Download - Pain Lec 3rd Year
Pain
Dr.Mohammad Shaikhani.
Pain
An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described
in terms of such damage.
International Association for the Study of Pain
Clinical Terms For The Sensory Disturbances Associated With Pain
Dysesthesia – An unpleasant abnormal sensation, whether spontaneous or evoked.
Allodynia – Pain due to a stimulus which does not normally provoke pain, such as pain caused by light touch to the skin
Hyperalgesia – An increased response to a stimulus which is normally painful
Hyperesthesia - Increased sensitivity to stimulation, excluding the special senses. Hyperesthesia includes both allodynia and hyperalgesia .
Approach To Pain Control
1. Thorough assessment by skilled and knowledgeable clinician
– History
– Physical Examination
2. Discuss with patient/family the goals of care, hopes, expectations, anticipated course of illness,with consideration of investigations and interventions
3. Investigations – X-Ray, CT, MRI, etc - if they will affect approach to care
4. Treatments – pharmacological and non-pharmacological; interventional analgesia (e.g.. Spinal)
5. Ongoing reassessment and review of options, goals, expectations, etc.
TYPES OF PAIN
NEUROPATHICNOCICEPTIVE
Deafferentation Sympathetic Maintained
Peripheral
Somatic• bones, joints• connective tissues• muscles
Visceral• Organs –
heart, liver, pancreas, gut, etc.
Acute vs. ChronicAcute Chronic
Onset Abrupt Gradual
Duration 1 second to 6 months Longer than 6 months
Intensity Mild, moderate, severe Mild, moderate, severe
Etiology Biologically identifiable May not be easily identified
Physical response
Increased BP, HR, RR, dilated pupils, pallor, nausea and vomiting, increase muscle tension and dry mouth
No autonomic nervous system symptoms
Somatic Pain
• Aching, often constant• May be dull or sharp• Often worse with movement• Well localized
Eg/– Bone & soft tissue– chest wall
Visceral Pain
• Constant or crampy• Aching• Poorly localized• Referred
Eg/– CA pancreas– Liver capsule distension– Bowel obstruction
Neuropathic pain
•A variety of mechanisms:• Sensitized primary afferent nociceptors, damaged primary afferents, including nociceptors, become highly sensitive to mechanical stimulation and begin to generate impulses in the absence of stimulation.• There is evidence that this increased sensitivity and spontaneous activity is due to an increased concentration of sodium channels. •Damaged primary afferents may also develop sensitivity to norepinephrine&spinal cord pain-transmission neurons cut off from their normal input may also become spontaneously active. •So both central &peripheral NS hyperactivity contribute to neuropathic pain.
COMPONENT DESCRIPTORS EXAMPLES
Steady, Dysesthetic
• Burning, Tingling
• Constant, Aching
• Squeezing, Itching
• Allodynia
• Hypersthesia
• Diabetic neuropathy
• Post-herpetic neuropathy
Paroxysmal, Neuralgic
• Stabbing
• Shock-like, electric
• Shooting
• Lancinating
• trigeminal neuralgia
• may be a component of any neuropathic pain
FEATURES OF NEUROPATHIC PAIN
Referred Pain:
PainAssessment
“Describing pain only in terms of its
intensity is like describing music
only in terms of its loudness”
von Baeyer CL; Pain Research and Management 11(3) 2006; p.157-162
Pain AssessmentSubjective Data
• Comprehensive pain history includes COLDERR– Character– Onset– Location– Duration– Exacerbation– Relief– Radiation
PAIN HISTORY
Description: severity, quality, location, temporal features, frequency, aggravating & alleviating factors
Previous history
Context: social, cultural, emotional, spiritual factors
Meaning
Interventions: what has been tried?
Example Of A Numbered Scale
• Dose
• Route
• Frequency
• Duration
• Efficacy
• Adverse effects
Medication(s) Taken
Physical Exam In Pain Assessment Inspection / Observation
Overall impression.?
