Transcript Staporn Pain and Cancer Pain Management 20060402

Pain and Cancer Pain
Management
Dr.Staporn Leelanuntakit
Definition of Pain
“An unpleasant sensory and emotional
experience associated with actual or potential tissue
damage or described in terms of such damage. Pain
is always subjective. Each individual learns the
application of the word through experiences related
to injury in early life…. It is unquestionably a
sensation in a part or parts of the body but it is also
always unpleasant and therefore an emotional
experience”
International Association for the Study of Pain,1979
The Perception of
Pain
The processes involved in
perception of pain are no longer
viewed as a simple hard wired
system with a pure stimulus
response relationship.
Neurobiology and
Neurophysiology of
Pain
Neurotransmitters
Involved in Pain Pathways





Serotonin
GABA
Glutamate
Substance P
Opioid peptides
Reisine T, Pasternak G. In: Goodman & Gilman’s. 9th ed. 1996;521-555.
Ollat H, Cesaro P. Clin Neuropharmacol.1995;18:391-404.
Neurotransmitter that play
a role in Pain Modulation





Alpha-2-adrenergic agonists
N-methyl-d-aspatate (NMDA)
antagonists
Sodium channel blockers
Calcium channel blockers
Gamma-aminobutyric agonists (GABA)
Pain Behaviour
Pain Behaviour
Suffering
Pain
Nociception
Composition of Pain
Physiological Pain ----
(Functional)
PAIN
------- Pathological Pain
(Nociceptive;Neuropathic)
^
|
|
Psychological Pain
Other symptoms adverse
effects of treatment
Physical
Depression
Loss of social position
Loss of job prestige and income
Loss of role in family
Insomnia and chronic fatigue
Sense of helplessness
Disfigurement
Anger
TOTAL PAIN
Bereaucratic bungling
Delays in diagnosis
Unavailable doctors
Therapeutic failure
Friends who do not visit
Anxiety
Fear of hospital or nursing home
Fear of Pain
Worry about family and finance
Fear of death
Spiritual unrest, uncertainty about future
Robert Taycross; 1944
Pain related to Cancer
PHYSICAL PAIN
Pain Unrelated
to cancer
Pain
+
Other physical symptom +
Psychological problem +
Social difficult
+
Cultural issue
+
Spiritual concern
+
What the patient says it is
Pain related to
cancer treatment
- Pain
- Other physical symptom
- Psychological problem
- Social difficult
- Cultural issue
- Spiritual concern
CLINICAL PAIN
The Concept of Clinical Pain
What has to be treated
Types of Pain



Acute Pain
Chronic Pain
Cancer Pain
Difference between Acute
and Chronic Pain
Patients:
Acute pain
Transcient
Acts as a warning sign
Decreases
Obviously in pain
Complains loudly of pain
Understand pain
Primarily affect patients
Doctors:
Treatment straightforward
Parenteral analgesics
Analgesic side effects
acceptable
Chronic pain
Persistent
Serve no useful purpose
Tends to increase
May only seem depressed
May only complain of discomfort
See pain as unending and
meaningless
Pain overflows to affect family
Treatment may be complex
Oral analgesics preferable
Side effects unacceptable
Pain in Cancer Patient





Direct tumor involvement
Complications of cancer treatment or of antalgic
therapy
Cancer related physiologic and biochemical
alterations, and those associated with chronic
illness, such as muscle weakness and other disorder
known as “paraneoplastic syndrome”
Painful disorders unrelated to cancer and cancer
therapy
A combination of these
What is Cancer Pain?
By nature cancer pain is:
 Recurrent acute pain because there is continual
tissue damage.
 If there is nerve damage, cancer pain can be
very severe and persistent.
Rarely, there may be associated chronic pain.
Particularly when there is nerve damage and the
patient has a long history.

