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Pain Management
Dr. Lamya Alnaim
Pain is a Very Significant ProblemPain is a Very Significant Problem
Pain has negative effects on sleep, work, enjoyment of activities, sexual function, and personal interactions
Multiple studies show pain of all types is under treated
Pain is a Very Significant Problem
Good medications and treatments are available
Barriers (patient and caregiver) include lack of education, attitudes (myths, cultural differences), and regulatory/legal issues
Definition: Acute Pain An unpleasant sensory and emotional
reaction/sensation secondary to tissue damage Arises from injury, trauma, spasm, or disease
of the skin, muscles, somatic structure or viscera.
Corresponds to the degree of injury Self limiting- limited duration
Definition: Acute Pain Serves a purpose
By inducing an organism to withdraw from or avoid a noxious stimulus.
Responds to conventional therapy. Decreases in intensity as the damaged area
heals and tissue repair takes place.
Definition of Chronic Pain
Any pain that Persists beyond the expected time after a physical
or emotional injurySubjective complaints are magnifiedPain is out of proportion to clinical signsIs accompanied by severe psycho-social issuesResponds poorly to conventional therapy
PAIN
SUFFERING
DEPRESSION
LOSS OF FUNCTION
DRUG ABUSE
FINANCIAL LOSS
DOMESTIC DISRUPTION
Persistent Pain
Who Gets Persistent Pain ? Systemic disease
Diabetes mellitushypothyroidismHIV/AIDSHepatitis CMalignancyNeurological disease….ALS, MSRheumatoid related syndromes
Obesity Psychiatric co-morbidity
ACUTE PAIN Meaningful, linear,
reversible
Well defined, recent onset, clear definable cause
Observable responses
Readily responds to analgesics
Usually nociceptive in origin
CHRONIC PAIN Meaningless, cyclical,
irreversible
Persists over time
Adaptation
Less amenable to analgesics alone
Multiple etiologic componentsnts
Cancer Pain 20-50 % at time of diagnosis
Incidence varies with tumor type
55-95% with advanced disease
50-70% report pain of moderate to severe intensity
30% report excruciating pain
Pain Experience in Ambulatory Cancer Patient Population
Disease Pain Pain due to Disease
Worst Pain > 5
Negative PMI
Breast 71% 83% 60% 43%
GI 61% 91% 58% 41%
GYN 55% 80% 71% 54%
GU 64% 84% 66% 38%
Lymphoma 53% 66% 63% 63%
Lung 74% 85% 63% 34%
Other 74% 85% 64% 42%
Pain Classification Schemes1-Neurophysiologic:
Nociceptive (somatic, visceral) Neuropathic
2-Duration: acute vs. chronic3-Temporal pattern:
continuous intermittent
incident Breakthrough End-of-dose failure
Pain Classification Schemes4-Severity
5-Specific cancer pain syndromes (etiology):
Tumor infiltration of bone, nerve, viscera.
Treatment related.
Types of Persistent Pain Nociceptive
Musculo skeletalJointLigamentousVisceral
NeuropathicCentralSomaticSympathetic
Psychogenic Mixed
Types of Pain: Nociceptive vs. Neuropathic
Nociceptive Mediated by normal nervous system: Inflammatory pain: in response to activation
of peripheral nociceptors by either mechanical pressure, high or low temperature or chemical mediators.
Usually acute
Types of Pain: Nociceptive vs. Neuropathic
Nociceptive Somatic –
arising from skin, bone, joint, muscle, or connective tissue
dull, aching, well-localized. Bone metastasis, invasion of soft tissue
Types of Pain: Nociceptive vs. Neuropathic
Nociceptive Visceral –
vague distribution, referred. Bowel obstruction, carcinomatosis, pleural effusion
arising from internal organs such as the large intestine or pancreas
Types of Pain: Nociceptive vs. NeuropathicNeuropathic mediated by damaged nervous system: Localized to an area of sensory abnormality Pain in response to non-painful stimuli Pain in the absence of ongoing tissue damage Painful peripheral neuropathy, post mastectomy
pain, brachial plexopathy
Mixed TypeCaused by a
combination of both primary injury and secondary effects
Nociceptive vs Neuropathic PainNociceptive
PainCaused by activity in neural pathways in
response to potentially tissue-damaging stimuli
Neuropathic Pain
Initiated or caused by primary lesion or dysfunction in the nervous system
Postoperativepain
Mechanicallow back pain
Sickle cellcrisis
Arthritis
Postherpeticneuralgia
Neuropathic low back pain
CRPS*
Sports/exerciseinjuries
*Complex regional pain syndrome.
