Professional Documents
Culture Documents
Management
Vanny Le, MD
Assistant Professor
Department of Anesthesiology
Basics of Pain Management
Definitionof Pain
Pain Processing
Pharmacologic Management of Pain
PO medications
PCA
PCEA
Addiction Medicine vs. Pain Medicine
Definition of Pain
“An unpleasant sensory and emotional experience
associated with actual or potential tissue damage,
or described in terms of such damage.” (IASP)
Sensory experience
Cognitive experience
Acutepain generally resolves after 1 month
Chronic pain is pain occurring ≥ 3 months
Definition of Pain
Nociception vs. Pain
Nociception
Physiologic process of activation of neural pathways
by stimuli that are potentially or currently damaging
to tissue
Pain
Conscious experience: perception of pain
Composite of alterations in somatosensory
processing following injury to tissues and/or nerves
and psychosocial factors
Pain Processing
Anatomy of Nerve Fibers
Activation of
Nociceptive Action
Voltage-sensitive
Stimulus Potential
Cation Channel
• Thermal • NaV
• Chemical • CaV
• Mechanical
Pain Processing
Perception
• Subjective sensation of
pain
Modulation • Activation of primary and
• Neural activity altered secondary somatosensory
and limbic cortices
along pain pathway
• Attenuation or
enhancement of pain signal
Transmission
• Action potential is
conducted through nervous
system
• Periphery (1st order) to
Spinal neurons (2nd order) to
Brainstem/Thalamus to
Transduction Cortex
• Peripheral terminals of
primary afferents
• Stimuli converted to
action potentials
Pain Processing
Transition from Acute to Chronic Pain
Continued noxious stimulation
Produces greater noxious sensation
Reduces the stimulus threshold or intensity
necessary to perceive noxious sensation
PersistentC fiber activation at Laminae I and V
enhances response to subsequent stimulation and
augments size of receptive field
Pain Processing
Spinal Modulation
Central sensitization
Neuronal plasticity
Previous innocuous stimuli is perceived as painful
Afferent input from adjacent dermatomal areas now
produces neuronal excitation
Cellular damage and migration of inflammatory cells
increases inflammatory soup
Axonal sprouting and the formation of neuroma
Increased neuronal activation by cytokines, prostaglandins,
etc.
Pain Processing
Spinal Modulation
Wind-up phenomenon
Repeated stimulation of C fibers activates laminae I and V
Progressive increase in number of discharges
Expansion of receptive field
Increase in spontaneous discharge rate
Non-noxious stimuli can activate nociceptive neurons
Phenotypic switch
Activation of large-diameter Aβ fibers following injury
A beta fibers now express substance P
Transmit noxious stimulation from periphery
Different Types of Pain
Somatic Pain Neuropathic Pain Visceral Pain
• Constant, well- • Diffuse or follows • Vague distribution
localized pain nerve distribution and quality
• Aching, throbbing, • Shooting, burning, • Deep, dull, aching,
sharp, or gnawing electricity-like dragging,
• Tingling and squeezing, or
numbness pressure-like
sensation
Pharmacologic Management
Pharmacologic Management
Pharmacologic Management
Adjuvants
NSAIDs
Acetaminophen
Muscle relaxants
Tizanidine
Baclofen
Ketamine
Lidocaine patch
Capsaicin
Pharmacologic Management
Adjuvants
Antidepressants – TCAs and SNRIs
Duloxetine (Cymbalta)
Nortriptyline, amitriptyline
Anticonvulsants
Gabapentin (Neurontin) and Pregabalin (Lyrica)
Oxcarbazepine (Trileptal)
Lamotrigine (Lamictal)
Topiramate (Topamax)
Zonisamide (Zonegran)
Opioids
Morphine
Hydromorphone (Dilaudid)
Hydrocodone (Vicodin)
Oxycodone
Fentanyl
Methadone
Buprenorphine (Butrans, Subutex, Suboxone)
Tramadol
Tapentadol (Nucynta)
Equianalgesic
Drug Duration Half-life Route
Dosage
Codeine 4–6 h 3h IM 120 mg
PO 200 mg
Fentanyl 1–2 h 1.5–6 h IM 0.1 mg
Hydrocodone 4–8 h 3.3–4.5 h PO 30 mg
Hydromorphone 4–5 h 2–3 h IM 1.3–1.5 mg
PO 7.5 mg
Levorphanol 6–8 h 12–16 h IM 2 mg
PO 4 mg
Meperidine 2–4 h 3–4 h IM 75 mg
PO 300 mg
Methadone 4–6 h 15–30 h IM 10 mg
PO 10–20 mg
Morphine 3–7 h 1.5–2 h IM 10 mg
PO 30–60 mg
Oxycodone 4–6 h NA PO 15-30 mg (20 mg)
Oxymorphone 3–6 h NA IM 1 mg
PR 10 mg
130-200 mg *
Propoxyphene 4–6 h 6–12 h PO
(Inconclusive data)
Opioid equivalents
Morphine IV to Morphine PO = 1:3
Dilaudid to Morphine
Naïve 1:7
Tolerant 1:5
Dilaudid IV to Dilaudid PO
Naïve 1:7.5
Tolerant 1:5
Morphine to Oxycodone = 1:1.5
Fentanyl patch conversion
Converting Opioids
IV to PO or Changing Opioids
Calculate the total daily dose of the original opioid (add
long-acting and rescue doses).
Use the Conversion Chart to convert from an IV to PO
dose.
Or use the Conversion Chart to convert original opioid to
an alternative opioid.
Adjust the dose for incomplete cross tolerance by
reducing dose by 25%-50%.
Divide adjusted dose by 24 to obtain hourly opioid
infusion rate.
Converting Opioids
A patient is taking sustained-release oxycodone,
100 mg every 12 hours, but has developed
intolerable sedation. She would like to try an
immediate-release opioid agent, hydromorphone.
What is the equivalent dose of hydromorphone?
Converting Opioids
Oxycodone 100 mg Q12 = 200 mg total/day
Oxycodone to Morphine = 1:1.5
Oxycodone 200 mg = Morphine 300 mg
Morphine to Dilaudid = 5:1
Morphine 300 mg = Dilaudid 60 mg
Dilaudid 60 mg x .75 = 45 mg/day
Dilaudid 45 mg/day / 6 doses per day = 7.5 mg
~Dilaudid 8 mg Q4 hours
Patient Controlled Analgesia
PCA nomenclature
Basal/demand dose/lockout/4 hour lockout
Morphine PCA - 0/1/6/0
Dilaudid PCA – 0/0.2/6/0
Morphine
Morphine
Remifentanil
Remifentanil
Long-Acting Opioid for Baseline Pain
Long Acting Opioids
Pharmacologically long-acting Pharmaceutically long-acting
>Oxycodone (Oxycontin)
Oxymorphone (Opana ER)