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Acute Pain: Assessment and Treatment

Elsa Wuhrman, MS, FNP, Maureen F. Cooney, DNP, FNP Jan 03, 2011

Acute Pain Overview

In recent decades, technological advances have refined the clinical assessment and management of adult
patients in the acute care setting. However, nurses must rely heavily on knowledge, interviewing techniques,
and physical assessment skills to competently assess and manage patients with acute pain, because these
skills have not been replaced by technology. Pain is a common reason for patients to seek healthcare and be
admitted to hospitals. According to the National Center for Health Statistics, 46 million Americans undergo
inpatient surgical procedures each year and experience acute surgical pain.[1] In 2006, pain was a frequent
"chief complaint" for adults who presented to emergency departments (EDs), and pain severity was reported as
moderate to severe by 45% of patients in the ED.[1]

Such organizations as the American Society for Pain Management Nursing (ASPMN), the American Pain
Society (APS), the American Society of Anesthesiologists (ASA), and the American Society of PeriAnesthesia
Nurses (ASPAN) have attempted to improve the quality of pain management in the United States through
formulation and publication of pain-related position statements and clinical practice guidelines.[2-5] Accreditation
agencies, such as the Joint Commission, have developed standards for the assessment and management of
pain.[6] Despite recognition of the widespread prevalence of pain and increased efforts to promote effective pain
management, numerous studies document that pain remains inconsistently and inadequately addressed.[7]

In a national telephone survey about postoperative pain, 59% of patients reported concern about experiencing
postoperative pain and 80% of patients rated acute pain as moderate to severe in the first hours to days
following surgery.[8]

"Pain" is defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional
experience arising from actual or potential tissue damage or described in terms of such damage"[9] Although
this is a technical description of pain, it recognizes both the physiologic and affective nature of the pain
experience. Pain is a highly personal, subjective experience 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 of patient 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] This definition,
which has endured for more than 40 years, has allowed healthcare providers to intervene 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 person's inability to verbally communicate does not preclude the possibility that pain is
present or negate the responsibility 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 pain results from activation of the pain
receptors (nociceptors) at the site of tissue damage. This type of pain generally accompanies surgery, traumatic
injury, tissue damage, and inflammatory processes. Acute pain plays the vital role of providing a warning signal
that something is wrong and in need of further examination. Acute pain is typically self-limited and resolves over
days to weeks, but it can persist for 3 months or longer as healing occurs. Acute pain can activate the
sympathetic branch of the autonomic nervous system and produce such responses as hypertension,
tachycardia, diaphoresis, shallow respiration, restlessness, facial grimacing, guarding behavior, pallor, and pupil
dilation.[11] Although pain in response to tissue damage is a normal phenomenon, it may be associated with
significant, unnecessary physical, psychological, and emotional distress.[8,13] Inadequate relief of acute pain
can contribute to hypercoagulability and impaired immunity, leading to such complications as venous
thromboembolic disease and infections.[14,15] Inadequately controlled acute pain can be a factor in the

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development of chronic pain,[12,13,15-19] extended hospital stay, readmission, and patient dissatisfaction.[8,20,21]

Acute Pain Physiology

Pain 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 nerve endings are activated by tissue
damage or inflammation.[10] Neuropathic pain involves the abnormal processing of stimuli from the peripheral or
central nervous systems and is thought to serve 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 can aid understanding of pain mechanisms and pain interventions. First, tissue damage releases
chemical mediators, such as prostaglandins, bradykinin, serotonin, substance P, and histamine. These
substances then activate nociceptors, resulting in transduction, or the generation of an action potential (an
electrical impulse). In the second process -- transmission -- the action potential moves from the site of injury
along afferent nerve fibers to nociceptors at the spinal cord. Release of substance P and other
neurotransmitters carry the action potential across the cleft to the dorsal horn of the spinal cord, from where it
ascends the spinothalamic tract to the thalamus and the midbrain. Finally, from the thalamus, fibers send the
nociceptive message to the somatosensory cortex, parietal lobe, frontal lobe, and the limbic system, where the
third nociceptive process -- perception -- occurs.[11]