Unique Aspects of
Cancer Pain






More than one site of pain
More than one syndrome
More than one etiology
Acute and/or chronic
Varied pattern, intensity, and durations
More than one treatment
Prevalence of Cancer Pain



Approximately 25% of patients with
localized disease report pain
Prevalence of pain can be as high as 90%
in patients with advanced cancer
Adequate pain control can be achieved in
as many as 88% of patients with cancerrelated pain, but in reality many patients
have inadequate pain management
Cause of Cancer Pain



Somatic (Bone)
Viscera
Nervous system
Types of Pain : Somatic
Pain
When nociceptors are activated in
cutaneous or deep tissues, somatic
pain results, typically characterized by
a dull or aching but well-localized pain.
Metastatic bone pain, postsurgical
incisional pain, and myofascial and
musculoskeletal pain are common
examples of somatic pain.
Types of Pain : Visceral
Pain
Visceral pain results from activation of nociceptors
from infiltration, compression, extension or stretching of
the thoracic, abdominal or pelvic viscera. This typically
occurs in patients with interperitoneal metastases and is
common with pancreatic cancer. This type of pain is
poorly localized; is often described as deep, squeezing,
and pressure-like, and when acute is often associated
with significant autonomic dysfunction, including nausea,
vomiting and diaphoresis. Visceral pain is often referred
to cutaneous sites that may be remote from the site of
lesion (e.g. shoulder pain with diaphragmatic irritation).
It may be associated with tenderness in the referred
cutaneous site.
Types of Pain :
Neuropathic Pain
Neuropathic pain result from injury to
the peripheral or central nervous system
as a consequence of tumor compression
or infiltration of peripheral nerves or the
spinal cord, or from chemical injury to the
peripheral nerve or the spinal cord caused
by surgery, radiation therapy or
chemotherapy.
Types of Pain :
Neuropathic Pain
Pain from nerve injury is often severe and is
described as burning or dysesthetic, with a vicelike quality. The pain is typically most common in
the site of sensory loss and may be associated
with hypersensitivity to non-noxious (allodynia)
and noxious stimuli. Intermittently patients
complain of paroxysms or burning or electric
shock-like sensations. The latter symptoms
result from the phenomenon of central
sensitization.
Principle of Treating
Cancer Pain


Aim of treatment
- relief and prevention of pain
General principles
- through assessment
- good communication
- reassurance about pain relief
- discourage acceptance of pain
- encourage patient participation
Principle of Treating
Cancer Pain

Principle of treatment
- integrated part of a multidisciplinary
plan of care
- should be appropriate to the stage of
the disease
- use the appropriate treatment modalities
- must be consistent, and variable
- requires continuity of care
- involves repeated reassessment
Examples of two females and one male actor showing neutral, anger and
pain faces (from left to right column). Five time points in the clip are displayed.
ASSESSMENT of PAIN
Clinical Evaluation
1.Pain is what the patient says-so believe and
treat.
2.Assess the pain carefully
- history (especially result from the
previous treatment)
- examination
- investigation
Clinical Evaluation (cont..)
3. Assess each pain (most cancer
patients have more than one pain)
- type of pain
- cause of pain
- intensity of pain
- characteristic of pain
Clinical Evaluation (cont..)
4. Assess the extent of the patient’s disease
- The pain
Site
Where’s it?
Radiation
Present since
Progressive
Severity
Quality
Frequency
Duration
Precipitating factors
Aggravating factors
Relieving factors
Impact on – activity
- sleep
- mood
Does it spread to anywhere else?
How long have you had it?
Has it got worse?
How bad is it? (use tools)
What is it like?
How often does it occur?
How long does it last?
What brings it on?
What make it worse?
What helps the pain?
Does it stop patient doing things?
Does it disturb patient sleeping?
Does it make patient unhappy or depressed?
Clinical Evaluation (cont..)
4. Assess the extent of the patient’s disease (cont..)
- Effect of previous medication
Medication
Dose
Route
Frequency
Duration
Effect
Side effects
What did patient take?
How much?
By mouth? or others?
How often?
For how long?
Did it help?
Did it upset patient?
5. Assess the other factors which may influence pain-physical, psychological,
social, culture, spiritual
6. Reassessment especially for the new or more extensive pain.
MANAGEMENT
OF
CANCER PAIN
Modalities of Treatment (I)





Treatment of underlying cancer
Analgesics
Adjuvant analgesics
Neurostimulatory treatment
Anesthetic, neurolytic and
neurosurgical procedures
Modalities of Treatment (II)



