Pain Management Flashcards
Pathophysiology of Pain Transmission
Pain transmission starts at nociceptors, which are stimulated by leukotrienes, prostaglandins, and histamine
Nerve fibers of the spinal cord initiate pain sensation by exciting pain transmission neurons.
Pain is modulated by nerve fibers in the spinal cord that inhibit spread of action potentials caused by nociceptors. Also modulated by the brain by the endogenous opiate system made up of 3 kinds of endogenous endorphins: enkephalins, dynorphins, and beta-endorphins.
Types of Pain
- Nociceptive
- Inflammatory
- Neuropathic
- Functional
Nociceptive
- Transient pain in response to noxious stimulus at nociceptors that are located in cutaneous tissue, bone, muscle, connective tissue, vessels and viscera
- prevents further tissue damage due to autonomic withdrawal reflex
Inflammatory
- Contributes to pain hypersensitivity to prevent contact or movement of injured part until healing is complete, thus reducing further damage
Neuropathic
- Spontaneous pain and hypersensitivity associated with damage to PNS
Functional
- Pain hypersensitivity due to an abnormal processing or functioning of the CNS
Classification of Pain
acute chronic chronic malignant chronic nonmalignant neuropathic
Acute
- occurs as result of injury or surgery and is usually self-limited, subsiding when injury heals
Chronic
- persists beyond the time of the expected healing and serves no useful physiologic purpose
Chronic Malignant
- associated with progressive disease that is usually life threatening (i.e. CA)
Chronic Nonmalignant
- not associated with life threatening disease and lasting more than 6 months beyond the healing period
Neuropathic
- a type of chronic nonmalignant pain involving disease of the central and peripheral nervous systems
Incorrect assumptions/attitudes/pain assessment that lead to the undertreatment of pain
There is a correct amount of pain for a given injury
People become easily addicted to narcotics (Truth: people are more likely to become addicted when they are inadequately tx’d)
Pain is necessary and builds character or using analgesics builds character
Inadequate assessment fosters undertreatment because prn dosing is based on pts report of need for analgesics
Pain is difficult to evaluate in young children and elderly with dementia
Limited information on pain management in medical training
Predictors of Inadequate Pain Management
Age
Non-Caucasian
Low cognitive performance
Multiple other medications
Principles of Effective Pain Assessment
Measure pain using self report +/- behavioral observation tools
- interpret behaviors cautiously (people in chronic pain will have fewer behavioral/physiologic changes)
Use physiologic measures only as adjuncts to self report and behavioral observation
Tailor assessment to developmental level and situation
Pain is 5th vital sign
Principles of Effective Pain Management (4)
Assess pain intensity and relief at regular intervals
Respect pt preferences (not necessarily drug seeking)
Evaluate effectiveness of pain management and medication side effects and adjust as needed
Suspect pain – pt may not be able to report
Nonpharm Therapy
Psychological interventions and PT
Psychological Interventions
- Acute: controlled mental imagery, controlled attention or distraction
- Chronic: relaxation training, biofeedback, cognitive behavioral therapy, psychotherapy, support groups, spiritual counseling
Physical therapy
- US therapy, TENS, massage, therapeutic exercises, heat, cold
Steps for treating acute pain
Step 1:
- mild pain (1-3/10)
- +non-opioid +/- adjuvants
Step 2:
- moderate pain (4-6/10)
- weak opioid + non-opioid +/- adjuvants
Step 3:
- severe pain 7-10/10
- strong opioid + non-opioid +/- adjuvents
Acetaminophen
Indication
MOA
Usual/Max Dose
AE (6)
Indication
- tx mild-moderate pain
- analgesic effect = ASA
MOA
- inhibits pg synthesis in CNS and peripherally blocks pain impulse generation
Usual dose 325-650 mg q4-6hrs
Max dose 4000 mg/day
AE
- usually well tolerated
- hepatotoxicity
- analgesic nephropathy
- anemia
- blood dyscrasias
- rare skin rxns (SJS/TEN)
- OD ==> serious/fatal hepatotoxicity
Hepatotoxicity Mechanism
- small amount of APAP is metabolized by CYP450 into NPAQI, a hepatotoxic metabolite
- NPAQI is usually bound by glutathione and excreted, but OD/misuse leads depletes glutathione
NSAID Efficacy
Most nonselective NSAIDs are more effective than full dose ASA or APA
Some have greater than or equal to analgesic effect of oral opioid combos
Some pts respond better to one NSAID than another
Celecoxib is less effective than ibuprofen or naproxen
NSAID Adverse Effects
Broad Categories
GI Renal Hematologic Cardiovascular Hepatotoxicity - rare CNS - high doses can cause sedation and dec'd cognition in older adults Derm - rare SJS or TEN
NSAID GI Side Effects
MOI
High Risk Patients
Spectrum of GI toxicity
MOI
- direct irritation of gastric epithelium
- systemic inhibition of endogenous GI mucosal PG synthesis
High Risk Patients
- > 60 y.o.
