Cancer pain

SYAFRUDDIN GAUS
DEPARTMENT OF ANESTHESIOLOGY, INTENSIVE
CARE AND PAIN MANAGEMENT
FACULTY OF MEDICINE, HASANUDDIN
UNIVERSITY

Magnitude of Cancer Pain
Etiology of Cancer Pain
Pathophysiologic of Cancer Pain
Clinical Characteristic of Cancer Pain
Evaluation of Cancer Pain
Management of Cancer Pain
CPD Perioperative IDSAI, Medan Juli 2010

 Bonica 1985
 50 % of patient of all stage reported pain
 > 70 % with advanced cancer
 Faley 1985
 50 % of patient with non metastatic cancer had significant
pain
 60-90 % of patient with advanced cancer reported debilitating
pain
 WHO 1986
 70 % of patient with advanced cancer has pain
 3,5 million people suffering from cancer pain with or without
satisfactory treatment every day
 Paice, 2006
 20-75% have pain at first diagnosis
 23- 100% report pain in advance stage

TOTAL
PAIN
SOMATIC SOURCE
ANXIETY
ANGERDEPRESSION
Non-cancer pathology
Cancer
Symptoms of debility
Side-effects of theraphy
Loss of social position
Loss of job prestige and income
Loss of role in family
Chronic fatigue and insomnia
Sense of helpessness
Disfigurement
Bureaucratic bungling
Friends who do not visit
Delay in diagnosis
Unavailable doctors
Irritability
Therapeutic failure
Fear of hospital or nursing home
Worry about family
Fear of death
Spiritual unrest
Fear of pain
Family finances
Loss of dignity and bodily control
Uncertainty about future
WHO 1986

 TUMOR-RELATED PAIN
 TREATMENT-RELATED PAIN
 DEBILITY-RELATED PAIN
 NON-MALIGNANT CONCURRENT DISEASE

 Surgical procedures
 Chemotherapy
 Immediate acute pain : iv infusion pain
 Painful sequelae : arthralgia, headache,
mucositis
 Radiotherapy
 Soft tissue injury : mucositis, proctitis,
peripheral neurophaty, ets

 NOCICEPTIVE PAIN
 SOMATIC PAIN
 VISCERAL PAIN
 NEUROPHATIC PAIN
 NERVE COMPRESSION
 DEAFFERENTATION NERVE INJURY
 SYMPATHETICALLY MEDIATED
 PSYCHOGENIC PAIN

1. Nociceptive pain
 Somatic pain :
 aching, stabbing, throbbing
 Well localized
 Visceral pain :
 obstruction : gnawing, cramping
 Organ capsule : aching, sharp, throbbing
 Diffuse and difficult localize
 May referred to somatic structure

2. Neuropathic pain
 Nerve compressions
 Burning, prickling, electric like
 Area innervated nerve
 Malignancy compression
 Deafferentation nerve injury
 Same nerve compressions + shooting,stabbing
 allodynia
 Often loss afferent sensory function
 Superficial burning pain

 Sympathetically mediated
 Cutaneous vasodilatation, increased skin temperature,
abnormal sweating, tropic cahanges and allodynia
 Nondermatomal pattern pain
 Diagnostic sympathetic block
3. Psychogenic pain
- after pathology pain generating excluded
- can contribute but pure psychogenic etiology is
rare

 REFLECT
 TUMOR SIZE
 LOCATION
 EXTENT TISSUE DESTRUCTION
 MECHANISM OF PAIN
 PAIN INTENSITY USED TO GUIDE ANALGESIC
THERAPY

 MEDICAL HISTORY
 PAIN HISTORY
 PAIN ASSESSMENT :
 LOCATION
 CHARACTER
 SEVERITY
 ONSET
 DURATION
 TEMPORAL PATTERN
 RELIEVING AND EXACERBATION FACTOR
 ASSOCIATED SYMPTOMS
 PREVIOUS ANALGESIC THERAPY
 SPECIFIC CANCER TREATMENT

 ORIGINALLY INTRODUCED IN 1986
 SIMPLE
 THREE STEP
 WIDELY AVAILABLE AND INEXPENSIVE ANALGESIC
 GLOBALLY DISTRIBUTED AND CURRENTLY
CONSIDERED AS STANDARD FOR MANAGEMENT
CANCER PAIN

 Mainstay of cancer pain
 Multiple routes
 Enteral
 Parenteral ( iv, sc )
 Spinal delivery
 Transdermal
 Transmucosal
 Several formulation :
 sustained release eg. MS Contin, Kadian, Avinza.
 Rapid release : not available in Indonesia

