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Lewis Chapter 10: Pain
Key Terms
 Analgesic ceiling: a dosage at which no additional analgesia is produced regardless of further dosage increases
 Breakthrough pain: moderate to severe pain that occurs despite treatment
 Ceiling effect: a phenomenon wherein increasing dosage of a given medication produces progressively smaller
effects
 Dermatomes: areas on the skin that are innervated primarily by a single spinal cord segment
 Equianalgesic dose: a dose of one analgesic that is equivalent in pain-relieving effect compared with another
analgesic
 Imagery: a structured technique that uses the client’s own imagination to develop sensory images that divert focus
away from the pain sensation and emphasize other sensory experiences and pleasant memories
 Modulation: involves the activation of descending pathways that exert inhibitory or facilitatory effects on the
transmission of pain
 Neuropathic pain: pain caused by damage to nerve cells or changes in spinal cord processing
 Nociception: the activation of the primary afferent nociceptors with peripheral terminals (free nerve endings) that
respond differently to noxious (tissue-damaging) stimuli
 Nociceptive pain: pain caused by damage to somatic or visceral tissue
 Pain: as defined by the International Association for the Study of Pain (IASP) – an unpleasant sensory and emotional
experience associated with actual or potential tissue damage or described in terms of such damage
 Pain perception: occurs when the pain is recognized, defined, and responded to by the individual experiencing the
pain
 Patient-controlled analgesia: a system to provide analgesia using a pump that allows the client to self-administer a
dose of opiod when needed
 Physical dependence: an expected physiological response to ongoing exposure to pharmacological agents, this is “a
state of adaptation that is manifested by a drug class specific withdrawal syndrome and can be produced by abrupt
cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist”
 Suffering: the state of severe distress associated with events that threaten the intactness of the person
 Titration: dosage adjustment based on assessment of the adequacy of analgesia effect versus the side effects
produced
 Transduction: the conversion of a mechanical, thermal, or chemical stimulus to a neuronal action potential
 Transmission: the movement of pain impulses from the site of transduction to the brain
 Trigger point: a circumscribed hypersensitive area within a tight and of muscle that is caused by acute or chronic
muscle strain
 Windup: part of a constellation of changes in dorsal horn excitability that results in central sensitization – peripheral
tissue damage or nerve injury can cause central sensitization, and continued nociceptive input from the periphery is
necessary to maintain it – with ongoing stimulation of slowly conducting unmyelinated C-fibre nociceptors, firing of
specialized dorsal horn neurons gradually increases
Magnitude of the Pain Problem
 11-12% of Canadians aged 12 and over report moderate to severe pain that interferes with daily activities
 Over 50 million people are affected with musculoskeletal pain such as back pain and arthritis that goes unrelieved
for 5 years or more
 3-6 productive work days/year are lost for those with mild-moderate and severe pain
 Total cost of lost productive work time from common pain conditions among active workers in US: $61.2
billion/year
 80% of people seeking care in the ER experience some relief of pain and 34% continue to have pain at discharge
 Elderly, female, and minority cultural groups have been found most at risk for inadequate or inaccurate
assessment
o The prevalence of unrelieved pain in older adults living in the community is almost 50%, and 70-80% of
those living in nursing homes report pain
 Studies of terminally ill patients reveal that unrelieved pain exists during the last month of life
o Persons living with cancer, institutionalized older adults all have inadequate pain treatment
 In acutely ill client, unrelieved pain can result in increased morbidity as a result of respiratory dysfunction,
increased heart rate and cardiac workload, increased muscular contraction and spasm, decreased GI motility and
transit, and increased catabolism
 Reasons for undertreatment
o Some health care professionals fear that aggressive pain management of pain may hasten or cause
death
o Underreporting and undertreatment of pain
o
o
Fear of addiction, tolerance, and side effects often makes clients reluctant to report pain or comply with a
regimen that involves opioid drugs
Belief that pain is inevitable and a result of worsening disease, and the expectation that the drugs will not
relieve pain
Definitions of Pain
 McCaffery and Pasero: whatever and whenever the person says it is
 IASP definition: one can experience pain in the absence of identifiable tissue damage
 Important to differentiate pain that involves perception of a noxious stimulus from nociception, which may not be
perceived as painful
 Nociception: activation of the primary afferent nociceptors with peripheral terminals (free nerve endings) that respond
differently to noxious (tissue-damaging) stimuli
o Nociceptors: function primarily to sense and transmit pain signals
o If nociceptive stimulus are blocked, pain is not perceived
 Suffering: state of severe distress associated with events that threaten the intactness of the person
o Can occur in the presence or absence of pain
o Pain can also occur with or without suffering
