Pain Management PDF

PAIN MANAGEMENT CLASSIFICATION OF PAIN Nociceptive vs. neuropathic ○ Nociceptive - transfer of info from location of tissue damage to CNS Pain from chemical, thermal, and/or mechanical sources 2 types...

PAIN MANAGEMENT CLASSIFICATION OF PAIN Nociceptive vs. neuropathic ○ Nociceptive - transfer of info from location of tissue damage to CNS Pain from chemical, thermal, and/or mechanical sources 2 types Somatic (musculoskeletal) - superficial or deep ○ Originate in peripheral ○ Sharp, stabbing pain, dull ache, usually pinpoint location Visceral - originate in organs ○ Cramping, pressure like, deep squeezing ○ Often difficult to localize ○ Neuropathic - damage/disorders of central or peripheral nervous system Pain perception without tissue damage, nerve impulses due to trauma, metabolic diseases, infection, tumor invasion, neurotoxins Burning, shooting, pricking, pins and needles, numbness touch/cold evoked Allodynia (pain due to stimulus that doesn't usually provoke pain), hyperalgesia (increased pain from stimulus that normally provokes pain), sensory loss possible Acute vs. chronic ○ Acute - sharp, dull, tingling, shooting, radiating Timely relationship with obvious stimuli, short duration Signs: HTN, tachycardia, tachypnea, pallor infants/dementia - change in eating habits, inconsolable Ex: surgery, trauma, medical procedures ○ Chronic - occurs without temporal relationship with obvious stimuli Sharp, dull, tingling, shooting, radiating lasts/recurs for more than 3 months Comorbid conditions often present Ex. cancer treatment, fibromyalgia, arthritis, lower back pain Mild vs. moderate vs. severe ASSESSMENT OF PAIN History and physical exam - underlying/contributing factors Characterize pain at baseline - OLDCARTS, SOCRATES, SCHOLAR-MAC, PQRSTU Ongoing assessment of pain - wong baker faces scale, brief pain inventory, numeric rating scale OLDCARTS - onset, location, duration, characteristics, alleviating/aggravating factors, radiating/relieving factors, timing severity SOCRATES - site, onset, character, radiation, associations, time course, exacerbating/relieving factors, severity SCHOLAR-MAC - symptoms, characteristics, history, onset, location, aggravating, remitting, medication, allergies, conditions PQRSTU - provoking/palliating factors, quality of pain, region/radiation of pain, severity, timing, understanding Wong baker cant be completed by third party Brief pain inventory - severity of pain and impact on daily functioning GOALS OF THERAPY Acute pain - recovering from underlying disease ○ Reduce pain and prevent chronic pain Chronic pain - improve/maintain function ○ Decrease pain perception, reduce medication when possible, improve QoL, minimize ADE NONPHARMACOLOGIC THERAPY Exercise, PT, diet, weight loss Cognitive behavioral therapy Tai chi, yoga, acupuncture PRINCIPLES OF PAIN MANAGEMENT Mild (1-3) ○ APAP/NSAID ○ Around the clock regimens ○ PRN breakthrough pain ○ Titrate max dose & adjuvant analgesics Moderate (4-6) ○ Opioid & APAP/NSAID ○ Consider ATC regimen ○ PRN breakthrough pain ○ NSAID ATC w/ opioid PRN ○ Adjuvant analgesics PRN Severe (7-10) ○ Opioid consider ATV ○ PRN breakthrough ○ Pain assessment tool and titrate to relief ○ Adjuvant analgesic PRN PHARMACOLOGIC THERAPY Non opioid - APAP/NSAID Co-analgesic/adjuvants - anticonvulsant, antidepressant, skeletal muscle relaxant, topical agent, regional anesthesia Opioid - morphine like agonists, meperidine like agonists, methadone like agonists, centrally acting agents, agonist-antagonist derivatives, opioid antagonists NON-OPIOID ANALGESICS - NOCICEPTIVE PAIN Acetaminophen - analgesic & antipyretic ○ Oral, IV, rectal ○ Indications - 1st line mild to mod pain, mod to severe pain in combo w opioids ○ CI: severe hepatic impairment ○ ADE: hepatotoxicity, GI upset ○ 325-1000mg q4–6h max 4000mg/day NSAID - analgesic, antipyretic, anti-inflammatory, antiplatelet ○ Indications - 1st line mild to moderate pain, preferred in osteoarthritis & low back pain ○ CI: active GI bleed, renal impairment, unstable CV disease ○ ADE: GI (celecoxib only COX2), renal, cardiac toxicity ○ Clinical pearls: may need PPI for chronic use Ketorolac max 5 days bc CV concerns, renal failure, ulcers CO-ANALGESICS/ADJUVANTS Anticonvulsants - primarily for neuropathic pain, possible multimodal pain control ○ Decrease neuronal excitability ○ Gabapentinoids - gabapentin/pregabalin MOA Inhibit Ca channel to decrease release excitatory neurotransmitters ADE Dizzy, drowsy, respiratory depression Pregabalin - visual disturbance P>G: peripheral edema, weight gain Clinical pearls Renal dose adjust, pregabalin schedule 5, risk of abuse 1st line neuropathic pain Postherpetic neuralgia, diabetic peripheral neuropathy Pregabalin in fibromyalgia ○ Carbamazepine & oxcarbazepine Drug of choice for trigeminal neuralgia MOA Inhibit