Opioid Half live Equipotent IV
dose
( mg/kg)
Equipotent
PO dose
( mg/kg )
Duration
( hr )
Morphine
Fentanyl
Pethidine
Alfentanyl
Sufentanyl
Codeine
Oxycodone
2-4 hrs
1 – 7 min
3 – 4 hrs
1.4 min
1.4 min
3 hrs
2 – 6 hrs
0.1
0.001
1
0.05
0.0001
1.2
N/A
0.3 – 0.5
0.001-0.005
transmucosal
1.5 – 2
N/A
N/A
2
0.1
3-5
0.75 – 1
2 – 3
0.5
1
4 - 6
4 – 6

 Least lipid soluble
 Metabolites M6G and M3G ( longer half lifes )
 M6G more potent than morphine
 M3G ( no analgesic effect ) role in tolerance
 Slow release ( controlled release or sustained
release ) use for chronic and cancer pain
 Slow onset, prolonged duration  fast
titration its impossible

 Highly lipid soluble synthetic opioid
 Rapid onset and short duration
 Metabolite inactive (safe for renal impairment)
 Suitable for transdermal administration

 Synthetized as a potential substitute for
atropine  ( atropine like effect )
 Weak affinity for NMDA receptor
 Pethidine superior in renal and biliary colic
but evidenced show that all opioids are
equally effective
 Metabolite is norphetidine ( normeperidine )
with long half-life ( 15-20 hrs )
 analgesia ( µ receptors ) but neurotoxicity
( CNS excitation : anxiety, mood changes,
tremors, twitching, myoclonic , convulsion )

 Treatment
 Discontinue pethidine
 Substitue to alternative opioid
 Symptomatic treatment
 DO NOT administer naloxone
 Suggest
 Dose limit : 1000 mg in first 24 hrs and 600-700
mg/day thereafter, Reduced in elderly
 Should be avoided in renal impairment

 Centrally acting synthetic analgesia
 µ receptors activity ( by main metabolite M1
( O-desmethyl-tramadol ))
 Inhibit reuptake NE and serotonine (5HT ) in
nerve terminal
 Advantages of equianalgesic dose opioid
 Less sedation
 Less repiratory depression
 Less constipation
 Nausea and vomiting similar
 Not a controlled drug

 Epilepsy was relatively contra indication
 Seizure have been reported but probably
similar with other opioid
 Accumulation M1 in renal failure can cause
respiratory depression
 Total daily dose : 600 mg

 Naturally alkaloid like morphine
 Metabolized in liver by CYP 2D6
 converted to morphine (2-10%)
 analgesic effect of Codeine
( ineffective prodrug of morphine )
 Usually for mild to moderate pain
 Combine with non-opioid agents like
acetominophen or aspirin
 increased analgesic efficacy but also
decreased opioid relate adverse effect

Oral dose
( mg )
Opioid Parenteral iv/sc/im
( mg )
400 Meperidine 100
100 Tramadol 100
200 Codeine 130
30 Morphine 10
- Fentanyl 0.15 – 0.20
- Sufentanyl 0.02
Morphine 50 mg PO in 24 hrs = fentanyl patch 25 mcg/hr

 Analgesic antipyretic
 Used in all steps in Stepladder WHO
 Recommend dose 4000 mg/d
 Dose adjustment in hepatic dysfunction

 Analgesic, antipyretic and anti-inflammatory
 Nonselective agents and selective COX-2
inhibitors
 Effective component in multimodal therapy
 Carefully selected patients due to adverse
effect
 COX-2 inhibitors proveide protection adverse
effect but concern in Cardiovascular effect

 Antidepressant
 Inhibition NE and serotonin reuptake
 For neurophatic pain
 Delays onset day to week
 Mood elevating and sleep enhancing effect
 Adverse effect on cardiac , glaucoma n prostatic
 Amitriptyline, Nortryptiline and Despiramine
 Anticonvulsant
 For neurophatic pain eg. Chemotherapy
 Na channel blocker : Carbamazepine and clonazepam
 Gabapentin : Ca Channel and can act as NMDA
antagonist . 900 – 3600 mg/d

 Corticosteroids
 Inhibit prostaglandin synthesis and reduce
edema
 For neuropathic pain syndrome
 Bone pain , malignant intestinal obstruction
 Dexamethasone 12 – 24 mg once daily
 NMDA antagonist
 Bind EAA glutamat
 For severe neuropathic pain
 Routine use limited due to cognitive changes

 Local anesthetic
 Inhibiting ions across neural membrane
 Relieving neuropathic pain
 Orally, topically, intravenously, subcutaneously,
spinally
 For Intractable neuropathic pain :
Lidocaine intravenous 1 – 2 mg/kg ( max 500 mg )
over 1 hour then 1 -2 mg/kg/h continuous infusion

 Nerve block
 Sympathetic nerve block
 Myofacial trigger point
 Neurolytic block : celiac plexus block
 Epidural or intratechal drugs

 Physical therapy
 TENS
 Accupuncture
 Counterirritation
 Psychological approach
 Depression and anxiety most often
 Cognitive intervention : relaxation

Cancer pain

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Cancer pain