o Ex. woman awaiting breast biopsy may suffer because of anticipated loss of her breast – after biopsy, she
may have pain without suffering if the biopsy is negative, or pain with suffering if the biopsy is positive for
malignancy
o Some interventions for suffering are inadequate for pain, and vice versa
Dimension of Pain and the Pain Process
 Gate control theory (GCT): developed by Melzack and Wall - limited to providing a basic understanding of acute
pain mechanisms, it is seminal work that remains critical to our basic understanding of the pain process, including
transduction, transmission, modulation, and perception of pain
 Physiological dimension of pain
o Neural mechanism by which pain perceived consists of 4 major steps:
 1) transduction
 2) transmission
 3) perception
 4) modulation
o Transduction
 Conversion of a mechanical, thermal, or chemical stimulus to a neuronal action potential
 Occurs at level of the peripheral nerves, in particular the free nerve endings or nociceptors
 Noxious stimuli (tissue damaging): thermal damage, mechanical damage, or chemical damage
 Cause release of numerous chemicals into the peripheral microenvironment of the primary
afferent nociceptor (PAN)
 Some chemicals (histamines, bardykinin, prostaglandins, nerve growth factor, and
acids): activate or sensitize the PAN to excitation
 If PAN activated or excited, it will fire an action potential to the spinal cord
 Action potential necessary to convert the noxious stimulus to an impulse and move from the periphery
to the spinal cord
 Pain action potential can result from 2 sources:
 A release of the sensitizing and activating chemicals (nociceptive pain)
 Abnormal processing of stimuli by the nervous system (neuropathic pain)
 Both produce change in charge along the neuronal membrane
 When PAN membrane becomes depolarized – sodium enters the cell, and potassium exits the cell,
generating an action potential – action potential then transmitted along the entire length of the neuron
to cells in the spinal cord
 Sensitization: inflammation and release of above-named chemical mediators lower excitation
threshold of PANs and increase the likelihood of transduction
 Chemicals involved in process of sensitization: leukotrienes, prostaglandins, and
substance P
 Substance P: stored in distal terminals of the PAN – release causes sensitization of PAN
and dilates nearby blood vessels with production of edema, and release of histamine from
mast cells
 Therapies directed at altering either PAN environment or the sensitivity of the PAN are used to
prevent transduction and initiation of an action potential
 Decreasing the effects of chemicals released at the periphery is the basis of several pharmacological
approaches to pain relief
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o
Ex. NSAIDs and corticosteroids exert their analgesic effects by blocking pain-producing
chemicals – NASIDs block action of cyclo-oxygenase and corticosteroids block action of
phospholipase, interfering with production of prostaglandins
Transmission
 Movement of pain impulses from site of transduction to the brain
 Three segments are involved in nociceptive signal transmission
 1) transmission along nociceptive fibres to level of spinal cord
 2) dorsal horn processing
 3) transmission to the thalamus and the cortex
 Transmission to spinal cord
 One nerve cell extends entire distance from periphery to the dorsal horn of the spinal cord
with no synapses
 AP: once generated, travels all the way to the spinal cord unless blocked by a sodium
channel inhibitor or disrupted by a lesion at the central terminal of the fibre
 Two types of peripheral nerve fibres responsible for the transmission of pain impulses
from the site of transduction to the level of the spinal cord: the A fibres (alpha, beta, and
delta) and the C fibres
 First-order neurons: neurons that project from the periphery to the spinal cord
 Each type of fibre has different characteristics, which determines its conduction rate
o A-alpha (sensory muscle) and A-beta (sensory skin) fibres: large fibres enclosed
with myelin sheaths, allowing them to conduct impulses at a rapid rate
 Transmit non-painful sensations such as light pressure to deep muscles, soft
touch to skin, and vibration
o A-delta fibres: smaller with thinly myelinated sheaths – they conduct at a slower rate
than the larger A-alpha and A-beta fibres
 Stimulation of these fibres results in pain described as pricking, sharp, well
localized and short in duration
o C fibres: smallest fibres and are unmyelinated – conduct at slowest rate
 Activation pain described as a dull, aching, burning sensation and is
characterized by its diffuse nature, slow onset, and relatively long duration
o All of these fibres extend from peripheral tissues through the dorsal toot ganglia to
the dorsal horn of the spinal cord – enter spinal cord through dermatomes
 Dermatomes: areas on skin that are innervated primarily by a single spinal cord segment
 Drugs that stabilize the neuron membrane and inactivate sodium channels disrupt the
transmission of the AP along the PAN axon
 Local anaesthetics prevent transmission via this type of mechanism
o In diluted concentrations, local anaesthetics are effective in blocking small-fibre
transmission without affecting nonpainful sensation (pressure) or motor function
o Large concentrations are required to block large fibres
 Dorsal horn processing
 Nociceptive signal arrives in CNS  processed within the dorsal horn of the spinal cord
 Includes release of neurotransmitters from the afferent fibre into the synaptic cleft