Physical therapy
Lifestyle modification
Treatment of other aspects of suffering
which cause or aggravate pain:
physical, psychological, social, cultural,
spiritual
“Analgesic drugs are the
mainstay for control cancer
pain”
“All pain do not respond
equally to analgesic”
Analgesics



Non-Opioid Analgesic
Opioid Analgesic
- Weak opioid
- Strong opioid
Adjuvant Drugs
The Use of Analgesics for
Cancer Pain

Choice of Drug
- appropriate drug for choice of pain
- appropriate drug for severity of pain
- use of combinations of drugs not
combined drugs
- follow the analgesic ladder
- use adjuvant analgesics
- never use placebo
The Use of Analgesics for
Cancer Pain

Administration
- give in adequate dosage
- titrate the dose for each individual patient
- schedule administration according to
drug pharmacology
- strict scheduling to prevent pain, not PRN
- give written instructions for patients on
multiple drugs
The Use of Analgesics for
Cancer Pain


Administration
- warn of, and give treatment to prevent,
side effect
- keep the analgesic program as simple as
possible
- use the oral route whenever possible
Review and reassess
Help patient survives to live
with pain and inspite of pain
Type of Pain: Implications for treatment
Nociceptive
Bone, soft tissue
mild,modulate
severe
Visceral
mild
severe
non-opioid
(opioid if required)
opioid + non-opioid
non-opioid
(opioid if required)
opioid ± non-opioid
Type of Pain: Implications for treatment
Neuropathic
Nerve compression
:opioid + corticosteroid
anticonvulsant
or tricyclic antidepressant
or oral local anesthetic drug
Sympathetic-type pain :sympathetic nerve block
Type of Pain: Implications for treatment
Other
Raised intracranial pressure
:corticosteroid
Muscle spasm
:muscle relaxant
Non-Opioid Analgesics



Aspirin
Paracetamol
Nonsteroidal Anti-inflammatory Drugs
(NSAIDs)
NSAIDs


The realization that NSAIDs may have
a central action.
The cyclo-oxygenase enzyme
differentiates into two types, COX-1
and COX-2.
Development of safer
NSAIDs



Preferential inhibitor of COX-2
- nabumetone
- etodolac
- meloxicam
Highly selective COX-2 inhibitor
- celecoxib, etoricoxib,valdecoxib,
parecoxib
NSAIDs containing nitric oxide
The new classification of
NSAIDs as COX-2 concepts
1. Classical NSAIDs
2. Preferential COX-2 inhibitors
(selective COX-2 inhibitor)
3. Highly specific COX-2 inhibitors
(COX-2 inhibitor, specific COX-2
inhibitors)
Selective (nonacidic)
COX-2 inhibitors
-
COX-2
COX-2
COX-2
COX-2
and
and
and
and
the gastrointestinal tract
kidney functions
the cardiovascular system
the other body functions
OPIOIDS
Classification of Opioids



“Weak” or “Strong”
Mechanism of action
The chemical derivation of drug
- naturally occuring opium alkaloids
- semisynthetic derivatives of opium
alkaloids
- synthetic opioids
Effects of Activation of
Opioid Receptors
µ
: Analgesia, supraspinal
: Dependence (withdrawal signs, drugseeking behaviour)
: Sedation
: Euphoria
: Respiratory depression
Effects of Activation of
Opioid Receptors
K
: Analgesia, spinal
: Sedation
S
: Dysphoria
: Psychomotor stimulation
(not clinically useful)
: Hallucination
Opioid Analgesics I
Optimal use of opioid analgesics requires
a sound understanding of the general
principles of opioid pharmacology, the
pharmacological characteristics of each of
the commonly used drugs and principles of
administration, include:
Opioid Analgesics II
1.
2.
3.
4.
Drug selection
Routes of administration
Dosing and dose titration
Adverse effects and their management
NO SINGLE OPIOID IS
RIGHT FOR ALL PATIENTS
IN ALL SITUATIONS
Weak-Opioids



