deck_7034093 Flashcards
(120 cards)
1
Q
Acute pain
A
-short duration-injury, illness, surgery-<6 months-usually disappears when underlying condition treated-unrelieved - can become chronic
2
Q
chronic pain
A
-persistent pain associated with long-term incurable/intractable condition or disease ->6 months-exists beyond expected healing time-risk dependence/tolerance
3
Q
malignant pain
A
-pain of terminal illness-goals: improve function and QOL, comfort, acceptable level (to pt) of consciousness-opiates should not be withheld for fear of addition/high doses-continually assess-tachyphylaxis/tolerance more of an issue than addiction
4
Q
non-malignant pain
A
-very rare that nonmalignant should require opiates-should fail adequate trials of non-opiates first
5
Q
nociceptive pain
A
-regular pain - cut your arm and it hurts-injury/inflammation of somatic/visceral tissues-somatic: skin, bone, joint, connective tissues nociceptor activation-visceral: internal organ nociceptor activation, often referred pain-descriptors: stiff, throbbing, dull ache, sore, squeezing, “just hurts”-typically respond well to opioids-opioids are entirely ineffective on nerve pain
6
Q
neuropathic pain
A
-due to changes in function/physiology in peripheral or CNS-causes: tumor infiltration into nerves, chemo/radiation, nerve damage (amputation, compression), conditions (diabetic neuropathy, post-herpetic)-descriptors: numbness, tingling, cold or on fire, burning, “like my foot fell asleep,” shock-like, shooting, come and go-poor or partial response to opioids, often managed with adjuvant meds-delayed response to therapies - most important thing that you educate patient on!-6-8 weeks to start seeing an effect and roughly 12 weeks to see full effect-side effects will come early and fade
7
Q
stimulation/transduction of pain
A
-sensitization/stimulation of nociceptors (free nerve endings)-release of neural chemicals such as bradykinins, potassium ion, prostaglandins, histamine, leukotrienes, serotonin (5-HT), substance P-generation of AP
8
Q
transmission of pain
A
-dorsal horn of spinal cord-spinothalamic tract to CNS (medulla, midbrain, cortex)
9
Q
perception of pain
A
-conscious experience of pain (different for everyone = SUBJECTIVE)
10
Q
modulation of pain
A
-inhibition of nociceptive impul-neurons from brain stem descend to spinal cord and release susbstance tha inhibit transmission of nociceptive impulse (endogenous opioids, serotonin, gamma-aminobutyric acid (GABA), norepinephrine)
11
Q
drugs that affect the perception of pain in the brain
A
-opioids-alpha-agonists-TCAs-SSRIs-SNRIs
12
Q
drugs that affect modulation
A
-TCAs, SSRIs, SNRIs
13
Q
drugs that affect transmission
A
-LAs, alpha2 agonists, opioids
14
Q
drugs that affect transduction
A
-LAs, capsaicin, anticonvulsants, NSAIDs, ASA, acetaminophen, nitrate
15
Q
MOA of Opioids
A
-G protein (opioid receptors), decrease cAMP/Ca2+-decrease release of neurotransmitters (DA/Ach/NE/5HT/sub P)
16
Q
opioid receptor types
A
-(mu-1): mostly analgesia-(mu-2): sedation, constipation, antidiuretic, respiratory depression, bradycardia, euphoria, physical dependence (All of the bad side effects)-δ (delta): analgesia, mood, reinforcement, breathing, tolerance to mu-κ (kappa): analgesia, miosis, sedation, constipation-s (sigma): autonomic stimulation, dysphoria, hallucinations, confusion-(epsilon): analgesia-These other (delta, kappa, sigma, epsilon) are not really ones we are targeting-Ideally you want heavy effect on 1 and little effect on 2 to reduce side effects
17
Q
analgesic ladder
A
-Step 1: non-opioid +/- adjuvant analgesic-Step 2: opioid for mild to moderate pain +/- non-opioid and/or adjuvant analgesic-step 3: opioid for moderate to severe pain +/- non-opioid and/or adjuvant analgesic
