This document provides information on pain management in nursing, including: - Objectives related to neurophysiology of pain pathways, pharmacological and non-pharmacological interventions, chronic pain, and nursing contributions to pain management. - Details on the pain process including transduction, transmission, modulation, and perception. - Descriptions of various pharmacological interventions for pain including analgesics, local anesthetics, anticonvulsants, and opioids.

1. Pain Management in
Nursing
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2. Objectives:
Basic Neurophysiology of Pain Pathways
Pharmacological and Non-pharmacological
Interventions of Pain Pathways
Matching neurophysiology with pharmacology
Pathophysiology of Pain
When Pain becomes Chronic or Persistent Pain
Interventions of Chronic or Persistent Pain
Nursing Contributions to Pain Management
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3. Combination Analgesics
Rationale
Multimodal analgesia
Multiple sites of action target multiple pain
pathways
Complementary pharmacokinetic activity
Potentially synergistic analgesic effect
Reduced adverse event profile with comparable
efficacy
Raffa, RB, 2001

4. Pain Process
The neural mechanisms by which pain is perceived
involves a process that has four major steps:
Transduction
Transmission
Modulation
Perception
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6. Facilitating Transduction
Biochemical mediators: “Chemical Soup”
Prostaglandins
Bradykinins
Serotonin
Histamines
Cytokines
Leukotrienes
Substance P
Norepinephrine
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8. Peripheral Excitatory Mediators
(Pain)
Substance Receptor Mechanism
Substance P
(SP)
NK1 ↑ neuronal excitability, edema
Prostaglandin
(PG)
? Sensitize nociceptors,
inflammation, edema
Bradykinin B2 (normal)
B1 (inflammation)
Sensitize nociceptors
↑ PG production
Histamine H1 C-fiber activation, edema,
vasodilatation
Serotonin 5-HT3 C-fiber activation, release SP
Norepinephrine
(NE)
α1 Sensitize nociceptors
Activate nociceptors

9. Peripheral sensitization
Peripheral opioid receptors
Management of histamine
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11. Diclofenac

13. Acetaminophen (Tylenol)
Analgesic, antipyretic
Inhibits prostaglandin synthetase in the CNS, weak
peripheral anti-inflammatory activity
Serotonergic effect at descending pathway
Used to treat osteoarthritis
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14. Acetaminophen (Tylenol)
American Pain Society: Maximum dose 4,000
mg/day,
American Liver Foundation: 3,000 mg/day
Risk of hepatotoxicity with higher doses
Antidote – acetylcysteine (Mucomyst, Acetadote)

15. Transmission of pain
Defined as:
Projection of pain
into the
Central Nervous System
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16. Transmission
A synapse contains three
elements:
the presynaptic terminal
the synaptic cleft
the receptive membrane
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18. Transmission
The presynaptic terminal is the
axon terminal of the presynaptic
neuron
Here that the presynaptic
neuron releases
neurotransmitters which are
found in vesicles
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21. Peripheral Nerves:
Transmission of Action Potential
αA
δA
C
peripheral
nerve
myelin
spinal
cord
K+
Na+

23. Capsaicin
Hot peppers
May deplete & prevent re-
accumulation of substance P
in primary afferent neurons
responsible for transmitting
painful impulses from
peripheral sites to the CNS.
Absorption, distribution,
metabolism & excretion, half
life – unknown
May produce transient
burning with application,
usually disappears in 2-4
days, but may persist for
several weeks.
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25. Transmission
The synaptic cleft is the narrow
intercellular space between
neurons.
Neurotransmitters cross the
synaptic cleft and bind to specific
receptors on the postsynaptic
neurons
This will excite or inhibit the
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28. Muscle Pain
Correlated with Lactic acid levels
Lactic acid levels in the blood vessels of the muscle
influence neuronal noxious stimuli
What might that tell us about intervening with
muscle pain?
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30. Neuropathic Pain Features
Burning, prickling, tingling
Shock-like
May or may not be lancinating
Paresthesia
May be associated with
– Allodynia
– Hyperalgesia
– Hyperethesia
– Referred Pain
– More intense at noc
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31. Local Anesthetic Agents
On-Q delivery
Synera patch (topical)
Emla: Lidocaine and Prilocaine 1:1 (topical)
LMX 4% lidocaine (topical)
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32. Local Anesthetics
Blocks conduction of nerve impulses by
decreasing or preventing an increase in
the permeability of excitable membranes
to Na+.
Inhibits depolarization of nerve
Blocks neuronal firing
Challapalli, V., et. al., 2005
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33. Lidoderm 5% Patch