o Bind to receptors on nearby cell bodies and dendrites of cells that may be located
elsewhere in the dorsal horn
o Some produce activation, whereas others inhibit activation of nearby cells
o Nearby cells: release other neurotransmitters
 Effects of complex neurochemistry can facilitate or modulate transmission of noxious stimuli
 Exogenous and endogenous opioids: bind to opioid receptors and block the release of
neurotransmitters, particularly substance P
 Endogenous opioids: include enkephalins and B-endorphins – chemicals that are
synthesized and secreted by the body – capable of producing effects that are similar to those
of exogenous opioids (ex. morphine)
 Wide dynamic range neurons (WDR): specialized cells in dorsal horn
o Receive input from noxious stimuli primarily carried by A-delta and C fibre afferent,
nonnoxious stimuli from A-beta fibres, and indirect input from dendritic projections
o Provides a neural explanation of referred pain as receive inputs from noxious and
innocuous stimuli from distant areas
o Inputs from nociceptive fibres and A-beta fibres converge on the WDR neuron 
when message transmitted to brain, the originating area of body poorly localized
(referred pain)
 Sensitization: can occur at level of spinal neurons – known as central sensitization
o

Caused by: peripheral tissue damage or nerve injury, and continued nociceptive
input from periphery is necessary to maintain it
o Windup: with ongoing stimulation of slowly conducting unmyelinated C-fibre
nociceptors, firing of specialized dorsal horn neurons gradually increases dependant on the activation of N-methyl-D-aspartate (NMDA) receptors
 NMDA receptors: produce alterations in neural processing of afferent stimuli
that can persist for long periods
 Commonly used NMDA antagonist: anaesthetic agent ketamie (Ketalar) –
side effects of hallucinations
 Transmission to the thalamus and the cortex
 Dorsal horn  third-order neurons primarily in thalamus and several other areas of the brain
 Fibres of dorsal horn projection cells enter the brain through several pathways, including
spinothalamic tract (STT) and spinoreticular tract (SRT)
 Distinct thalamic nuclei receive nociceptive input from spinal cord  projections to several
regions of cerebral cortex where perception of pain occurs
o Perception
 Occurs when pain is recognized, defined, and responded to by the individual experiencing the pain
 In brain: nociceptive input perceived as pain – no single location where pain perception occurs –
several brains structures where pain perception occurs
 Reticular activating system: responsible for autonomic response of warning the individual to attend
to the pain stimulus
 Somatosensory system: responsible for localization and characterization of pain
 Limbic system: responsible for the emotional and behavioural response to pain
 Cortical structures: crucial to constructing the meaning of pain
o Modulation
 Activation of descending pathways that exert inhibitory or facilitatory effects on the transmission of
pain
 Nociceptive stimuli may or may not be perceived as pain depending on type and degree of
modulation
 Can occur at level of periphery, the spinal cord, the brainstem, and the cerebral cortex
 Centrally: modulation of nociceptive impulses occurs via descending fibres that influence dorsal horn
neuronal activity
 Neurochemistry: excitatory and inhibitory neurotransmitters such as enkephalin, GABA, serotonin,
and norepinephrine – involved in nociceptive modulation, resulting in inhibition of pain transmission
 Many pain management drugs exert their effects through modulatory system – interfere with reuptake
of serotonin and norepinephone increases their availability to inhibit noxious stimuli and produce
analgesia
Sensory, affective, behavioural, cognitive, and sociocultural dimensions of pain
o Sensory component: recognition of the sensation as painful
 Elements: pattern, area, intensity, and nature (PAIN)
o Affective component: emotional responses to the pain experience – anger, fear, depression, and anxiety
o Behavioural component: observable actions used to express or control the pain
 Facial expressions, posturing
o Cognitive component: beliefs, attitudes, memories, and meaning of pain for individual
 Pain-related beliefs and cognitive coping strategies that people use
 Cognitions about pain contribute to clients’ goals for an expectations of pain relief and treatment
outcomes
 Factors that affect cognition, such as sedation, dementia, delirium, and mental disability, alter the
pain experience and responses to pain
o Sociocultural component: demographics, support systems, social rules, past pain experiences ,and cultural
aspects that contribute to the pain experience
 Ex. sex – influences nociceptive processes and the acceptability and usage of an response to
analgesics such as NSAIDs and opioids
 Families and caregivers also influence the client’s response to pain through their own beliefs and
behaviours
Etiology and Types of Pain
 Nociceptive, neuropathic, or both
 Nociceptive pain
o Caused by: damage to somatic or visceral tissue
o Somatic pain: aching or throbbing that is well localized, arises from bone, joint, muscle, skin, or connective
tissue
o

Visceral pain: result from stimuli such as tumour involvement or obstruction, arises from internal organs such
as intestine and bladder
o Examples: pain from surgical incision or broken bone, arthritis, or cardiac ischemia
o Usually responsive to nonopioids as well as opioids
Neuropathic pain
o Caused by: damage to nerve cells or changes in spinal cord processing
