Acute Pain Assessment and Treatment

7/9/2014 www.medscape.
com/viewarticle/735034_print
http://www.medscape.com/viewarticle/735034_print 1/14
www.medscape.com

January 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assessment skills to competently assess and manage patients with acute pain, because these skills have not been
replaced by technology.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]
Acute Pain: Assessment and Treatment
Elsa Wuhrman, MS, FNP, Maureen F. Cooney, DNP, FNP
7/9/2014 www.medscape.com/viewarticle/735034_print
Inadequately controlled acute pain can be a factor in the 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
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 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]
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.
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 (mu) agonist opioids because they bind primarily to the opioid receptors to produce both wanted
(analgesia) and unwanted (adverse) effects. The 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
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 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]
If respiratory depression develops, the nurse must be familiar with proper administration of the receptor antagonist
naloxone (Narcan
), which will reverse the sedating and respiratory depressant effects of 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 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 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 receptor. Unlike
other opioid medications, except tramadol, its receptor activity is supplemented by its inhibition of norepinephrine
reuptake, believed to enhance the inhibition of pain signal transmission.
Methadone is a 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.
References
1. Centers for Disease Control and Prevention. National Center for Health Statistics. FastStats. Inpatient
Surgery. 2010. Available at: http://www.cdc.gov/nchs/fastats/insurg.htm Accessed December 16, 2010.
2. American Society for Pain Management Nursing. Position Papers. Available at:
http://www.aspmn.org/Organization/position_papers.htm Accessed December 16, 2010.
3. American Pain Society. Clinical Practice Guidelines. Available at: http://www.ampainsoc.org/ Accessed
December 21, 2010.
4. American Society of Anesthesiologists. Practice Parameters. Available at:
http://www.asahq.org/publicationsAndServices/practiceparam Accessed December 21, 2010.
5. American Society of PeriAnesthesia Nurses. Clinical Guidelines. Available at: http://www.aspan.org/
Accessed December 16, 2010.
6. Joint Commission on Accreditation of Healthcare Organizations. Implementing the new pain management
standards. Oakbrook Terrace, Ill.: JCAHO; 2000.
7. Gordon DB, Pellino TA, Miaskowski C, et al. A 10- year review of quality improvement monitoring in pain
management: Recommendations for standardized outcome measure. Pain Manag Nurs. 2001;3:116-130.
8. Apfelbaum JL, Chen C, Mehta SS, Gan TJ. Postoperative pain experience: results from a national survey
suggest postoperative pain continues to be undermanaged. Anesth Analg. 2003;97:534-540. Abstract
9. International Association for the Study of Pain. IASP proposed taxonomy change. 2008. Available at:
http://www.iasp-pain.org/AM/Template.cfm?
Section=Home&Template=/CM/ContentDisplay.cfm&ContentID=6633 Accessed December 21, 2010.
10. Pasero C, McCaffery M. Pain Assessment and Pharmacologic Management. St. Louis, Mo: Mosby; 2011.
11. Sipos Cox D, Karapas ET. Taxonomy for pain management nursing. In: St. Marie B, ed. Core Curriculum for
Pain Management Nursing. 2nd ed. Dubuque, Ia: Kendall Hunt Professional; 2010.
12. Carr DB, Goudas LC. Acute pain. Lancet. 1999;353:2051-2058. Abstract
13. Joshi GP, Ogunnaike BO. Consequences of inadequate postoperative pain relief and chronic persistent
postoperative pain. Anesthesiol Clin North Am. 2005;23:21-36.
14. Dunwoody CJ, Krenzischek DA, Pasero C, Rathmell JP, Polomano RC. Assessment, physiological
monitoring, and consequences of inadequately treated acute pain. Pain Manag Nurs. 2008;9(1 Suppl):11-21.
15. Rosenfeld BA, Faraday N, Campbell D, Dise K, Bell W, Goldschmidt P. Hemostatic effects of stress hormone
infusion. Anesthesiology. 1994;81:1116-1126. Abstract
16. Desai PM. Pain Management and pulmonary dysfunction. Crit Care Clin. 1999;15:151-166. Abstract
17. Callesen B., Kehlet H. Prospective study of chronic pain after hernia repair. Br J Surg. 1999;86:1528-1531.
Abstract
18. Keller SM, Carp NZ, Levy MN, Rosen SM. Chronic post thoracotomy pain. J Cardiovasc Surg. 1994;35:161-