36. Mentholatum
Menthol generates
analgesic
activity through:
Ca2+ channel blocking
activity
Binding to kappa opioid
receptors
Stanos, S.P., 2007
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37. Methyl Salicylate Toxicity
Salicylic acid derivative (a.k.a. wintergreen oil,
sweet birch oil)
Lipid solubility increases toxicity
More toxic than aspirin
1 teaspoon (5ml) wintergreen oil contains 4,000 mg
salicylate
30ml wintergreen oil is a fatal dose in adults
Risk of toxicity reduced with use for acute pain,
limited to a small area of dermal application
Chyka, P.A., et al., 2007
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38. Anticonvulsants
1) Inhibit sustained high-frequency neuronal firing by
blocking Na+ channels after an action potential,
reducing excitability in sensitized C-nociceptors.
2) Blockade of Na+ channels and increase in synthesis
and activity of GABA, in inhibitory neurotransmitter,
in the brain.
3) Modulates Ca+ channel current and increases
synthesis of GABA.
Deglin, J.H. & Vallerand, A.H., 2001
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39. Antiepileptic Agents
Broad clinical actions in
the CNS:
Reduce seizures
Neuropathic pain
Bipolar disorder
Anxiety
Schizophrenia
Agitation
Impulse dyscontrol
Dementia
Delirium
Three proposed
mechanisms of action:
Blockade of voltage gated
sodium channels
(↓ glutamate release)
Blockade of voltage gated
calcium channels – alpha 2
delta subunits (reduces
excessive neurotransmitter
release)
Enhancement of GABA
actions
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40. Lyrica Pregabalin
Schedule V

41. Modulation
Sympathetic Chain ganglion
Substantia gelatinosa
Post synaptic jct
Contralateral spinothalamic
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43. Ascending Pain Pathways
Ascending
fibers
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44. Perception
Review:
Impulses go through the postsynaptic junction
Cross the dorsal horn
To the spinothalamic tract
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47. Meperidine (Demerol)
Duration 2-3 hrs
PO doses 1/4 analgesic effect
 Toxic metabolite - normeperidine
dysphoria, irritability, seizures
t1/2 =12-15 hrs; not reversible with Narcan
Do not use Demerol for more than 48 hrs or at
doses >600 mg/24hr
Only indications: rigors, short term use, i.e.
endoscopy.
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49. Reference: Am Family Physician, 71(7), 2005
Methadone
FDA Indications: Severe pain, narcotic detoxification,
and temporary maintenance of narcotic addiction
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50. Methadone
Inexpensive
Accumulates with repeated dosing
85% protein bound
Slowly released up to 10 days after dose increase
Available in 10 mg tablet or oral solution, use of 40 mg
diskette no longer available for pain mgt use
Patient may be subjected to scrutiny, stigma &
misconceptions
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51. Federal Regulation
Prevention of withdrawal in opioid addiction
Special annual registration with DEA
Use only in an established addiction treatment
program
Maintenance patients may continue tx when
admitted to acute care facility
Treatment for pain
Any clinician licensed to prescribe Schedule II drugs
may prescribe methadone for pain
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52. Methadone
Incomplete Cross-Tolerance
Inverse relationship with dosing
Monitor ekg for QT prolongation
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53. Schmittner, J., 2006
Clinical Indications for Electrocardiogram in
Patients Receiving Methadone
 History of long-QT syndrome or torsades de pointes
 Family history of long-QT syndrome or early sudden cardiac death
 Cardiac arrhythmia and heart block (2nd or 3rd degree AV block)
 Anorexia nervosa
 Frequent electrolyte depletion (K, Ca, Mg)
 HIV patients on multiple-antiretroviral therapy
 Methadone dosages greater than 150mg/day
 Initiation of a P-450 inhibitor
 Initiation of medications associated with QTc prolongation
 Presyncopal or syncope symptoms
 Unexplained tonic-clonic seizures with abnormal
electroencephalogram
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54. Routhier, D., et al., 2007The Nurses and attendants staff we provide for your healthy recovery for bookings
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55. Methadone Black Box Warning
 Deaths during initiation and conversion from
other opioids
 Respiratory depression – chief hazard
 Use of concomitant sedatives including alcohol
 Self-titration – iatrogenic overdose
 QTc prolongation
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56. Key Teaching Points
Careful of mix up between long acting and short
acting with same mg amount (ex. MS Contin and
MSIR)
Remove old patch before new one put on
Safe disposal issues
Drinking, driving issues
Tell all of your healthcare providers everything that
you take, always
Careful about buying on the Intranet
Sleepers, sedatives
Teach S & S of withdrawal
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57. Key Teaching Points
Never take more or less than prescribed without
calling us
Only you take your pain medication, do not share!
Never alter the medication, i.e. splitting sustained
release medications
Keep in a safe place always!
Medication parties
Middle & High School students; #1 medicine cabinet
thefts
– Inciardi, J.A., et al., 2007
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59. Some of our biggest safety issues
Careful of look alike names and sustained release
versus immediate release
Only witness waste when you see it first, protect your
hard earned license
Careful of which line is which
PCA pumps; double check, double check and double
check-settings and syringe concentration, medication
and document
Instruct patient only to press button
ISMP, February 2007
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60. Descending Pathway
Anatomic path
From cerebral cortex
Brain stem
To dorsal horn
Pain inhibition
Enkephalin excites inhibitory interneurons in the dorsal
horn
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62. Descending Pathway
Mediates voluntary and involuntary motor control
Regulates somatic sensory processing
Regulates the autonomic nervous system
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64. Coexisting CD and Pain
Unique experiences
Anatomic paths of the nervous system have
commonalities
Addictive responses are altered by the physiological
presence of pain
Pain responses are altered by the physiological
presence of addiction.
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66. Endocannabinoids
Research on the adaptations of cells continue with the
recent discover of the cannabinoid receptor and the
subsequent searching and findings of the endogenous
cannabinoids.
Two endocannabinoids, anandamine and 2-
arachidonyl glycerol or 2-AG.
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67. Endocannibinoids
Found in most brain function
Equal balance between endocannibinoids and their
receptors occur (Fride, 2005)
Role in brain plasticity leading to
long term effects on movement and coordination
habit formation
reward and addiction
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68. Figure 5. Concept map of endocannabinoids.