Central post-stroke pain
Trigeminalneuralgia
Distalpolyneuropathy (eg, diabetic, HIV)
Manifestations of PainAcuteIncreased BP, P,
R.Dilated pupils.Sweating.Focuses on painReports pain Crying, moaning restlessGrimace
ChronicNormalNormalDry skin
Easy distractionNo reportQuiet, sleep, rest Blank or normal
facial expression
Behavio
ral
Physi
olo
gic
Key Principles in Assessment Pain is a multidimensional, subjective, and
uniquely personal experience
Pain is what ever the person says it is, occurring whenever the person says it does
Reliance on observable physiologic and behavioral manifestations in order to verify existence and severity of pain is inadequate
Goals of Assessment Estimate severity of pain (0-10 scale, visual
analog scale)
Form clinical impression regarding etiology
Determine need for additional diagnostic testing
Formulate therapeutic recommendations which take into account the patient’s medical and psychosocial status
Symptom Assessment Site Onset Temporal pattern Quality Relieving/Provoking
factors Associated signs/
symptoms
Impact of function and QOL.
Impact on psychological state.
Response to prior therapy.
Treatment preferences.
Pain Intensity Rating Scales
• Visual Analogue Scale (VAS)
No painNo pain ----------------------------------- ----------------------------------- Worst painWorst pain
• Categorical Scale
None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10) None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10)
• Numerical Rating Scale
-------------------------------------------------------------------------------------- 00 No painNo pain
1010Worst pain Worst pain imaginableimaginable
Guidelines in Pain Therapy Assess the pain frequently Pain assessment must be dynamic and not static Use around the clock therapy (ATC) Treat and assess breakthrough pain
aggressively Where possible use oral route Consider age, previous drug usage, hepato-
renal function Monitor for abuse Monitor and treat side effects
Treatment Goals Decrease Intensity and duration of pain Decrease conversion from acute to chronic Decrease suffering and disability Decrease psychological and socioeconomic of
sequel of untreated pain.
Treatment Goals Optimize drug therapy Improve quality of life and optimize ability to
perform activities of daily living Minimize adverse effects of therapy Minimize inappropriate use
Overall Treatment Strategies
Analgesic and adjuvant medications
Physical therapies
Psychological interventions
Anesthetic and neurolytic procedures
WHO Analgesic “Ladder” for Cancer Pain
WHO 3-StepWHO 3-StepAnalgesic Analgesic
LadderLadder
Proposed 4th StepProposed 4th Step
Freedom from Pain
Intrathecal Opioid Delivery
Pain persisting or increasing
Step 3Opioid for moderate to severe pain
± Nonopioid ± Adjuvant
Pain persisting or increasing
Step 2Opioid for mild to moderate pain
± Nonopioid ± Adjuvant
Pain persisting or increasing
Step 1± Nonopioid± Adjuvant
Pain
Algorithm for Medication Selection in Various Pain Syndromes
Cancer
Cancer Pain Cancer: Tumor expansion, nerve compression,
infiltration by tumor, malignant obstruction,
infection of malignant ulcers.