Facial expression: Grimacing; furrowed brow; appears anxious; flat affect
Body position and spontaneous movement: there may be positioning to protect painful areas, limited movement due to pain
Diaphoresis – can be caused by pain
Areas of redness, swelling
Atrophied muscles
Gait
Myoclonus – possibly indicating opioid-induced neurotoxicity
“You can observe a lot just by watching” Yogi Berra
Physical Exam In Pain Assessment Palpation
Localized tenderness to pressure or percussion
Fullness / mass
Induration / warmth
Physical Exam In Pain Assessment Neurological Examination
Important in evaluating pain, due to the possibility of spinal cord compression, and nerve root or peripheral nerve lesions
Sensory examination– Areas of numbness / decreased sensation– Areas of increased sensitivity, such as allodynia or hyperalgesia
Motor (strength) exam - caution if bony metastases (may fracture)
Deep tendon reflexes – intensity, symmetry– Hyperreflexia and clonus: possible upper motor neuron lesion,
such as spinal cord compression or cerebral metastases.– Hyoporeflexia - possible lower motor neuron impairment,
including lesions of the cauda equina of the spinal cord or leptomeningeal metastases.
Sacral reflexes – diminished rectal tone and absent anal reflexes may indicate cauda equina involvement of by tumour
Physical Exam In Pain Assessment Other Exam Considerations
Further areas of focus of the physical examination are determined by the clinical presentation.
Eg: evaluation of pleuritic chest pain would involve a detailed respiratory and chest wall examination.
PainTreatment
Non-Pharmacological Pain Management
Acupuncture
Cognitive/behavioral therapy
Meditation/relaxation
Guided imagery
TENS
Therapeutic massage
Others…
+/- adjuvantNon-opioid
Weak opioid
Strong opioid
Pain persist
s or in
creases
By the
Clock
W.H.O. ANALGESIC LADDER
+/- adjuvant
+/- adjuvant
1
2
3
STRONG OPIOIDS
• most commonly use: – morphine– Hydromorphone (Dilaudid ®)– transdermal fentanyl (Duragesic®)– oxycodone– Methadone
• DO NOT use meperidine (Demerol) long-term– active metabolite normeperidine seizures
OPIOIDS andINCOMPLETE CROSS-TOLERANCE
• Tolerance to a specific opioid is fully “crossed over” to other opioids.
• cross-tolerance unpredictable, especially in:– high doses– long-term use
• divide calculated dose in ½ and titrate
TITRATING OPIOIDS
• Dose increase depends on the situation• Dose by 25 - 100%
EXAMPLE: (doses in mg q4h)
Morphine 5 10 15 20 25 30 40 50 60
Hydromorphone 1 2 3 4 5 6 8 10 12
TOLERANCE
PHYSICAL DEPENDENCE
PSYCHOLOGICALDEPENDENCE /
ADDICTION
TOLERANCE
A normal physiological
phenomenon in which increasing
doses are required to produce
the same effect
Inturrisi C, Hanks G. Oxford Textbook of Palliative Medicine 1993: Chapter 4.2.3
PHYSICAL DEPENDENCE
A normal physiological
phenomenon in which a withdrawal
syndrome occurs when an opioid
is abruptly discontinued or an
opioid antagonist is administered
Inturrisi C, Hanks G. Oxford Textbook of Palliative Medicine 1993: Chapter 4.2.3
PSYCHOLOGICAL DEPENDENCEand ADDICTION
A pattern of drug use characterized
by a continued craving for an opioid
which is manifest as compulsive
drug-seeking behaviour leading to
an overwhelming involvement in the
use and procurement of the drug
Inturrisi C, Hanks G. Oxford Textbook of Palliative Medicine 1993: Chapter 4.2.3
po / sublingual / rectal routes
SQ / IV / IM routes
reduce by ½
Changing Route Of Administration In Chronic Opioid Dosing
Using Opioids for Breakthrough Pain
• Patient must feel in control, empowered• Use aggressive dose and interval
Patient Taking Short-Acting Opioids:• 50 - 100% of the q4h dose, given q1h prn
Patient Taking Long-Acting Opioids:• 10 - 20% of total daily dose given, q1h prn with short-acting opioid preparation
Opioid Side Effects
Constipation – need proactive laxative use
Nausea/vomiting – consider treating with dopamine antagonists and/or prokinetics (metoclopramide, domperidone, prochlorperazine [Stemetil], haloperidol)
Urinary retention Itch/rash – worse in children; may need low-dose naloxone
infusion. May try antihistamines, however not great success
Dry mouth Respiratory depression – uncommon when titrated in
response to symptom
Drug interactions Neurotoxicity (OIN): delirium, myoclonus seizures
OIN: Treatment
Switch opioid (rotation) or reduce opioid dose; usually much lower than expected doses of alternate opioid required… often use prn initially
Hydration
Benzodiazepines for neuromuscular excitation
Adjuvant Analgesics
First developed for non-analgesic indications
Subsequently found to have analgesic activity in specific pain scenarios
Common uses:– Pain poorly-responsive to opioids (eg. neuropathic
pain), or– With intentions of lowering the total opioid dose
and thereby mitigate opioid side effects.