164.
19. Wallace MS, Wallace AM, Lee J, Dobke MK. Pain after breast surgery: a survey of 282 women. Pain
1996;66:195-205.
20. Gupta A, Daigle S, Mojica J, Hurley RW. Patient perception of pain care in hospitals in the United States. J
Pain Res. 2009;2:157-164
21. Roth W, Kling J, GockelI I. Dissatisfaction with post-operative pain management - a prospective analysis of
1071 patients. Acute Pain. 2005;7:75-83
22. Arnstein P. Clinical Coach for Effective Pain Management. Philadelphia, Pa: F.A. Davis Company; 2010.
23. Shyu BC, Vogt BA. Short-term synaptic plasticity in the nociceptive thalamic-anterior cingulate pathway. Mol
Pain. 2009;5:51- 71. Abstract
24. Jensen MP. The validity and reliability of pain measures in adults with cancer. J Pain. 2003;4:2-21. Abstract
25. Taylor S, Voytovich AE, Kozol RA. Has the pendulum swung too far in postoperative pain control? Am J Surg.
2003;186:472-475.
26. Flaherty SA. Pain measurement tools for clinical practice and research. AANA J. 1996;64:133-140. Abstract
27. Herr K. Pain in the older adult. Pain Manag Nurs 2010;11(Suppl 2):S2-S10.
28. Herr K, Spratt KF, Garand L, Li L. Evaluation of the Iowa Pain Thermometer and other selected pain intensity
scales in younger and older adult cohorts using controlled clinical pain: a preliminary study. Pain Med.
2007;8:585-600. Abstract
29. Herr K, Coyne PJ, Key T, et al. Pain assessment in the nonverbal patient: position statement with clinical
practice recommendations. Pain Manag Nurs. 2006;7:44-52. Abstract
30. Pasero C. Challenges in pain assessment. J Perianesth Nurs. 2009;24:50-54. Abstract
31. Bjoro K, Herr K. Assessment of pain in the nonverbal or cognitively impaired older adult. Clin Geriatr Med.
2008;24:237-262. Abstract
32. Pasero C, McCaffery M. No self-report means no pain-intensity rating. Assessing pain in patients who cannot
provide a report. Am J Nurs. 2005;105:50-53.
33. Glinas C, Johnston C. Pain assessment in the critically ill ventilated adult: validation of the critical-care pain
observation tool and physiologic indicators. Clin J Pain. 2007;23:497-505. Abstract
34. Payen J, Bru O, Bosson J, et al. Assessing pain in critically ill sedated patients by using a behavioral pain
scale. Crit Care Med. 2001;29:2258-2263. Abstract
35. Hutchison RW, Tucker Jr. WF, Kim S, Gilder R. Evaluation of a behavioral assessment tool for the individual
unable to self- report pain. Am J Hosp Palliat Care 2006;23:328-331.
36. American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain. 6th ed.
Glenview, Ill: American Pain Society; 2008.
37. Pasero C. Around-the-clock (ATC) dosing of analgesics. J Perianesth Nurs. 2010;25:36-39. Abstract
38. Vadivelu N, Mitra S, Narayan D. Recent advances in postoperative pain management. Yale J Biol Med.
2010;83:11-25. Abstract
39. Eksterowicz N, Quinlan-Cowell A, Vanderveer B, Menez J. Acute pain management. In: St. Marie B, ed. Core
Curriculum for Pain Management Nursing. 2nd ed. Dubuque, Ia: Kendall Hunt Professional; 2010:343.
40. Buvanendran A, Kroin JS. Multimodal analgesia for controlling acute post operative pain. Curr Opin
Anaesthesiol 2009; 22:588- 593.
41. White PF, Kehlet H, Liu S. Perioperative analgesia: what do we still know? Anesth Analg. 2009;108:1364-
1367.
42. American Society of Anesthesiologists Task Force on Acute Pain Management Practice guidelines for acute
pain management in the perioperative setting: an updated report by the American Society of Anesthesiologists
Task Force on Acute Pain Management. Anesthesiology. 2004;100:1573-1581. Abstract
43. Hutchison RW, Tucker WF Jr, Gilder R. A comparison of a fentanyl, morphine, and hydromorphone patient-
controlled intravenous delivery for acute postoperative analgesia: a multicenter study of opioid-induced adverse
reactions. Hosp Pharm. 2006;41:659-663.
44. D'Arcy Y. One opioid does not fit all. Nurse Pract. 2007;32:7-8.
45. Somogyi AA, Barratt DT, Coller JK. Pharmacogenetics of opioids. Clin Pharmacol Ther. 2007;81:429-444.
Abstract
46. Ltsch J, Geisslinger G. Current evidence for genetic modulation of the response to analgesics. Pain.
2006;121:1-5. Abstract
47. Medscape Drug Reference. Acetaminophen. Available at: http://www.medscape.com/druginfo/dosage?
drugid=78503&drugname=Acetaminophen+%28Bulk%29+Misc&monotype=default Accessed December 16,
2010.
48. Bayer Healthcare. History of aspirin. Available at: http://www.wonderdrug.com/pain/asp_history.htm Accessed
on December 16, 2010.
49. Medscape Drug Reference. Aspirin. Available at: http://www.medscape.com/druginfo/dosage?
