1. Acute and chronic pain
Management
k/Mariam Tamrat

2. Pain lecture
 Module Title: Anaesthesia Management III
 Course Title:- ICU and Pain Management
 Course Number:- Anst 5172
 Credit Hours:- 3
 Course Description:- This course is designed to enable the anaesthetist to
effectively assess and manage pain as well as identify, assess and manage
patients who are critically ill.
21/08/09 2

3. Cont..
 Course Objectives:-
 By the end of the course the student will be able to:
 Define pain & explain the physiology of pain
 Competently assess & manage acute post operative and non post-operative
pain.
 Understand the basics of chronic pain management
21/10/20
09 3

4. Pain…
What is the real definition of pain?
And what is pain management??
How can this information help me???
18/8/09
4

5. Group Assignment
 G1. Describe the characteristics and genesis of pain
 G2. Explain the categories of pain
 G3.Manage pain Effectively
 G4.Consequences of untreated pain
Submit after a week.

6. Definition of Pain
An Unpleasant Sensory and Emotional
Experience Associated with Actual or
Potential Tissue Damage, or Described
in Terms of Such Damage.

7. Physiology of Pain
INTRODUCTION
 Pain is defined by the International Association for
the Study of Pain (IASP) as ‘an unpleasant sensory
and emotional experience associated with actual
or potential tissue damage or described in terms of
such damage’.
 Pain has objective, physiological sensory aspects
as well as subjective, emotional and psychological
components.
 The term ‘nociception’ is used only to describe the
neural response to traumatic or noxious stimuli.

8. What areas in the CNS are involved
in pain generation and perception?
 Afferent pathways,
 CNS and efferent pathways.
 Nociceptors transmit pain sensation to
the dorsal horn of the spinal cord
(substantia gelatinosa, laminae) across
to the contralateral spinal cord and
through spinothalamic tracts to the
thalamus 21/o8/20
09
8

9. PERIPHERAL TRANSMISSION
 Transmission occurs from the peripheral
receptor to the brain as one continuous
process, for convenience this section is divided
into peripheral and central transmission.
 Peripheral transmission of pain consists of
production of electrical signals at pain nerve
endings (transduction) followed by
propagation of those signals through the
peripheral nervous system (transmission).

10. Transduction
 The primary sensory structure that
accomplishes transduction is the nociceptor.
Most nociceptors are free nerve endings that
sense heat, mechanical and chemical tissue
damage. Several types are described:
 1. mechanoreceptors, which respond to
pinch and pinprick,
 2. silent nociceptors which respond only in
the presence of inflammation, and
 3. polymodal mechano-heat nociceptors.

11. Physiology of Pain
 Nociceptors
 Stimulus Transmission
 Termination
 Modulation

12. The pain experience begins with the
nociceptors.
 These are afferent nerves that respond to
noxious stimulation.
 Different nociceptors may preferentially react
to a specific kind noxious stimuli, such as
mechanical or temperature sensation.
 Different types of nociceptors may be found
in different sites: for example, the most
common cutaneous receptor is the polymodal
C fiber, which responds to pressure,
temperature and chemical stimuli, whereas
skeletal muscle contains mostly
chemoreceptors.

13. Cont..
 All nociceptors have an initial high threshold
to noxious stimuli, which decreases with
repeated stimuli.
 It is tempting to stop at this point and treat
pain as a simple reflex, in which the
nociceptor receives a noxious response and
transmits it to the brain. Much pain
treatment is based on this naive assumption.
 It is, in reality, a long and complicated
journey between the nociceptor and the
brain. Signals from the nociceptor are
transmitted to the spinal cord.

14. Cont..
 This is done mainly by two fibers: Ad fibers
and C fibers.
 Ad fibers are myelinated and provide the
initial pain response.
 C fibers are unmyelinated and probably
cause the slower response felt several
seconds after an injury.
 Most of these fibers enter the spinal cord
through the dorsal root ganglion and
terminate in the dorsal horn of the spinal
cord.

15. cont
 Generally they terminate ipsilaterally, but a
small number will cross to the contralateral
side.
 The clinical significance of this is not clear, but
it may explain the incomplete pain relief seen
after unilateral surgical ablation of this area.
 The dorsal horn is organized into areas, called
laminae, and certain pain fibers will
predictably go to specific laminae

16. Cont..
In the laminae the fibers synapse with
second order neurons, which take various
pathways to the brain.
 The best understood pathways are the
spinothalamic and spinoreticular
pathways.
 These pathways are named after their
points of origin and termination.

