IASP definition of pain
unpleasant sensory and emotional experience associated with or resembling that associated with, actual or potential tissue damage
understanding of pain
- personal experience that is influenced by biological, psychological and social factors
- pain and nociception are two distinct concepts (pain is more than just sensory receptor activation)
- people learn about pain throughout their life experiences
- a person’s report of pain should always be respected
- pain usually serves an adaptive role (it may have adverse effects on function and social/psych well-being)
- verbal description is only one of several behaviours to express pain (inability to communicate doesn’t negate the possibility of pain)
consequences of unmanaged pain
a) neurologic: depression, anxiety and sleep disturbances
b) respiratory: atelectasis (collapse of the lung), clotting (hypercoagulable state), pneumonia, hypoxemia
c) blunted immune response
d) changes in cognitive fn or mood
e) extended hospital stays/readmissions
pain screening and assessment- inpatient
- at hospital admission/inpatient admission
- new reports of pain
- changes in medical conditions
- during vital sign check
pain screening and assessment- outpatient
- whenever there is a change in health status
- before and after any procedure or intervention
- brief screening at every encounter with a HCP
- during routine assessments (LTC)
importance of pain assessment
- individuals may not always disclose pain
- explore the patients previous experiences and expectations with pain management, as this can influence their beliefs regarding pain
validated pain tools: OPQRSTUV
a) onset: when did it begin? how long/often?
b) provocation/palliation: what makes it worse/better?
c) quality: describe it?
d) region/radiating: where? is it spreading?
e) severity: 1-10
f) timing/treatment: always present/intermittent? when is it the worst? using meds/treatments? how effective are they? side effects?
g) understanding: what do you think is the root of the pain? how is pain impacting your life/family?
h) value/deja vu: what is your acceptable pain level? are there views about this pain that are important to your family?
validated pain tools: faces
- validated in kids 5-12
- choose the face that shows how bad your pain is
validated pain tools: numeric rating scale
- used in individuals >8
- individuals score their pain from 0-10
validated pain tools: verbal rating score
- list of adjectives/phrases to describe different levels of pain intensity
- can range from 3-6 descriptors
- usually mild (1-2), moderate (4-6), severe (7-10)
- people often have difficulty differentiating between the words
validated pain tools: nonverbal pain indicators
- six behaviours scored at rest and on activity in cognitively impaired adults and post operatively
- presence of any of the behaviours may indicate that the individual is in pain, requiring further assessment
- includes vocal complaints (groans, gasps) , facial grimaces/winces, bracing, restlessness, rubbing, vocal complaints (words)
validated pain tools: critical care pain observation
- used with patients who are unable to communicate in an ICU
- 4 categories, each score 0-2
- a score >2 indicates the presence of pain
opioids
- any drug, natural or synthetic, that has actions like morphine
- any opiate describes compounds that are present in opium
- endogenous opioid peptides include endorphins, enkephalins and dynorphins
function of opioids in the body
- endogenous opioid peptides function similarily to opioids in our body
- they inhibit pain transmission and decrease pain perception
- they have a role in how our body responds to pain, emotional regulation and stress response
opioid receptor classes
a) mu: opioid analgesics act primarily by activating the mu receptor
b) kappa: opioid analgesics cause a weak activstion of the kappa receptor
c) delta: not activated by opioid analgesics
opioid peptides bind to all three receptors
classification of opioids
- classified based on how they affect mu/kappa receptor function
a) pure opioid agonist: leads to mu and kapp activation (morphine, codeine, meperidine, hydromorphone)
b) agonist-antagonist opioids: partial mu agonist and kappa antagonist (nalbuphine, buprenorphine) - some pain relief, small doses can cause dec AE of opioids
c) pure opioid antagonists: mu and kappa antagonist (naloxone, naltrexone) - used to reverse overdoses
morphine
- remains gold standard (all opioids converted to morphine milliequivalent)
- strong opioid, used to treat moderate to severe pain
- derived from seed pod of poppy plant
morphine: MOA
- relieves pain by mimicking actions of endogenous opioid peptides at the mu receptor
- acts in the CNS and periphery (associated with the perception of pain)
morphine: PK
- predominantly metabolized in the kidney and liver
- conjugated with glucaronic acid to form metabolites, which are excreted in the urine
a) morphine-3-glucuronide (75-85%): causes neuroexcitation
b) morphine-6-glucuronide: causes analgesia and respiratory depression - undergoes first pass effect, so oral dose has to be much larger
- longer effects in patients with liver disease, poor clearance can lead to toxicity
morphine: AE (resp depression)
- resp drive dec from mu activation
- symptom onset is dependent on route of admin
- tolerance to resp depression can dev with LT use
- important to complete resp assessment prior to admin (hold w RR<10-12)
- inc with concurrent CNS depressant meds (benzos, alc)
- treated with opioid antagonist
morphine: AE (constipation)
- activation of mu receptors present in the GI tract lead to slow gastric motility, intensification on non-propulsive contractions (cramping), increased tone of the anal sphincter and dec fluid into the intestinal lumen (dry poops)
- can lead to fecal impaction, bowel obstruction, bowel perforation and heorrhoids
- managed pharmacologically (stool softeners and laxatives) and with lifestyle modifications (high-fibre diet, increase fluid intake, exercise)
morphine: AE (POTS)
- diminishes baroreceptor reflex
- dilates peripheral arterioles and veins, leading to blood pooling
- education is important (ie. stand up/change positions slowly)
- synergistic occurence with antihypertensive medications, perform med reconciliation
morphine: AE (other)
a) urinary retention: inc bladder sphincter tone (harder to pass urine), inc bladder detrusor tone (inc pressure in bladder), suppresses awareness of bladder stimuli
- encourage voiding q4h, inc urinary retention with AC drugs
b) cough suppression: can lead to build-up of mucous, encourage coughing
c) emesis: activation of chemoreceptors in medulla, common in ambulatory pts and pts new to opioids
d) sedation: important to discuss with outpatients, admin smallest effective dose
morphine: AE (other) cont’d
e) neurotoxicity: delirium, agitation, confusion, myoclonus
- more common with renal impairement (poor excretion of metabolites)
- administer smallest effective dose, reduce dose, switch opioid drug
f) euphoria: from activation of mu receptors, can contribute to misuse of med
- can also contribute to dysphoria (sense of anxiety and unease)
g) birth defects: inc risk for congenital heart defects in pre-conception & first trimester
- avoid during preganancy if possible