18
Q
aspirin, choline salicylate (arthropan), magnesium salicylate (Doan’s pills, trilisate), salsalate (disalcid), sodium salicylate, diflunisal (dolobid)
A
salcylates
19
Q
ibuprofen, fenoprofen, flubiprofen, ketoprofen, suprofen, naproxen, oxaprozin
A
-propionic acids
20
Q
indomethacin, sulindac
A
indoles
21
Q
diclofenac, ketorolac (toradol), tolmentin
A
acetic acid
22
Q
nabumetone
A
naphthylakanone
23
Q
piroxicam
A
oxicam
24
Q
etodolac
A
pyranocarboxylic acid
25
meclofenamate, mefenamic acid
fenamates
26
NSAIDs
-widely used for chonic treatment of arthritis and pain-not as efficacious analgesics as opioids (ceiling effect, no addicition potnential-no evidence iof delayed healing in acute injuries (sprains, back injuries, etc.) and shown to work as well as opioids for these minor injuries
27
NSAID MOA
-decrease CNS pain impulses receieved -inhibit prostaglandin synthesis and release-Reduces inflammation → Inhibit leukocyte migration and lysosomal enzyme release-Block hypothalamus pain impulses-Decrease body temperature → Antipyretic
28
NSAID use
-Analgesic → Mild-moderate pain, Severe pain: opioid combination, Metastatic bone pain, Musculoskeletal syndromes (strains, sprains, low back pain), Dysmenorrhea, Migraines -Anti-inflammatory → Rheumatoid arthritis, Osteoarthritis, Ankylosing spondylitis, Nonrheumatic inflammation, Acute gout attacks (except tolmentin)-Antipyretic-Often preferred over opiates in the treatment of acute mild to moderate pain
29
dosing for ibuprofen (motrin, advil)
200-800 mg tid/qid, max dose 3200mg-peak onset 1-2 hrs
30
dosing for naproxen
250-500mg bid/tid, max does 1250mg-peak onset 2-4 hrs
31
Adverse effects of NSAIDs
-“Nuisance” symptoms: nausea, dyspepsia: NSAIDs are the most likely cause of these symptoms-Mucosal lesions: endoscopic: Up to 80% NSAIDs users, Usually asymptomatic, Heal & redevelop with continued NSAID use-Serious GI complications-Clinical Pearl: less than max dose may provide same analgesic effect with less GI irritation (i.e. ibuprofen 600mg tid instead of 800mg)-Daily NSAID use may increase CV risk factor (exception naproxen)-From ARAMIS database –Endoscopic evidence of mucosal damage can occur without symptoms, symptoms without obvious mucosal damage, serious GI complications can occur without prior sx or prior evidence of mucosal damage-It is increasingly recognized that a reduction in the incidence of endoscopic ulcers in clinical trials cannot be directly translated into a comparable reduction in clinically significant GI complications
32
Serious GI complications risk factors
-Advanced age (especially > 60 yrs)-History of GI problems (PUD and GIB)-Concomitant corticosteroid or anticoagulant use-Serious underlying disease (CV, DM)-Chronic NSAID use and high-dose NSAID
33
ASA and bronchospasm
-ASA sensitivity triad (~20% of asthmatics are sensitive to aspirin and other NSAIDs-rhinosinusitis (sinusitis with nasal polyps-low dose ASA inhibits platelet aggregation for life of platelet (~7 days)-begins 30mins - 3hrs after dose-NSAIDs that inhibit COX1 can induce non-allergic hypersensitivity reactions that cause sinusitis or asthma in pts
34
ASA drug interactions
-Lithium → increase lithium levels-warfarin → increase GI bleed risk, platelet aggregation inhibition-ACE inhibitors → increase renal disease-loop, K sparing, thiazide diuretics → DECREASE diuretic effect
35
adverse effects of aspirin
-painless GI bleed-low doses may potentiate gout-reyes syndrome (hepatic ecephalopathy → esp in children)
36
aspirin toxicity
-hyperthermia-hyperventilation-respiratory alkalosis
37
aspirin kinetics