Treatment: radiation → mucositis pain
Principles of Analgesia for cancer-Related pain Follow WHO Ladder ATC dosing for continuous pain Rescue dosing for intermittent pain Oral route unless contraindicated No PRN
It is reactive not preventive Requires larger doses to reestablish control which may lead
to side effects
Principles of Analgesia for cancer-Related pain
ATC dosing
Small fixed doses on a schedule to prevent pain
Rescue (Breakthrough) dosing
Fixed doses on a flexible schedule Analgesia is administered in response to pain
or to prevent predictable pain Key to success of pain management Similar to NG in angina Use immediate release opioid or NSAIDs
Calculating Rescue dosing
1. 25-50% of the 4hrly ATC If ATC is 60 mg MS q 4 hrs, rescue can be 15
mg
2. 2-5% of the 24 hr ATC dose
3. Based on response, 50% relief from 2 mg morphine →4 mg should provide ≈ 100% relief
All rescue should be prescribed q 4 hrs
Titrating dosage If 3 or more rescue doses in 24 hr
Calculate ↑ based upon total opioid dose ( ATC+ rescue) taken in the previous 24 hrs.
↑ both the ATC and breakthrough Increase by the following guidelines
Pain > 7 , ↑ dose by 50-100%Pain 4-7, ↑ dose by 25-50%Pain < 4, ↑ dose by 25%
When patient uses < 2 rescue, sustained release opioid should be started
Non Opioid Analgesics
NSAIDS Acetominophen
NSAIDS Mechanism of action
- Inhibition of prostaglandin synthesis
- Synergism with opioid analgesics
Mild to moderate pain
Different side effect profile from opioids
No tolerance or dependence
Ceiling effect
Limited routes
NSAIDS Pain from injury, surgery, trauma, arthritis, or
cancer
Very effective for bone pain
Predominant effect on PNS→synergistic
All are equipotent
Patient response varies
Selective COX-2
Inhibitor
The Arachidonic Acid Cascade and COX-1 and COX-2 Inhibition
X XTraditional NSAID X
Arachidonic acid
COX-1 COX-2
Body Homeostasis• Gastric integrity• Renal function• Platelet function
InflammationPain
The COX 2 Inhibitors
Rofecoxib 25-50 mg daily (Vioxx) →W Celecoxib 100-200mg daily (Celebrex) Valdecoxib 10-20 mg daily (Bextra) →W Etrocoxib Paracoxib (iv use)
The COX 2 Inhibitors
Minimal effect onGastric integrityRenal functionPlatelet function
Potent inhibition of PGI2 →↑ risk if CV events (MI)
Contraindications to COX2 I Previous side effects with COX2 inhibitors Allergy to sulpha drugs History of previous GI bleed pregnancy History of perforated gastric ulcer Esophageal varices Bronchospastic disease Renal dysfunction Coronary artery disease needing aspirin Congestive heart failure
Acetaminophen Same analgesic potency as ASA No neuropsychological and little GI SE Orally, or rectally For musculoskeletal or visceral pain Can be used in 3 ways
1. ATC 1g q 4 hrs as 5 doses in 24 hrs
2. As rescue with ATC opioid 1g q4 PRN
3. As an adjuvant analgesic
Opioids Morphine Sulphate Hydromorphone (Dilaudid) Demerol Fentanyl Methadone Buprenorphine Pentazocine Oxycodone (Roxycodone, Tylox, Percocet) Hydrocodone (vicodin, lortab, Norco) Propxyphene ( Darvon, Darvocet) Codeine
Strong Opioids
Partial agonists
Weak
opioids
Opioids Opioid Agonist: bind w/ opioid receptor site in
PNS & CNS = pain relief
No Ceiling
Titrate to pain relief or side effects
Opioid Antagonist: blocks relief. Naloxone
Opioid Agonist-antagonist: + pain relief. Stadol, Nubain, Talwin (not recommended)
Opioids No rationale for combining two opioids, use
same agent for ATC and rescue pain.
Potent Opiates: Morphine, Hydromorphone. µ-receptors, κ-receptors Treat acute, chronic, sever, or terminal
malignant pain Orally, rectally, IV Infusion, epidural ,
intrathecal Immediate release analgesic effect 4 hrs
Morphine, Hydromorphone. Doses according to
Prior exposurePain severityHepatic, renal functionRoute of administration
Oral: parental, 5:1
Morphine Opioid of choice
Available in multiple routes and formulationsExtensive clinical experience in dosing, route
change and side effects.
