pain management for residents - hospital.tu.ac.th management for... ·...
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Pain management
Preeyaphan Arunakul MD FRCAT
Department of Anesthesia
Faculty of Medicine, Thammasat University
“An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage.”
Definition
• Acute pain
- Pain less than 12 weeks
• Chronic pain
- Pain longer than 12 weeks
Classification of pain by time
Nociceptive Nonnociceptive
Somatic Visceral Neuropathic Psychogenic
sharp, dull
achingPoorly localized,
deep squeezing,
crampy
Burning, electrical
(lancinating),
numbing,
allodynia,
hyperalgesia
-Rarely pure
-No nociceptive or
neuropathic mechanism
can be identified
-With sufficient
psychogenic symptoms
-Myofascial
-Metastatic
bone pain
-Postsurgical
-Arthritis
-Small bowel
obstruction
-Carcinomatosis
peritonii
-Trigeminal neuralgia
-Postherpetic neuralgia
-Painful peripheral
neuropathy
-CRPS I,II
-Phantom limb pain
Antidepressants
Psychological therapy
Anticonvulsants
Antidepressants
Interventions
Multimodalities
TCA/SSRI
Gabapentin
Opioids
Interventions
Psychotherapy
NSAIDs
Opioids
Muscle relaxants
Aniline deriv.
Multimodalities
ผู้ ป่วยมีอาการปวดเฉียบพลนั
มีสาเหตทุี่ท าให้เกิดอาการปวด
ประเมินระดบัความปวด
อาการปวดต้องการการรักษาหรือไม่
รักษาโดยใช้ยารักษาโดยไม่ใช้ยารักษาแบบผสมผสาน
รักษาสาเหตุ
เคร่ืองมือท่ีใช้ประเมินความปวด- VAS/VRS/NRS- FACE/FLACCs- CHEOPS
ไม่ต้องการ
ต้องการ (PS ≥ 4 หรือปวดปานกลางขึน้ไป)
ประเมินซ า้และบนัทกึ
การรักษาได้ผลดีหรือไม่
เกิดภาวะแทรกซ้อนจากการรักษาหรือไม่
ประเมินซ า้และบนัทกึ
รักษาภาวะแทรกซ้อน
ไม่ได้ผล ปรึกษาผู้ เชี่ยวชาญ
เกิดได้ผลดี
ไม่เกิด
“5th Vital sign”
Postoperative pain
• Acute pain
• Choices:
- iv bolus/iv PCA/oral opioids
- neuraxial opioids (spinal & epidural)
- peripheral nerve blocks with LAs
- NSAIDs and other medications
• Effects of pain on systems
CNS & Neuroendocrine
1. Secretes enkephalins, endorphins
2. Reflex escape response “Fight or Flight”
- stimulated sympathetic nervous system
- increased E and NE
- inhibit peristalsis and secretion of digestive enzymes
3. Increasing CRH, ACTH, Cortisol from hypothalamus
4. Increasing glucagon and reduce insulin level
CNS & Neuroendocrine
5. Increasing E & NE from adrenal medulla
6. Decreasing ADH = Na & water retention
7. Increasing renin & AT II secretion from adrenal gland
8. Increasing protein breakdown = reduce wound healing
9. Increasing IL-1 level = increase inflammatory effect
Cardiovascular system
Increasing sympathetic activity
Hypertension increase myocardial
Tachycardia O2 consumption
Myocardial ischemia
GI and Immune system
• Depress immune system
• Impaired GI function
- delayed gastric emptying
- reduce bowel motility, potential paralytic ileus
- nausea & vomiting (also from CTZ)
Limiting movement of thoracic & abdominal muscles
Respiratory dysfunction
Retained sputum and secretion
(reluctant to cough)