-protein binding: low dose 90% bound-high dose 76% bound-interaction with protein bound drugs (warfarin, phenytoin)-plasma levels increase disproportionately as dosage increases
38
aspirin for CV risk
-non-selective NSAIDs may have negative interaction with ASA for cardiovascular prevention (ibuprofen, naproxen) → ASA exhibits antiplatelet effects for CV risk reduction by irreversible acetylation of the active site of COX in platelets. NSAIDs may attenuate this effect (competitive binding)-advise patient to take ASA at least 2 hrs before NSAID or use APAP instead (interaction not seen with celecoxib or diclofenac)
39
combination therapy
-attack pain on two fronts: prostaglandins and opiate receptors (enhances pain relief, lower doses of each agent, better SE profile)-very effective in treating bone metastatic cancer
40
opiates
-naturally present in opium (morphine)
41
opioids
-manufactured-semisynthetics are derived from an opiate (heroin from morphine, buprenorphine from thebaine)-synthetics are completely man made, dsigned to work like opiates (methadone, fentanyl)
42
opioid analgesics
-morphinans-benzomorphans-phenantrenes-phenylpiperidines-phenylheptylamines-tramadol
43
morphinans
-opioid analgesics-levolphanol (resembles morphine)-Butorphanol
44
benzomorphans
-opioid analgesics-pentazocine (K agonist, weak mu antagonist or partial agonist) - irritant, do not administer subq
45
phenantrenes
-opioid analgesics-morphine, hydromorphone, oxymorphone, diacetylmorphine-nalbuphine - K receptor agonist and mu antagonist (parenteral route, resistant to naloxone reversal)-buprenorphine
46
phenylpiperidines
-opioid analgesics-fentanyl-sufentanil, alfentanil, remifentanil-meperidine-diphenoxylate-loperamide (limited access to the brain, low abuse potential, available OTC for diarrhea)
47
phenylheptylamines
-opioid analgesics-methadone (t1/2 = 25-52 hrs, QT prolongation, close monitoring of dose initially)-propoxyphene (pulled from market)
48
tramadol
-opioid analgesics-partial mu agonist
49
opioid absorption/distribution
-most are well absorbed-high first-pass metabolism (fentanyl has low oral bioavailability - this is why it doesn't come in tablets)-codeine and oxycodone have reduced 1st pass-meperidine has larger Vd in the elderly
50
opioid metabolism
-converted mostly to glucuronides which are excreted by the kidneys-morphine → active metabolites M3G and M6G accumulation may lead to adverse effects in reduced kidney function or very large doses-diacetylmorphine → monoacetyl IM → morphine-mepiridine → normeperidine (neurotoxic/seizures)-codeine → morphine (codeine converted by liver to morphine, relies on enzymes that are genetically linked, approximately 2% of the population does not have the enzyme that converts codeine to morphine and 2% more have too much enzyme so they get higher dose with one dose
51
opioid excretion
-polar metabolites-as glucuronide conjugates → urine (hydromorphine 75% renally excreted, morphine 90% renal)
52
routes of administration - opioid
-epidural (morphine, fentanyl)-rectal (morphine, hydromorphone)-transdermal (fentanyl, buprenorphine)-intranasal (butorphanol, fentanyl)-buccal transmucosal (fentanyl lozenges)-PCA (fentanyl, morphine, hydromorphone)-IV, IM, subq, PO
53
Short-acting vs long acting opioid
-LAs have fewer peak/trough fluctuations-LAs have less end of dose failure-LAs increased interval → increased adherence-SAs may have fewer ADE
54
opioid mechanism of action
-opioid agonists inhibit the release of excitatory transmitters from the primary afferents and directly inhibit the dorsal horn pain transmission neuron
55
opioid receptor types