Meperidine…….Demerol Used for traumatic and postoperative pain 1/10 potency of morphine Oral or parenteral Short acting Toxic metabolites: nomeperidine
Can accumulate in renal dysfunction and cause CNS stimulation and seizures
Metabolites with long half life >12 hrs High addiction potential Expensive
Methadone Equivalent potency to morphine Orally, IV, rectally, epidurally/intrathecally Long acting adjust dose q 5-7 days Lower addiction and tolerance potential Cheap No active or toxic metabolites 8-12 hour analgesic action ( give Q8-12 hrs)
Longer intervals in hepatic failure
Methadone CNS depression lasts for 36 hrs after overdose
Needs CIVI Naloxone for reversing effect. No renal excretion Dependence on hepatic function (p-450)
Watch for drug-drug interaction
Fentanyl >100 potent than morphine IV, intraspinally as preoperative anesthetic
agent Rapid onset, short duration of action
Transdermal patch: Consistent dosing Oral lollipop
The Fentanyl Patch Indications for use
Severe nausea and vomiting Unable to swallow Children Patients with poor compliance Concern of drug diversion
Beware Opioid naïve Febrile patient Elderly Drug abuser
The Fentanyl Patch disadvantages
Delay in onset of analgesiaResidual activity after the patch is removed
25,50,75,100 mcg Duration 72hrs Steady state requires 24 hrs, use supplemental
short acting to cover initial period.
Weak Opioids Codiene, oxycodone, propoxyphene For mild to moderate pain
Oxycodone Analgesic effect 4 hrs High bioavailability compared to MSO4 No toxic metabolites Less tolerance compared to MSO4 Higher incidence of euphoria Expensive
Tramadol Activity against opioid and serotonergic and
noradrenergeric pathways in CNS. Moderate to sever pain Advantages
Lower abuse liabilityLower risk of respiratory depression
DisadvantagesDizziness, dry mouth, sedation, constipation.
Use lower doses in elderly
3-5.75200130Codeine
4-6200Hydrocodone
2-4430075Meperidine
3-515Oxycodone
3-657.51.5Hydromorphone
4-533010Morphine
DURATIONRATIOPOIVMEDICATION
Equianalgesic Dosing
Dose Conversion
Equianalgesic dose of current opioid
24 hrs dose current opioid
Equianalgesic dose of desired opioid
24 hrs dose current opioid
=
Drug Delivery No evidence that other routes are superior or
have less SE. Choice of route depends on pragmatic
consideration e.g. inability to swallow Can only be done safely with knowledge of
equianalgesic dosing.
OralRoute of choice Simple, noninvasive Reasons for failure: inadequate dose,
parenteral to oral conversion made too quickly, dosing intervals too long
Formulation and dose dependent upon pattern of pain and severity
Long Acting Combined with Short Acting for Chronic Pain
Sublingual, buccal
Simple, noninvasive Unable to tolerate oral dosing, unable to
swallow rapid onset, drug not subject to first-pass effect
fentanyl
Intravenous Most efficient for rapid titration, dose finding,
immediate analgesic effect. Bolus, continuous, PCA. Steady state better maintained with CI. Full effects of increase CI will not be felt until
steady state or approximately 5-6 half-lives. Therefore with IV Morphine 12-18 hours.
Morphine, hydromorphone, fentanyl, methadone
Rectal Morphine, hydromorphone Conversion from oral at 1:1 ratio Sustained release tablets of morphine can be
used by this route.
Subcutaneous Morphine, hydromorphone Equivalent to IV in efficacy and side effects
Conversion to Oral Calculate total daily requirement with PCA Convert to IV morphine Convert to Oral morphine Convert to alternate opioid 75 % as ATC 25% as rescue
Prior to Oral Conversion
Patient able to tolerate oral fluids Oral therapy started prior to removal of PCA Pain control predictable and stabilized IV to oral conversion calculated Side effects under control
Example of Conversion Total morphine for 24 hours on PCA= 60mg
Want to convert to Oxycodone.
60 mgm of MS IV( x 3) = 180 mgm oral.