Reduction in vital capacity
Hypoxia
Cardiac complication, disorientation,
confusion, and delayed wound healing
Respiratory system
Increasing CAs, aldosterone, ADH, cortisol, AT-II, and PGs
(regulate urinary output, fluid & electrolyte balance, blood volume, and BP)
Na & water retention
Increase K+ excretion
Fluid overloadIncrease cardiac workload
Hypertension
KUB system
Reflex muscle spasm, impaired muscle function
Muscle fatigue
Immobility
Venous stasis
Increase coagulability
Increase risk of developing DVT
Musculoskeletal system
Acute stress-induced hormonal changes
1. Anxiety interrupt sleep pattern (insomnia)
Depression interfere daily activity
2. Distressing cognitive impairment
- disorientation
- mental confusion
- reduce ability to concentrate
3. Poorly-controlled acute pain --> chronic pain
Psychological & Cognitive function
Definition
• “Pain caused by a lesion
or disease of the somato-
sensory nervous system”
• Clinical description
(not a diagnosis) ; requires
demonstrable lesion or disease
that satisfies established neurological diagnostic criteria
• Central and peripheral neuropathic pain
• Pharmacotherapy
• Physical and Psychotherapy
• Interventions
• Surgery
• Lifestyle modifications
• Alternatives
• Neurostimulation (SCS)
Management
Pharmacotherapy
• Gabapentin/Pregabalin (Neurontin®/Lyrica®)
• Amitriptyline/Nortriptyline
• Carbamazepine/Oxcarbazepine (Tegretol®/Trileptal®)
• Duloxetine/Venlafaxine (Cymbalta®/Effexor®)
• Tramadol (for acute exacerbation only)
Medications
• Opioids
• Gabapentin and pregabalin
• NSAIDs (for bone metastasis)
• Antidepressants/antianxiety
ยาNociceptive
painNeuropathic cancer pain
Cancer-induced
bone pain
Tumor-induced
headache
Visceral pain MBO*
Opioids ดีมาก ปานกลาง ดีมาก ดีดีมากส าหรับอาการปวดตลอดเวลา
NSAIDs ดีมาก ไม่ดี ดีมาก ดี ไม่แนะน าAntidepressants TCAsและSNRIs
นอ้ย ดีมาก ปานกลาง ไม่แนะน า ไม่แนะน า
Gabapentinoids นอ้ย ดีมาก ดี ไม่แนะน าดีส าหรับ visceral
hyperalgesia
Carbamazepine ไม่ดีดีส าหรับ paroxysmalsharp shooting pain
นอ้ยนอ้ย ยกเวน้ใชเ้ป็นยา
กนัชกัไม่ดี
Bisphosphonates ไม่ดี ไม่ดี ดีเม่ือใหร้ะยะยาว ไม่ดี ไม่ดี
Corticosteroids ไม่แนะน าดีมากส าหรับ
nerve/cord compression
ปานกลาง ดีมากดีส าหรับ liver capsule
distension
Strong opioids
• Morphine (Morphine, MST, Kapanol)
• Meperidine (Pethidine)
• Fentanyl (Fentanyl, Duragesic, Durogesic)
• Methadone
• Oxycodone
Visceral pain
Clinical features :
• Diffuse localization, deep, squeezing, crampy
• Unreliable association with pathology
• Referred sensation to cutaneous structures
• Cutaneous or deep tissue hyperalgesia
• Strong autonomic and emotional response may be
evoked with minimal sensation
Referred pain
• Pain referred from a deep somatic or visceral structure to
a distant region within the same segment
• With/without hyperalgesia and hyperesthesia, deep
tenderness, muscle spasm, and autonomic disturbances.