Perception, the conscious experience of pain, involves both the sensory and affective components of pain.
Clinical research in recent years has yielded greater understanding of the limbic system at the area of the
anterior cingulated gyrus and its role in the emotional response to pain.[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, including endorphins, enkephalins, serotonin (5-HT), and dynorphin, descend to lower
areas in the central nervous system; these neurons stimulate the release of additional neurotransmitters, which
ultimately trigger the release of endogenous opioids and inhibit transmission of the pain impulse at the dorsal
horn. Improved understanding of nociception has promoted the development of new treatment options and
enabled the use of various medications and interventions to target nociceptive processes.[11,22]

Assessment of Acute Pain

Accurate assessment of acute pain is essential for the development of an effective pain management plan.
Nurses play a pivotal role in the assessment of pain, owing to the nature of their relationship with patients. Pain
assessment can be challenging because of the subjectivity and multidimensionality of the pain experience. The
patient's self-report of pain includes the sensory, emotional, psychological, and cultural components of the pain
experience, which cannot be captured on the unidimensional tools typically used in practice.[11] A
comprehensive pain assessment includes pain location and quality, aggravating and alleviating factors, timing
and duration, pain relief and functional goals, and intensity.[10,11] The effectiveness of any previous pain
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 the healthcare
setting and at the onset of new acute pain. To determine treatment effectiveness and guide 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 for the patient population in which they are used.

Unidimensional pain intensity scales. Unidimensional scales are quick and easy to use, provide rapid
feedback about the effectiveness of interventions, and are valid and reliable measures of pain intensity.[24]
Because the unidimensional scales measure only intensity, they cannot substitute for a comprehensive pain
assessment.[25] The unidimensional pain intensity scales used most often in the clinical setting are:

Numeric Rating Scale (NRS), also known as the Numerical Pain Intensity Scale (NPI);

Visual Analog Scale (VAS); and

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Verbal Descriptor Scale (VDS).

Numeric Rating Scale. The NRS can be used graphically (visually) or verbally.[26] When used graphically, the
NRS consists of a vertical or horizontal line that is anchored by the number 0 on the bottom or the left side and
the number 10 on the top or the right side. Patients are instructed to rate the intensity of their pain on this scale,
with "0" indicating no pain, and "10" indicating the worst pain imaginable.

Visual Analog Scale. The VAS is a 10-cm (100-mm) line on which the patient is asked to place a mark that
corresponds with his or her current pain intensity. The line is then measured from the beginning to the patient's
mark, and this distance is translated into a pain intensity score ranging from 0 to 10. The format of scale,
coupled with the need for a marking implement and for the patient to be able to clearly visualize and mark the
line, make the VAS impractical to use in the clinical 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 be administered verbally or visually, and the
patient is instructed to pick the words that best describe his or her current pain intensity.[10,11]

Pain assessment in older adults. Older adults deserve special consideration in a discussion of pain
assessment. As the number of older adults in society increases, it is important to understand the effect of pain
on this population and determine the appropriate assessment and management techniques. 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, the Faces Pain Scale-Revised (FPS-R) and the Iowa Pain Thermometer
(IPT) have been validated for 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 Measures

In 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 otherwise cognitively impaired may be
unable to report pain.[10,29,30] The assessment of pain in this population is challenging because no single
objective strategy, such as observation of behaviors or 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
many other factors.

In response to this challenge, the ASPMN published a position statement that recommends a comprehensive,
hierarchical approach to the assessment of pain in nonverbal patients,[29] which provides the framework for a
decision-making process that can be used to manage pain in nonverbal 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 patient's 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 patient's self-report is the most reliable
indicator of pain and the sole indicator of pain intensity. Ascertaining the patient's report of pain should always

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be attempted first. Reliability of the patient's self report may diminish with advancing cognitive impairment, but
many valid and reliable tools are available that may be effectively used with cognitively impaired persons. No
method has been identified to establish a patient's ability to reliably use a self-report tool; it is therefore helpful
to have several tools available in the clinical setting so that the tool that yields the most consistent results for the
individual 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 in the hierarchy is
to consider whether the patient has a condition that is typically associated with pain or is undergoing procedures
that are generally considered painful. In such cases, the nurse should "assume that pain is present"
(abbreviated "APP" for documentation when approved by facility policy and procedure) and provide the
appropriate treatment.[10] It is never appropriate to assume that a patient who is unresponsive, nonverbal,
confused, demented, or delirious cannot feel or is not feeling pain. Similarly, pain must be assumed to be
present and treated if the patient who is receiving paralytics or sedatives has an underlying painful condition or
is undergoing painful procedures.