o Burning, shooting, stabbing, or electrical in nature – can be sudden, intense, short-lived, or lingering
o Difficult to treat and management includes: opioids, anti-seizure drugs and antidepressants
o Centrally generated pain
 Deafferentation pain: injury to either peripheral or CNS
 Sympathetically maintained pain: associated with dysregulation of ANS
o Peripherally generated pain
 Painful peripheral neuropathies: pain felt along distribution of multiple peripheral nerves
 Painful mononeuropathies: pain felt at least partly along distribution of the damaged nerve
o Examples: postherpetic neuralgia, phantom limb pain, diabetic neuropathies, and trigeminal neuralgia
o Acute pain: postoperative pain, labour pain, pain from trauma and infection, angina
 Treatment: analgesics for symptom control and treatment of underlying cause
 Diminishes over time as healing occurs
o Persistent pain: persists beyond normal time expected for healing
 Can be disabling and often is accompanied by anxiety and depression
 Further subdivided into cancer and noncancer pain
 Cancer pain separate because its cause can be determined, its course differs from nonmalignant pain and use of opioids in treating cancer pain more widely accepted than for
treatment of noncancer pain
 Causes: disease progression, diagnostic procedures, anticancer therapies, and infection
Pain Assessment
 Sensory component
o Pattern, area, intensity, and nature (PAIN) of pain
o Must recognize that pts may use words other than “pain”
o Pattern of pain: pain onset and duration
 Acute pain: increases during wound care, ambulation, coughing, deep breathing
 Acute pain associated with surgery or injury tends to diminish over time, with recovery as
tissues heal
 Persistent pain: ongoing, episodic, or both
 Breakthrough pain: moderate to severe pain that occurs despite treatment – experience by many
cancer pts
 Rapid in onset, brief in duration, with highly variable intensity and frequency of occurrence
 Episodic, procedural, or incident pain is a transient increase in pain that is caused by a
specific activity or event that precipitates the pain
 Examples: dressing changes, movement, eating, position changes, certain procedures such
as catheterization
o Area of pain: location of pain may be referred from its origin to another site
 May radiate from its origin to another site
o Intensity of pain: scales used – adjusted to age and cognitive development
 Numeric scales, verbal descriptor scales, or visual analog scales can be used by most adults to rate
intensity of their pain
 For those unable to respond to other pain intensity scales, a series of faces ranging from “smiling” to
“crying” can be used
o Nature of pain: quality or characteristics of pain
 Captures qualitative and affective components of pain in addition to present pain intensity
 Assists in identifying type of pain
 Neuropathic pain: burning, cold, shooting, stabbing, or itchy sensation
 Nociceptive pain: sharp, aching, throbbing, and cramping
 Different types of pain are more responsive to some therapies than others
 Ex. antiseizure drug gabapentin found to be more effective in MS pain
 Affective, behavioural, cognitive, and sociocultural components
o Effects of pain on the pts sleep and daily activities, relationships with others, physical activity, emotional wellbeing, past pain experiences, meaning of pain for the pt, ways in which the pt expresses the pain, strategies
that the pt has used to control the pain, should be assessed
Pain Treatment

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Client must always be believed
Treatment based on pts goals – pain intensity, functional goal, etc.
Treatment plans should use combination of drug and nondrug therapies – all therapies should be evaluated to ensure
that they are meeting pt’s goals – individualized for each pt
Pt and family teaching should be a cornerstone in treatment plan – causes of pain, pain assessment methods,
treatment goals and options, expectations for pain management, instruction regarding the proper use of drugs, sideeffects management and of drug and self-help pain relief measures
Drug Therapy for Pain
 Equianalgesic dose
o Dose of one analgesic that is equivalent in pain-relieving effects compared with another analgesic
o Equianalgesic doses are provided for opioids and are important because there is no upper dosage limit for
many of these drugs
o Are approximate, and individual client response must be routinely assessed
 Scheduling analgesics
o Focus on preventive or ongoing control of pain rather than providing analgesics only after the pt’s pain has
become moderate to severe
o Premedicated before procedures
o Titration: dose adjustment based on assessment of the adequacy of analgesic effect vs. side effects
 Wide variability in amount of analgesic needed to manage pain, and titration is an important strategy
in addressing this variability
 Can be titrated upward or downward, depending on situation
 Goal: to use smallest dosage of analgesic that provides effective pain control with fewest side effects
 Analgesic ladder
o Step 1: nonopioids +/- adjuvant – for mild pain
o Step 2: opioids for mild to moderate pain +/- nonopioid and adjuvant
o Step 3: opioids for moderate to severe pain +/- nonopioid and adjuvant
o Drug therapy for mild pain
 1-3/10 – nonopioid analgesics may be used
 Characterized by following:
 1) there is a ceiling effect to their analgesic properties – increasing dose beyond an upper
limit provides no greater analgesia
 2) they don’t produce tolerance or physical dependence