• No changes in reflexes, no weakness or atrophy
• Segments involved are identified (all somatic and visceral
structures innervated are carefully examined for a
pathologic process)
• Ex: Shoulder pain in subphrenic abscess
Visceral pain etiologies
• Inflammation (acute and chronic), including inflammation
caused by mechanical irritants (kidney stone)
• Infection
• Disruption of normal mechanical process (GI dysmotility)
• Neoplasms (benign or malignant)
• Alterations in nerves carrying sensations from the viscera
• Ischemia
• Opioid for cancer in origin
• Antidepressants
• Gabapentin/pregabalin
• Sympathetic plexus block/neurolysis
Medications & Interventions
Oral medications
- Acetaminophen (paracetamol)
- NSAIDs
- opioids = tramadol, codeine
- tramadol + paracetamol (Ultracet®)
- antidepressants/anticonvulsants
IV medications
- Opioids = morphine, pethidine, tramadol, fentanyl
- NSAIDs = Parecoxib (Dynastat®), Ketorolac
Patient-controlled analgesia (PCA)
Patient-controlled epidural analgesia (PCEA)
1. Improved pain control
2. Receive immediate
delivery of pain med.
3. Patient control
4. Frequent but smaller
dose, less side effects
PCA variables
• Bolus dose or PCA dose or demand dose
(self-administered intermittently)
• Lock out interval (time between dose)
• Loading dose
• Background infusion
• Dose limit in 1 or 4 hour
Using PCA
- Patient education
- Monitor O2 saturation (in high risk patient)
1. Pain scores at rest/movement
2. Side effects
Sedation, N/V, pruritus, respiratory depression,
urinary retention
3. Total amount of opioids delivered
Neuraxial Opioids
Spinal/epidural morphine
- duration 18-24 hours/it depends
- no sedatives or sleeping pills (except for order
from anesthesiologist)
- side effects :
respiratory depression
nausea and vomiting
pruritus
urinary retention
Local anesthetic for epidural
0.0625% - 0.15% Bupivacaine/Levobupivacaine
1-2% Lidocaine with or without adrenaline
Opioids
• Morphine 1-5 mg bolus or epidural infusion at
0.005-0.02 mg/ml
• Fentanyl 1-2 mcg/ml epidural infusion
- Local anesthetics only
- Single shot or catheter
- US-guided and/or peripheral
nerve stimulator
- 18-24 hours
- Side effects :
motor weakness
catheter migration
Peripheral nerve blocks
Acetaminophen (paracetamol)
• tablet 500 mg 1 tab oral prn/every 4-6 hrs
• tablet 650 mg 1 tab oral prn/every 8 hrs
• FDA Liver warning:
Severe liver damage may occur if you take
- more than 4,000 mg of acetaminophen in 24 hours
- with other drugs containing acetaminophen
- 3 or more alcoholic drinks everyday while using this
product
• FDA reminds health care professionals to stop dispensing
prescription combination drug products with more than 325
mg of acetaminophen (4/28/2014)
• Acetaminophen in both OTC and prescription products
and the risk of attention deficit hyperactivity disorder
(ADHD) in children born to women who took this
medicine at any time during pregnancy.
Liew Z, Ritz B, Rebordosa C, Lee PC, Olsen J. Acetaminophen use during
pregnancy, behavioral problems, and hyperkinetic disorders. JAMA Pediatr
2014;168:313-20.
NSAIDs
Role of NSAIDs
• Acute postoperative pain
• Chronic musculoskeletal pain
• Cancer-induced bone pain
Evidence-based practice
• Prevent and treat postoperative pain in ambulatory surgery
• Decrease: opioid consumption
early return of bowel function
early recovery of physical activity
increase patient satisfaction
• No difference if given before or after surgery
Drug mg FrequencyMaximum
dose/day
Parecoxib (dynastat®) 40 IV q 12 h 80
Ketorolac 15, 30 IV q 8 h 90
Ibuprofen 200,400,600 q 4-6 h 2400
Diclofenac25,50 q 8 h
150SR75,100 q 12-24 h
Indomethacin 25 q 8-12 h 200
Naproxen 250 q 12 h 1000
Piroxicam 10,20 q 24 h 20
Meloxicam 7.5 q 12-24 h 15
Celecoxib 200,400 q 12 or 24 h 400
Etoricoxib 30,60,90,120q 24 h
120120 mg < 8 days
Compounds appearing above the line are COX-1-selective, those
below the line COX-2-selective.