To convert to oxycodone x by 1.5 = 120 mg oxycodone
75% as ATC = 90 mg = 40 mg Q 12 , but factor in 50% less for ICT = 20 mg q 12 hourly
25% as rescue = 30 mg or 5 mg Q 4-6 hourly PRN
One 25 mcg/h transdermal
fentanylpatch/3 days
(72 hours)
Conversion Chart for Starting Dose of Transdermal Fentanyl
Fixed-combination short-acting opioids (6/day):
–Lorcet 5 mg/500 mg–Lortab 5 mg/500 mg–Percocet 5 mg/325 mg–Percodan 5 mg/325 mg–Tylenol + Codeine 30 mg/325 mg–Tylox 5 mg/500 mg–Vicodin 5 mg/500 mg
Long-acting opioids(2/day):– OxyContin 20 mg– MS Contin 30 mg
Multiple patches may be used for doses exceeding 100 mcg/h. Doses up to 6oo mcg/h have been evaluated in clinical trials.
Renal Failure
Methadone Dilaudid Oxycodone Hydrocodone Morphine Fentanyl Demerol
NEUROTOXICITY
SEDATION
TOLERANCE
Liver Failure
Methadone Dilaudid Oxycodone Hydrocodone Morphine Fentanyl Demerol
All pretty much OK, but halve dose
Side effects of opioids Constipation Sedation Mental clouding Respiratory depression Nausea and vomiting Orthostatic hypotension Urinary retention Pruritus Myoclonus
Constipation Decreased gastric,
pancreatic, biliary secretions.
Decrease motility Delayed passage
Tolerance does not develop
Dose dependent Preventative
approach Bulk and stimulant
laxatives
Sedation Common with start,
increase, change drug, pain relief in sleep deprived.
Tolerance to sedative effects 2-7 days.
Other causes: sedatives, sepsis, metabolic imbalances, hypoxia.
Strategies: change dose,
frequency, type of opioid
Stimulants: Caffeine, dextroamphetamines, methylphenidate
Respiratory Depression Direct action on brain Direct action on brain
stem respiration stem respiration receptors; decreased receptors; decreased responsiveness to responsiveness to CO2 levels CO2 levels
Pain is physiologic Pain is physiologic antagonistantagonist
Risk factorsRisk factors
Rapid tolerance Short acting Goal: gradual reversal
without analgesic withdrawal
Naloxone 0.4 mg/10cc; 0.5 cc q 2-3 mins
Nausea - Vomiting Common with start or increase dose
Tolerance within 2-3 days
Rule out other causes
Treatment:
treat constipation, use antiemetics, change opioid
Withdrawal
Physical dependence Causes: abrupt discontinuation, rapid
dose reduction, antagonist, agonist- antagonist
Onset dependent upon elimination half-life
Signs and symptoms 25% of daily dose
Dependence
Physical dependence Psychological dependence Pseudo addiction
Definitions Physical Dependence: involuntary,
adaptation, withdrawal with abrupt reduction or discontinuation
Psychological Dependence (addiction): compulsive use despite harm, for effects other than pain relief
Adjuvant Medications Enhance analgesic
effect of opioids Treat concurrent
symptoms Provide independent
analgesia
Antidepressants Neuroleptics Anticonvulsants Local anesthetics Antispasmodics Muscle relaxants Psychostimulants Corticosteroids NMDA receptor
antagonism Anticholinergics Bisphosphonates
Antidepressant TCA, MAOIs, Clinical effects
Improve moodImprove sleepAnoxiolyticsDecreased pain perception
TCA more easier to use
Antidepressant TCA inhibit reuptake of serotonin and
norepinephrineSerotogergic processes are part of endogenous
pain inhibitory mechanisms TCA have analgesic properties related to
ability to increase pain tolerance Faster onset than antidepressant effect Have local anesthetic properties
Antidepressant Improve sleep disturbances and depression
associated with chronic pain. 1-3 weeks for effect Amitriptyline most commonly used for painful
conditions 50-150 mg/day Anticholinergic side effects
TCA: Adverse EffectsCommonly reported AEs
(generally anticholinergic):blurred visioncognitive changesconstipationdry mouthorthostatic hypotensionsedationsexual dysfunctiontachycardiaurinary retention