Na channels potentiating GABA ADE Dizzy, drowsy, unsteady, N/V BBW carbamazepine: BBW serious derm reaction (HLA B1502 allele) Rare: aplastic anemia, agranulocytes Clinical pearls Carb: DDI induce 3A4, 1A2, 2B6, 2C9, pgp Oxcarb: improved tolerability, less DDI Monitor CBC, LFT, sodium ○ Lamotrigine MOA Inhibit Na channels ADE BBW serious skin rash, nausea Rare: aseptic meningitis, hemophagocytic lymphohistiocytosis (HLH) Clinical pearls D/c first sign of rash ○ Topiramate MOA Inhibit Na channels, increase activity GABA-A, block glutamate receptors, inhibit carbonic anhydrase ADE Dizzy, drowsy, fatigue, paresthesia, ocular effects, weight loss Clinical pearls Caution in renal impairment ANTIDEPRESSANTS Inhibit reuptake of serotonin and norepinephrine to enhance pain inhibition First line for neuropathic pain Analgesic effect independent of analgesic effects at doses less than depression tx Low back pain & fibromyalgia Tricyclic antidepressants ○ Amitriptyline, nortriptyline, desipramine, imipramine ○ 10-25 mg QHS titrate every 7 days as necessary ○ ADE: anticholinergic, sedation, weight gain, orthostatic hypotension, cardiac conduction abnormalities Serotonin norepinephrine reuptake inhibitors (SNRI) ○ Duloxetine, venlafaxine, milnacipran - generally more well tolerated ○ ADE: nausea, somnolence, dry mouth, ED, anorexia, constipation, inc BP, risk of bleed SKELETAL MUSCLE RELAXANTS CNS depression decreases transmission of reflexes at spinal level Antispasmodic +/- antispasticity to reduce muscle spasms ○ Spasticity - stiffness, hypertonicity, hyperreflexia Ex. MS, cerebral palsy, spinal cord injury ○ Spasmodic - involuntary contractions of muscle Pain, fibromyalgia, lower back pain, sciatica ADE: CNS depression, long term leads to withdrawal symptoms (taper) Clinical pearls: should only be used short term & with caution in elderly Medication Mechanism ADE Clinical pearls Baclofen Inhibit transmission at Withdrawal, CNS Renal dose adj, give spinal cord depression intrathecal as cont infusion cyclobenzaprine Decrease excitability Anticholinergic, CNS Caution arrhythmias alpha and gamma motor depression neurons at brainstem level Diazepam Postsynaptic inhibition of Withdrawal syndrome, Avoid in renal impair GABA in spinal cord CNS depression, sedation Methocarbamol unknown Urine discoloration, CNS depression Tizanidine Central acting alpha 2 Withdrawal, agonist hypotension, hepatotoxicity TOPICAL AGENTS Address local symptoms while minimizing systemic exposure & ADE Capsaicin - neuropathic/muscle/joint pain MOA Transient receptor potential vanilloid 1 receptor (TRPV1) agonist, nociceptor defunctionalization ADE Burning, increase BP w/ 8% patch, avoid contact w mucus membranes Clinical pearls OTC require 2-4 weeks continuous therapy for results OTC & RX Cream, gel, liquid, lotion, patch - 3-4x/day 8% - apply to most painful area 60 mins, up to 4 patches at a time, do not apply more than every 3 months, apply by HC professional Topical NSAIDs - mild to moderate localized pain ○ Strains, sprain, confusion, osteoarthritis ○ Can penetrate muscle, synovium, joint tissue ○ Diclofenac: gel, patch, topical solution - use dose card for gel ○ ADE similar to NSAID but absorption low Topical lidocaine - local anesthetic ○ MOA: inhibit voltage gated sodium channels ○ Neuropathic pain including postherpetic neuralgia ○ Formulations: cream, gel, ointment, liquid, lotion Patch - 4%OTC, 5% RX Apply 1-2 patches to site for 12 hours on then 12 hours off Menthol, trolamine - bengay, icyhot, salonpas, aspercreme ○ Minor aches and pains of muscles and joints ○ Rubefacients - produce redness of skin, dilate blood vessels causing sensation followed by analgesic effect REGIONAL ANESTHESIA Neural blockade using local anesthetics for acute/chronic pain (primarily nociceptive) Injection - in joint, epidural, intrathecal space along nerve root Procaine, tetracaine, bupivacaine, lidocaine, prilocaine ○ Risk CNS excitation & depression, CV effects MISCELLANEOUS AGENTS Corticosteroids ○ Bone pain, joint/connective tissue disease, inflammatory conditions ○ PO, IV, joint injection ○ Hyperglycemia, weight gain, mood changes, osteoporosis, insomnia, GI bleeding Cannabinoids ○ Chronic pain, possibly neuropathic Ketamine ○ Analgesic/anesthetic used in acute/chronic pain ○ Non competitive NMDA glutamate receptor antagonist w/ CNS, CV, psychiatric adverse events OPIOID ANALGESICS Oral opioids - onset 45 mins, peak in 1-2 hours ○ Start with IR, ER for long term patients, around the clock MORPHINE LIKE AGONISTS Morphine - standard opioid to which others are compared ○ Active metabolites: morphine-3-glucuronide & morphine-6-glucuronide M3G - side effects / M6G - analgesia - potential accumulation in renal impairment CrCl 30-59: consider other agents OR 50-75% usual dose CrCl 15-29: avoid is possible (25-50%) CrCl