Acute pain medscape


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Acute pain medscape

  1. 1. Acute Pain: Assessment and TreatmentAcute Pain OverviewIn recent decades, technological advances have refined the clinical assessment and managementof adult patients in the acute care setting. However, nurses must rely heavily on knowledge,interviewing techniques, and physical assessment skills to competently assess and managepatients with acute pain, because these skills have not been replaced by technology. Pain is acommon reason for patients to seek healthcare and be admitted to hospitals. According to theNational Center for Health Statistics, 46 million Americans undergo inpatient surgicalprocedures each year and experience acute surgical pain.[1] In 2006, pain was a frequent "chiefcomplaint" for adults who presented to emergency departments (EDs), and pain severity wasreported as moderate to severe by 45% of patients in the ED.[1]Such organizations as the American Society for Pain Management Nursing (ASPMN), theAmerican Pain Society (APS), the American Society of Anesthesiologists (ASA), and theAmerican Society of PeriAnesthesia Nurses (ASPAN) have attempted to improve the quality ofpain management in the United States through formulation and publication of pain-relatedposition statements and clinical practice guidelines.[2-5] Accreditation agencies, such as the JointCommission, have developed standards for the assessment and management of pain.[6] Despiterecognition of the widespread prevalence of pain and increased efforts to promote effective painmanagement, numerous studies document that pain remains inconsistently and inadequatelyaddressed.[7]In a national telephone survey about postoperative pain, 59% of patients reported concern aboutexperiencing postoperative pain and 80% of patients rated acute pain as moderate to severe in thefirst hours to days following surgery.[8]"Pain" is defined by the International Association for the Study of Pain as "an unpleasant sensoryand emotional experience arising from actual or potential tissue damage or described in terms ofsuch damage"[9] Although this is a technical description of pain, it recognizes both thephysiologic and affective nature of the pain experience. Pain is a highly personal, subjectiveexperience which can only be accurately described by the individual who is experiencing pain.Recognition and acceptance of the subjectivity of pain are among the most challenging aspects ofpatient care; concepts that have evolved since 1968 when Margo McCaffery first defined pain as"whatever the person experiencing says it is, existing whenever he says it does."[10,11] Thisdefinition, which has endured for more than 40 years, has allowed healthcare providers tointervene and treat patients on the basis of the self-report of the pain experience. In recent years,definitions of pain have been further refined to include the fact that a persons inability toverbally communicate does not preclude the possibility that pain is present or negate theresponsibility of healthcare providers to treat it.Acute pain is "the normal, predicted physiologic response to an adverse chemical, thermal,or mechanical stimulus ... associated with surgery, trauma, or acute illness."[12] Acute painresults from activation of the pain receptors (nociceptors) at the site of tissue damage. This type 1
  2. 2. of pain generally accompanies surgery, traumatic injury, tissue damage, and inflammatoryprocesses. Acute pain plays the vital role of providing a warning signal that something is wrongand in need of further examination. Acute pain is typically self-limited and resolves over days toweeks, but it can persist for 3 months or longer as healing occurs. Acute pain can activate thesympathetic branch of the autonomic nervous system and produce such responses ashypertension, tachycardia, diaphoresis, shallow respiration, restlessness, facial grimacing,guarding behavior, pallor, and pupil dilation.[11] Although pain in response to tissue damage is anormal phenomenon, it may be associated with significant, unnecessary physical, psychological,and emotional distress.[8,13] Inadequate relief of acute pain can contribute to hypercoagulabilityand impaired immunity, leading to such complications as venous thromboembolic disease andinfections.[14,15] Inadequately controlled acute pain can be a factor in the development of chronicpain,[12,13,15-19] extended hospital stay, readmission, and patient dissatisfaction.[8,20,21]Acute Pain PhysiologyPain is often classified by its pathophysiology into 2 major types: nociceptive and neuropathic.Nociceptive pain involves the normal neural processing of pain that occurs when free nerveendings are activated by tissue damage or inflammation.[10] Neuropathic pain involves theabnormal processing of stimuli from the peripheral or central nervous systems and is thought toserve no useful purpose.