Desipramine
Nortriptyline
Imipramine
Doxepin
Amitriptyline
FewestAEs
Most AEs
Caveats With the Antidepressants•Start at lowest dose available
•Escalate slowly…every 10 -14 days
•Slow weaning, over a week
•Beware of drug interactions
•Check for
•Glaucoma
•Prostatic obstruction
•Heart block
Drug Interactions With Antidepressants Coumadin Alcohol ( cold medications) Appetite suppressants Quinolone antibiotics Antihistamines Tramadol Anti epileptics Bronchodilators
Neuroleptics Fluphenazine, methotrimeprazine For mild to moderate pain Improve sleep Similar analgesic effects to morphine without
addictive properties or respiratory depression Side effects
High sedative and anticholinergic effectsExtrapyramidal
Anticonvulsants Carbamazapine (Tegretol) Gabapentin (Neurontin) Oxcarbezapine (Trileptal) Topiramate ( Topramax) Zonisamide ( Zonergan) Levetiracetam( Keppra) Lamotragine ( Lamictal) Valproate ( Depakote)
Anticonvulsants
Carbamazapine and valproate for lancinating, burning pain. (neuropathic)
Neural invasion by cancerous tumorSurgical scarringTrigeminal neuralgia
For opioid induced myoclonus dosing start at 100-200mg/d in cancer pain Plasma levels need to be monitored
Anticonvulsants
Carbamazapine and valproate Side effects
Bone marrow suppressionAtaxia, diplopia, Nausea lymphadenopathy, hepatic dysfunction
MonitoringLFTsCBCSerum Drug levels
Gabapentin in Neuropathic Pain Disorders FDA approved for postherpetic neuralgia Neuropathic pain in patients who do not respond to
CBZ and TCA. Neuropathy, multiple sclerosis, migraine Usually well tolerated; serious adverse effects rare
dizziness and sedation can occur No significant drug interactions Peak time: 2 to 3 h; elimination half-life: 5 to 7 h Usual dosage range for neuropathic pain up to 1200-
4800 mg/d
Gabapentin Start as low as possible…..100 mgm q HS Increase slowly by 100 mgm every three days Caution regarding driving ( sedation) Increase to 1200 mgm and assess pain relief If > 50% relief, wait two weeks and reassess Increase to maximum of 3600 mgm Do not exceed 1200 mgm in elderly Elixir in children mgm/kilo
Local anesthetics Lidocaine For neuropatheic pain
Short duration Mexiletine longer acting Doses same as antiarrhythmic dose Side effects
Dizziness, lightheadedness, ataxia, N/VHigh dose lead to tremor and convulsion
Lidocaine available as patches which have lower SE
Local anesthetics Ketamine
At the N-methyl-D-aspartate (NMDA) receptorAnalgesic at subanesthetic dosesFor neuropathetic pain25 mg q 6 hrs , titrate by 25 mg q 24-48hrsSide effects
Psychotomimetic, tachycardia, high BP , ↑ intracranial pressure
Benzodiazepines Diazepam, midazolam Skeletal muscle relaxant and anxiolytic → ↑
pain threshold. Side effects
Sedation, cognitive impairment, depressionAddictiveSerious withdrawal symptoms such as seizures
Corticosteroids Prednisone, Dexamethasone No ceiling effect Opioid sparing effect Dexamethasone
4-16 mg/d in divided dosesOral or IV
Other non-analgesic effectsRelief of nausea and vomitingIncrease energy
Corticosteroids Indications
Bone metastasesVisceral painNeuropathic painNerve compression from tumorSoft tissue or musculoskeletal pain from
inflammatory lesionsHeadache from ↑ intracranial pressurePain from spinal cord compression
Bisphosphonates Analgesic and prevents skeletal complications
of malignancy Treatment of hypercalcemia Indications
Wide spread painful bone metastases at risk of complications
Multiple painful sites of disease at risk of hypercalcemia
Osteolytic bone disease where radiation is CI
Bisphosphonates Pamidronate, zoledronic acid given IV q 4 wks
Nonpharmacologic therapy Surgery Neuroablative blocks and neurolysis Central and peripheral nervous system
stimulation Physical therapy