-Mu receptor → associated with opiate addiction, activation produces analgesia or euphoria, respiratory depression, sedation, and miosis, slowed GI transit-Kappa receptor → activation also produces analgesia, psychosis (still has abuse potential), slowed GI transit-delta receptor → activation in humans not well characterized
56
Full mu agonists
-highly reinforcing, therefore most abused opioid type-no ceiling to analgesic efficacy - there is no max dose, its whatever the pt can tolerate - the number should not scare you, its about what the pt can handle-will not reverse or antagonize effects of other opioids within this class - they will just have an additive effect-morphine, hydromorphone, codeine, oxycodone, methadone, fentanyl
57
tolerance
-repeated mu receptor activation results in neuronal adaptation-Diminished effect over time from same dose-Need for larger doses to produce the same analgesia -Diminished SE as well, except for eye/GI effects -Cross tolerance and cross dependence develop-can be reversed - titrate down
58
physical dependence
-physical adaptation-Immediate cessation produces withdrawal-Normal process with opioids-can be reversed - titrate down
59
hyperalgesia
-increased pain sensation
60
psychological dependence
-euphoria, sedation-IV use-5 C’s (Chronic, loss of Control, Compulsive use, Craving, Continued use despite personal harm)-Aberrant behaviors
61
pseudo-addiction
-drug seeking behavior as a need to diminish poorly managed pain-Fear of pain, PTSD
62
diversion
-diverting drugs from original purpose, recreational use.-Street value: Oxycontin $1/mg (prior to reformulation)
63
risk for chronic opioid use
-Personal or family history of substance abuse-Co-morbid psychiatric conditions-Aberrant behaviors-Use of opioids to treat other symptoms (depression, anxiety, sleep)-Requesting specific medications-? Aggressive requests for higher dose-50% of patients who continue opioids for 3 months will still be taking them 5 years later
64
degrees of opioid tolerance
high: Analgesia, Euphoria, Dysphoria, Mental clouding, Sedation, Resp. depression, Antidiuresis, Nausea/vomiting, Cough suppressionmoderate: bradycardiaminimal/none: miosis, constipation, convulsions
65
order of strength for codeine, meperidine, methadone, hydromorphone and oxymorphone, and methadone and fentanyl
Order of Strength (IM): codeine< meperidine < methadone < hydromorphone & oxymorphone < methadone & fentanyl
66
acute opioid use effects
-euphoria, vomiting, constricted pupils, depressed respiration, drowsiness, decreased pain sensation, decreased awarenes, decreased consciousness
67
large dose opioid acute effects
-non-responsive, pinpoint pupils, if severe anoxia pupils may dilate, bradycardia and hypotension, skin cyanotic, skeletal muscle flaccid, pulmonary edema in ~50%, slow or absent respiration
68
chronic opioid use effects
-physical dependence, psychological dependence, lethargy and indifference, reduction in bowel movement
69
conversions between opioids
-convert to total daily dose equivalent-reduce by 25-50% for cross-tolerance
70
levels of control
-if something is not scheduled, it is not a legal drug -CI: something that doesnt have medical purposes in most cases-CII: has addictive properties-CIII-V: not as addictive, can get refills
71
opioid tolerance
-FDA definition: Patients receiving, for one week or longer, at least-60mg oral morphine/day,-25mcg transdermal fentanyl/hour, -30mg oral oxycodone/day, -8mg oral hydromorphone/day,-25mg oral oxymorphone/day, -or an equianalgesic dose of another opioid.
72
fentanyl pre-screening
-Due to several cases of over-sedation requiring naloxone reversal-Is pt currently on patch Strength? Date and time last patch was placed?-Is pt on other opioid pain meds? Drug? Strength? Total daily dose (TDD)?-Are you treating acute pain with fentanyl?-Is patient opioid-naïve?