Codeine
Dextropropoxyphene
Tramadol
Strong Opioids



Morphine
Methadone
Pethidine



Buprenorphine
Hydromorphine
Levorphanol
Pentazocine
Not a control drug
It is an agonist-antagonist of the nalophine
type. It has agonist properties at the kappa and
sigma receptors but an antagonist effect at the
mu receptor, analgesics of this type produce
psychomimetic side effects such as dysphoria,
depersonalization, vivid day- dreams,
nightmares and hallucinations. As a partial
agonist it may attenuate the effects of pure
agonist given concurrentally.
It has no place in the relief of cancer pain.
Buprenorphine
Sublingual and injection
Not controlled drug
6 to 8 hourly regimen
Partial agonist at the mu-opioid receptor
Analgesic celling dose of about 5 mg, which
equivalent to about 50 mg of oral
morphine 4 hourly.
Pethidine




Pethidine has no real place in cancer pain
management.
It often need to be given every two to three
hour to maintain relief.
It has a toxic metabolite, norpethidine, with
a plasma half-life of some 17 hours
compared with 3.5 hours of pethidine itself.
Norpethidine is excitatory and causes
tremor, twitching, agitation and convulsions
of high plasma concentration.
Pethidine


Appreciable cumulation occurs with doses of
pethidine of 200-300 mg particularly if
taken by mouth when the ratio of pethidine
to norpethidine in the blood shifts in favour
of the latter.
In patients with severe renal failure, toxic
effects are seen at much lower doses.
Methadone



Methadone is slightly more potent than morphine
in single doses but use repeatedly; it is
considerably more potent on account of
cumulation.
With chronic use, the plasma half-life increases
from 15 hours to two to three days, the use of
methadone is more complicated than the use of
morphine.
It is not advisable to use methadone in the very
elderly and severity debilitated, in patients with
appreciable liver, renal or respiratory failure or in
patients with intracranial tumours.
Morphine is generally the
standard against which other
opioids are compared and is
considered by many to be the
analgesic of choice for severe
pain associated with terminal
illness.
Opioid agonist drugs
Drug
Dose (mg)
equianalgesic to 10
mg IM Morphine
IM
PO
Half-life
(hrs)
Duration of action
(hrs)
Codeine
130
200
2-3
2-4
Oxycodone
12
30
2-3
2-4
Propoxyphene
50
100
2-3
2-4
Morphine
10
2-3
3-4
Hydromorphone
1.5
2-3
2-4
Methadone
10
20
15-190
4-8
Meperidine
75
300
2-3
2-4
Oxymorphone
1
2-3
3-4
Heroine
5
60
0.5
3-4
Levorphanol
2
4
12-15
4-8
Fentanyl transdermal
system
NA
NA
30(repeated dose)
60(single dose)
7.5
10 (PR)
48-72
Morphine is not the
Panacea
Morphine sulphate




Strong narcotic of choice
Usual starting dose 10 mg 4 hourly
With frail elderly patients, it may be
wise to start on a suboptimal dose.
If changing from alternative strong
narcotic, a considerably higher dose
may be need
Morphine sulphate




Adjust upwards after first-dose if not more
effective than previous medication.
Adjust after 24 hours if pain not 90%
controlled
Most patients are satisfactorily controlled on
doses of between 5 and 30 mg 4 hourly
Giving a larger dose at bed times (1.5 or
2xdaytime dose)
Oral-to-Parenteral potency
ratio of Morphine
1.2: 1.3 or 1.6
Morphine
Dose (titrate up or down based on patient
response)
Initial dose
PO
IM
IV
SR
CR
10-30 mg q 3-4 h.
5-10 mg q 3-4 h.
1-2.5 mg q 5 min PRN
15-30 mg q 12 h
30-60 mg q 24 h
Use immediate-release product with SR or CR product to control
“breakthrough” pain.
Morphine sulphate






Use co-analgesic medications as appropriate
Prescribe an antiemetic for regular use should
nausea or vomiting develop
Prescribe laxative
Warm patient of possibility of initial drowsiness
Controlled release morphine sulphate, B.I.D. or
sustained release morphine sulphate, O.D. should
be considered in long term treatment.
Subcutaneous, intramuscular injection only in
patient who becomes difficult in swallowing or
vomiting persists.
Route of Drug Administration
Oral
Internasal
Buccal
Subcutaneous
Sublingual
Intravenous
Rectal
Epidural
Transdermal
Intrathecal
and Intracerebroventricular
Durogesic® : Fentanyl Transdermal
System Delivers fentanyl direct to
circulation
and alcohol
silicone
(Ethylene-vinyl
acetate copolymer)
D-trans Matrix Durogesic
Mechanism of Action
Technology of D-TRANS®
Drug-in-Adhesive Matrix Technology
D-TRANS®
Reservoir System
Reservoir
....................
.....................
Layers :