drugid=77678&drugname=Aspirin+%28Bulk %29+Misc&monotype=default Accessed December 16, 2010.
50. Ghafoor V, St Marie B. Overview of pharmacology. In: St. Marie B., Ed. Core Curriculum for Pain Management
Nursing. 2nd ed. Dubuque, Ia: Kendall Hunt Professional; 2010:236-242.
51. Trescot AM, Datta S, Lee M, Hansen H.. Opioid pharmacology. Pain Physician. 2008;11: S133-S153..
Abstract
52. Krenzischek DA, Dunwoody CJ, Polomano RC, Rathmell JP. Pharmacotherapy for acute pain: implications for
practice. J Perianesth Nurs. 2008;23:S28-S42. Abstract
53. Dietis N, Guerrini R, Calo G, Salvadori S, Rowbotham DJ, Lambert DG.. Simultaneous targeting of multiple
opioid receptors: a strategy to improve side-effect profile. Br J Anaesth. 2009;103:38-49. Abstract
54. Hader CF. Epidural analgesia in the critically ill. Nursing 2007 Critical Care. 2007;2:20-30.
55. Pasero C. Assessment of sedation during opioid administration for pain management. J Perianesth Nurs.
2009;24:186-190. Abstract
56. Dempsey SJ, Davidson J, Cahill D, et al. Selection of a sedation assessment scale for clinical practice: inter-
rater reliability, ease of use and applicability testing of the Richmond Agitation-Sedation and Pasero Opioid-
Induced Sedation scales. Program and abstracts of the National Association of Orthopedic Nurses Congress;
May 6-10, 2009; Tampa, Florida.
57. Nisbet A, Mooney-Cotter F. Comparison of selected sedation scales for reporting opioid-induced sedation
assessment. Pain Manag Nurs. 2009;10:154-165. Abstract
58. Weetman C, Allison W. Use of epidural analgesia in post-operative pain management. Nurs Stand.
2006;20:54-64.
59. Medscape Drug Reference. Lidoderm. Available at: http://www.medscape.com/druginfo/patienthandout?
cid=med&drugid=17549&drugname=Lidoderm+Top&monotype=patienthandout. Accessed on December 16,
2010.
60. Habib AS, Polascik TJ, Weizer AZ, et al. Lidocaine patch for postoperative analgesia after radical retropubic
prostatectomy. Anesth Analg. 2009;108:1950-1953. Abstract
61. Saber AA, Elgamal MH, Rao AJ, Itawi EA, Martinez RL. Early experience with lidocaine patch for
postoperative pain control after laparoscopic ventral hernia repair. Int J Surg 2009;7:36-38.
62. Dreschnack PA. Transdermal Lidoderm for acute headache? Headache. 2006;46:692.
63. Kivitz A, Fairfax M, Sheldon E, et al. Comparison of the effectiveness and tolerability of lidocaine patch 5%
versus celecoxib for osteoarthritis-related knee pain: Post hoc analysis of a 12-week, prospective, randomized,
active-controlled, open-label, parallel-group trial in adults. Clin Ther. 2008;30:2366-2377. Abstract
64. Burch F, Codding C, Patel N, Sheldon N. Lidocaine patch 5% improves pain, stiffness, and physical function
in osteoarthritis pain patients. A prospective, multicenter, open-label effectiveness trial. Osteoarthritis
Cartilage. 2004;12:253-255. Abstract
65. Gammaitoni AR, Alvarez NA, Galer BS. Safety and tolerability of the lidocaine 5% patch, a targeted peripheral
analgesic: a review of the literature. J Clin Pharm. 2003:43:111-117.
66. Pasero C. Lidocaine patch 5%. Am J Nurs. 2003;103:75,77-78.
67. Pasero C. Perineural local anesthetic infusion. When close is almost perfect. Am J Nurs. 2004;104:89-93.
68. Amr YM, Yousef AA. Evaluation of efficacy of the perioperative administration of venlafaxine or gabapentin on
acute and chronic postmastectomy pain. Clin J Pain. 2010;26:381-385. Abstract
69. Clarke H, Pereira S, Kennedy D, et al. Gabapentin decreases morphine consumption and improves functional
recovery following total knee arthroplasty. Pain Res. Manag. 2009;14:217-222.
70. Dauri M, Faria S, Gatti A, Celidonio L, Carpenedo R, Sabato AF. Gabapentin and pregabalin for the acute
postoperative pain management. A systematic-narrative review of the recent clinical evidences. Curr Drug
Targets. 2009;10:716-733. Abstract
71. Grover VK, Mathew PJ, Yaddanapudi S, Sehgal S. A single dose of preoperative gabapentin for pain reduction
and requirement of morphine after total mastectomy and axillary dissection: randomized placebo-controlled
double-blind trial. J Postgrad Med. 2009;55:257-260. Abstract
72. Sen H, Sizlan A, Yanarates O, et al. The effects of gabapentin on acute and chronic pain after inguinal
herniorrhaphy. Eur J Anaesthesiol. 2009;29:772-776.
73. Agarwal A, Gautam S. Evaluation of a single preoperative dose of pregabalin for attenuation of postoperative
pain after laparoscopic cholecystectomy. Br J Anaesth. 2008;101:700-704. Abstract
74. Mathiesen O, Miniche S, Dahl JB. Gabapentin and postoperative pain: a qualitative and quantitative
systematic review, with focus on procedure. BMC Anesthesiol. 2007;7:6.

