NURS 116 Pain and Pain management

Assessment of pain

pain is a symptom(subjective) and a vital sign, goal is to know the story of the pain

Location of pain

Associated signs and symptoms e.g. fever

Timing of pain

Exposure/environmental factors

Reliving factors

Severity→ “How bad is your pain on a scale of 1-10, 1 being no pain at all and 10 being the worst pain you have ever felt”

Nature→ sharp, dull, stabbing

Aggravating factors

Patient perspective

Significance to patient

afferent pathway

sensory information from the parasympathetic nervous system to CNS is afferent

• starts at the sensory receptor in a specific body part and ends in the CNS’s somatosensory cortex

• sensory impulse must be strong enough to reach threshold and initiate an action potential( must reach -50mV)→ not strong enough, no action potential= no pain message

• nociceptor in skin, bones, blood vessels, visceral organs→ 1st order neuron(PNS)

visceral pain

deep organ related pain

cutaneous pain

superficial, surface related pain

referred pain

due to body surface innervated by the same spinal nerve/nerve plexus and interneuron communication

that causes pain to be perceived in a different location from the source of injury

• nerve plexuses covers large area and can lead to confusion in identifying the actual site of injury

• interneuron communication can carry the message forward→ ask patient “does the pain radiate or move anywhere?” e.g. cardiac pain radiating over down the arm

neuropathic pain

persistent nerve irritation that is difficult to treat

• allodynia→ pain caused by a non-painful stimulus

• hyperalgesia→ hypersensitivity to a painful stimulus

• paresthesias→ pins and needles

phantom pain

neuropathic pain post amputation

• spinal cord neurons are still active despite the lack of stimulus(no nociceptor)

• interneurons are still communicating pain

• often leads to chronic pain

acute pain

less than 10 days

• self-limiting and typically resolves with healing of the underlying injury

• sympathetic nervous system responses are active

• innate protective mechanism

• appropriate treatment is effective→ the pain can be improved

chronic pain

pain lasting more than 6 months

• usually travels along C fibers

• is slower pain

• not self-limiting→ endogenous pieces trying to get rid of it don’t work anymore

• endogenous modulators are absent

• destructive mechanisms is not beneficial to the host and yields other dysfunctions e.g. insomnia, anxiety, anorexia

• this is when we use other treatment modulations e.g. CBT

• sympathetic nervous system is not active

sensory homunculs

maps the cortex region per anatomical body part(based on number of innervation) somatosensory association

• then links the sensation to previous experience→ first time patient feels pain it is less traumatic but if it the associated with a traumatic experience than 2nd exposure can be worse(because you anticipate the pain)

• somatosensory cortex is in the parietal lobe

• different regions in the body have different threshold of pain→ some have nociceptors(large body part)

what happens when a large stimuli triggers many receptors?

it causes a high awareness of pain

• more nerves triggered= bigger experience of pain

• e.g. trauma(tissue tearing)

non-pharmacological techniques

• decrease inflammation and sensation( involves PNS) → ice

• alleviate the trigger(PNS)→ massage, physiotherapy

• distraction/behaviour modulation(CNS)

  • Cognitive behaviour therapy(CBT)→ alter behaviours that have to do with perception of pain

  • treat pain to avoid chronic pain

Non-pharmacological techniques- Ice

decrease inflammation and sensation involve PNS

• decrease perfusion to tissue

• decrease excitability of nociceptor(decrease cellular function)

• 20 minutes of ice(2-3x) but protect the tissue→ put over a shirt, paper towel, plastic bag

Cognitive behaviour therapy(CBT)

alter behaviours that have to do with perception of pain

• treat pain to avoid chronic pain

• activities modulate pain by distractions( make you think about something else why the pain is happening)→ especially for anticipated pain

reflexes→ flexor withdrawl reflex

• stimulus(sharp pain)→ reflex to withdraw without cerebral control

• there is an activation of a sensory neuron(afferent)

• then interneuron(at level of stimulus in CNS)→ they do not have an inhibitor but have an induction function(induce pattern)