[10] Nociception involves the 4 processes of transduction, transmission,perception, and modulation.[10,22] These processes are highly complex, but a simple summary canaid understanding of pain mechanisms and pain interventions. First, tissue damage releaseschemical mediators, such as prostaglandins, bradykinin, serotonin, substance P, and histamine.These substances then activate nociceptors, resulting in transduction, or the generation of anaction potential (an electrical impulse). In the second process -- transmission -- the actionpotential moves from the site of injury along afferent nerve fibers to nociceptors at the spinalcord. Release of substance P and other neurotransmitters carry the action potential across thecleft to the dorsal horn of the spinal cord, from where it ascends the spinothalamic tract to thethalamus and the midbrain. Finally, from the thalamus, fibers send the nociceptive message tothe somatosensory cortex, parietal lobe, frontal lobe, and the limbic system, where the thirdnociceptive process -- perception -- occurs.[11]Perception, the conscious experience of pain, involves both the sensory and affectivecomponents of pain. Clinical research in recent years has yielded greater understanding of thelimbic system at the area of the anterior cingulated gyrus and its role in the emotional response topain.[23] The final nociceptive process -- modulation -- results from activation of the midbrain.Multiple types of neurons from this area that have a variety of neurotransmitters, includingendorphins, enkephalins, serotonin (5-HT), and dynorphin, descend to lower areas in the centralnervous system; these neurons stimulate the release of additional neurotransmitters, whichultimately trigger the release of endogenous opioids and inhibit transmission of the pain impulseat the dorsal horn. Improved understanding of nociception has promoted the development of newtreatment options and enabled the use of various medications and interventions to targetnociceptive processes.[11,22] 2
  3. 3. Assessment of Acute PainAccurate assessment of acute pain is essential for the development of an effective painmanagement plan. Nurses play a pivotal role in the assessment of pain, owing to the nature oftheir relationship with patients. Pain assessment can be challenging because of the subjectivityand multidimensionality of the pain experience. The patients self-report of pain includes thesensory, emotional, psychological, and cultural components of the pain experience, which cannotbe captured on the unidimensional tools typically used in practice.[11] A comprehensive painassessment includes pain location and quality, aggravating and alleviating factors, timing andduration, pain relief and functional goals, and intensity.[10,11] The effectiveness of any previouspain treatment, as well as the effects of pain on quality of life, should also be determined.The comprehensive pain assessment should be performed when patients present with pain to thehealthcare setting and at the onset of new acute pain. To determine treatment effectiveness andguide further interventions, subsequent pain assessments should focus on the nature of the pain,pain intensity, and responses to treatment. Pain assessment tools should be valid and reliable forthe patient population in which they are used.Unidimensional pain intensity scales. Unidimensional scales are quick and easy to use, providerapid feedback about the effectiveness of interventions, and are valid and reliable measures ofpain intensity.[24] Because the unidimensional scales measure only intensity, they cannotsubstitute for a comprehensive pain assessment.[25] The unidimensional pain intensity scales usedmost often in the clinical setting are: • Numeric Rating Scale (NRS), also known as the Numerical Pain Intensity Scale (NPI); • Visual Analog Scale (VAS); and • Verbal Descriptor Scale (VDS).Numeric Rating Scale. The NRS can be used graphically (visually) or verbally.[26] When usedgraphically, the NRS consists of a vertical or horizontal line that is anchored by the number 0 onthe bottom or the left side and the number 10 on the top or the right side. Patients are instructedto rate the intensity of their pain on this scale, with "0" indicating no pain, and "10" indicatingthe worst pain imaginable.Visual Analog Scale. The VAS is a 10-cm (100-mm) line on which the patient is asked to placea mark that corresponds with his or her current pain intensity. The line is then measured from thebeginning to the patients mark, and this distance is translated into a pain intensity score rangingfrom 0 to 10. The format of scale, coupled with the need for a marking implement and for thepatient to be able to clearly visualize and mark the line, make the VAS impractical to use in theclinical setting.Verbal Descriptor Scale. The VDS uses the verbal descriptors "no pain," "mild pain,""moderate pain," "severe pain," "very severe pain," and "worst pain possible." This scale can beadministered verbally or visually, and the patient is instructed to pick the words that bestdescribe his or her current pain intensity.[10,11] 3