17. Modulation of the Stimulus.
Local chemicals.
 No "pain transmitter" has been identified. However,
many substances can modulate a nociceptor's response
to noxious stimuli.
 The best understood is substance P, which may work
indirectly through vasodilatory effects.
 Other chemicals that have a role in pain modulation
include prostaglandin, serotonin, histamine,
acetylcholine, bradykinin, slow-reacting substance of
anaphylaxis (SRS-A), calcitonin-gene-related peptide
(CGRP), and potassium.

18. Higher down-modulation.
 Virtually every part of the pain system can
reciprocally affect other parts, and the
system should be envisioned as bidirectional.
The cortex, in particular, can influence all
previous stages of pain transmission through
a variety of means.
 The most obvious is through attentional
processes. Most of us are familiar with
stories of combat victims who performed
heroic acts after injury, apparently unaware
of their pain until hours later.

19. Cont..
 More common are reports from chronic pain
patients that their pain seems to get worse
at night, presumably when there is less
distraction.
 The meaning of pain can also influence its
perception--for example, pain perceived as
jeopardizing health (e.g.. cancer pain) can
seem worse than pain that is not life
threatening.
 Finally, a variety of learned phenomena,
such as cultural factors, can affect one's
perception and expression of pain.

20. Physiology of Pain
 Multiple
 Redundant
 Reciprocal
 Complex

21. Assessment of Pain
Immediate Pain, Physical Functioning, Psychological Factors Pain
Behaviors, Objective Correlates and Pain is always subjective.
 It is the result of a variety of factors.
 The assessment of pain, therefore, must rely on methods that are
necessarily subjective and multidimensional.
 Currently there is no universal "gold standard" for pain assessment,
and it is not the purpose here to outline a blueprint for such an
assessment.
 However, any approach must acknowledge the many different
dimensions of the pain experience.
 These dimensions are discussed in the following slides and include
the areas bulleted above.

22. Cont..
 Thus, the take home is that pain is very
complex.
 It is not like other senses. There are
multiple systems involved, and they are
reciprocally influenced by what appears
to be a central control over the
process.

23. Assessment: Immediate Pain
 Intensity
 Location
 Affective Response
 Composite Measures

24. Intensity.
 Most commonly, we wish to quantify the intensity of the pain.
 We might give the patient a list of adjectives to describe
the pain, usually listed in order of increasing intensity.
 Alternately, we might ask the patient to give a numerical
value to the pain intensity.
 In the latter case, we often ask patients to rate the pain
from one to 10, one being no pain and 10 the most pain
they can imagine.
 The latter approach is particularly practical in that it
rapid and easy to do, and most patients can readily
understand the task.
 This can help us track changes in intensity over time, for
example, in response to treatment.

25. Introduction
Classification of Pain
 Acute or Chronic
 Nociceptive or Neuropathic

26. Introduction
Pain Signal Processing:
Pain perception is a complex phenomenon
involving sophisticated transmission
pathways in the nervous system
 With many pain signal transmission points,
there exists opportunity!

27. Acute Pain
 Pain in Perioperative Setting
 Pain in Patients with Severe or Concurrent
Medical Illnesses (Pancreatitis)
 Acute Pain Related to Cancer or Cancer
Treatment
 Labor Pain

28. Acute Perioperative Pain
Pain that is Present in a
Surgical Patient Because of
Preexisting Disease, the
Surgical Procedure, or a
Combination of Both

29. Why Treat Pain?
 Basic human right!
 ↓ pain and suffering
 ↓ complications –
 ↓ likelihood of chronic pain development
 ↑ patient satisfaction
 ↑ speed of recovery → ↓ length of stay → ↓
cost
 ↑ productivity and quality of life

30. Adverse Effects of Poor Pain Control
 CVS: MI, dysrhythmias
 Resp: atelectasis, pneumonia
 GI: ileus, anastomotic failure
 Endocrine: “stress hormones”
 Hypercoagulable state: DVT, PE
 Impaired immunological state
Infection, cancer, wound healing
 Psychological:
Anxiety, Depression, Fatigue

31. Importance of
Pain Management
 Adequate Pain Control
 Reduce the Risk of Adverse
Outcomes
 Maintain the Patient’s Functional
Ability, as well as Psychological Well-
being
 Enhance the Quality of Life
 Shortened Hospital Stay and Reduced
Cost