Warner TD, Mitchell JA. FASEB J 2004; 18: 790-804
“NSAIDs cause an increased risk of serious
gastrointestinal adverse events including inflammation,
bleeding, ulceration, and perforation of the stomach or
intestines, which can be fatal. These events can occur
at anytime during use and without warning symptoms.
Elderly patients are at greater risk for serious
gastrointestinal events.”
FDA Black box warnings
GI toxicity
Relative Risk in developing
NSAIDs-induced Gastropathy
• History of complicated ulcer 13.5
• Multiple NSAIDs (including ASA) 9.0
• High dose of NSAIDs 7.0
• Use of anticoagulant 6.4
• Age > 70 5.6
• Use of corticosteroids 2.2
Tannenbaum, et al. J Rheum 2006
NSAID-induced small bowel injury
• Rebamipide (Mucosta®)
• Gastroprotective effect by modulate gene expression of protein
-increases growth factors thus accelerates healing
-reduces inflammatory cytokines
-acts as free radical scavengers
-increases PGs production
• Peak serum concentration at 2.4 hrs
• Distribute mostly to GI mucosa
• Does not require CYP450, less drug interaction
J Gastroenterl 2009; 44:879-88
Role of COX-2 inhibitors
• Developed to reduce GI complications
• CLASS trial1
- Symptomatic ulcer and ulcer complications
2.1% in Celecoxib group
3.5% in conventional NSAIDs group (p=0.02)
- Presence of aspirin negated GI benefit
- After 1 year, no difference in GI events2
1.Silverstein FE, et al. JAMA 2000; 284: 1247-55
2. Wright JM, et al. JAMA 2001; 286:2398-400
What if patients also taking aspirin
• Risk of GI complications
ASA + coxib = nonselective NSAID alone
• Risk of hospitalization for adverse GI event
ASA + coxib = 0.86 (hazard ratio)
ASA + NSAIDs = 1.61 (hazard ratio)
FDA Black box warning
Cardiovascular risk
“NSAIDs and COX-2 inhibitors may cause an increase
risk of serious cardiovascular thrombotic events,
myocardial infarction, and stroke, which can be fatal.
Patients with cardiovascular disease or risk factors for
cardiovascular disease may be at greater risk.”
Fosbol. Clinical Pharm Ther 2009; 85(2):190-7
Cox proportional hazard ratios for the composite end point of death and
myocardial infarction associated with exposure to NSAIDs in a study population
of 1,028,437 individuals characterized by no prior concomitant pharmacotherapy
and no comorbidity.
2.01
0.97
1.01
1.63
2.13
Healthy Individuals
NSAID alone NSAID +
PPI/Misoprostol/Rebamipide or
Coxib +
PPI/Misoprostol/Rebamipide
Naproxen (if no ASA) Avoid NSAIDs if possible
Naproxen +
PPI/Misoprostol
(if ASA)
Naproxen +
PPI/Misoprostol/Rebamipide
(regardless of ASA use)
AVG
CV risk
High
CV risk
AVG GI risk High GI risk
Chan Am J Gastroenterol 2008; 103: 2908-2918
Serious side effects
• Myocardial ischemia/infarction
• Hypertension, stroke
• Heart failure (fluid retention)
• Renal insufficiency
• Bleeding & ulcers
• Life-threatening skin & allergic reactions
• Liver failure
• Induce asthmatic attacks in asthmatic patients
Contraindications for NSAIDs
• Cardiovascular thromboembolic events
• CrCl < 30 ml/min
• Active GI bleeding
• Thrombocytopenia from chemotherapy
• Active liver disease (enzymes rising > 3 times)
• Allergic to Sulfonamides
• Pseudo-allergic reactions from NSAIDs
Prolonged use of NSAIDs
• Baseline
- Serum Cr
- Hepatic function
- K+
- CBC
- BP, pulse, BW
• 2 weeks after starting
- Serum Cr
- K+
• Periodically
- Serum Cr
- K+
- BP, pulse, BW
- Hepatic function
Other drug interactions
• Celecoxib metabolized by CYP2D6, 2C9
- Celecoxib + warfarin = increase INR
- Conventional NSAIDs + warfarin/clopidogrel
= increase risk of bleeding
• SSRIs itself increase risk of GI complications
- SSRI + NSAIDs even more risk
Do NSAIDs interact with aspirin??
