Cancer Pain Management
Ann L. Janer
Pain Management
• Pain is an unpleasant sensation, a symptom, a
subjective experience, a complex interaction of
neuro-systems with the interaction of biochemical,
physiological, psychological, and neocortical
processes. It is influenced by attention, anxiety,
suggestion, fatigue, prior conditioning and the
extent of tissue damage.
Pain Receptors
• found in abundance in the superficial layers of
skin
• found in periosteum, arterial walls, joint surfaces
and parts of the cranial vault
• Deep internal structures have few to no pain
receptors
Pain Sensation
• Pain receptors do not adapt to stimulation as other
sensory receptors;
• with repeated stimulation, pain receptor sensitivity
and sensation may actually increase;
• intensity of pain is correlated to rate of tissue
damage
Causes of Pain
Ischemia...as blood flow to a tissue is decreased and
blocked, pain results, caused by…
• lactic acid (anaerobic metabolism)
• cell damage leads to accumulation of bradykinin
and proteolytic enzymes
Causes of Pain
Muscle Spasm as a Cause of Pain
• spasm stimulates mechanical pain receptors
AND
• compression of blood vessels by the spasm
induces ischemia
Stimulation of Pain Receptors
Mechanical
• excessive mechanical stretch triggers the response
• e.g. inflammation, edema, tumor
Thermal
• extremes of heat (>45°C) or cold
Stimulation of Pain Receptors
Chemical
• usually responsible for stimulating slow, aching
pain which follows an injury.
• some chemicals excite the chemical pain receptors
and some enhance the sensitivity of pain nerve
endings.
Pain Message Control
Gate Control
• The transmission of painful information can be
modulated by afferent input from the periphery,
descending inhibitory systems, cognitive and
emotional factors.
Pain Message Control
Corticifugal Signals
• Inhibitory signals from the cerebral cortex to lower
"relay stations" of the thalamus, medulla and spinal
cord.
• Control the sensitivity of the sensory input. (When
input intensity becomes too great, corticifugal signals
automatically decrease the transmission.)
Pain Message Control
Corticifugal Signals cont.
• This decreases the lateral spread of sensory signals to
adjacent neurons and it keeps the sensory system operating
in a range of sensitivity so that signals are neither too low
(ineffective) or too high (unable to differentiate sensory
patterns).
Endogenous Opioids
• Enkephalins act at peripheral neural sites occur at
the dorsal root ganglion, spinal cord, midbrain,
hypothalamus, periaquaductal gray area and
rostral medulla.
Endogenous Opioids
• Enkephalin is believed to cause presynaptic inhibition of
both incoming type C and A delta fibers where they
synapse in the dorsal horns. The probable mechanism is
via calcium channel blockade in the nerve terminals. The
inhibition apparently lasts for prolonged periods of time as
analgesia lasts from minutes to hours.
Other Pain Inhibition
Pathways
Adrenergic Pathways
• Norepinephrine acts at the dorsal horn (descending
impluses) to inhibit pain;
• By a different mechanism (enhancing
prostacycline production), it can also enhance
peripheral pain.
Other Pain Inhibition
Pathways
Serotonin Pathways
• Centrally mediated pain modulation via a descending
pathway along the spinothalamic tract
• Presynaptic reuptake inhibition of serotonin and
norepinephrine (amitriptyline-Elavil) is key. SSRI's
(fluoxetine-Prozac) not as effective modulating
neurogenic pain as TCA’s
Other Pain Inhibition
Pathways
Cholinergic Pathway
• Binding sites responsive to acetylcholine have
been found in the dorsal horn.
Other Pain Inhibitory
Pathways
GABA-ergic Pathway - 2 types of receptors
• GABAA sensitive to muscimol
and
• GABAB which is sensitive to baclofen (Lioresal)
• Greatest effect - C fibers; baclofen is effective in treating
central pain syndromes especially associated with muscle
spasms.
Pain Management Goal
• The goal is to identify the specific origin and
cause of the pain so that medical, surgical or drug
treatment may be implemented. The pain
threshold can be lowered by fear, anxiety,
depression, fatigue, or anger. It can also be raised
by rest, mood elevation, sympathy, diversion or
understanding.