- Prior PUD or UGI bleed
- High dose or more toxic NSAIDs
- concurrent corticosteroid, bisphosphonate, or SSRI use
- Anticoagulant use or coagulopathy
- Antiplatelet use (e.g ASA or clopidogrel)
- Chronic illness
Spectrum of GI toxicity
ibuprofen < naproxen < ketorolac
Diclofenac/Misoprostol available to prevent PUD
NSAIDs and Nephrotoxicity
MOI
RFs
MOI
- NSAIDs decrease renal blood flow
- more pronounced in pts with pre-existing kidney disease
Risk factors
- older age
- HF
- renal insufficiency
- ascites
- volume depletion
- diuretic therapy
NSAIDs and Hematologic Toxicity
MOI
- may prolong bleeding times due to anti-platelet affects
ASA inhibits platelet aggregation for lifetime of platelets (7-10 days)
Other N-NSAIDs affect platelet aggregation to a lesser degree and only when drug is on board
These do not affect INR, but do increase bleeding risk when used with anticoagulants
NSAIDs and Cardiovascular Toxicity
May increase CV risk (depends on type)
Risk is greater with higher doses, prolonged duration, and greater COX-2 selectivity
Selective inhibition of COX-2 may decrease endothelial production of prostacyclin, leaving platelet thromboxane A2 mediated by COX-1 relatively unopposed, which may increase vasoconstriction, platelet aggregation, and thrombosis
Highest CV with celecoxib; naproxen is lowest
All NSAIDs can inhibit ASA’s antiplatelet effect
- *NSAIDs also inc BP b/c decreased renal perfusion
- *Avoid NSAIDs after MI indefinitely
Acetylated Salicylates
Representative drug
Indication
MOA
AE
Aspirin
Indication
- mild-moderate pain
- prevention of MI, CVA
MOA
- same as N-NSAID
AE
- platelet inhibit for life of platelet
- ASA sensitivity (asthma, bronchospasm, urticaria) related to COX-1 inhibition–> inc leukotriene production –> inc histamine release
- Do not use in pts with angioedema and bronchospasm with ASA
- Reye’s Syndrome (don’t use in <19 y.o. esp with flu/mono)
Nonacetylated Salicylates
Salsalate, Trisalicylate
AE:
- less GI toxicity than N-SAIDs
- no antiplatelet effects
- otherwise same as N-NSAIDs
- occassional cross-reactivity with ASA sensitive pts
- Reye’s syndrome
Opioid MOA and AE
MOA: stimluates opioid receptors (mu, kappa, and delta) in the CNS
Most common:
- somnolence–>drowsiness
- stimulation of CTZ–>N/V
- decreased GI motility–>constipation (docusate)
- histamine release –> pruritis
Most severe
- respiratory depression
Opioid Withdrawal Symptoms
Minor
- rhinorrhea
- lacrimination
- excessive yawning
- mild irritability or restlessness
- mild N/V
Major
- increasing restlessness or irritability
- tremors
- abdominal cramps
- anxiety
- persistent N/V
- increased HR, BP, hot or cold flashes, fever
Opioids and Receptor Activity
Agonists
- best analgesic effect by binding mu receptor
Partial agonists
- submaximal response at the receptor even at high doses
Agonists/antagonists
- mu agonist, kappa antagonist
- lower abuse potential, ceiling effect on respiratory depression
- only used in certain populations
Antagonists
- reverse or inhibit the effect of agonists by preventing receptor access
Opioids for Moderate Pain (6)
Codeine/APAP
- gastritis frequent; metabolized to morphine
Hydrocodone/APAP
- also antitussive; less gastritis than codeine
Oxycodone/APAP
- less hallucinations than morphine; CYP3A4 substrate–>black box warning
Others:
- Meperidine (Dermerol)
- Tramadol (efficacy = codeine/APAP)
- Trapentadol
Opioids for Severe Pain (5)
Morphine - gold standard Hydromorphone - high potency, terminal pain syndromes Oxymorphone
Others:
- Fentanyl