Layers :
Backing layer
Reservoir with permeation
membrane
–
Fentanyl embedded in a gel
–
Contains ethanol to enhance
permeation
Adhesive layer

Backing layer

Solid drug-in-adhesive matrix:
– Contains and releases fentanyl
(in dissolved state)
– Simultaneously functions as
adhesive
.....
Technology of D-TRANS® Summary
Durogesic Reservoir
Durogesic
Matrix
Patch structure
Reservoir system with gel
Flexible matrix
Patch size
25 µg/h – 18.7 cm2
50 µg/h – 34 cm2
75 µg/h – 44.2 cm2
100 µg/h – 57.0 cm2
-
Adhesive
Silicone-adhesive
Polyacrylate polymer
Fentanyl
Embedded in gel of
water/ethanol/
hydroxyethyl cellulose
Dissolved in the adhesive layer
(diffusion through matrix and
skin = rate limiting)
Permeation enhancer
Ethanol
None
Protective liner
Without slit
Provided with an S-shaped slit
Packaging
10.5
21
31.5
42

cm2
cm2
cm2
cm2
Child-resistant
D-TRANS
Matrix smaller
Comparison of Patches
Characteristics
Fentanyl transdermal patch
Fentanyl Matrix
Dosage
Strengths
25, 50, 75, and 100 mcg/h 25, 50, 75, and 100
mcg/h
Rate Control
Membrane and skin
stratum corneum provide
drug delivery rate control.
No membrane.
Ethanol included as
permeation enhancer.
No permeation enhancer.
Skin stratum corneum
provides drug deliver
rate-control.
Side effects and Complications
of Opioid Analgesics







Constipation
Central nervous system side effects
Euphoria
Confusion
Sedation
Dizziness
Drowsiness
Nausea, vomiting and puritus
Respiratory depression
Tolerance
Physical Dependence
Addiction
Tolerance VS Addiction
TOLERANCE
≠
≠
ADDICTION
(Psychological Dependence)
PHYSICAL
DEPENDENCE
Signs and Symptoms of Opioid
Intoxication and Withdrawal

Intoxication
Euphoria
Dysphoria
Apathy
Motor retardation
Sedation
Attention Impairment
Miosis
Slurred speech

Withdrawal
Lacrimation
Rhinorrhea
Mydriasis
Piloerection
Diaphoresis
Diarrhea
Yawning
Fever
Insomnia
Muscle aching
Adjuvant Analgesics
Adjuvant use for
Multipurpose Symptoms




Corticosteroids
Antihistamines
Muscle relaxants
Neuroleptics




Anticholinergics
Psychostimulants
Antibiotics
Etc.
Adjuvants used for Bone Pain




Anti-inflamatory drugs (NSAIDs,
corticosteroids)
Bisphosphonates
Radiopharmaceuticals
Calcitonin
Adjuvants used for
Neuropathic Pain





Antidepressants
Oral local
anesthetics
Clonidine
Capsicine
Adjuvant drugs for
sympathetically
maintain pain