32. Adverse Outcomes Associated with
Management ofAcute Pain
 Respiratory Depression
 Circulatory Depression
 Sedation
 Nausea and Vomiting
 Pruritus
 Urinary Retention
 Impairment of Bowel Function

33. Adverse Outcome of Undertreatment
of Acute Pain
Thromboembolic or Pulmonary
Complications
Needless Suffering
Development of Chronic Pain

34. Adverse Effects of Poor Pain Control
“… it remains a common misconception amongst
clinicians that acute postoperative pain is a
transient condition involving physiological
nociceptive stimulation, with a variable
affective component, that differs markedly in its
pathophysiological basis from chronic pain
syndromes.”

35. Pain Assessment
Pain History
O – Onset
P – Provoking / Palliating factors
Q – Quality / Quantity
R – Radiation
S – Severity
T – Timing

36. Pain Assessment
Origin of Pain
Acute Pain
ie. Incisional pain, acute appendicitis
Chronic Pain
ie. Chronic back pain
Acute on Chronic Pain
Acute and chronic causes may or
may not be related to each other

37. Pain Assessment Tools
 In Pediatric Patients:
Physiologic and Behavioral Indicators
of Pain ( Infants, Toddlers, Nonverbal
or Critically Ill Children)
Face Scale (Age 3-10 yrs)
Visual Analogue Scales (Age 10-18)

38. Pain Assessment .VAS,VPIS,0-10 NPIS &
FACES SCALE
Visual Analogue Scale

41. Pain Assessment
Current Pain Medications
 Accuracy and detail are very important!
 Name, dose, frequency, route
 ie. Oxycontin 10mg PO TID
 Don’t forget to re-order or factor in patient’s pre-
existing pain Rx usage when writing orders
Conflicts with HPI(Hx, of pr. Illness) PMH(past med. Hx)
 Renal disease → avoid morphine, NSAID’s
 Vomiting → avoid oral forms of medication
 Short gut/high output stomas → avoid CR
formulations

42. Pain Assessment
Allergies / Intolerances
 Drug allergies
 Document drug, adverse reaction and
severity
 Intolerances
 Nausea / vomiting, hallucinations,
disorientation, etc.
Very important to differentiate between an allergy and an intolerance!

43. Methods to Treat Pain
Pharmacologic manegement
 Alter Nerve Conduction (Local
Anesthetics)
 Modify Transmission in the Dorsal Horn
(Opioids, Antidepressants)

44. Routes of Administration
 PO
 PR
 IV
 IM
 Transdermal
 Transmucosal
 Epidural
 Intrathecal

45. Methods to Treat Pain
 Pharmacologic
 Medications (po, iv, im, sc, pr, transdermal)
 Acetaminophen
 NSAIDs
 Opioids
 Gabapentin
 NMDA antagonists
 Alpha-2 agonists
 Procedures
 Regional Anesthesia
 LA infiltration at incision site
 Surgical Intervention
 Non-Pharmacologic / Non-Surgical

46. WHO Analgesic Ladder

47. Non-Opioid Analgesics
Acetaminophen
NSAIDs (Aspirin, Ibuprofen,
Ketorolac,
COX-2 Inhibitors)
Lidocaine Patch (Lidoderm)

48. NSAIDs
 Relieve of Mild to Moderate Pain
 Complication:
GI Discomfort
GI Bleeding (Inhibition of COX-1)
Nephrotoxicity
Inhibition of Platelet Aggregation
Osteogenesis

49. Ketorolac
Potent Analgesic
Parenteral (IV or IM)
15-30 mg Q 6hr
Patients Older than 16 yrs
Should not Exceed 5 days

51. Multimodal Analgesia
Using more than one drug for pain control
 Different drugs with different mechanisms/sites
of action along pain pathway
 Each with a lower dose than if used alone
 Can provide additive or synergistic effects
 Provides better analgesia with less side effects
(mainly opiate related S/E)
Always consider multimodal analgesia when
treating pain

52. Acetaminophen
 First-line treatment if no contraindication
 Mechanism: thought to inhibit prostaglandin
synthesis in CNS → analgesia, antipyretic
 Typical dose: 650 to 1000 mg PO Q6H
 Max dose: 4 g / 24 hrs from all sources
 Warning: ↓ dose / avoid in those with liver damage

53. NSAIDs
 Also, first-line treatment
 Mechanism
 Block cyclooxygenase (COX) enzyme
→ ↓ prostaglandin synthesis
 COX-2 → Prostaglandins → pain,
inflammation, fever
 COX-1 → Prostaglandins → gastric
protection, hemostasis

54. NSAIDs
 Warnings: ↓dose / avoid if
 GI ulceration
 Bleeding disorders / Coagulopathy
 Renal dysfunction
 High cardiac risk – COXII inhibitors
 Asthma
 Allergy
 ?Avoid celecoxib if allergic to Sulpha
Concern for anastomotic leaks?