Acute Pain
• Injury, trauma, spasm or disease to skin, muscle, somatic
structures or viscera;
• Perceived and communicated via peripheral mechanisms
(pathways) A delta and C fibers
• Usually with autonomic response as well (tachycardia,
blood pressure, diaphoresis, pallor, mydriasis (pupil
dilation);
Acute Pain
• Usually subsides quickly as pain producing stimuli
decreases
• Associated with anxiety-(decreases rapidly)
• Can be understood or rationalized as part of the
healing process.
Acute Pain
Somatic-Superficial
• Initiated in skin, subcutaneous or mucous tissues
• Characterized by throbbing, burning, or pricking
sensations; associated with tenderness, allodynia
(pain from a usually non-pain stimulus) or
hyperalgesia
Acute Pain
Somatic-Deep
• Generally initiated in musculoskeletal tissue
• Characterized by dull, aching pain which CAN be
localized; pain may radiate
Acute Pain
Visceral
• Initiated in the abdomen or thorax difficult to
localize
• Frequently associated with referred pain sites
Referred Pain
•
•
•
•
Appendix > Umbilicus
Esophagus > Neck, Pharynx, Middle Chest, Arm
Gallbladder > Right shoulder, Central abdomen
Heart > Lower neck, shoulders; Radiates down either arm
(left more common than right)
Referred Pain
•
•
•
•
•
Kidneys > Lower back, Flank
Stomach > Upper abdomen, Chest
Ureters > Anterior abdominal wall, Back, Flank
Urinary Bladder > Lower abdomen, Vagina
Uterus > Lower abdomen, Back, Groin, Pelvis
Chronic Pain
•
•
•
•
Non-malignant
Pain persists beyond the precipitating injury
Rarely accompanied by autonomic symptoms
Sufferers often fail to demonstrate objective evidence of
underlying pathology.
• Characterized by location-visceral, myofacial, or
neurologic causes.
Chronic Pain
• Malignant
• Has characteristics of chronic pain as well as
symptoms of acute pain (breakthrough pain).
• Has a definable cause, e.g. tumor recurrence
• In treatment, narcotic habituation is generally not
a concern.
Pain Perception
Pain perception and response are different • actual tissue injury (mech., thermal, or chemical)
• intensity & duration of the insult
• function of nerves’ spinothalamic paths
• central nervous system pain mediators & neurotransmitters
• social, religious, psychological & cultural factors
Initial Pain Assessment
•
•
•
•
Patient Interview including PQRST for pain
Intervention History
Physical Exam (include MMS)
Labs & Radiology (thyroid profile, CBC, ESR,
Radiograph, ECG)
• Functional Assessment (ADL) & Psychological
Assessment
• Treatment Access
ABCDE of Pain Management
•
•
•
•
A Ask about pain regularly; Assess systematically.
B Believe pt. & family’s report of pain & relief.
C Choose pain control appropriate for pt.& family.
D Deliver interventions in a timely, logical &
coordinated manner.
• E Empower pts. & families; Enable them to have as much
control as possible.
Pain Evaluation
PQRST
• P palliative/provocative
• Q quality
• R region/radiation
• S subjective/severity
• T temporal/time factors
Severity Assessment
Visual Analog Scale (VAS)
• No Pain ---> 10 cm line ---> As bad as it can be
• Faces of Pain (Ouchers) - similar to the visual
analog scale J ------->L
Severity Assessment
Numerical Rating Score (NRS - similar to VAS)
|----|----|----|----|----|----|----|----|----|----|
0 1 2 3 4 5 6 7 8 9 10
• (for children or adults who understand numerical
relationships)
Severity Assessment
McGill Pain Questionnaire
• 0 ----------> 5
• None -------------------> Excruciating
• Mild, Discomforting, Distressing, Horrible, in
between.
WHO Pain Management Scale
Step 3
Step 2
Step 1
NSAIDS,
+ adjuvants
NSAID
+ mild
opioids
+ adjuvant
strong
opioids +
NSAIDS
+ adjuvants
VAS vs WHO
VAS
1-3
4-6
7 - 10
WHO Steps
Step 1
Step 2
Step 3