Behavioral indicators of pain. The third step in the hierarchy requires the nurse to observe the patient 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 or her 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 Alzheimer's 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 been developed for the
assessment of pain in nonverbal patients. Validity and reliability have not yet been fully established for some of
these tools. As with pain intensity scales, behavioral tools should be used only in the patient populations for
which they were intended and in patients who are able to respond with the requisite behaviors for each tool.
Although many tools have been developed to aid in the assessment of pain, the patient's self-report of pain
intensity remains the most dependable method of pain assessment.[36]

Step 4: Solicit information from caregivers and family members. A surrogate who knows the patient's usual
behavioral responses can provide input about pain behaviors, which can be valuable in identifying the patient's
unique responses to pain.[10,30]

Step 5: Analgesic trial. The last step of the hierarchy of measures is an analgesic trial, which involves
observing the patient's behavior before and after administration of a low dose of analgesic medication. An
improvement in behaviors after the analgesic dose helps confirm the presence of pain and serves as the basis
for a pain treatment plan. If the patient does not respond to the trial, an increase of the analgesic dose or trial of
a different analgesic should be attempted. If the behaviors do not improve despite optimal titration of the
analgesic regimen, causes of the behaviors other than pain should be considered.[30]

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Treatment of Acute Pain: Overview

Proper pain relief in any setting continues to be a major goal but is often elusive. It is incumbent upon the nurse
to understand the principles of pain management and to understand and assess for adverse effects of
pain-relieving therapies, especially pharmacologic therapies.

Several important principles guide the successful management of acute pain.[36,37] Chief among these is the
need to prevent pain whenever possible by administering analgesics before pain occurs. Another is to try to
achieve a level of comfort that allows the patient to function adequately. 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, goals may include going to work or walking the dog. At the end of life, the focus may
be to help the patient enjoy the last moments of life with loved ones. An overriding principle of safe and effective
pain management is to individualize therapy on the basis of the patient's unique characteristics.

Pain relief can be achieved by pharmacologic and nonpharmacologic measures. Optimal pain relief seems to
result from a multimodal approach,[38-42] combining a variety of medications and possibly nonpharmacologic
measures. With multimodal analgesia, also known as "balanced analgesia," the patient is given 2 or more
analgesic agents and/or analgesic measures. Each agent acts by a different mechanism and at a different site in
the nervous system. This method provides maximal pain relief while minimizing adverse effects of any single
agent. The analgesic agents prescribed for a patient will depend on the cause and type of the patient's pain and
on the individual's response to treatment.

Research has consistently shown great individual variability in response to analgesics. Recent research
indicates much of this occurs as a result of genetic differences.[36,43-46] A patient may experience better pain
relief or more adverse effects with a certain opioid or NSAID versus another opioid or NSAID. If a patient is not
experiencing expected relief or is experiencing adverse 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 patient's pain is constant 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 be maintained. It is best to prevent incidental pain whenever
possible by giving an analgesic before pain develops. For example, administration of pain medication 30-60
minutes before physical therapy will help to minimize therapy-associated pain and maximize the patient's
participation. Pain that increases above the patient's controlled baseline level of pain is referred to as
"breakthrough pain." Incidental pain can occur as the patient's only pain, or it can occur as a breakthrough
pain.[10] Patients receiving ATC analgesics for continuous pain and patients with 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 patient advocate and offer the patient these interventions for pain.

Reassessment of the patient's response to treatment is paramount. After a patient has been given a medication
and/or a nonpharmacologic measure has been used, the nurse must check the patient in a timely manner
(depending on expected time of action of intervention) to assess for the efficacy of the treatment and for any
adverse effects that may have occurred.

Nonopioid Pharmacologic Treatments

Nonopioid analgesics include acetaminophen, aspirin, and nonsteroidal anti- inflammatory drugs (NSAIDs).
Used individually, these medications are effective for mild to moderate pain. In conjunction 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 adverse effects.