55. Opioid Analgesics
 Bind to Opioid Receptors:
 Mu, Delta and Kappa
 Morphine, Hydromorphone, Meperidine,
Fentanyl, Codeine, Methadone,
Oxycodone, Hydrocodone, Tramodol
 Opioids may be Combined with NSAIDs
to Enhance the Opioid Analgesic Effect

56. Opioids
Key Points:
 Centrally acting on opioid receptors
 No ceiling effect
 High dose/response variability in non-opiate
users
 Previous dependence creates a challenge in
acute on chronic pain management cases
 Balancing safety and efficacy can be difficult
(OSA patients)
 Side effects may limit reaching effective dose

57. Opioids
Side Effects
 Nausea / Vomiting
 Sedation
 Respiratory Depression
 Pruritus
 Constipation
 Urinary Retention
 Ileus
 Tolerance

58. Opioids
 Morphine
 Most commonly prescribed opioid in hospital
 Metabolism:
 Conjugation with glucuronic acid in liver and kidney
 Morphine-3-glucuronide (inactive)
 Morphine-6-glucuronide (active)
 Impaired morphine glucuronide elimination in renal failure
 Prolonged respiratory depression with small doses
 Due to metabolite build-up (morphine-6-glucuronide)

59. Opioids
 Hydromorphone (Dilaudid)
 Better tolerated by elderly, better S/E profile
 Preferred over morphine for renal disease
patients
 Low cost, IV and PO forms available
 Oxycodone
 Good S/E profile, but $$
 PO form only
 Percocet (oxycodone + acetaminophen)

60. Opioids
 Codeine
 1/10th Potency of morphine
 Metabolized into morphine by body
 Ineffective in 10% of Caucasian patents
 Challenge with combination formulations
 Meperidine (Demerol)
 Not very potent
 Decreases seizure threshold, dystonic reactions
 Neurotoxic metabolite (normeperidine)
 Avoid in renal disease

61. Opioids - Formulations
 Short acting forms
Need to be dosed frequently to maintain
consistent analgesia
 Controlled Release forms
Provides more consistent steady state level
Helpful for severe pain or chronic pain situations
Never crush / split / chew controlled release pills

62. Opioids
Drug PO
mg
IV
mg
Starting
Oral Dose
mg
Comments
Morphine 30 10 15-30 MS Contin, Release 8-12 hrs
MSIR for BTP
Hydro-
morphone
7.5 1.5 4-8 Duration Slightly Shorter
than Morphine
Meperidine 300 75 Duration Slightly Shorter
than Morphine
Normeperidine Causes CNS
Toxicity
Methadone 20 10 5-10 Qd Long Half-Life, 24-36 hrs
Accumulates on Days 2-3
Fentanyl 0.02-
0.05
Fentanyl Patch, 12 hrs Delay
Onset and Offset

63. Dose Regimens for PCA
Drug Bolus Dose
(mg)
Lock-Out
(Minutes)
Morphine 0.5-2 5-15
Hydromorphone 0.1-0.2 5-10
Fentanyl 0.01-0.02 5-10

64. Opioid Equianalgesic Table
Drug Equianalgesic Dose Initial Adult Dose (>50kg)
IV/SC/IM Oral IV/SC/IM Oral
Morphine 10 mg 20-30 mg 2-10 mg q4h 5-20 mg q4h
Hydromorphon
e
1.5 mg 4-7.5 mg 0.5-2 mg q4h 1-4 mg q4h
Oxycodone N/A 10-20 mg N/A 5-10 mg q4h

65. Opioids – PCA

66. Opioids – PCA
 Allows patient to reach their own
minimum effective analgesic
concentration (MEAC)
 Rapid titration (Morphine 1mg IV
every 5 min)
 Better analgesia and less side
effects than IM prn

