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...