  4. 4. Pain assessment in older adults. Older adults deserve special consideration in a discussion ofpain assessment. As the number of older adults in society increases, it is important to understandthe effect of pain on this population and determine the appropriate assessment and managementtechniques. Older adults with mild to moderate cognitive impairment can self-report pain.[27]Many unidimensional pain tools have been tested in older adults, and several of these tools,including the NRS, have been validated for use in this population.[28] In addition to the NRS, theFaces Pain Scale-Revised (FPS-R) and the Iowa Pain Thermometer (IPT) have been validatedfor use with older adults. When compared with other commonly used pain intensity scales (NRS,VAS, VDS, and FPS-R), the IPT was the scale most preferred by both younger and older adults,supporting findings that older adults prefer scales with verbal descriptors.[27]Hierarchy of Importance of Pain MeasuresIn many situations, particularly in the acute care setting, it is not possible to obtain a patient self-report of pain intensity. Patients who are critically ill, sedated, confused, delirious, or otherwisecognitively impaired may be unable to report pain.[10,29,30] The assessment of pain in thispopulation is challenging because no single objective strategy, such as observation of behaviorsor vital signs, provides sufficient information to assess pain. Nurses often rely on heart rate,respiratory rate, blood pressure, and other physiologic data to confirm the presence of pain;however, these variables are the least sensitive indicators of pain and may be affected by manyother factors.In response to this challenge, the ASPMN published a position statement that recommends acomprehensive, hierarchical approach to the assessment of pain in nonverbal patients,[29] whichprovides the framework for a decision-making process that can be used to manage pain innonverbal patients.[10,29] The hierarchical approach has 5 key steps: 1. When possible, obtain self-report. 2. Look for possible pathologies, procedures, or other causes of pain. 3. Observe for behaviors that may indicate the presence of pain. 4. Obtain input from caretakers who know the patient and the patients usual behaviors and responses to pain. 5. Use an analgesic trial and observe for changes in behavior.[10,29,31]Step 1: Patient self-report of pain. The hierarchy affirms that the patients self-report is themost reliable indicator of pain and the sole indicator of pain intensity. Ascertaining the patientsreport of pain should always be attempted first. Reliability of the patients self report maydiminish with advancing cognitive impairment, but many valid and reliable tools are availablethat may be effectively used with cognitively impaired persons. No method has been identified toestablish a patients ability to reliably use a self-report tool; it is therefore helpful to have severaltools available in the clinical setting so that the tool that yields the most consistent results for theindividual patient may be selected. Once identified, this tool should be used at each assessment.[10,29,31]Step 2: Assumption of pain. If a reliable self-report of pain cannot be elicited, the next step inthe hierarchy is to consider whether the patient has a condition that is typically associated with 4
  5. 5. pain or is undergoing procedures that are generally considered painful. In such cases, the nurseshould "assume that pain is present" (abbreviated "APP" for documentation when approved byfacility policy and procedure) and provide the appropriate treatment.[10] It is never appropriate toassume that a patient who is unresponsive, nonverbal, confused, demented, or delirious cannotfeel or is not feeling pain. Similarly, pain must be assumed to be present and treated if the patientwho is receiving paralytics or sedatives has an underlying painful condition or is undergoingpainful procedures.Behavioral indicators of pain. The third step in the hierarchy requires the nurse to observe thepatient for possible indicators of pain, such as grimacing or other indicative facial expressions,bracing, rocking, or changes in activity.[28] Recognizing that certain behaviors may indicate pain,researchers have developed behavioral pain assessment tools for use in patients who cannot self-report. Many of these tools yield a behavioral score that can help determine the presence of pain,and when changes are noted, can be used to evaluate the effectiveness of interventions; however,a behavioral score is not a pain intensity score. If the patient cannot report the intensity of his orher pain, then the intensity is unknown.