67. Gabapentin
 Anti-epileptic drug, also useful in:
Neuropathic pain, Postherpetic neuralgia,
CRPS
 Blocks voltage-gated Ca channels in CNS
 Additive effect with NSAIDs
 Reduces opioid consumption by 16-67%
 Reduces opioid related side effects
 Drowsiness if dose increased too fast

68. Management of Side Effects
 Nausea / Vomiting
 Ondansetron (Zofran)
 Dimenhydrinate (Gravol)
 Metoclopramide (Maxeran)
 Changing medication(s) / ↓ dose
 Pruritus
 Diphenhydramine (Benadryl)
 Changing medication(s) / ↓ dose

69. Regional Anesthesia

70. Interventional
Management
Epidural Analgesia (Continuous
Lumbar or Thoracic Epidural
Catheter Placement, PCEA)
Spinal Analgesia
Peripheral Nerve Block ( Single
Shot or Continuous)

71. Regional Anesthesia
 Neuraxial Techniques
Spinal (subarachnoid) anesthesia
Epidural anesthesia (lumbar and
thoracic)

72. Anatomy of
Epidural Space
 Surrounds the Dural
Sac
 Anteriorly: Post.
Long. Ligament
 Posteriorly:
Ligamentum Flavum
 Laterally: Pedicles and
Intervertebral Foramina

73. Anatomy of Epidural Space
 AP Dimension of the Epidural Space is Largest
in the Lumbar Region, 5-6 mm
 In Thoracic Region the AP Dimension
Decreases but the Space is More Continuous

74. MIDLINE SAGITTAL VIEW OF THE LUMBAR SPINE

75. x

80. Regional Anesthesia
 Involves blockade of nerve impulses using local anesthetics (LA)
 LA bind sodium channels preventing propagation of action potentials
along nerves
 Wide variety of LA with different characteristics:
 ie. Lidocaine – fast onset, short duration of action
 ie. Bupivacaine (Marcaine) – slow onset, longer duration

81. Regional Anesthesia
 Peripheral Nerve Blocks
 Upper Limb: Brachial plexus
 Lower Limb: Femoral, sciatic, popliteal, ankle
 Abdomen: TAP blocks
 Thoracic: Paravertebral, intercostal blocks
 Use of Ultrasound Imaging has revolutionized peripheral
nerve blockade
 Safety?
 Accuracy / Improved Success
 Efficiency

82. Benefits of
Epidural Analgesia
 Superior analgesia to IV PCA in open abdominal procedures &
specifically in colorectal surgery
 Reduce incidence of paralytic ileus
 Blunt surgical stress response
 Improves dynamic pain relief
 Reduces systemic opiate requirements
 Facilitates early oral intake, mobilization and return of bowel fx
when part of fast track protocols

83. Epidural Analgesia
 Recommended as part of ERAS/fast track protocols for
colon/colorectal surgery
 Increased incidence of hypotension and urinary retention
 Management of postoperative hypotension?

84. Contraindications to
Neuraxial Blockade
 Absolute:
 Pt refusal or allergy to LA
 Uncorrected hypovolemia
 Infection at insertion site
 Raised ICP
 ? Coagulopathy
 Relative:
 Uncooperative patient
 Fixed cardiac output states
 Systemic infection/sepsis
 Unstable neurological disease
 Significant spine abnormalities or surgery

85. Management of
Opioid Overdose

86. Management of
Opioid Overdose
 For ↓LOC, somnolent patient:
 Stimulate patient
 Vitals/Monitors/Lines
 Airway
 Breathing
 Circulation
 CODE BLUE? CCRT? ICU? APS

87. Opioid Overdose Management
 Opioid Reversal
 Naloxone - opioid antagonist
 Reverses effects of opioid overdose (for 30-45min)
 MUST BE diluted before use:
 0.4mg ampule
 Dilute: 1mL Naloxone + 9mL Saline = 0.04 mg/mL
 Give 0.04 to 0.08 mg (1 to 2 mL) IV q3-5 minutes
 If no change after 0.2mg, consider other causes

88. Opioid Overdose Management
 Ddx:
 Seizure, stroke
 Hypoxia, Hypercarbia
 Hypotension
 Other medication effect
 Severe electrolyte or acid base abnormalities
 MI
 Sepsis
 …..etc.