 3) many are available without a prescription
 Number of nonopioid analgesics such as aspirin, and NSAIDs inhibit chemicals that activate the PAN
– PAN is transduced less often or a larger stimulus needed to produce transduction
 Aspirin: effective for mild pain but its use limited by its common side effects – GI upset and bleeding
 Tylenol: has analgesic and antipyretic effects but no anti-platelet or anti-inflammatory effects – doses
greater than 4000mg/d, acute overdose, or use by clients with alcoholism or liver disease can result
in severe hepatotoxicity
 NSAIDs: possess equal analgesic efficacy as aspirin, whereas others have somewhat higher efficacy
 Pts vary in responses to a specific NSAID
 Inhibit cyclo-oxygenase-1 and -2 enzymes, which produce prostaglandins involved in
inflammation
o Prostaglandins: have role in protecting lining of stomach from acids – side effects of
NSAIDs can be serious and include bleeding tendencies secondary to decrease
platelet aggregation, GI problems ranging from dyspepsia to ulceration and
hemorrhage, renal insufficiency, and occasionally CNS dysfunction
 COX-2 enzyme: doesn’t play a role in protecting stomach or intestinal tract so its selective
inhibition not associated with same risk of injury to these organs as inhibition of COX-1
o Drug therapy for mild to moderate pain
 4-6/10 – opioids – bind to receptors to produce effects
 Opioid receptors are found in CNS, on terminals of sensory nerves and on surface of immune cells
 3 receptors: mu, kappa, and delta
 Recently receptors classified as OP1 (delta), OP2 (kappa), and OP3 (mu)
 Most clinically useful opioids bind to OP3 (mu): morphine, oxycodone, hydromorphone, and
methadone
 Opioid agonists: bind to receptors and cause analgesia
 Opioid antagonists: bind to receptors but don’t produce analgesia – also block other effects of
opioid receptor activation such as sedation and respiratory depression

o
o
Mixed agonist-antagonists: should not be used since they bind as agonists on the kappa receptor
and as weak antagonists or partial agonists on the mu receptor
 When given to someone taking an antagonist, it will act as an agonist-antagonist such as
Naloxone, and reverse any analgesic effect
 Cause more dysphoria and agitation
 Analgesic ceiling: dosage at which on additional analgesia is produced regardless of further
dosage increases
 Can precipitate withdrawal if used in a client who is physically dependent on agonist drugs
 At step 2: commonly used opioids are often prescribed in products combining an opioid with a
nonopioid analgesic which may limit the opioid dose that can be given
 Oxycodone: for severe pain as well
 Propoxyphene (Darvon): included as step 2 drug but not recommended in analgesia guidelines
because of its limited effectiveness and toxic metabolite that can cause seizures
 Tramadol (Ultram): for moderate pain – weak mu-agonist and is thought to inhibit reuptake of
norepinephrine and serotonin – same efficacy as Tylenol #3 – common side effects similar to those of
other opioids (nausea, constipation, dizziness, sedation)
Drug therapy for moderate to severe pain
 Most commonly used step 3 analgesics: mu-agonists – these drugs also bind with other receptors
 Effective for moderate to severe pain because they are potent, have no analgesic ceiling, and can be
delivered via many routes of administration
 Morphine: standard of comparison for all other opioid analgesics
 Equianalgesic charts: present dosages in equivalent morphine doses
 Fentanyl (Duragesic), hydromorphone (Dilaudid), methadone (Metadol), and oxycodone (Percocet)
 MS Contin: long-acting morphine formulation – for pts who need around-the-clock therapy for
extended period of time
 Meperidine (Demerol, Pethidine): mu-agonist – no longer recommended for acute or persistent pain
because of high incidence of neurotoxicity (ex. seizures) associated with accumulation of its
neurotoxic metabolite, normeperidine
 Any adverse effects cannot be reversed by Naloxone which potentiates the effect of
normeperidine
 A hyperpyrexic syndrome with delirium which can cause death, can occur if meperidine is
given to pts taking monoamine oxidase inhibitors
 Step 3 opioids: no analgesic ceiling – people can experience dose limiting side effects
 Side effects: constipation, nausea, vomiting, sedation, respiratory depression, and pruritus
 With continued use, most side effects disappear except constipation
 Less common side effects: urinary retention, myoclonus, dizziness, confusion, and
hallucinations
 Most common: constipation
 Metoclopramide: effective when a client complains of gastric fullness – opioids delay gastric
emptying
 Sedation: resolved with development of tolerance
 Respiratory depression: rare in opioid-tolerant clients when opioids are titrated to analgesic
effect
o At risk pts: opioid-naïve clients, older pts, and pts with underlying lung disease
o Naloxone can be administered - not used if pt taking opioids for more than a few
days as can precipitate severe, agonizing pain, profound withdrawal symptoms, and
seizures – has short half life (60-90 minutes)
 Itching: when opioids administered via intraspinal routes
Adjuvant analgesic therapy
 Drugs used in conjunction with opioid and nonopioid analgesics
 Sometimes referred to as coanalgesics
 Include drugs that enhance pain therapy through one of three mechanisms:
 1) enhancing the effects of opioids and nonopioids
 2) possessing analgesic properties of their own
 3) counteracting the side effects of other analgesics
 Antidepressants