[32]Tools for pain assessment include: 1. The Critical Care Pain Observation Tool (CPOT) was designed to assess pain in critically ill adults. It uses facial expression, body movement, muscle tension, and ventilator compliance or vocalization as pain indicators.[33] 2. The Payen Behavioral Pain Scale, which uses facial expression, upper extremity movement, and ventilator compliance as pain indicators, may also be used for critically ill adults who are intubated.[34] 3. The Pain Assessment in Advanced Dementia (PAINAD) is used to assess pain in patients who have dementia or Alzheimers disease and are nonverbal.[35] It uses breathing, negative vocalization, facial expression, body language, and consolability as pain measures.City of Hope provides a brief summary and critique of many of the tools that have beendeveloped for the assessment of pain in nonverbal patients. Validity and reliability have not yetbeen fully established for some of these tools. As with pain intensity scales, behavioral toolsshould be used only in the patient populations for which they were intended and in patients whoare able to respond with the requisite behaviors for each tool. Although many tools have beendeveloped to aid in the assessment of pain, the patients self-report of pain intensity remains themost dependable method of pain assessment.[36]Step 4: Solicit information from caregivers and family members. A surrogate who knows thepatients usual behavioral responses can provide input about pain behaviors, which can bevaluable in identifying the patients unique responses to pain.[10,30]Step 5: Analgesic trial. The last step of the hierarchy of measures is an analgesic trial, whichinvolves observing the patients behavior before and after administration of a low dose ofanalgesic medication. An improvement in behaviors after the analgesic dose helps confirm thepresence of pain and serves as the basis for a pain treatment plan. If the patient does not respondto the trial, an increase of the analgesic dose or trial of a different analgesic should be attempted. 5
  6. 6. If the behaviors do not improve despite optimal titration of the analgesic regimen, causes of thebehaviors other than pain should be considered.[30]Treatment of Acute Pain: OverviewProper pain relief in any setting continues to be a major goal but is often elusive. It is incumbentupon the nurse to understand the principles of pain management and to understand and assess foradverse effects of pain-relieving therapies, especially pharmacologic therapies.Several important principles guide the successful management of acute pain.[36,37] Chief amongthese is the need to prevent pain whenever possible by administering analgesics before painoccurs. Another is to try to achieve a level of comfort that allows the patient to functionadequately. For example, in postoperative patients, functional goals may be deep breathing,ambulating, and being able to participate in physical therapy. In patients with chronic pain, goalsmay include going to work or walking the dog. At the end of life, the focus may be to help thepatient enjoy the last moments of life with loved ones. An overriding principle of safe andeffective pain management is to individualize therapy on the basis of the patients uniquecharacteristics.Pain relief can be achieved by pharmacologic and nonpharmacologic measures. Optimal painrelief seems to result from a multimodal approach,[38-42] combining a variety of medications andpossibly nonpharmacologic measures. With multimodal analgesia, also known as "balancedanalgesia," the patient is given 2 or more analgesic agents and/or analgesic measures. Each agentacts by a different mechanism and at a different site in the nervous system. This method providesmaximal pain relief while minimizing adverse effects of any single agent. The analgesic agentsprescribed for a patient will depend on the cause and type of the patients pain and on theindividuals response to treatment.Research has consistently shown great individual variability in response to analgesics. Recentresearch indicates much of this occurs as a result of genetic differences.