89. Acute Pain Service
 Consult service for complex / specialized pain
management
 Anesthesia Staff + Advanced Practice Nurses
 Many post-op patients will be followed by APS
 If APS involved, APS must write all pain Rx
 Call for:
 Advice
 Difficult to manage cases

90. Summary
 Accurate pain assessment
 Make sure to continue or account for patient’s pre-hospital pain regimen
 Use Multimodal pain management
 Discharge pain management plan
 Acute Pain Service available 24 hrs/day

91. Summary
 Superior analgesia, ↓ side effects means:
 Improved patient satisfaction
 Better rehabilitation
 Earlier functional return
 Earlier discharge from hospital
 ↓ likelihood of chronic pain
 Reduced health care costs

92. Why Treat Pain?
 Basic human right!
 ↓ pain and suffering
 ↓ complications –
 ↓ likelihood of chronic pain development
 ↑ patient satisfaction
 ↑ speed of recovery → ↓ length of stay → ↓ cost
 ↑ productivity and quality of life

93. Adverse Effects of Poor Pain
Control
 CVS: MI, dysrhythmias
 Resp: atelectasis, pneumonia
 GI: ileus, anastomotic failure
 Endocrine: “stress hormones”
 Hypercoagulable state: DVT, PE
 Impaired immunological state
 Infection, cancer, wound healing
 Psychological:
 Anxiety, Depression, Fatigue

94. Importance of
Pain Management
 Adequate Pain Control
 Reduce the Risk of Adverse Outcomes
 Maintain the Patient’s Functional Ability, as well as
Psychological Well-being
 Enhance the Quality of Life
 Shortened Hospital Stay and Reduced Cost

95. Chronic pain management

96. Outline
 Definition
 Common Pain Syndromes
 Oral therapy
 Opioids
 Antidepressants
 Anticonvulsants
 Epidural Steroid injections
 Trigger Point Injections
 Non pharm: TENS unit, heat/cool
 Spinal cord stimulator
 Cancer Pain

97. Definition
 Chronic Pain: pain that persists beyond the usual course
of an acute disease or after a reasonable time for
healing to occur
 Often complex with patients having biologic disease that
coexists with congnitive, behavioural, and social factor
 May be nociceptive, neuropathic, or both
 Nociceptive: due to noxious stimulation of tissue that
activates nociceptors
 Neuropathic: due to prolonged injury of the nerve
fiber/neural structures

98. Common Pain Syndromes
 Low Back Pain
 Neuropathic Pain
 Diabetic Neuropathy
 Post-herpetic neuralgia
 Chronic Regional Pain Syndrome (CRPS)
 Type I and Type II

99. Low Back Pain
 One of the most common reasons people seek medical
attention
 Between T12 to sacro-coccygeal joint
 Conservative management
 60-70% patients recover in 6 weeks
 90% patients recover in 12 weeks
 After 12 weeks, recovery in uncertain

100. Low Back Pain
 Lumbosacral pain – localized to the back
 Radicular pain – distributed in the area of a nerve

102. Radicular Pain
 Signs: numbness, weakness, loss of deep tendon
reflexes in area of affected nerve root
 Acute Radicular Pain:
 usually due to a herniated nucleus pulposus (“herniated
disc”) or foraminal narrowing that causes inflammation of
the nerve root
 Chronic Radicular Pain:
 requires indepth diagnostics to find source, often with MRI

103. Lumbosacral Pain
 Acute: ususally due to myofascial injury
 Chronic: may arise from injury of many parts of the
vertebral unit
 i.e. sacroiliac joint, lumbar facts, intervertebral discs
 Diagnostic nerve blocks into these areas by pain specialist
with local anesthetic may help figure out cause

106. Neuropathic pain
 Pain following injury to the nervous system
 Two common examples
 Diabetic neuropathy
 Postherpetic neuralgia

107. Diabetic Neuropathy
 Occurs in advanced diabetes mellitus (both Type I and
Type II)
 Peripheral – usually first presents in the feet
 Pt having numbness, tingling, burning sensation

108. Postherpetic Neuralgia
 Occurs 3-6 months after acute infection of herpes zoster
(also called varicella zoster or Shingles)
 Usually in immunocompromised or elderly patients
 Pts have episodic sharp pain in a dermatomal
distribution
 Zoster infection can now be prevented by a vaccine

109. Complex Regional Pain
Syndrome (CRPS)
 Due to a known injury
 Pain disproportionate to original injury
 Pain often severe and burning, pt may have joint stiffness,
atrophic changes in muscle
 Accompanied by sympathetic nerve dysfunction
 Changed in vasoconstriction and vasodilation, changes in
temperature, loss of hair in the affected region
 2 Types
 CRPS I: absence of known nerve injury
 CRPS II: known nerve injury