Adjuvants Analgesics
General / Non-specific– corticosteroids– cannabinoids
Neuropathic Pain– Gabapentin– Antidepressants– Ketamine – Topiramate– Clonidine
Bone Pain– Bisphosphonates– (Calcitonin)
InflammationEdema
Spontaneous nerve depolarization
tumor mass effects
CORTICOSTEROIDS AS ADJUVANTS
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IMMEDIATE LONG-TERM
Psychiatric
Hyperglycemia
risk of GI bleedgastritisaggravation of
existing lesion (ulcer, tumor)
Immunosuppression
Proximal myopathy often >15 days
Cushing’s syndrome
Osteoporosis
Aseptic / avascular necrosis of bone
CORTICOSTEROIDS: ADVERSE EFFECTS
DEXAMETHASONE
• Minimal mineralcorticoid effects
• po/iv/sq/?sublingual routes
• perhaps can be given once/day; often given more frequently
• If an acute course is discontinued within 2 wks, adrenal suppression not likely
Treatment of Neuropathic Pain
Pharmacologic treatment• Opioids• Steroids• Anticonvulsants – gabapentin, topiramate• TCAs (for dysesthetic pain, esp. if depression)• NMDA receptor antagonists: ketamine, methadone• Anesthetics
Radiation therapy
Interventional treatment• Spinal analgesia• Nerve blocks
Gabapentin
Common Starting Regimen
– 300 mg hs Day 1, 300 mg bid Day2, 300 mg tid Day 3, then gradually titrate to effect up to 1200 mg tid
Frail patients
– 100 mg hs Day 1, 100 mg bid Day 2, 100 mg tid Day 3, then gradually titrate to effect
Incident Pain
Pain occurring as a direct and
immediate consequence of a
movement or activity
Circumstances In Which Incident Pain Often Occurs
• Bone metastases
• Neuropathic pain
• Intra-abd. disease aggravated by respiration» “incident” = breathing» ruptured viscus, peritonitis, liver hemorrhage
• Skin ulcer: dressing change, debridement
• Disimpaction
• Catheterization
Time
Incident Incident Incident
Pai
n
Having a steady level of enough opioid to treat the peaks of incident pain...
...would result in excessive dosing for the periods between incidents
Fentanyl and Sufentanil
Synthetic µ agonist opioids
Highly lipid soluble• Transmucosal absorption; effect in approx 10 min• rapid redistribution, including in / out of CSF; lasts approx
1 hr.
fentanyl » 100x stronger than morphine
sufentanil » 1000x stronger than morphine
10 mg morphine 10 µg sufentanil 100 µg fentanyl
INCIDENT PAIN PROTOCOL
Step #Medication (50
g/ml)# Micrograms Sublingually
1 Fentanyl 50
2 Sufentanil 25
3 Sufentanil 50
4 Sufentanil 100
(see also http://palliative.info)
• Fentanyl or sufentanil is administered SL 10 min. prior to anticipated activity
• Repeat q 10min x 2 additional doses if needed
• Increase to next step if 3 total doses not effective
• Physician order required to increase to next step if within an hour of last dose
• the Incident Pain Protocol may be used up to q 1h prn
INCIDENT PAIN PROTOCOL ctd...