[36,43-46] A patient mayexperience better pain relief or more adverse effects with a certain opioid or NSAID versusanother opioid or NSAID. If a patient is not experiencing expected relief or is experiencingadverse effects, a trial of another agent in the same analgesic class is warranted.Pain medications can be divided into 3 categories[36]: nonopioid analgesics, opioid analgesics,and coanalgesics (or adjuvant analgesics).To use pain medications correctly, it is important to find out whether the patients pain isconstant or incidental. Constant pain is best treated with an "around the clock" (ATC) regimen;[36,37] by giving the patient medications regularly, an adequate blood level of analgesic can bemaintained. It is best to prevent incidental pain whenever possible by giving an analgesic beforepain develops. For example, administration of pain medication 30-60 minutes before physicaltherapy will help to minimize therapy-associated pain and maximize the patients participation.Pain that increases above the patients controlled baseline level of pain is referred to as"breakthrough pain." Incidental pain can occur as the patients only pain, or it can occur as abreakthrough pain.[10] Patients receiving ATC analgesics for continuous pain and patients with 6
  7. 7. pain that occurs incidentally are provided with short-acting, "as-needed" (PRN) analgesics.Because some patients do not request PRN medication,[37] the nurse must act as a patientadvocate and offer the patient these interventions for pain.Reassessment of the patients response to treatment is paramount. After a patient has been givena medication and/or a nonpharmacologic measure has been used, the nurse must check thepatient in a timely manner (depending on expected time of action of intervention) to assess forthe efficacy of the treatment and for any adverse effects that may have occurred.Nonopioid Pharmacologic TreatmentsNonopioid analgesics include acetaminophen, aspirin, and nonsteroidal anti- inflammatory drugs(NSAIDs). Used individually, these medications are effective for mild to moderate pain. Inconjunction with opioid medications, these agents can have an opioid dose-sparing effect.Lowering the opioid requirement for a patient reduces the potential for opioid-related adverseeffects.Acetaminophen. The mechanism by which acetaminophen (N-acetyl-para-aminophenol) exertsits analgesic effects is unknown.[47] Its potency is similar to that of aspirin, but it does not causedamage to the gastric mucosa.[36] The current dose limit is 4000 mg/day for adults who do nothave liver disease or renal insufficiency.[22,47] Doses exceeding 4000 mg/day can cause hepaticdamage and may cause renal problems. For patients with liver disease, the dose limit is 2000 mg/day.[47] The nurse must be aware of all sources from which the patient is receivingacetaminophen; for example, acetaminophen is included in combination opioid/nonopioidmedications, such as Percocet® (oxycodone/acetaminophen) or Fioricet®(acetaminophen/butalbital/caffeine). The nurse should notify the prescriber and not administerdoses that exceed the daily limit.Aspirin. Aspirin, or acetylsalicylic acid, is an NSAID that was discovered almost a centuryearlier than other NSAIDs.[48] Aspirin, like other NSAIDs, exerts its analgesic action byinhibiting prostaglandin synthesis.[49] Aspirin irreversibly inhibits platelet aggregation and canalso cause gastrointestinal distress and mucosal damage. For these reasons, acetaminophen isused more often than aspirin, especially in the hospital and postoperative setting when bleedingmight be a major concern. Some patients have important hypersensitivity reactions to aspirin,including bronchospasm and anaphylaxis.[22,49] Aspirin is effective for mild and possibly formoderate pain, and it is used in conjunction with opioids to treat moderate to severe pain. Likeacetaminophen, aspirin can be found in combination pills, such as Percodan®(oxycodone/aspirin) or Fiorinal® (aspirin/butalbital/caffeine). The maximum dose for adults is4000 mg/day.[49] Exceeding the daily dose can result in acetylsalicylic acid toxicity, which canaffect the liver, kidneys, and central nervous system.[22]NSAIDs. Similar to acetaminophen and aspirin, NSAIDs provide opioid dose-sparing effects.[41]NSAID medications exert their analgesic effects by interfering with the inflammatory response.[22,36,39] They are especially useful for pain caused by surgery, infection, or trauma. NSAIDsinhibit the cyclooxygenase (COX) enzyme, reducing the synthesis of prostaglandins.Cyclooxygenase has 2 known forms: COX-1 and COX-2. The earlier (traditional) NSAIDs 7
  8. 8. interfere with both forms of the enzyme. As a result of COX-1 inhibition, traditional NSAIDscan cause platelet inhibition, gastric mucosal irritation, and renal blood flow compromise.[22,36,50]COX-2 inhibition is responsible for the desired effects of reducing pain and inflammation.Newer NSAIDs (COX-2 agents) selectively block COX-2. Because the effects of COX-1 are notinhibited, platelet function is maintained with COX-2 inhibitors. Likewise, the gastric mucosalprotective effects of COX-1 are not impeded. Thus, fewer untoward gastrointestinal effects occurwith COX-2 selective agents than with traditional NSAIDs.[36] However, COX-2 agents are nosafer for the kidneys than nonselective agents and have been associated with prothromboticeffects.