73
Propoxyphene alternatives
-episodice pain (acetaminophen, NSAIDs, some studies show no better than APAP or NSAIDs, more severe pain: hydrocodone/APAP or oxycodone IR)-chronic pain (sustained release morphine, methadone, sustained release oxycodone, fentanyl)
74
antitussives
-opioid like compounds-antitussives: opioid analgesics are most effective; low doses-Dextromethorphan – dextrorotatory stereoisomer of levorphanol derivative (No addictive properties; less constipation than codeine, Abuse potential: “Robo-tripping”, Dose: 15-30mg 3-4 times daily, OTC (Robitussin DM, Delsym))-Codeine/guaifenesin – 10mg/100mg po q4hours prn cough
75
antidiarrheals
-Diphenoxylate/atropine (Lomotil) & Loperamide (Imodium)-Dose: 2 tabs initially, then 1 tablet after each loose stool-Tincture of opium (10mg morphine/ml) – 0.3-1 ml q 2-6 hours (6ml/24 hour MAX)-Paregoric (0.4mg morphine/ml)– 5-10ml 1-4 times daily (aka camphorated tincture…)-Caution! Opium tincture v.s. camphorated tincture of opium 25 fold overdose
76
CNS effects of opioids
-Analgesia: reduce both sensory and affective components-Dysphoria/euphoria-Sedation-Respiratory depression-Antitussive (anti-cough)-Miosis (constriction of pupils)-Nausea/vomiting: activate chemoceptor trigger zone
77
CV effects of opioids
Cardiovascular effects: peripheral vasodilation (histamine release), cerebral vasodilation (increase intracranial pressure), orthostatic hypotension
78
GI effects of opioids
Gastrointestinal effects: increased tone, decreased activity (constipation), smooth muscle spasm
79
potential patient risks using opioids
-Use in patients with head injuries – CO2 retention → increased intracranial pressure-Use during pregnancy (avoid if possible)Impaired pulmonary function (OSA, etc)-Impaired hepatic/renal function-Endocrine disease – Addison’s disease or hypothyroidism may have prolonged and exaggerated responses to opioids
80
impaired renal function and opioids
-Opioids to avoid in renal failure/ highly impaired renal function: Morphine, hydromorphone, codeine -Not enough data: Oxycodone-Appears safe: Methadone—start low and go slow-Probably safe: fentanyl
81
acute opioid intoxication
-Miosis (pin point pupils), resp. depression-Excessive sedation, stupor, coma-Treat with Naloxone (pure antagonist)
82
opioid REMS plan
-REMS: Risk Evaluation & Management Strategies (July 9, 2012)-Misuse is a wide-spread problem-FDA targeting extended-release products-Affects all LA/ER Opioid analgesics-Prescriber training-Patient counseling (required med guide)
83
opoid medication errors
-Mix-up w/ hydromorphone (NOT the generic for morphine, NOT equipotent doses)-Programming parenteral pumps (decimal errors)-Failure to remove old fentanyl patch when placing new patch-Unfamiliarity with oral to parenteral dosing equivalence-Concentration error mix-ups (select 10 mg/ml rather than 2 mg/ml)-Dangerous abbreviations MSO4 vs. MgSO4-Administration line confusion (IV vs. epidural)-Meperidine use in elderly (seizures, nervousness)
84
drug interactions with opioids
-Sedative-hypnotics-Antipsychotic drugs-MAO inhibitors-Anything that causes: respiratory depression, CNS depression
85
Mu receptor partial agonist
1. activates receptor at lower levels2. relatively less reinforcing3. less abused opioid type4. includes bupenorphine
86
receptor affinity
-affinity is the strength with which a drug physically binds to a receptor-buprenorphine's affinity is very strong and it will displace full agonists like heroin and methadone-receptor binding is NOT the same as receptor activation
87
receptor dissociation
-speed of disengagement or uncoupling of a drug from the receptor-buprenorphine's dissociation is slow-therefore stays on the receptor for a long time and blocks heroin or methadone binding
88
opioid agonists/antagonists and partial agonists
-Side Effects: similar to opioids-Drug Interactions: opioids (full agonists)-Contraindications/Precautions: Can precipitate opioid withdrawal in chronic opioid users, Should not be co-administered with opioid
89
opioid withdrawal syndrome
-dysphoric mood-N/V/D-body aches-lacrimation-rhinorrhea-pupillary dilation-sweating-piloerection-yawning-mild fever-insomnia-irritability-opioid craving
90
spontaneous withdrawal syndrome
-develops if a physically dependent person suddenly stops, or decreases, opoid use-severity usually less with longer half-life drugs-duration depends on half-life
91
blind abrupt discontinuation of buprenorphine
-only minor elevation of withdrawal scale scores-less intense than heroin withdrawal-less intense and briefer than methadone withdrawal
92
precipitated withdrawal syndrom
-precipitated in a physically dependent person, by administration of either: an opioid antagonist (naloxone, naltrexone) or an opioid partial agonist (buprenorphine)-qualitatively similar to spontaneous withdrawal but faster onset-duration depends on the half-life of drug
93
repeated administration and withdrawal
-Withdrawal precipitated by a partial agonist is more likely if there is:-High level of physical dependence-Short time interval between administration of full agonist and partial agonist-High dose of partial agonist