• Other NSAIDs (naproxen) also have been
considered to attenuate the effect of aspirin.
Ibuprofen Aspirin30 mins
8 hrs
Risk Reduction
• Avoid NSAIDs in pts with existing renal dysfunction,
CHF, resistant hypertension
• Monitor BP and serum Cr in high risk patients
Elderly, cirrhosis, HT, DM, hypovolemia
“Lowest effective dose with shortest duration”
Eperisone (Myonal)
Tolperisone (Biocalm, Mydocalm)
Orphenadrine (Pormus)
Baclofen
Tizanidine (Sirdalud, Zanaflex, Tizan)
Cyclobenzaprine (Flexeril)
Benzodiazepines (Diazepam)
Contraindications: Myasthenia gravis
Muscle relaxants
Eperisone (Myonal)
• Centrally-acting skeletal muscle relaxant used to improve
myotonic symptoms
• Should be taken with food. Take after meals
• Weakness, dizziness, insomnia, drowsiness, hepatic and
renal dysfunction
• Avoid concomitant use with Tolperisone
• Muscle spasm
• Adult: 50 mg 3 times/day
Tolperisone (Biocalm)
• Centrally-acting muscle relaxant
• Adult: PO 50-150 mg 3 times/day with food
• Well absorbed from GI tract.
• Bioavailability: 20%
• Extensively metabolized by liver and kidney
• Excreted mainly via urine as metabolites
• Side effects: muscular weakness, headache, hypotension, N/V,
sedation, drowsiness, ataxia, dizziness, confusion
• Concomittant use with levodopa in Parkinson pts may result in
confusion, agitation, hallucinations
• Orphenadrine 35 mg + Paracetamol 500 mg
• Dosage: PO BID, Duration: 4-6 h
• Indications: Adjunctive treatment for acute, painful
musculoskeletal conditions.
• Contraindications:
Glaucoma, pyloric/duodenal obstruction, PU,
prostatic hypertrophy, obstruction of bladder neck, and
esophageal achalasia.
Pormus
Norgesic
Orphenadrine 35 mg + Paracetamol 450 mg
Multilayer: Orphenadrine 25 mg + Aspirin 385 mg +
caffeine 30 mg
Orphenadrine citrate
• Derivative of diphenhydramine, acts on brainstem
• Pharmacology:, antihistamine and anticholinergic
• Onset 1 hr, duration 4-6 hrs
• Maximum 100 mg divided into BID
• Pharmacokinetics: good GI absorption, T max is 2 hrs
• Side effects: tachycardia, lightheaded, N/V, dry mouth
• Caution in renal and liver impairment
Baclofen
• GABA derivative binds to GABAB, antispastic
• Inhibits Glu and SP release at both monosynaptic and
polysynaptic reflexes at spinal level
• Onset 3-4 days, variable duration
• 5 mg PO TID (40-80 mg/day)
• Side effects: drowsiness, slurred speech, hypotension,
constipation, urinary retention, short-term memory loss
Tizanidine (Sirdalud, Tizan)
• α2-adrenergic receptor agonist
• Decrease spinal excitatory amino acid release
• FDA-approved for mx of increased muscle tone
• Onset 2 wks, 2-8 mg PO TID-QID
• Clearance is reduced >50% in pt with CrCl<25 mL/min
• Side effects: bradycardia, dose-related hypotension,
dizziness, lightheadedness but rarely syncope
Diazepam
• GABA agonist
• Onset 30 min, variable duration
• 2-10 mg PO TID
• Side effects:
Sedation, fatigue, hypotension, ataxia,
respiratory depression
• Must be slowly tapered after long-term use to
avoid withdrawal symptoms
Alters perception of pain
Mesolimbic dopamine system = reinforcing and
rewarding properties (euphoria)
Modulates nociceptive pathways, enhancing
effects of endogenous opioids
Opioid Pharmacodynamics
How does opioid inhibit pain transmission??
