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 receptorsAND

• 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 isgenerally 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 ------->

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 1NSAIDS, + adjuvants

Step 2NSAID + mild opioids+ adjuvant

Step 3strong opioids +NSAIDS+ adjuvants

VAS vs WHO

VAS1 - 34 - 67 - 10

WHO StepsStep 1Step 2Step 3