110. Oral Pain Medications
 Opioids
 Antidepressants
 Anticonvulsants

111. Opioids
 See “Acute Pain” lecture for mechanism
 Oral Opioids include:
 Morphine sulfate
 Codeine
 Hydromorphone
 Tramadol
 Oxycodone
 Some opioids (morphine, oxycodone) come in
immediate and sustained release formulations

112. Opioids
 Pt develop tolerance quickly and can require escalating
doses
 May need to “rotate” opioids to have continued effect
 Manage side effects
 Constipation
 Nausea, Vomiting

113. Antidepressants
 Have an analgesic effect that occur at lower doses than
needed for their antidepressant action
 Often helpful for neuropathic pain
 Mechanism: blockade of presynaptic reuptake of
serotonin, norepinephrine, or both
 Older tricyclic antidepressants are more effective
analgesics than newer SSRIs (selective serotonin
reuptake inhibitors)
 Commonly use tricyclic antidepressants
 Nortryptiline
 Amitryptiline

114. Anticonvulsants
 Useful for neuropathic pain
 Mechanism: block voltage-gated sodium channels and
suppress spontaneous neural discharges
 Examples:
 Gabapentin
 Carbamezapine (first line for trigeminal neuralgia, which
is a distinct syndrome from post-herpetic neuralgia)

115. Epidural Steroid Injections
 Useful for patients with radicular back pain
 Usually a combination of local anesthetic (lidocaine 1%)
and a steroid is given
 Local Anesthetic provides rapid relief of pain
 Steroid takes a couple days to work, but will reduce
inflammation of nerve root and provide more long term
relief
 Typical Steroids: methylprednisolone or triamcinolone
 Usually done with x-ray/fluoroscopy by pain specialist
 Epidural needle is usually smaller gauge than typically
used in the OR.

116. Trigger Point Injection
 Indication: Myofascial pain – often in upper or lower
back
 Technique:
 Identify “trigger points”: areas of the back that are
particularly tender to palpation and reproduce the back
pain
 Mixture of lidocaine and bupivacaine
 Syringe with 25g needle injects ~2ml of local anesthetic
into trigger point
 While doing so, move the needle in many directions to
break up the muscle fibers
 The main benefit is from the needle breaking up the
contracted muscle fibers.

117. Non-pharmacologic
 Heat/Cool to affected area
 Transcutaneous Electrical Nerve Stimulation (TENS Unit)
– a device that provides external vibration to the painful
area
 Stimulates large afferent fibers
 Thought to be a distracting input that will reduce the
amount of pain sensed

118. Management contd..
Non-pharmacological
interventions
 Massage
 Diversion therapy
 Relaxation therapy
 Heat & cold
applications
 Yoga
18/08/2009
118

119. Non-pharmacologic
 Heat/Cool to affected area
 Transcutaneous Electrical Nerve Stimulation (TENS Unit)
– a device that provides external vibration to the painful
area
 Stimulates large afferent fibers
 Thought to be a distracting input that will reduce the
amount of pain sensed

120. Spinal Cord Stimulator
 A small device is surgically implanted with electrodes in
the epidural space
 Mechanism: activation of descending modulating
systems and inhibition of sympathetic outflow
 Indications:
 Spinal cord lesions, phantom limb pain, ischemic lower
extremity pain
 Still an area with much research.

121. Cancer Pain
 Pain is the most common presenting symptom of
undiagnosed malignancy
 May be due to cancer invasion or cancer treatment
 Infiltration into bone or nerves is especially painful
 May also have pain from chemotherapy, radiation, or surgical
treatment
 Primary focus is treatment of malignancy but may
require specific treatment of symptoms as well

122. Cancer Pain Treatment
 Multimodal
 Includes
 Opioids – mainstay
 Many routes of administration – pills, liquid, transdermal
patch, buccal, IV
 Tricyclic antidepressants
 Anticonvulsants
 Implantable intrathecal drug delivery
 Palliative sugery
 Nerve blocks with agents that permanently lyse the nerves
 Celiac plexus block for pancreatic cancer

123. hhhhhhhhhhhhhhhhh
define
pain
nociception
acute
NSAID
ADJUVANTS
OPIOIDS
chronic
Non-
pharmacologic
HeatTranscutaneous
Electrical Nerve
Stimulation (TENS Unit) pharmacologic