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Acetaminophen. The mechanism by which acetaminophen (N-acetyl-para-aminophenol) exerts its analgesic

effects is unknown.[47] Its potency is similar to that of aspirin, but it does not cause damage to the gastric
mucosa.[36] The current dose limit is 4000 mg/day for adults who do not have liver disease or renal insufficiency.
[22,47]
Doses exceeding 4000 mg/day can cause hepatic damage 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 receiving acetaminophen; for example, acetaminophen is included in combination opioid/nonopioid
medications, such as Percocet® (oxycodone/acetaminophen) or Fioricet® (acetaminophen/butalbital/caffeine).
The nurse should notify the prescriber and not administer doses that exceed the daily limit.

Aspirin. Aspirin, or acetylsalicylic acid, is an NSAID that was discovered almost a century earlier than other
NSAIDs.[48] Aspirin, like other NSAIDs, exerts its analgesic action by inhibiting prostaglandin synthesis.[49]
Aspirin irreversibly inhibits platelet aggregation and can also cause gastrointestinal distress and mucosal
damage. For these reasons, acetaminophen is used more often than aspirin, especially in the hospital and
postoperative setting when bleeding might 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 for
moderate pain, and it is used in conjunction with opioids to treat moderate to severe pain. Like acetaminophen,
aspirin can be found in combination pills, such as Percodan® (oxycodone/aspirin) or Fiorinal® (aspirin/butalbital
/caffeine). The maximum dose for adults is 4000 mg/day.[49] Exceeding the daily dose can result in
acetylsalicylic acid toxicity, which can affect 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. NSAIDs inhibit the cyclooxygenase (COX)
enzyme, reducing the synthesis of prostaglandins. Cyclooxygenase has 2 known forms: COX-1 and COX-2.
The earlier (traditional) NSAIDs interfere with both forms of the enzyme. As a result of COX-1 inhibition,
traditional NSAIDs can 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 not inhibited, platelet
function is maintained with COX-2 inhibitors. Likewise, the gastric mucosal protective effects of COX-1 are not
impeded. Thus, fewer untoward gastrointestinal effects occur with COX-2 selective agents than with traditional
NSAIDs.[36] However, COX-2 agents are no safer for the kidneys than nonselective agents and have been
associated with prothrombotic effects.[36] All NSAIDs, including COX-2 agents, have a "ceiling effect"[22,36,50]
beyond which no further analgesic action will be exerted, but exceeding that dose will produce more adverse
effects. Aspirin and acetaminophen also have ceiling effects.

The nurse should be aware of NSAID-related risks and should address concerns with the prescriber if a
traditional NSAID is ordered for a patient who is receiving anticoagulation, who has 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 not work for a patient, another might be effective.

All nonopioid medications can be given orally. Acetaminophen, aspirin, and some NSAIDs are also available as
suppositories for rectal administration. The NSAIDs ketorolac and ibuprofen are available in a parenteral form
for intravenous administration. Some NSAIDs are available in topical forms, either as a cream or a patch.

Opioid Pharmacologic Treatments

Opioid analgesics act by binding to and activating specific receptor sites in the central and peripheral nervous
systems.[36,51,52] Once these receptor sites are activated, pain signal transmission is blocked through several
mechanisms, producing analgesia. The first-line opioid analgesics, such as morphine, fentanyl, hydromorphone,
and oxycodone, are µ (mu) agonist opioids 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 severe acute 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] although milligram for

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milligram, morphine is not the most potent of these drugs. Opioid medications are available in combination with
nonopioid: for example, oxycodone/acetaminophen (Percocet®) and hydrocodone/ibuprofen (Vicoprofen®). The
maximum daily recommended dose of the nonopioid in these combination products makes them appropriate
only for management of mild to moderate acute pain.[36] In contrast, with the exception of codeine, which may
be limited by side effects, there are no ceiling doses for µ agonist-only agents; dose titration can continue until
adequate pain relief is achieved or intolerable and unmanageable adverse effects occur. Opioids commonly
used to treat moderate to severe acute pain include morphine, fentanyl, oxycodone, and hydromorphone.