94
abuse potential characteristics
-Route of administration– Faster route has a greater abuse potentialInjecting IV → Injecting SQ/IM → Oral -Drug Half life– Shorter half-life has a greater abuse potentialHeroin → Methadone-Lipophilicity (faster across blood brain barrier)– Higher lipophilicity has a greater abuse potential- Heroin → Morphine → Methadone -Degree of mu agonist activity
95
Controlled substances CA
-Provider needs a DEA number -C III – V may have 5 refills in a 6-month period for a total of 120 days supply-C II has NO refills: order may NOT be given over telephone, may fax (followed by special form) -Require special prescription forms-NEW: e-prescribing of all CIII-CV
96
Drug addiction treatment act (DATA)
-Must meet qualifications and apply to treat patient for addiction (wavier of separate registration)-Methadone can be used for pain or addiction, so rx must say “FOR PAIN” to fill in outpatient RX-Buprenorphine prescribers get X in DEA number-“legitimate medical purpose”
97
California controlled substance special forms
-No more triplicate form; now need the new controlled substance form for ANY controlled substance-Approved Security Prescription Printers: Prescribers must order the new tamper-resistant forms from pre-approved security prescription printer companies -Oral or faxed okay for schedule III-V: Prescribers must order the new tamper-resistant forms from security prescription printer companies that have been pre-approved by the Board of Pharmacy and the Department of, Justice to produce the forms.
98
Who may prescribe in Ca
-Physicians, Dentists, Podiatrists-Veterinarians-Physician’s Assistant - under protocol-Pharmacists – under protocol + clinical training-Nurse Practitioner – in collaboration with or under supervision of a physician-Optometrists – limited to certain agents affecting the eyes-Licensed Naturopaths-may issue non C-II drugs-"Prescriber," as used in this section, means a person, who holds a physician's and surgeon's certificate, a license topractice optometry, a license to practice naturopathic medicine, a license to practice dentistry, a license to practice veterinary medicine, or a certificate to practice podiatry, and who is duly registered by the Medical Board of California, the State Board of Optometry, the Bureau of Naturopathic Medicine, the Dental Board of California, the Veterinary Medical Board, or the Board of Osteopathic Examiners of this state.
99
Biopsych/Neuropsych model
-Multi-disciplinary team for difficult chronic non-malignant pain-Pain Specialist, MD-Pain psychologist-Physical/Occupation Therapy-Mid-Level practitioner with specialized training-Clinical Pharmacist-Pain-related thoughts-Behavioral responses-Patient’s ability to achieve relaxation and comfort-A patient-centered, multifactorial, comprehensive care plan is necessary, one that includes addressing biopsychosocial factors. Addressing spiritual and cultural issues is also important. It is important to have a multidisciplinary team approach coordinated by the primary care physician to lead a team including specialty areas of psychology and physical rehabilitation.
100
geriatric dosing
-Renal changes with age: Blood flow to the kidney decreases by up to 10% per decade of life, Number and size of “filtering units” (nephrons) decrease with age, Kidneys filter blood slower with age-Decrease in muscle mass: Decrease in creatinine production (falsely low SCr)-Increase in body fat decrease in body water (distribution)-Digestion rate decreases: Drug absorption takes longer-Liver mass and blood flow to the liver decrease: Slower metabolism
101
opioid rotation
-Recommended by American Pain Society (APS) guidelines for chronic opioid use in non-cancer pain-Used when patients experience inadequate response despite increased doses-In general, after chronic use a switch to a new drug should be accompanied by a moderate (25-50%) reduction in calculated equianalgesic dose: Theory of cross-tolerance-Usually recommended at about 200mg/day of morphine PO equivalent-Keep in mind individual response to different opioids vary widely (Your plan must be patient specific!)-start with lower end of conversion dose , add IR product prn for total requirements: titration-Monitoring and patient education is key, genetic factors?-Opioid-induced Hyperanalgesia (OIH): Opiates lower pain threshold, manifests as opioid tolerance, Worsening pain despite accelerating dose, Abnormal pain symptoms: allodynia (pain from non-painful stimulus)
102
Breakthrough Pain (BTP) treatment
-Used for ‘spikes’ in pain-Should be agent with fast onset-Ideally should be same agent as being used in long-acting form (prevents cross-tolerance)-Originally used mostly for malignant pain (now seeing it more often for non-malignant- controversy?)-Give roughly 10-20% of total 24hr dose for each breakthrough dose
103
Patient controlled analgesia
-Gives patients a sense of their pain control-Usually morphine, hydromorphone, sometimes fentanyl-Safety issues—mis-programmed, use of different concentrations, patients not monitored?