[36] All NSAIDs, including COX-2 agents, have a "ceiling effect"[22,36,50] beyond which nofurther analgesic action will be exerted, but exceeding that dose will produce more adverseeffects. Aspirin and acetaminophen also have ceiling effects.The nurse should be aware of NSAID-related risks and should address concerns with theprescriber if a traditional NSAID is ordered for a patient who is receiving anticoagulation, whohas renal compromise, or who has a known allergy or sensitivity to aspirin or other NSAIDs.Response to a particular anti-inflammatory agent is highly individual: If one NSAID does notwork for a patient, another might be effective.All nonopioid medications can be given orally. Acetaminophen, aspirin, and some NSAIDs arealso available as suppositories for rectal administration. The NSAIDs ketorolac and ibuprofenare available in a parenteral form for intravenous administration. Some NSAIDs are available intopical forms, either as a cream or a patch.Opioid Pharmacologic TreatmentsOpioid analgesics act by binding to and activating specific receptor sites in the central andperipheral nervous systems.[36,51,52] Once these receptor sites are activated, pain signaltransmission is blocked through several mechanisms, producing analgesia. The first-line opioidanalgesics, such as morphine, fentanyl, hydromorphone, and oxycodone, are µ (mu) agonistopioids because they bind primarily to the µ opioid receptors to produce both wanted (analgesia)and unwanted (adverse) effects. The µ agonist opioids are the cornerstone of moderate to severeacute pain management and are added to nonopioids as part of a multimodal treatment approach.Opioid analgesics. Morphine is considered the gold standard of opioid analgesics,[53] althoughmilligram for milligram, morphine is not the most potent of these drugs. Opioid medications areavailable in combination with nonopioid: for example, oxycodone/acetaminophen (Percocet®)and hydrocodone/ibuprofen (Vicoprofen®). The maximum daily recommended dose of thenonopioid in these combination products makes them appropriate only for management of mildto moderate acute pain.[36] In contrast, with the exception of codeine, which may be limited byside effects, there are no ceiling doses for µ agonist-only agents; dose titration can continue untiladequate pain relief is achieved or intolerable and unmanageable adverse effects occur. Opioidscommonly used to treat moderate to severe acute pain include morphine, fentanyl, oxycodone,and hydromorphone.Two opioid medications require particular mention: Meperidine and propoxyphene have fallenout of favor in recent years. Both medications have metabolites that are neurotoxic and can cause 8
  9. 9. serious detrimental effects,[22,36,52] including seizures. Because so many alternative analgesics areavailable, many facilities had elected to remove these drugs from their formularies. As ofNovember 19, 2010, the FDA asked that propoxyphene be removed from the US marketaltogetherOpioid analgesics are available in several formulations and can be administered by a variety ofroutes, the most common of which are oral, subcutaneous, and intravenous (IV). Oral opioids areavailable in short-acting and long-acting (modified, controlled, or extended-release) preparations.Parenteral formulations of opioids are available for subcutaneous, intramuscular, or intravenousadministration. Intravenous patient-controlled analgesia allows patients to manage their pain byself-administering opioid doses and is one of the most commonly used methods to treat acutepain, particularly postoperative pain. Preservative-free preparations are available for epidural andintrathecal delivery.[54] These preparations can be administered as single injections or in solutionsfor epidural analgesia, with or without the capability for patient-controlled analgesia.Intramuscular injections are no longer recommended for the management of any type of pain.The American Pain Society[36] describes the disadvantages of intramuscular opioid injections,noting that they are painful and have highly variable absorption, with a 30- to 60-minute lag topeak effect.Adverse effects of opioid analgesics. Patients should be assessed systematically for adverseeffects during opioid therapy and, if these are present, treated with appropriate therapies. Themost common adverse effects of opioids are nausea, vomiting, pruritus, constipation, andsedation.[22,36,43] Whenever possible, these adverse effects should be prevented. For example, astool softener plus a laxative should be administered to prevent constipation as soon as thepatient can take oral medications. With the exception of constipation, opioid adverse effects aredose-related. Thus, that the best way to treat an adverse effect is to reduce the dose of the opioid.The lowest effective dose should always be administered; use of a multimodal approach to painmanagement makes this easier. For example, an opioid dose-sparing effect is produced whennonopioid analgesics are routinely added to the opioid treatment plan. Another measure toconsider is rotation to a different opioid.