 Tricyclic antidepressants have analgesic properties at doses lower than those effective for
depression
 Enhance the descending inhibitory system by preventing synaptic reuptake of serotonin and
norepinephrine

o
Higher levels of serotonin and norepinephrine in the synaptic cleft inhibit the transmission of
nociceptive signals in the CNS
 Have been shown to be effective for a variety of pain syndromes, especially those involving
neuropathic pain
 Their anticholinergic side effects (dry mouth, urinary retention, sedation, and orthostatic
hypotension) can decrease client acceptance and adherence to regimen
 Selective serotonin reuptake inhibitors: not been as effective in treating pain
 Antiseizure agents: gabapentin (Neurontin), carbamazepine (Tegretol), and clonazepam (Rivatril) –
stabilize the membrane of the neuron and prevent transmission
 Effective for some neuropathic pain and prophylactic treatment of headaches
 Corticosteroids: dexamethasone (Decadron) and methylprednisolone (Medrol) – used for several
pain problems, including acute and persistent cancer pain, pain secondary to spinal cold or brain
compression, and some neuropathic pain syndromes
 Decrease edema and inflammation
 Side effects: hyperglycemia, fluid retention, dyspepsia and GI bleeding, impaired healing,
muscle wasting, osteoporosis, and susceptibility to infection
 Local anaesthesia: oral, parenteral, and topical applications of local anaesthetics used to interrupt
transmission of pain signals to brain
 Used for acute pain resulting from surgery or trauma
 Controls persistent neuropathic pain
 Side effects: dizziness, paresthesias, seizures, affect cardiac conductivity thereby causing
dysrhythmias and myocardial depression
Administration routes
 Oral
 Route of choice for person with a functioning GI system
 To obtain equivalent analgesia to doses administered IM or IV, larger oral doses are needed
o First pass effect: oral opioids initially are absorbed from the GI tract into the portal
circulation and shunted to the liver – partial metabolism in the liver occurs before the
drug enters systemic circulation and becomes available to peripheral receptors or
can cross blood-brain barrier and access CNS opioids receptors, which is necessary
to produce analgesia
 Made in short-term and long-term acting preparations
 Sustained-released preparations: should not be crushed, broken, or chewed
o Ex. oxycodone
o Range of effectiveness: 8-24 hours
 Sublingual and buccal
 Under the tongue or held in mouth and absorbed into systemic circulation – exempt from firstpass effect
 Intranasal
 Allows delivery of medication to highly vascular mucosa and avoids first-pass effect
 Ex. Butorphanol (Stadol) – one of few intranasal analgesics that is available – for migraines
 Rectal
 Useful when pts cannot take an analgesic by mouth
 Ex. hydromorphone (Dilaudid), oxymorphone (Numorphan), and morphine
 Transdermal
 Ex. Fentanyl (Duragesic)
 Useful for pts who cannot tolerate oral analgesic drugs not suitable for rapid dose titration but
can be effective if the pt’s pain is stable and the dose required to control it is known
 Changed every 48 hours rather than the recommended 72 hours
 Ex. Lidocaine-impregnated transdermal patch (Lidoderm patch)
o On area of postherpetic pain – in place for up to 12 hours – not left in place for 24
hours continuously because toxic accumulations can occur
 Several precautions taken for pts receiving class I antidysrhythmic drugs or products
containing local anaesthetic agents because their effect will be additive and my induce
toxicity
 Creams and lotions containing 10% trolamine salicylate: for joint and muscle pain –
aspirin like substance – avoids GI irritation but other side effects of high-dose salicylate not
prevented
 Ointments, lotions, gels, liniments, and balms: applied to skin to achieve pain relief
o Common ingredients: methyl salicylate combined with camphor, menthol, or both
o
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Produce strong hot or cold sensation and should not be used after massage or a
heat treatment when blood vessels already dilated
 Others: capsaicin and prilocaine plus Lidocaine (EMLA) – provide analgesia
o From red chilli peppers – depletes and prevents reaccumulation of substance P in the
peripheral sensory neurons
o Can control pain associated with postherpetic neuralgia, diabetic neuropathy, and
arthritis
o EMLA: useful for control of pain associated with venipunctures, ulcer debridement,
and possibly postherpetic neuralgia
 Areas to which EMLA applied, should be covered in plastic wrap for 30-60
min before painful procedure
Parenteral routes
 Subcutaneous (SC) and intravenous (IV) administration
 Meperidine: only opioid requiring IM injection – not recommended because its toxic
metabolite, normeperidine, can accumulate with repeated administration, causing CNS
excitation
 IM route: not recommended because causes pain – unreliable absorption, and with chronic
use can result in abscesses and fibroses
 SC route: onset of analgesia is slow – rarely used for acute pain management
o Continuous SC infusions are effective for persistent cancer pain
o Helpful for ppl with abnormal GI function and limited venous access
 IV route: best when immediate analgesia and rapid titration are necessary
Intraspinal delivery
 Epidural or intrathecal: involves inserting a catheter into a subarachnoid space (for
intrathecal delivery) or the epidural space (epidural delivery) and injecting an analgesic, ether
by intermittent bolus doses or continuous infusion
 Percutaneously placed temporary catheters: used for short-term therapy (2-4 days)