Anticonvulsants
Baclofen
Calcitonin
Pimozide
Commonly used Adjuvant Analgesics
(1/4)
Class (example) Usual Indication
Anticonvulsant
Gabapentin
Phenytoin
Carbamazepine
Oxcarbazepine
Clonazepam
Neuropathic pain
Particularly
Lancinating or
Proxysmal pain
Antidepressants
Neuropathic pain
Amitryptylline
Nortriptylline
Imipramine
Desipramine
Trazodone
Approximate
Adult Daily Dose
Range
Route of
Administration
900-3600 mg
300-500 mg
200-1600 mg
600-2400 mg
1-8 mg
PO
PO
PO
PO
PO
10-300 mg
10-100 mg
20-100 mg
25-300 mg
50-225 mg
PO
PO
PO
PO
PO
Commonly used Adjuvant Analgesics
(2/4)
Class (example) Usual Indication
Local
Anesthetics
Mexiletine
Neuropathic pain
Corticosteroids
Dexamethasone Tumor invasion of
Prednisone
neural tissue,elevated
intracranial pressure
spinal cord
compression
additional effect (mood
elevation, antiemesis,
appetite stimulation)
Approximate
Adult Daily
Dose Range
Route of
Administration
450-600 mg
PO
16-96 mg
40-100 mg
PO
PO
Commonly used Adjuvant Analgesics
(3/4)
Class (example)
Antihistamine
Hydroxyzine
Muscle relaxants
Orphenadrine
Carisoprodol
Methocarbamol
Chlorzoxazone
Cyclobenzaprine
Neuroleptics
Methotrimeprazine
Fluphenazine
Usual Indication
Coanalgesic,
Antiemetic
Occasional useful for
musculoskeletal pain
Neuropathic pain
Approximate
Adult Daily
Dose Range
75-450 mg
Route of
Administration
PO or IM
75-200 mg
800-1400 mg
4000-6000 mg
1500-3000 mg
20-60 mg
PO
PO
PO
PO
PO
15-100 mg
1-10 mg
PO
PO
Commonly used Adjuvant Analgesics
(4/4)
Class (example)
Other drugs for
Neuropathic pain
Baclofen
Clonidine
Calcitonin
Capsicine topical
Anticholinergics
Glycopyrolate
Psychostimulants
Caffeine
Methylphenidate
Dextroamphetamine
Usual Indication
Neuropathic pain
Approximate
Adult Daily
Dose Range
Route of
Administration
20-120 mg
0.1-0.6 mg
50-100 mg
PO
PO or TD
SC, IM, NS
Visceral pain
resulting from bowel
obstruction
2-6 mg
PO
Decreased sedations
resulting from opioid
analgesia
50-1000 mg
10-15 mg
5-10 mg
PO
PO
PO
Pharmacologic Management
of Neuropathic Pain
Drug class
Example
Antidepressants
Amitriptyline, desipramine,
nortriptyline, imipramine
Anticonvulsants
Carbamazepine, Oxcarbezepine,
phenytoin, valproic acid, gabapentin,
clonazapam
Antiarrhythmias and local Lidocaine, mixelitine
anesthetics
Topical formulations
Capsaicin, EMLA cream, aspirin
Baclofen

Dissociative anesthetics
Ketamine
Dextorphan
Delsym
Anticonvulsants as Adjuvant
Analgesics
Drug
Carbamazepine
Phenytoin
Valproate
Clonazepam
Gabapentin
Site of Action
Decreases sodium channel activity
Decreases sodium channel activity
Decreases sodium channel activity,
possibly increases GABA
Increases GABA function
Increases GABA levels, decreasing
sodium channel function
Upton N. Trends Pharmacol Sci. 1994;15:456-463.
Petroff O, et al. Ann Neurol. 1996;39:95-99.
Am Fam Physician. 1996;55:2534. Family Practice International.
Pharmacologic Properties of
Second-Generation Anticonvulsants
Gabapentin





Increases GABA in brain, possibly by enhancing rate
of synthesis from glutamate
Binds to specific site localized to brain regions
associated with major excitatory inputs
Inhibits sodium currents by mechanism distinct from
phenytoin and carbamazepine
Inhibits branched-chain amino acid transferase,
possibly reducing glutamate concentration
No effect on GABAA or GABAB receptors
GABA
Upton N. Trends Pharmacol Sci. 15;456-463.
Chadwick D. Lancet. 1994;343:89-91.
Petroff O, et al. Ann Neurol. 1996;39:95-99.
Goldlust A, et al. Epilepsy Res. 1995;22:1-11.
Oxcarbazepine
The pharmacological activity of oxcarbazepine is
primarily exerted through the metabolite (MHD) of
oxcarbazepine.
The mechanism of action of oxcarbazepine and MHD
is thought to be mainly based on blockade of voltagesensitive sodium channels, thus resulting in stabilisation of
hyperexcited neural membranes, inhibition of repetitive
neuronal firing and diminishment of propagation of synaptic
impulses; and increased potassium conductance and
modulation of high-voltage activated calcium channels may
also contribute to the anticonvulsant effects of the drugs.
CAUTION ! ! !
ADVERSE REACTIONS
Examples of Nonpharmacologic
Approaches to Cancer