Two opioid medications require particular mention: Meperidine and propoxyphene have fallen out of favor in
recent years. Both medications have metabolites that are neurotoxic and can cause serious detrimental effects,
[22,36,52]
including seizures. Because so many alternative analgesics are available, many facilities had elected
to remove these drugs from their formularies. As of November 19, 2010, the FDA asked that propoxyphene be
removed from the US market altogether

Opioid analgesics are available in several formulations and can be administered by a variety of routes, the most
common of which are oral, subcutaneous, and intravenous (IV). Oral opioids are available in short-acting and
long-acting (modified, controlled, or extended-release) preparations. Parenteral formulations of opioids are
available for subcutaneous, intramuscular, or intravenous administration. Intravenous patient-controlled
analgesia allows patients to manage their pain by self-administering opioid doses and is one of the most
commonly used methods to treat acute pain, particularly postoperative pain. Preservative-free preparations are
available for epidural and intrathecal delivery.[54] These preparations can be administered as single injections or
in solutions for 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 to peak effect.

Adverse effects of opioid analgesics. Patients should be assessed systematically for adverse effects during
opioid therapy and, if these are present, treated with appropriate therapies. The most common adverse effects
of opioids are nausea, vomiting, pruritus, constipation, and sedation.[22,36,43] Whenever possible, these adverse
effects should be prevented. For example, a stool softener plus a laxative should be administered to prevent
constipation as soon as the patient can take oral medications. With the exception of constipation, opioid adverse
effects are dose-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 pain management
makes this easier. For example, an opioid dose-sparing effect is produced when nonopioid analgesics are
routinely added to the opioid treatment plan. Another measure to consider is rotation to a different opioid.[36] A
negative response by a patient to a certain opioid does 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 patient's respiratory status should be performed regularly, particularly during the first 24 hours of opioid
therapy. A comprehensive respiratory assessment includes counting respiratory rate and evaluating the
regularity of rhythm, depth, and sound of respirations. Snoring is a sign of respiratory obstruction and must be
attended to promptly with position changes and perhaps 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 as indicated.

Sedation is a sensitive indicator of respiratory depression.[55] Therefore, in conjunction with regular respiratory
assessments, routine and systematic assessment of the degree of patient sedation is vital. Reducing the opioid
dose when deepening sedation is detected can aid substantially in preventing respiratory depression. Opioid
orders should include the expectation that nurses will reduce or skip the opioid dose if a patient is significantly
sedated. The prescriber 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 the
administration of opioids for pain management, are recommended and have been shown to be valid and reliable
for this purpose.[55-57]

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If respiratory depression develops, the nurse must be familiar with proper administration of the µ receptor
antagonist naloxone (Narcan®), which will reverse the sedating and respiratory depressant effects of µ receptor
agonist opioids.[39] The aim of treatment with naloxone is to reverse respiratory depression and sedation
without reversing analgesia. Therefore, the drug should be diluted (0.4 mg in 10 mL saline) and administered in
small doses frequently (every 1 to 2 minutes), until the patient's respiratory status improves and the patient
starts to arouse.[36] Of note, the duration of action of naloxone is shorter than that of most opioid analgesics,
and another dose may be needed after initial administration. Close monitoring of the patient is necessary 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 sedation level.

Pharmacologic Treatments: Coanalgesics/Adjuvant Analgesics

Coanalgesics, as described by the American Pain Society,[36] are a diverse group of medications that enhance
the effects of typical analgesic medications or provide analgesia for certain types of pain. 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 nerve impulses.[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 Drug Administration-approved indication for the treatment of
postherpetic neuralgia.[59] Several studies from the past 10 years, as well as individual reports, have found the
lidocaine 5% patch to be safe and effective for the treatment of postoperative pain,[60,61] acute headache,[62]
and exacerbations of osteoarthritis.[63,64] The patch should be applied to intact skin over the painful area and
left on for several hours. Although the manufacturer recommends that the patch be placed for 12 hours on and
12 hours off during any 24-hour period, recent research has shown that the application of up to 4 patches at a
time, for as long as 24 hours per day, is safe for most adults.[65,66] Topical formulations are used primarily for
dermal analgesia.

