimension, and the

cognitive-evaluative dimension Unidimensional scales are

those that measure only one of these pain dimensions,

usually pain intensity as a component of the

sensory-discriminative dimension Multidimensional scales

attempt to measure the affective-motivational and

cognitive-evaluative dimensions of the pain experience,

in addition to the sensory dimension An example of aunidimensional scale is the NRS whereas the McGillPain Questionnaire (MPQ) is a multidimensional scalemeasuring all three pain dimensions Table9-1describesMelzack and Casey’s pain dimensions with examples ofscale measures

PAIN SCALESUnidimensional Pain ScalesNRS

NRSs consist of a range of numbers and are mostfrequently a 11-point (0–10) or 101-point (0–100) scale.With these instruments, a patient is simply told that 0represents ‘‘no pain’’ and 10 or 100 represents ‘‘the worstpossible’’ or ‘‘unbearable’’ pain The clinician then asks

Figure 9-1 Reliability vs validity.

the patient to choose a number that represents their

current pain intensity Many hospitals use the NRS in

rating pain as it offers several advantages including ease of

administration and scoring, multiple response options,

and no reported age-related difficulties in its utilization

Although the NRS is commonly administered verbally, it

may be administered in written form as well Figure9-2

depicts the 11-point NRS in its written format

VAS

The VAS is a 10-cm horizontal line anchored with a

written pain descriptor at each end The left-hand end of

the line is labeled ‘‘no pain,’’ whereas the opposing end

is labeled ‘‘worst possible pain’’ or ‘‘worst pain

imag-inable.’’ Here, a clinician shows the image to the patient

and asks the patient to make a vertical mark on the line

at the area that best represents their current pain

in-tensity The clinician then measures the distance from

the left-hand anchor to the patient’s mark

Although the VAS has been used extensively in

re-search and has been shown to be both reliable and valid

in the clinical setting, its disadvantages are that it can only

be used in its written form, it requires two steps to score,and the tool may be rendered invalid if multiple photo-copies of it are made Figure9-3represents the VAS

Verbal descriptor scale (VDS)Verbal descriptor or rating scales (VDS or VRS) aresimple scales made up of a list of phrases or adjectivesdescribing pain intensity, from least to most intense.Each phrase or descriptor is assigned a number andpatients are asked to choose the descriptor that mostaccurately describes their current pain intensity Thepatient’s pain score is the number associated with theirchosen descriptor or phrase Although many verbalscales exist, one of the most common in clinical practice

is the four-point scale labeled with the descriptors,

‘‘none,’’ ‘‘mild,’’ ‘‘moderate,’’ and ‘‘severe.’’ The point VDS is displayed in Figure9-4

four-In addition to describing pain intensity, similar scalesmay be used to assess a patient’s degree of pain relief,with common descriptors being ‘‘none,’’ ‘‘slight,’’

No pain 0 1 2 3 4 5 6 7 8 9 10 Worst possible pain

Figure 9-2 NRS.

Indicate the severity of your pain on the line above

Place a single mark through the line at the point that best

represents your pain.

No

pain

Worst possible pain

Figure 9-3 VAS.

Table 9-1 Dimensions of pain

‘‘moderate,’’ ‘‘lots,’’ and ‘‘complete.’’ Although VDSs

are simple to administer to patients who are literate and

without cognitive impairment, some researchers believe

that the small number of descriptor choices can limit the

precision of the instrument

The Wong-Baker FACES Pain Scale

The Wong-Baker FACES Pain Rating Scale is a pictorial

scale consisting of a series of six drawn faces with

expressions indicating the range of pain intensity from

no pain (no hurt) to the worst pain (worst hurt) Each

face is assigned a number from zero to five indicating

increasing pain intensity

A standard set of instructions explaining the meaning

of each face is included with the scale, and clinicians are

asked to read these instructions to the patient Following

the instructions, the clinician asks the patient to choose

the face that best describes how they are feeling Figure9-5

displays the Wong-Baker FACES Pain Rating Scale

Originally designed for use with school-aged children,

the FACES Scale has been studied extensively and is now

considered reliable and valid for toddler through

ado-lescent age children There is evidence to suggest validity

in adult, older adult, and cognitively impaired

popula-tions Additionally, this scale has been translated into

many different languages including Spanish, French,Italian, Portuguese, Romanian, Bosnian, Vietnamese,Japanese, Chinese, and German

The FACES Pain ScaleAnother commonly employed pictorial scale is theFACES Pain Scale, also referred to as the Bieri Scale Likethe Wong-Baker FACES Pain Rating Scale, Bieri’s FACESScale consists of a series of drawn faces representing thecontinuum from no pain to severe pain Patients areshown the scales faces and are asked to choose the facebest representing their pain state One key differencebetween the Wong-Baker and Bieri FACES scales is thatthe latter includes a neutral face as the ‘‘no pain’’ anchor

It has been suggested that a smiling face as an anchorcould potentially lead to the confusion of pain andhappiness Another key difference is the absence of tears

on the ‘‘most pain’’ Bieri face Some have felt that thepresence of tears may introduce bias for people fromcultures where crying in response to pain is not accept-able, or for male patients who may not be comfortablechoosing a face with tears to represent their pain.Figure9-6 represents the FACES Pain Scale

Like the Wong-Baker Scale, the Bieri Scale has beenshown to be reliable and valid in a wide variety of age

0

No hurt

1 Hurts little bit

2 Hurts little more

3 Hurts even more

4 Hurts whole lot

5 Hurts worst

Figure 9-5 The Wong-Baker FACES Pain Rating Scale (From Hockenberry MJ, Wilson D, Winkelstein ML Wong’s essentials of pediatric nursing, 7th edn St Louis, MO: Mosby, 2005, p 1259 Used with permission Copyright Mosby.)