Physical method
- Acupuncture
- Acupressure
- TENS (Transcutaneous Electrical
Nerve Stimulation)
- Electrode Implantation
Examples of Nonpharmacologic
Approaches to Cancer


Surgery
- Tumor debulking
- Adrenalectomy
- Hypophysectomy
Neurosurgery
- Cordotomy
- Rhizotomy
- Deep brain stimulation
- Placement of dorsal column stimulators
- Cingulotomy
Examples of Nonpharmacologic
Approaches to Cancer


Anesthesiology procedure
- Myofascial trigger point injection
- Nerve blocks
Psychological procedure
- Relaxation
- Hypnosis
- Biofeedback
- Brief psychotherapy
Palliative care for
Cancer Patients
Pain Team







Physician
Nurse
Social worker
Pharmacist
Patient and Family
Volunteer
Therapist
Case Study
Known case of 52-years-old Chinese male
patient with diagnosis of Ca floor of mouth stage
IV, Left cervical LN size 3x6 cm fixed post
radiation and chemotherapy.
Severe burning, spontaneous shooting pain at
left side of neck, left cheek with radiated to left
forehead.
Treatment on Oct19,2001
Codeine 60 mg PO q 4 h.
Paracetamol 2 tab q 4 h.
Neurontin 300 mg q 12 h.
MO solution 5 mg PO p.r.n. q 1 h.
MOM 20 ml PO hs.
Case Study
Oct 20,01 :
:
:
:
Nov 09,01:
:
Nov 12,01:
Dec 07,01:
Off Codeine
MST 30 mg p.o. q 12 h.
Neurontin to 600 mg p.o.q12 h.
MOM 30 ml p.o. hs
Neurontin to 900 mg p.o.q12 h.
Paracetamol 2 tab q 6 h.
Neurontin to 1200 mg p.o.q12h.
Add Ativan 1 mg p.o.
morning&hs
Case Study
Jan 08,02 :
Jan 17,02 :
:
:
Jan 24,02 :
Neurontin to 1800 mg p.o.q12h
(severe headache)
MST to 90 mg q12h
Dexamethasone 1 mg p.o. q6h
MST to 120 mg p.o. q12h
Last seen on Jan30,02 , No Pain at All
Case Study
Feb 12,02
Readmission with history of severe
burning pain at right side of the neck,
face, and scalp after developing some
groups of small vesicles and inflammatory
appearance at the skin of the right side of
the neck (harpes zoster to be diagnosed)
for 3 days.
Case Study
Treatment on Feb 12,02
MST 150 mg p.o. q 12 h
Neurontin 1800 mg p.o. q 12 h
Paracetamol 100 mg p.o. q 4 h
Amitryptylline 50 mg p.o. hs
MO 10 mg p.o. prn q 1 h
MOM 30 mg p.o. hs
Acyclovir 800 mg p.o. q 4 h for 7 days
(5 times/day)
Case Study
Feb 18,02 : Amitryptylline to 75 mg p.o. hs
: MO to 20 mg p.o. prn q 1 h
Feb 20,02 : Amitryptylline to 100 mg p.o.hs
Feb 21,02: MST to 210 mg p.o. q 12 h
: Dexamethasone to 2 mg p.oq6h
Feb 25,02: MST to 270 mg p.o. q 12h
: Neurontin to 2100 mg p.o.q12h
No pain at all on Feb28,02; and developing
some degree of dizziness and severe
drowsiness on Mar7,02
Case Study
Mar07,02 : Neurontin to 1800 mg p.o. q12h
Mar12,02 : MST to 210 mg p.o. q12h
: Neurontin to 1500 mg p.o. q12h
Mar14,02 : Due to developing some clonus at all
extremities, MST q12h dosage and MO solution
prn dosage were off, but all of the other adjuvant
pain medications are still further on adjuvant
pain medications are still further on
:Fentanyl patch 150 mcg/h q3days
:MO 5 mg SC. Inj. prn q 1 h
for breakthrough pain were substituted
Case Study
Patient tolerated well to the new
adjusted pain medication, and no any pain
recurred.
Patient expired peacefully on Mar17,02
Thank you for your
attention