Opioids
Opioid receptors (mu, kappa, delta)
Inhibits voltage-gated Ca2+ channels
Opens K+ channels causing hyperpolarization
Decreases synaptic transmission of pain signals
in the spinal cord dorsal horn
Tramadol
Dosage: 0.5-1 mg/kg iv (prn) q 4-6 H
50-100 mg oral (prn) q 4-6 H
max 400 mg/day
Forms : - Tramol 1-2 caps oral (prn) q 6 H
- Ultracet 1-2 caps oral (prn) q 6-24 H
(37.5 mg of Tramadol + 325 mg of paracetamol)
Side effects: dizziness, N/V, constipation
Cautions: Epilepsy, Serotonin syndrome (SSRI/SNRI),
liver or renal insufficiency
- mental status change
- autonomic instability (labile BP, tachycardia,
dizziness, diaphoresis, flushing, hyperthermia)
- neuromuscular changes (tremor, rigidity, myoclonus,
hyperreflexia, incoordination)
- seizure, use BZD
- GI symptoms (N/V/D)
Rx: Cyproheptadine in severe case
Serotonin syndrome
Codeine
• Tylenol with codeine (TWC)
• Codeine 15-60 mg + Tylenol 300 mg
• Q 4-6 H, max 240-360 mg of codeine/day
• metabolized by CYP2D6 to morphine (10%)
• extra careful in ultra-rapid or rapid metabolizer
• Analgesic effect is reduced when combined with
CYP2D6 inhibitor (fluoxetine, paroxetine)
• Side effects: drowsiness, N/V, constipation (>mo)
• Renal excretion
Strong opioids
• Morphine (Morphine, MST, Kapanol)
• Meperidine (Pethidine)
• Fentanyl (Fentanyl, Duragesic®)
• Methadone
• Oxycodone
* Commonly used in acute pain
Morphine
• binds to mu receptor
• Hepatic metabolism to M3G, M6G (active metabolite)
• consider other opioids in stage 4-5 CKD, dialysis pt
• respiratory depression in high risk pts :
1. respiratory problems
2. severe cardiovascular problems
3. renal dysfunction
(+ benzodiazepine)
Meperidine (pethidine)
• binds to mu and kappa receptor
• Short term use only!!!! ( < 72 hrs)
• prolonged use may lead to addiction and seizure
(toxic metabolites = Normeperidine)
• Delirium, myoclonus
• Reversal with naloxone can exacerbate convulsant
effect of normeperidine
Fentanyl
• potent mu agonist
• immediate onset, duration 30-60 min
• can also be used in epidural/spinal analgesia
Central effects of opioids
- Analgesia - Mood effect
- Sedation - N/V
- Respiratory depression - CNS excitation
- Pupil constriction - Tolerance
- Antitussive effect - Dependence
- Hypothalamic effects - Addiction
Constipation
Colon contains large population of mu opioid receptor
Inhibit peristalsis
Rx : Drink lots of water
Exercise
Stimulating laxatives/stool softener
Senokot 1-4 tabs oral hs
MOM 15-30 ml oral hs
Itching
Release of histamine from mast cells
Rx : Antihistamines
CPM 10 mg iv
Ondansetron 0.1 mg/kg IV prn q 6 h
Opioid Rotation
Nausea and vomiting
- stimulate CTZ in area postrema of medulla
- alter vestibular sensitivity
Rx - 5HT3 antagonist : Ondansetron
- Gastric prokinetic : Metoclopramide
Respiratory depression
- acts on brainstem and “dose-related”
- depress all phases of respiratory activity
(Rate, MV, TV)
- high risk pt: - impaired respiratory function
- opioid-naïve pt
- OSA
Rx - Naloxone (mu antagonist) (0.1 mg/ml iv titration)
titrated carefully (excessive saliva, bronchial spasm)
(in meperidine overdose : seizures)
Is your patient overdosed?