[36] A negative response by a patient to a certain opioiddoes not guarantee the same response to other opioids.One of the most dangerous adverse effects of opioid analgesics is respiratory depression.[22,36,55]Assessment of the patients respiratory status should be performed regularly, particularly duringthe first 24 hours of opioid therapy. A comprehensive respiratory assessment includes countingrespiratory rate and evaluating the regularity of rhythm, depth, and sound of respirations. Snoringis a sign of respiratory obstruction and must be attended to promptly with position changes andperhaps a respiratory therapy consultation and evaluation for the presence of sleep apnea.Changes from baseline respiratory status should be noted and discussed with the prescriber asindicated.Sedation is a sensitive indicator of respiratory depression.[55] Therefore, in conjunction withregular respiratory assessments, routine and systematic assessment of the degree of patientsedation is vital. Reducing the opioid dose when deepening sedation is detected can aidsubstantially in preventing respiratory depression. Opioid orders should include the expectationthat nurses will reduce or skip the opioid dose if a patient is significantly sedated. The prescriber 9
  10. 10. is then contacted for further orders. Such tools such as the Pasero Opioid-induced Sedation Scale(POSS), which is specifically designed to assess opioid-induced sedation during theadministration of opioids for pain management, are recommended and have been shown to bevalid and reliable for this purpose.[55-57]If respiratory depression develops, the nurse must be familiar with proper administration of the µreceptor antagonist naloxone (Narcan®), which will reverse the sedating and respiratorydepressant effects of µ receptor agonist opioids.[39] The aim of treatment with naloxone is toreverse respiratory depression and sedation without reversing analgesia. Therefore, the drugshould be diluted (0.4 mg in 10 mL saline) and administered in small doses frequently (every 1to 2 minutes), until the patients respiratory status improves and the patient starts to arouse.[36] Ofnote, the duration of action of naloxone is shorter than that of most opioid analgesics, andanother dose may be needed after initial administration. Close monitoring of the patient isnecessary to determine whether additional doses or a continuous infusion of naloxone is needed,and monitoring should continue until the patient is maintained at a stable, acceptable sedationlevel.Pharmacologic Treatments: Coanalgesics/Adjuvant AnalgesicsCoanalgesics, as described by the American Pain Society,[36] are a diverse group of medicationsthat enhance the effects of typical analgesic medications or provide analgesia for certain types ofpain. The types and number of coanalgesics are extensive. Local anesthetics, muscle relaxants,and certain anticonvulsants will be discussed here.Local anesthetics. Local anesthetics, including Xylocaine® (lidocaine), ropivacaine (Naropin®),and bupivacaine (Marcaine®), block sodium ion channels to prevent the conduction of nerveimpulses.[22,37,50,58] Local anesthetics are also available as creams and gels for topical application.A transdermal patch formulation of lidocaine, Lidoderm®, has a US Food and DrugAdministration-approved indication for the treatment of postherpetic neuralgia.[59] Several studiesfrom the past 10 years, as well as individual reports, have found the lidocaine 5% patch to besafe and effective for the treatment of postoperative pain,[60,61] acute headache,[62] andexacerbations of osteoarthritis.[63,64] The patch should be applied to intact skin over the painfularea and left on for several hours. Although the manufacturer recommends that the patch beplaced for 12 hours on and 12 hours off during any 24-hour period, recent research has shownthat the application of up to 4 patches at a time, for as long as 24 hours per day, is safe for mostadults.[65,66] Topical formulations are used primarily for dermal analgesia.Local anesthetics can also be infused near the spinal cord (intrathecal, epidural) or nearperipheral nerves (perineural)[58,67] or into surgical incision sites. Intravenous lidocaine issometimes used to treat refractory acute pain.Adverse effects can occur with local anesthetics and are usually dose-related. These includesensory and motor deficits when these agents are administered regionally or intraspinally.Neurologic or mental status change may signify systemic toxicity from increasing blood levels ofmedication. Dizziness, confusion, circumoral numbness, metallic taste, and seizures are some ofthe signs that suggest neurotoxicity.[50,67] Potential cardiovascular reactions include dysrhythmias; 10