 Surgically implanted catheters: for long-term therapy
 Lumbar region most common site of placement – epidural catheters may be placed at any
point along the neuroaxis (cervical, thoracic, lumbar, or caudal)
 Analgesics highly potent because they are delivered close to receptors in dorsal horn of the
spinal cord – much smaller doses needed
 Common symptoms: nausea, itching, and urinary retention
 Complications: catheter displacement and migration, neurotoxicity, and infection
 Catheter displacement: will cause decrease in pain relief with no improvement even with
additional analgesic
 Drugs which are neurotoxic when administered intraspinally: preservatives, antibiotics,
potassium, TPN
 Signs and symptoms of intraspinal analgesia: diffuse back pain, pain or paresthesias
during bolus injection, and unexplained sensory or motor deficits
 Acute bacterial infection (Meningitis): fever, headache, and altered mental status
Patient-controlled analgesia
 Infusion system in which the pt pushes a button to receive a bolus infusion of an analgesic
 Used for management of acute pain – postoperative and cancer pain
 Will also receive an additional continuous, basal infusion at a preset dose and rate
 Most common drugs used: morphine and hydromorphone
 Can’t overdose because pump is programmed to deliver a maximum number of doses/hour
Surgical Therapy
 Nerve block
o Used to reduce pain by temporarily or permanently interrupting transmission of nociceptive input by
application of local anaesthetics or neurolytic agents
o Used for perioperative pain
o For intractable persistent pain: used when more conservative therapies fail
o For more localized persistent pain states, such as peripheral vascular disease, trigeminal neuralgia,
causalgia, and some cancer pain
o Advantages: manages localized pain caused by malignancy and in debilitated clients who could not
withstand a surgical procedure for pain relief
 Interventional therapy
o Therapeutic nerve blocks

o
Involve one-time or continuous infusion of local anaesthetics into a particular area to produce pain
relief
 Aka. regional anaesthesia
 Interrupt all afferent and efferent transmission to the area and thus are not specific to nociceptive
pathways
 Include local infiltrate of anaesthetics into a surgical site and injection of anaesthetic into a specific
nerve or nerve plexus
 Used during and after surgery
 For intractable chronic pain: neuroablative nerve blocks with phenol or alcohol may be used
 Neuroablative techniques
 Performed for severe pain that is unresponsive to all other therapies
 Destroy nerves by surgical resection or thermocoagulation, including radiofrequency
coagulation
 Neurectomies, rhizotomies, and sympathectomies: neuroablative interventions that
destroy the sensory division of a peripheral or spinal nerve
 Cordotomies: neurosurgical procedures that ablate the lateral spinothalamic tract – if tract is
interrupted by in the spinal cord
 Tractotomies: neurosurgical procedures that ablate the lateral spinothalamic tract – if
interruption is in the medulla or the midbrain of the brainstem
Neuroaugmentation
 Involves electrical stimulation of the brain and spinal cord
 Spinal cord stimulation (SCS): performed much more often than deep brain stimulation
 Common uses: back pain secondary to nerve damage that is unresponsive to other therapies
 Potential complications: those related to surgery, migration of the generator (usually implanted in
subcutaneous tissues of upper gluteal or petoralis area), and nerve damage
Nonpharmacological Therapy for Pain
 Physical pain relief strategies
o Massage
 Specific techniques: acupressure and trigger-point massage
 Trigger point: circumscribed hypersensitive area within a tight band of muscle that is caused by
acute or chronic muscle strain
o Exercise
 Enhances circulation and cardiovascular fitness, reduces edema, increases muscle strength and
flexibility, and enhances physical and psychosocial functioning
o Transcutaneous electrical nerve stimulation
 Delivery of an electric current through electrodes applied to the skin surface over the painful region, at
trigger points, or over a peripheral nerve
o Percutaneous electrical nerve stimulation
 Stimulates deeper tissues near a large peripheral or spinal nerve through the insertion of a needle to
which a stimulator is attached
 If reduces pain, a permanent peripheral nerve stimulator is surgically implanted
 Effective in treatment of headaches, diabetic peripheral neuropathy, and low back pain
o Acupuncture
 Technique of traditional Chinese medicine in which very thin needles are inserted into body at
designated points
 Used for: musculoskeletal conditions, repetitive strain disorders, myofascial pain patterns,
postsurgical pain, postherpetic neuralgia, peripheral neuropathic pain, and headaches
 Complications: infection, pneumothorax, and bleeding
o Application of heat
 Superficial or deep
 Superficial: applied using an electric heating pad (dry or moist), a hot pack, hot moist compresses,
or a hot water bottle
 Deep heat therapy: short-wave diathermy, microwave diathermy, and ultrasound therapy
o Application of cold
 Dry cold: ice bag
 Moist cold: towels soaked in ice water, cold hydrocollator packs, or immersion in a bath or under
running cold water
 More effective than heat for a variety of painful conditions: acute pain from trauma or surgery,
acute flare-ups or arthritis, muscle spasms, and headache
 Cognitive Techniques
o Distraction and imagery
o
o
o
Hypnosis
 Enables a pt to achieve a state of heightened awareness and focused concentration that can be used