104
PCA safety measures
-Use of single, standard concentrations for drug-Precise, readable labeling-Match the MAR to the label—or use bar coded medication administration-Use smart pumps, capnography monitoring?-Assess opioid naïve vs. opioid tolerant:-Patient education prior to use (prior to surgery)
105
PCA monitoring
-Pain Assessment: Use of pain score/scales-Sedation Assessment: Richmond Agitation Sedation Scale (RASS), Pasero Opioid-induced Sedation Scale(POSS)-Respiratory Assessment: Rate—count for 30 seconds. If rate is less than 12/minute count for a full minute, Quality (Normal vs. shallow vs. deep, effort, sound)-Pulse Oximetry-RASS: +4 combative +3 very agitated +2 agitated +1 restless 0 calm -1 drowsy -2 light sedation -3 moderate sedation -4 deep sedation -5 unarousable
106
POSS scale
S = Sleep, easy to arouse Acceptable; no action needed; may increase opioid dose if needed 1. Awake and alert: Acceptable; no action needed; may increase opioid dose if needed 2. Slightly drowsy, easily aroused: Acceptable; no action necessary; may increase opioid dose if needed 3. Frequently drowsy, arousable, drifts off to sleep during conversation Unacceptable; monitor respiratory status and sedation level closely until sedation level is stable at less than 3 and respiratory status is satisfactory; decrease opioid dose 25% to 50% or notify prescriber or anesthesiologist for orders; consider administering a non‐sedating, opioid‐sparing nonopioid, such as acetaminophen or an NSAID, if not contraindicated. 4. Somnolent, minimal or no response to verbal or physical stimulation Unacceptable; stop opioid; consider administering naloxone; notify prescriber or anesthesiologist; monitor respiratory status and sedation level closely until sedation level is stable at less than 3 and respiratory status is satisfactory.
107
Conversion from PCA to PO meds
-Check actual administration records over the past few days-PCA requirements typically decline days out after surgery-Patient Example: KF is several days out from surgery and using a PCA dose of hydromorphone 0.2mg only 3 times/day the past 2 days and reporting pain on average of 6/10; What is an option for converting to po meds?
108
SE management: sedation
-Determine etiology-Decrease dose (25% reduction)-Increase interval-Stop medication-Consider reversal agent-Tolerance will develop but avoid dangerous sedation levels-Stimulants in chronic use patients?
109
SE management: respiratory depression
-Determine etiology-Decrease dose-Increase interval-STOP/HOLD medication-Consider reversal agent and titrate to effect
110
SE management: itching
-Caused by histamine release: Accompanying rash, swelling could mean allergic reaction true allergic reactions are RARE-Decrease analgesic dose-Consider antipruritics (additional sedation?)-Change analgesic: Some opioids more likely than other to cause histamine releaseMeperidine > codeine > morphine > hydrocodone > oxycodone > hydromorphone > fentanyl
111
Antipruritics options
-Diphenhydramine (Benadryl) is usually 1st choice (IV or PO): Additional sedation-Hydroxyzine (Atarax) (PO or IM)—caution sound-alikes!: Additional sedation (hydralazine is for hypertension)-Loratadine (Claritin) (PO)-Other antihistamine drugs.