  11. 11. [50 52] hypotension; and, if severe, cardiovascular collapse.[50] Allergic reactions to localanesthetics can occur but are rare; the prescriber should be notified immediately if a patient has arash, urticaria, or any difficulty breathing during use of local anesthetics.[50]Muscle relaxants. Skeletal muscle relaxants derive from several different drug classes,including benzodiazepines, antihistamines, and sedatives.[36,50] They are not considered effectiveanalgesics; benzodiazepines are analgesic only for pain associated with muscle spasm.[36]Depending on class, these drugs may be administered orally, parenterally, or rectally insuppository form. Mechanisms of action vary and are often nonspecific. All of these medicationsare associated with the adverse effect of sedation. The risk for respiratory depression is increasedin patients receiving concurrent muscle relaxants and opioid medications. The patients degree ofsedation and respiratory status must be carefully monitored.Anticonvulsants. Antiepileptic drugs are a group of diverse medications, each of which has adifferent mechanism of action.[36] Anticonvulsants are used primarily to treat persistentneuropathic pain, especially pain of a stabbing, shooting, or electric-like quality.[22] However,numerous studies have demonstrated an opioid dose-sparing effect of the anticonvulsantsgabapentin (Neurontin®) and pregabalin (Lyrica®) in the perioperative period[51,68-75] and ofgabapentin in the treatment of acute burns[76] Anticonvulsants act by stabilizing nervemembranes, reducing excitability, and reducing spontaneous neuronal firing.[22,36] They may havea role in the prevention of persistent postsurgical pain syndromes, such as postthoracotomy andpostmastectomy pain. Anticonvulsants can also be sedating,[22,36] and caution is required whenthey are administered concurrently with opioid medications.Miscellaneous medicationsTramadol (Ultra®) is a dual-mechanism analgesic. It binds to µ receptors and it also weaklyinhibits norepinephrine and serotonin reuptake,[77] which is believed to augment pain signaltransmission inhibition.Tapentadol (Nucynta®),[78] a newer medication, is considered an opioid agonist and binds to theµ receptor. Unlike other opioid medications, except tramadol, its µ receptor activity issupplemented by its inhibition of norepinephrine reuptake, believed to enhance the inhibition ofpain signal transmission.Methadone is a µ agonist opioid. However, it is also an N-methyl-D-aspartate (NMDA)antagonist[36,51] and produces excellent pain relief for some patients. Because methadone has avery long half-life, caution must be used in its administration and dosage adjustments must bemade slowly. It should be prescribed only by providers with substantial experience with its use.With proper monitoring, methadone can be a very effective analgesic for patients with difficultto control pain.Ketamine is an NMDA antagonist[37] that can also be used to provide analgesia. The use ofketamine at analgesic doses (doses much smaller than those used to induce anesthesia) and forparticular populations seems to be increasing. Because it lowers opioid requirements, ketamine isgenerally used in the postoperative setting for patients who require very high doses of opioids. 11
  12. 12. Patients who may have extensive opioid requirements include those with a history of long-termopioid use as a result of chronic pain, those with a history of heroin addiction, and those withneuropathic type pain that does not respond well to opioids. Use of ketamine may have beenlimited by reports of its psychotomimetic adverse effects, including hallucinations andnightmares.[36,37] However, a recent qualitative review of 11 studies[79] of ketamine administeredconcurrently with intravenous morphine demonstrated no significant increase in the risk foradverse effects with use of ketamine.Nonpharmacologic Treatment of PainNonpharmacologic therapies are as important as medications in relieving pain. They involvephysical modalities, such as acupuncture, massage, positioning, deep breathing, and applicationof heat or cold, and psychosocial modalities, such as distraction, biofeedback, and imagery.Nurses should be familiar with these essential treatments. A full discussion of these therapies isbeyond the scope of this article, so the reader is encouraged to seek further information on thistopicConclusionIf left untreated, acute pain can result in numerous negative physiologic and psychologicalsequelae to patients. As patient advocates, nurses must learn how to properly assess pain andhow to optimize safe pain management for all patients in their care. 12