69. Opioid-Induced Pain Hypersensitivity
Opioids may produce abnormally heightened pain
sensations
May share mechanisms with antinociceptive
tolerance
Possibly dose related?
Observed both with acute and chronic use
Current research indicates potential for targets for
new therapies
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70. Questions

71. Nursing Research in Pain Management
Peggy Compton, PhD, RN
Pain and Addiction
Christine Miaskowski, PhD, RN
Gender and Pain
Christine Kovach, PhD, RN
Elders and Pain
Margo McCaffrey, MSN, RN
“Pain is what the patient says it is”
Betty Morgan, PhD, RN
Pain and Addiction
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72. Nursing Research in Pain Management
Rosemary Polomano, PhD, RN
Pain, Rat lab
Keela Herr, PhD, RN
Geriatric Pain
Jo Eland, PhD, RN
Pediatric Pain
Donna Wong, PhD, RN
Smiley Faces, Faces Scale for Pain assessment
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73. What is Flare of Pain?
Same Pain as Chronic (Persistent) Pain
Same Location as Chronic (Persistent) Pain
Different Pain Intensity from Chronic (Persistent)
Pain
Temporary increase in pain intensity from a more
stable baseline pain with otherwise similar
characteristics.
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74. Pain Flare Study
2001-2002 Pain Flare Study
Descriptive study
N= 67
Location: University of Minnesota – Fairview Pain
Management Center
Survey mailed to 75 patients, 67 responses
IRB approval
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75. Pain Flare Study
Purpose of study
Describe the characteristics of and factors contributing
to pain flares in patients with chronic pain who receive
care from the nurse practitioner in Fairview Pain
Management Center
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76. Conclusions
Pain Flare definition: Same Pain, same location,
different intensity
This definition implies that
Pain flare should not represent new pathology
Patient has an ongoing pain problem that has been
relatively stable
No presumption of what baseline pain intensity was
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77. Conclusions
Studying flare gives meaning to the patients
experiences of flare of their pain
Gave patients a “voice”
Assurance that it is not permanent condition
Universality of flares in chronic pain
Pain intensity rating less important in chronic non-
malignant pain than changes in pain intensity
Once contributing factors to pain flares have been
resolved, chronic pain returns to baseline
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78. Envision the Future
Better pain control with fewer side effects
Genome pain management
Helping the brain erase persistent pain
Social Policy that enhances comprehensive approach
to pain management rather than reinforce procedures
to get rid of pain
Abuse deterrent opioid formulations that significantly
reduce diversion and are available for those who need
it.
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79. This platform has been started by Parveen Kumar Chadha with
the vision that nobody should suffer the way he has suffered
because of lack and improper healthcare facilities in India. We
need lots of funds manpower etc. to make this vision a reality
please contact us. Join us as a member for a noble cause.
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80. Our views have increased the mark of the 2,85,000
 Thank you viewers
 Looking forward for franchise,
collaboration, partners.
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81. Contact us:- 011-25464531, 9818569476
E-mail:- nursingcrusade@gmail.com
We are also available on
Justdial New Delhi.
Nursing Crusade Earlier Known
as Nursing Hi Nursing
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