- Methadone (only use if know how to dose)
Mixed mu Agonists/Antagonistsm (2)
Butorphanol
- 2nd line for mod-severe pain
Nalbuphine
- 2nd line for mod-severe pain, but IV/IM only
Mu Antagonist (1)
Naloxone
- reversal of respiratory depression; overdose
Pseudoallergy
True Allergy
Pseudoallergy
- flushing, itching, sweating, mild hypotension
- give nonopioid instead
- avoid codeine, morphine (strongly associated)
- more potent opioid that are less likely to release histamine
- if necessary give diphenhydramine
True Allergy
- give nonopioid
- opioid from different class
Adjuvant Analgesics
Caffeine
- may enhance APA, ASA, ibuprofen
Hydroxyzine
- may add to effect of opioids in postop and CA pain while reducing N/V
Corticosteroids
- can produce analgesia in pts with inflammatory disease or tumor infiltration of nerves
Signs and Sxs of Persistent Pain (3)
Big three: depression, anxiety, sleep disturbance
Also: Frustration Anger dec self-esteem dec involvement in social activities Financial stresses and concerns dec libido Work issues Inactivity Altered family dynamics Frequent use of meds Legal issues inc number of health care visits
Treatment Goals for Persistent Pain (6)
Inc tolerance for physical activity
Dec suffering and pain
Dec reliance on the health care system
Dec reliance on medications
Return to work or other functional role in society
Develop appropriate strategies for self-management
General Strategies for Txing Persistent Pain
Simultaneously address the various components of the problem
Taper use of inappropriate meds while initiating appropriate therapy
Provide education about chronic pain; correct any misconceptions
Focus on inc function and physical activity
Establish a time frame for achieving specific goals
Remind your patient and yourself that chronic pain is not the same as acute pain
Emphasize the multifactorial nature of chronic pain and avoid the distinction between physical and psychological causes
Nonpharm for persistent pain (3)
TENS
Biofeedback
PT
Pharm for persistent pain (4)
general
Nonopioids
Tramadol
Opioids
Adjuvant Analgesics
Adjuvant Analgesics
TCAs
AEDs
SNRI
Local anesthetic
TCAs
- amitriptyline
- inhibit NE & 5-HT reuptake
- onset: weeks
- SE: sedation
AEDs
- dec synaptic transmission
- Gabapentin, Carbamazepine, valproic acid
SNRI
- potent inhibit of NE and 5-HT reuptake
- duloxetine (cymbalta)
- tx: diabetic neuropathy, chronic m/s pain
Local anesthetic
- lidocaine patch
- 12h on, 12h off
- good bridging option
Pharm Mngmt of Chronic Noncancer Pain
Chronic low back pain
Fibromyalgia
Neuropathic Pain
Chronic low back pain
- Acetaminophen first; tramadol or opioids in selected patients; AEDs or TCAs if neuropathic symptoms (evidence weak)
Fibromyalgia
- Acetaminophen considered 1st (evidence weak); TCAs, AEDs, SNRIs (stronger evidence); tramadol better alternative than opioids; NSAIDs only with other agents
Neuropathic Pain
- TCAs, SNRIs, AEDs, 5% lidocaine patch considered 1st line, tramadol and opioids considered 2nd-line agents; capsaicins considered 3rd line
Guidelines for an Adequate Drug Trial
Discuss “trial and error” method with patient
Titrate only one drug at a time
Start at the low end of the dosing range and increase periodically (q3-7 days)
Increase dose if pain relief is inadequate, side effects are tolerable, and blood level is below toxic range
Weekly or biweekly communication with patient is needed to assure optimized trial and efficient titration
Continue titration until patient is satisfied with pain control or side effects are intolerable