to alter the pt’s pain perception
 Effective for many types of acute and chronic pain, particularly those types aggravated by tension and
stress
Relaxation strategies
 Reduces stress, decreases acute anxiety, distracts from pain, alleviates muscle tension, combats
fatigue, facilitates sleep, and enhances effectiveness of other pain relief measures
 Ex. breathing, music, imagery, meditation, and progressive muscle relaxation
Self-management
 Typically conduced in groups with a focus on helping participants increase their daily pain
management skills and decrease the negative consequences of persistent pain, such as social
isolation
 By structured rehearsal of various cognitive and behavioural self-management techniques (ex. energy
conservation, pacing, sleep promotion, relaxation, communication skills, and safe exercise), clients
and family members learn to set realistic weekly goals that are directed at increasing overall
functional capacity and emotional well-being
Barrier to Effective Pain Management
 Pain influenced greatly by: emotions, behaviours, misconceptions, and attitudes of clients and family members
about pain and the use of pain therapies
 Common barriers: tolerance, dependence, and addiction
 Tolerance
o State of adaptation in which exposure of a drug induces change that result in a diminution of one or more of
the drug’s effects over time
o Tolerance is characterized by need for an increased opioid dose to maintain the same degree of analgesia
o First sign: pt begins to experience regular end-of-dose failure
 If signs appear, appropriate evaluations should be made to rule out other causes of increased
analgesic needs, such as disease progression or infection
o Managing tolerance
 1) increase dosage of the analgesic
 2) substitute another drug in the same class (ex. changing from morphine to oxycodone)
 3) add a drug from a different drug class that will augment pain relief without increasing side effects
o No ceiling effect for opioid-agonist drugs
 Physical dependence
o State of adaptation that is manifested by a drug class specific withdrawal syndrome and can be produced by
abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an
antagonist
o When opioids are no longer needed to provide pain relief, a tapering schedule should be used in
conjunction with careful monitoring
 Beings with calculating the 24-hour dose used by the client and dividing by 2
 25% is given every 6 hours, after 2 days daily dose reduced by an additional 25% every 2
days until the 24-hour oral dose is 30mg/day – after 2 days on this minimum dosage, the
opioid is then discontinued
 Addiction
o Primary, chronic, neurobiological disease, with genetic, psychosocial, and environmental factors influencing
its development and manifestations – characterized by behaviours that include one or more of the
following:
 Impaired control over drug use, compulsive use, continued use despite harm and craving
o Tolerance and physical dependence are not indicators of addition – are normal physiological responses to
chronic exposure to certain drugs, including opioids
o Opiod addiction in acute care clients with no history of substance abuse is a risk estimated at less than 1%
o People with history of addiction: managed successfully on opiods for their pain - risk of addiction may be
higher
Institutionalizing Pain Education and Management
 The JCAHO Statement on Pain Management includes the following directives
o 1) to recognize the pt’s rights to appropriate assessment and management of pain
o 2) to identify pain in clients during their initial assessment and as needed during ongoing, periodic,
reassessments
o 3) to educate health care professionals in pain assessment and management and to ensure competency
o 4) to educate clients and their families about pain management
Ethical Issues in Pain Management
 Fear of hastening death by administering analgesics
o Rule of double effect: if an unwanted consequence (ex. hastened death) occurs as a result of an action
taken to achieve a moral good (ex. pain relief), the action is justified because the nurse’s intent is to relieve
pain and not to hasten death
o Unrelieved pain is one reason that clients make requests for assisted suicide; aggressive pain management
may decrease for the number of requests
 Age-related considerations
o Many older adults, even those with mild to moderate cognitive impairment, can use quantitative scales
accurately and reliably
o Some evidence that older adults have difficulty using visual analogue scales and that numerical rating scales
and verbal descriptor scales are preferable
o Older adults metabolize drugs more slowly than younger clients and thus are at greater risk for higher blood
levels and adverse effects
o Use of SNAIDs in older adults associated with high frequency of serious GI bleeding – acetaminophen should
be used whenever possible
o Cognitive impairment and ataxia can be exacerbated when analgesics such as opioids, antidepressants, and
anticonvulsant drugs are used
Special Populations
 Clients with substance abuse problems
o Opioids may be used effectively and safely in clients with substance dependence when indicated for pain
control
o Withholding opioids from chemically dependent clients with pain has not been shown to increase the
likelihood of recovery from addiction
o Opiod agonists-antagonists: should not be used in this population because they may precipitate withdrawal
o Use of potentiators and psychoactive drugs that don’t have analgesic properties should also be avoided