112
SE management: N/V
-Determine etiology-Decrease analgesic dose-Change route-Change analgesic-Consider antiemetic
113
Antiemetic options
-Metoclopramine (Reglan) 10mg IV q6h prn: Especially if nausea related to GI motility issues-Promethazine (Phenergan): Previously given IV, but now black box warning tissue injury including gangrene due to extravasation (policies often forbid), Can give oral, rectal, or deep IM-Ondansetron (PO or IV): Now preferred over promethazine, 4mg IV push every 8-12 hours prn, Can have higher doses with max 24mg/day (caution QT prolongation)
114
SE management: constipation
-Will always be present as long as the patient is on opioids: MUST prevent/manage it (tolerance does not develop)-1st Line: Increase fluids and fiber, increase activity if possible-Senna 2 tabs (17.2mg) daily to start-May add docusate 200mg daily or bid for hard stools-Other options: Milk of Magnesia, bisacodyl suppository, fleets enema prn, Consider polyethylene glycol or lactulose-Methylnaltrexone: GI mu antagonist, sub-q every other day ($$$ should be used as last resort): weight-based dosing, every other day injection; GI mu antagonist (cannot cross BBB)-Alvimopan: short-term hospital use only for post-op ileus; Mu antagonist in GI only, so does not block CNS effects of opioids
115
Adjuvant medications
-Drugs whose primary indications were not originally for pain, but are useful in combination with other pain medications-Tricyclic antidepressants (amitriptyline, nortriptyline)-SSRI/NRI (Cymbalta, Effexor) -Anticonvulsants (gabapentin, topamax, lyrica)-Steroids (prednisone, hydrocortisone)-Topical drugs (lidoderm, menthol)-Muscle relaxants (cyclobenzaprine, baclofen)-Alpha-2-Adrenergic Agonists (clonidine, tizanidine)
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adjuvant pain management: anticonvulsants
-for neuropathic pain-1st line: gabapentin (Neurontin) (not-FDA approved): Recent issues with evidence (Vedula et al NEJM 2009), Clinically many patients respond well-Pregabalin (Lyrica): FDA approved and being worked into guidelines, Controlled substance -Carbamazepine, lamotrigine (last line agents)-Consider slow titration to avoid adverse effects-Talk to patients about expectations with nerve pain!
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adjuvant pain management: antidepressants
-In chronic pain patients with co-morbid depression/neuropathic pain, fibromyalgia patients-TCAs have long track record: Have more anticholinergic side effects (anti-SLUD), Amitriptyline most commonly studied; others (nortriptyline) have less adverse effect profiles, Can use lower doses than those required for antidepressant effect-SSRIsSNRI’s:-Duloxetine (Cymbalta) is FDA approved – up to 60mg daily: Brand only – usually higher cost-Venlafaxine (Effexor) similar MOA but not FDA approved-All antidepressants require 4-6 week trial with titration to adequate tolerated dose (May see some relief as soon as 2 weeks)
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skeletal muscle relaxants
-Provide some short term relief-Approved for spasticity (baclofen, dantrolene, tizanidine) or musculoskeletal (carisoprodol, cyclobenzaprine, methocarbamol, chlorzoxazone)-Cyclobenzaprine (Flexeril) most studied: Has similar structure to amitriptyline: similar side effects-Carisoprodol (Soma) became controlled substance post-market-Sometimes use benzodiazepines for this effect
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topical pain relief
-Capsaicin cream: Alkaloid from chili peppers, Thought to deplete substance P, Apply tid-qid and give sufficient trial of at least 4 weeks-Topical NSAIDS: Diclofenac gel (Voltaren)-Lidocaine patches: Post-herpetic neuralgia, Back pain
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Non-pharm pain management
-Ice packs or heat: Typically ice for acute, heat for chronic, but patient specific, can alternate-Aromatherapy (peppermint oil, lavender)-Distraction techniques: All 5 senses, music , books, movies (happy subjects)-Smiling/laughter (endorphins increases pain threshold)-Meditation/Yoga (studies show efficacy in back pain)-Mobilization/Chiropractic/Accupuncture-physical therapy-massage therapy-TENS unit
