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Cancer Pain Management Ann L. Janer. Pain Management Pain is an unpleasant sensation, a symptom, a subjective experience, a complex interaction of neuro-systems

Jan 12, 2016



  • Cancer Pain ManagementAnn L. Janer

  • Pain ManagementPain 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 Receptorsfound in abundance in the superficial layers of skinfound in periosteum, arterial walls, joint surfaces and parts of the cranial vaultDeep internal structures have few to no pain receptors

  • Pain SensationPain 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 tissuedamage

  • Causes of Pain blood flow to a tissue is decreased and blocked, pain results, caused bylactic acid (anaerobic metabolism)cell damage leads to accumulation of bradykinin and proteolytic enzymes

  • Causes of PainMuscle Spasm as a Cause of Pain

    spasm stimulates mechanical pain receptorsANDcompression of blood vessels by the spasm induces ischemia

  • Stimulation of Pain ReceptorsMechanicalexcessive mechanical stretch triggers the responsee.g. inflammation, edema, tumor

    Thermalextremes of heat (>45C) or cold

  • Stimulation of Pain ReceptorsChemicalusually 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 ControlGate ControlThe transmission of painful information can be modulated by afferent input from the periphery, descending inhibitory systems, cognitive and emotional factors.

  • Pain Message ControlCorticifugal SignalsInhibitory 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 ControlCorticifugal 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 OpioidsEnkephalins act at peripheral neural sites occur at the dorsal root ganglion, spinal cord, midbrain, hypothalamus, periaquaductal gray area and rostral medulla.

  • Endogenous OpioidsEnkephalin 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 PathwaysAdrenergic PathwaysNorepinephrine 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 PathwaysSerotonin PathwaysCentrally mediated pain modulation via a descending pathway along the spinothalamic tractPresynaptic reuptake inhibition of serotonin and norepinephrine (amitriptyline-Elavil) is key. SSRI's(fluoxetine-Prozac) not as effective modulating neurogenic pain as TCAs

  • Other Pain Inhibition PathwaysCholinergic PathwayBinding sites responsive to acetylcholine have been found in the dorsal horn.

  • Other Pain Inhibitory PathwaysGABA-ergic Pathway - 2 types of receptorsGABAA sensitive to muscimolandGABAB 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 GoalThe 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 PainInjury, trauma, spasm or disease to skin, muscle, somatic structures or viscera;Perceived and communicated via peripheral mechanisms (pathways) A delta and C fibersUsually with autonomic response as well (tachycardia, blood pressure, diaphoresis, pallor, mydriasis (pupil dilation);

  • Acute PainUsually subsides quickly as pain producing stimuli decreases Associated with anxiety-(decreases rapidly)Can be understood or rationalized as part of the healing process.

  • Acute PainSomatic-SuperficialInitiated in skin, subcutaneous or mucous tissuesCharacterized by throbbing, burning, or pricking sensations; associated with tenderness, allodynia (pain from a usually non-pain stimulus) or hyperalgesia

  • Acute PainSomatic-DeepGenerally initiated in musculoskeletal tissueCharacterized by dull, aching pain which CAN be localized; pain may radiate

  • Acute PainVisceralInitiated in the abdomen or thorax difficult to localizeFrequently associated with referred pain sites

  • Referred PainAppendix > UmbilicusEsophagus > Neck, Pharynx, Middle Chest, ArmGallbladder > Right shoulder, Central abdomenHeart > Lower neck, shoulders; Radiates down either arm (left more common than right)

  • Referred PainKidneys > Lower back, FlankStomach > Upper abdomen, ChestUreters > Anterior abdominal wall, Back, FlankUrinary Bladder > Lower abdomen, VaginaUterus > Lower abdomen, Back, Groin, Pelvis

  • Chronic PainNon-malignantPain persists beyond the precipitating injuryRarely accompanied by autonomic symptomsSufferers often fail to demonstrate objective evidence of underlying pathology.Characterized by location-visceral, myofacial, or neurologic causes.

  • Chronic PainMalignantHas characteristics of chronic pain as well as symptoms of acute pain (breakthrough pain).Has a definable cause, e.g. tumor recurrenceIn treatment, narcotic habituation isgenerally not a concern.

  • Pain PerceptionPain perception and response are different - actual tissue injury (mech., thermal, or chemical)intensity & duration of the insultfunction of nerves spinothalamic pathscentral nervous system pain mediators & neurotransmitterssocial, religious, psychological & cultural factors

  • Initial Pain AssessmentPatient Interview including PQRST for painIntervention HistoryPhysical Exam (include MMS)Labs & Radiology (thyroid profile, CBC, ESR, Radiograph, ECG)Functional Assessment (ADL) & Psychological AssessmentTreatment Access

  • ABCDE of Pain ManagementA Ask about pain regularly; Assess systematically.B Believe pt. & familys 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 EvaluationPQRSTPpalliative/provocativeQqualityRregion/radiationSsubjective/severityTtemporal/time factors

  • Severity AssessmentVisual Analog Scale (VAS)No Pain ---> 10 cm line ---> As bad as it can beFaces of Pain (Ouchers) - similar to the visual analog scale J ------->L

  • Severity AssessmentNumerical 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 AssessmentMcGill Pain Questionnaire0 ----------> 5None -------------------> ExcruciatingMild, Discomforting, Distressing, Horrible, in between.

  • WHO Pain Management ScaleStep 1NSAIDS, + adjuvantsStep 2NSAID + mild opioids+ adjuvantStep 3strong opioids +NSAIDS+ adjuvants

  • VAS vs WHOVAS1 - 34 - 67 - 10WHO StepsStep 1Step 2Step 3


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