Instructions: Explain to the person that each face is for a person who feels happy because he has no pain (hurt) or sad because he has some or a lot of pain Face 0 is very happy because he doesn’t hurt at all Face 1 hurts just a little bit Face 2 hurts a little more Face 3 hurts even more Face 4 hurts a whole lot Face 5 hurts as much as you can imagine, although you don’t have to be crying to feel this bad Ask the person to choose the face that best describes how he is feeling.

Figure 9-6 The FACES Pain Scale (From Bieri D, Reeve RA, Champion GD, Addicoat L, Ziegler JB The Faces Pain Scale for the assessment of the severity of pain experienced by children: Development, initial validation, and preliminary investigation for ratio scale properties Pain 1990;41(2):144 Used with permission.)

groups, from toddlers to older adults The FACES Pain

Scale has also been used successfully with patients who

are cognitively impaired

Multidimensional Pain Scales

The Preverbal, Early Verbal Pediatric Pain Scale

Designed specifically for toddlers who are not yet to be

able to self-report their pain experiences using tools

such as the Wong-Baker FACES Pain Rating Scale, the

Modified Pre-Verbal, Early Verbal Pediatric Pain Scale

(M-PEPPS) is an important tool for clinicians who work

with this age group The full version of the PEPPS scalecontains seven assessment categories: heart rate, facial,cry (audible/visible), consolability/state of restfulness,body posture, sociability, and sucking/feeding

The scale authors modified these original categoriesfor use in the ED by eliminating the heart rate andsucking/feeding category as providers of emergency carewere concerned that elevated heart rate in febrile orscared toddlers and no oral intake status or the presence

of nausea in emergency patients would erroneouslyaffect pain scores in this population The modified

facial expression

Grimace, brows drawn together;

eyes partially closed, squinting

Severe grimace;

brows lowered, tightly drawn together;

eyes tightly closed

Sustained crying

Screaming

Consolability/State

of Restfulness

Pleasant, well integrated

Distractible, easy to console, intermittent fussiness

Able to console, distract with difficulty, intermittent restlessness, irritability

Unable to console, restlessness, sustained movement

rest, relaxed positioning

Clenched fists, curled toes and/or reaching for, touching wound or area

Localization with extension or flexion or stiff and non-moving

Intermittent or

sustained movement with our without periods of rigidity

Sustained arching, flailing, thrashing, and/or kicking

to voice and/or touch, makes eye contact and/or smiles, easy to obtain or maintain;

sleeping

With effort, responds to voice and/or touch, makes eye contact but difficult to obtain or maintain

Absent eye contact, no response to voice and/or touch

Total Score:

Figure 9-7 M-PEPPSª (From Schultz AA, Murphy E, Morton J, Stempel A, Messenger-Rioux C, Bennett K Perverbal, early verbal pediatric pain scale (PEPPSª): Development and early psychometric testing J Pediatr Nurs 1999;14(1):19–27 Used with permission of the author and Elsevier.)

version of the scale has been found to be reliable and

valid in ED pediatric patients

The M-PEPPS is displayed in Figure9-7 To score the

M-PEPPS, the emergency clinician observes the patient’s

behavior in each of the five categories, scoring each categoryand then summing the categories for a total score Theobservation period for the scale varies from patient topatient, but can typically be accomplished with under

CRIES Score Parameter 0 1 2

Requires Oxygen for

Coding Tips for Using CRIES

Crying The characteristic cry of pain is high-pitched

If no cry or cry which is not high-pitched, score 0

If cry high pitched but baby is easily consoled, score 1

If cry is high pitched and baby is inconsolable, score 2

If HR and BP are both unchanged or less than baseline, score 0

If HR or BP are increased by increase is <20% of baseline, score 1

If HR or BP are increased by increase is >20% over baseline, score 2

Expression The facial expression most often associated with pain is a grimace This may

be characterized by: brow lowering, eyes squeezed shut, deepening of the naso-labial furrow, open lips and mouth.

If no grimace is present, score 0

If grimace alone is present, score 1

If grimace and non cry vocalization grunt is present, score 2

Sleepless This parameter is scored based upon the infant’s state during the hour

preceding this recorded score.

If the child has been continuously asleep, score 0

If he/she has awakened at frequent intervals, score 1

If he/she has been awake constantly, score 2

Figure 9-8 The CRIES Scale (From Krechel SW, Bildner J CRIES: A new neonatal postoperative pain measurement score Initial testing of validity and reliability Pediatr Anesth 1995;5:53–61 Used with permission of Blackwell Publishing.)