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.
75. Tiippana EM, Hamunen K, Kontinen VK, Kalso E. Do surgical patients benefit from perioperative
gabapentin/pregabalin? A systematic review of efficacy and safety. Anesth Analg 2007;104:1545-1556.
76. Gray P, Williams B, Cramond T. Successful use of gabapentin in acute pain management following burn
injury: a case series. Pain Med. 2008;9:371-376. Abstract
77. Medscape Drug Reference. Tramadol. Available at: http://www.medscape.com/druginfo/monograph?
cid=med&drugid=4398&drugname=Tramadol+Oral&monotype=monograph&secid=6. Accessed December 16,
2010.
78. Medscape Drug Reference. Nucynta. Available at: http://www.medscape.com/druginfo/dosage?
drugid=152563&drugname=Nucynta +Oral&monotypeo=default. Accessed December 16, 2010.
79. Carstensen M, Mller AM. Adding ketamine to morphine for intravenous patient controlled analgesia for acute
postoperative pain: a qualitative review of randomized trials. Br J Anaesth. 2010;104:401-406. Abstract

Acute Pain Assessment and Treatment

Diunggah oleh

Informasi Dokumen

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Acute Pain Assessment and Treatment

Diunggah oleh

Hak Cipta:

Format Tersedia

7/9/2014 www.medscape.

(acetaminophen/butalbital/caffeine). The nurse should notify the

(aspirin/butalbital/caffeine). The maximum dose for adults is

) and hydrocodone/ibuprofen (Vicoprofen

(lidocaine), ropivacaine (Naropin

), block sodium ion channels to prevent the conduction of nerve impulses.

) and pregabalin (Lyrica

) in the perioperative period

) is a dual-mechanism analgesic. It binds to receptors and it also weakly inhibits norepinephrine

Anda mungkin juga menyukai