3 Pathognomonic signs :
1. Miosis (pinpoint pupil)
2. Respiratory depression (RR≤10/min)
3. Loss of consciousness
(sedation score ≥ 2)
Rx 1. Intubation
2. respiratory support
3. iv Naloxone
Chronic pain divided into 2 groups
1. Chronic non-cancer pain
1.1 Chronic neuropathic pain
antidepressant/anticonvulsant
gabapentin/pregabalin
1.2 Chronic musculoskeletal pain
muscle relaxant, α2-agonist
NSAIDs
interventions
2. Cancer pain – depend on causes of pain
Evidence of opioid efficacy
* A limitation of these trials was that the duration of opioid
therapy was a maximum of 3 months.
Evidence of opioid efficacy• Nociceptive pain of musculoskeletal origin
Only small-moderate benefits in improving
function and relieving pain
• Neuropathic pain
Only small-moderate benefits
• Migraine, tension headache, functional GI problems
Not indicated
• Widespread soft tissue pain
Only small benefit with weak opioid
MST
• MST 10, 30, 60 mg tablets oral q 8 or 12 h (not TID/BID)
• peak onset 2-4 h, duration 8-12 h
• no crushing/chewing
• IV 24-hr dose x 3 = oral maintenance dose per day
• then divide maintenance dose into q 8 or 12 h
Kapanol
• Sustained-release capsule of morphine sulfate
• 20, 50, 100 mg capsules with pellets
• peak onset 2-4 h, duration 24 h
• pellets can be dispersed in water, juice, yogurt,
custard, ice cream, and drink within 30 min without
crushing or chewing on pellets
Morphine for breakthrough pain
Syrup 10 mg/5 ml
• peak onset 30 min, duration 3-4 h
• always use exact measurement (syringe)
Immediate release tablet 10 mg
• Onset 15-30 min, duration 4-6 h (t1/2 2-4 h)
Fentanyl transdermal patch
• Release 12, 25, 50 microgram/hour topical patch
• Onset 8 h, duration 72 h
• NOT used in acute pain/ opioid-naive patient
• chest, back, flank, upper arm (no shaving)
• Need subcutaneous fat for absorption
• No sauna, hot bath, tanning, electric heating pad, or exercise
that may increase body temperature
• caution in MRI
Methadone
• tablet 5, 10 mg or syrup 1, 5 mg/ml
• binds to mu receptor, NMDA receptor antagonist,
inhibits serotonin reuptake transporter
• Not recommended as 1st line medication
• oral bioavailability 36-100%, half-life 8-59 h
• peak plasma concentration at 1-7.5 h
• Not dialyzed, inactive metabolites
Oxycodone
• moderate-severe pain if morphine is not tolerable
• Morphine : Oxycodone = 2:1
• binds to mu and kappa receptor
• controlled release (Oxycontin)
• metabolized by CYP3A4/CYP2D6 to
• noroxycodone : weak analgesic
• oxymorphone : strong analgesic (14 times potency)
Key principles of care
• pain reduction
• adverse effects
• daily activities and participation (such as ability to
work and drive)
• mood (depression and/or anxiety)
• quality of sleep
• overall improvement as reported by the person