Local anesthetics can also be infused near the spinal cord (intrathecal, epidural) or near peripheral nerves
(perineural)[58,67] or into surgical incision sites. Intravenous lidocaine is sometimes used to treat refractory
acute pain.

Adverse effects can occur with local anesthetics and are usually dose-related. These include sensory and motor
deficits when these agents are administered regionally or intraspinally. Neurologic or mental status change may
signify systemic toxicity from increasing blood levels of medication. Dizziness, confusion, circumoral numbness,
metallic taste, and seizures are some of the signs that suggest neurotoxicity.[50,67] Potential cardiovascular
reactions include dysrhythmias;[50 52] hypotension; and, if severe, cardiovascular collapse.[50] Allergic reactions
to local anesthetics can occur but are rare; the prescriber should be notified immediately if a patient has a rash,
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 effective analgesics;
benzodiazepines are analgesic only for pain associated with muscle spasm.[36] Depending on class, these
drugs may be administered orally, parenterally, or rectally in suppository form. Mechanisms of action vary and
are often nonspecific. All of these medications are associated with the adverse effect of sedation. The risk for
respiratory depression is increased in patients receiving concurrent muscle relaxants and opioid medications.
The patient's degree of sedation and respiratory status must be carefully monitored.

Anticonvulsants. Antiepileptic drugs are a group of diverse medications, each of which has a different
mechanism of action.[36] Anticonvulsants are used primarily to treat persistent neuropathic pain, especially pain
of a stabbing, shooting, or electric-like quality.[22] However, numerous studies have demonstrated an opioid
dose-sparing effect of the anticonvulsants gabapentin (Neurontin®) and pregabalin (Lyrica®) in the perioperative
period[51,68-75] and of gabapentin in the treatment of acute burns[76] Anticonvulsants act by stabilizing nerve

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membranes, reducing excitability, and reducing spontaneous neuronal firing.[22,36] They may have a role in the
prevention of persistent postsurgical pain syndromes, such as postthoracotomy and postmastectomy pain.
Anticonvulsants can also be sedating,[22,36] and caution is required when they are administered concurrently
with opioid medications.

Miscellaneous medications

Tramadol (Ultra®) is a dual-mechanism analgesic. It binds to µ receptors and it also weakly inhibits
norepinephrine and serotonin reuptake,[77] which is believed to augment pain signal transmission inhibition.

Tapentadol (Nucynta®),[78] a newer medication, is considered an opioid agonist and binds to the µ receptor.
Unlike other opioid medications, except tramadol, its µ receptor activity is supplemented by its inhibition of
norepinephrine reuptake, believed to enhance the inhibition of pain 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 a very long half-life, caution must be
used in its administration and dosage adjustments must be made 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 difficult to control pain.

Ketamine is an NMDA antagonist[37] that can also be used to provide analgesia. The use of ketamine at
analgesic doses (doses much smaller than those used to induce anesthesia) and for particular populations
seems to be increasing. Because it lowers opioid requirements, ketamine is generally used in the postoperative
setting for patients who require very high doses of opioids. Patients who may have extensive opioid
requirements include those with a history of long-term opioid use as a result of chronic pain, those with a history
of heroin addiction, and those with neuropathic type pain that does not respond well to opioids. Use of ketamine
may have been limited by reports of its psychotomimetic adverse effects, including hallucinations and
nightmares.[36,37] However, a recent qualitative review of 11 studies[79] of ketamine administered concurrently
with intravenous morphine demonstrated no significant increase in the risk for adverse effects with use of
ketamine.

Nonpharmacologic Treatment of Pain

Nonpharmacologic therapies are as important as medications in relieving pain. They involve physical modalities,
such as acupuncture, massage, positioning, deep breathing, and application of 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 is beyond the scope of this article, so the reader is encouraged
to seek further information on this topic

Conclusion

If left untreated, acute pain can result in numerous negative physiologic and psychological sequelae to patients.
As patient advocates, nurses must learn how to properly assess pain and how to optimize safe pain
management for all patients in their care.

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Topics in Advanced Practice Nursing eJournal. 2011;11(1) © 2011 WebMD, LLC

Cite this article: Elsa Wuhrman, Maureen F. Cooney. Acute Pain: Assessment and
Treatment. Medscape. Jan 03, 2011.

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