• results in automatic activation of a motor neuron(efferent) only after we become aware

• response by the effector then causes awareness

opium

naturally occurring milky extract from unripe seeds of the poppy plant contain morphine and codeine substances(and other 18 substances)

opiates

naturally occurring chemical compounds extracted from opium

• natural only

opioids

any drug that is derived from the opium formula synthetic or natural

• natural or synthetic

• remain therapeutic mainstay for moderate to severe pain management

• can be combined with other therapies to manage chronic or complicated pain

• most are schedule I some schedule II

• problem= they all cause dependence on the drug

narcotic

morphine like drugs that produce analgesia and CNS depression

• terminology associated with illegal use

• 2 people need to verify narcotics

• e.g. hallucinogen, heroin, amphetamines, marijuana

titration principle

most opioids have no ceiling doses(maximum dose of a drug that provides its full effect)

• titrate upward as needed

• all will cause dependence

• titrate downward as soon as patient can tolerate the pain

opioids mechanism of action

are agonists for receptors mu(1 and 2) , kappa, delta, sigma, and epsilon(opiate)

• when the synaptic knob at the primary or secondary synapse is activated by an opioid agonist it will inhibit release of pain neurotransmitters e.g. substance P and glutamate

substance P

involved in acute pain transmission

• opioids act at the mu or kappa receptors which inhibit the release of substance P

• this inhibition reduces depolarization of ascending pain neurons, thereby blocking pain transmission

opioids and dopamine

dopamine release in the mesolimbic reward pathway(ventral tegmental area→ nucleus accumbens→ prefrontal cortex) contributes to the rewarding and reinforcing effects of opioids

• results in a calming or pleasurable sensation

• however, dopamine is not directly responsible for analgesia but plays a role in addiction and reinforcement

how do we become aware of pain(PNS→ CNS)

• Nociceptor Activation → Detects harmful stimuli and converts them into electrical signals.

• First-Order Neuron (PNS) → A-delta or C fibers transmit signals to the spinal nerve via the dorsal root and dorsal root ganglion.

• Synapse in the Posterior Horn → Substance P neurotransmitter is released.

• Second-Order Neuron → Decussates (crosses over) to the opposite side of the spinal cord.

• Ascending Pathway → Travels up the lateral spinothalamic tract in the white matter of the spinal cord.

• Thalamus (Relay Station) → The signal reaches the thalamus, which processes and directs sensory information.

• then synapses with 3rd order neuron

• reaches somatosensory Cortex (Brain) → Localizes the pain to a specific body part on the sensory homunculus.

• Final Step → Conscious awareness of pain occurs.

thalamus

sensory relay station

• all sensory information goes through here

• it is a filter that gets rid of unimportant messaging to avoid overstimulation

• directs relevant signals to the appropriate areas of the brain for processing

C fibers

• type of nociceptive nerve fiber that transmits dull, aching pain signals

• has the slowest transmission(Gate control theory) is slower than A-delta fibers

• unmyelinated and play a significant role in chronic pain transmission

endogenous opioid peptides

natural molecules in the body that help control pain, stress, and emotions

→They work by attaching to opioid receptors in the brain, similar to pain-relief drugs e.g. F morphine

• endorphins

• enkephalins

• dynorphins

• they are automatically released during acute pain

serotonin and norepinephrine

• released from the CNS→ hypothalamus, limbic system, reticular formation

• descending (efferent) pathway bind opioid receptors(mu, kappa, delta) to inhibit substance P

substance P

excitatory CNS neurotransmitter

• propagates pain input

• is involved in the transmission of pain signals to the brain

substance P involvement with opioids

involved in acute pain transmission

• opioids act at the mu or kappa receptors which inhibit the release of substance P

• this inhibition reduces depolarization of ascending pain neurons which blocks the pain transmission

Dopamine

release in the mesolimbic reward pathway(ventral tegmental area→ nucleus accumbens→ prefrontal cortex)

• contributes to the rewarding and reinforcing of pleasurable sensations

• however, it is not directly responsible for analgesia but plays a role in addiction and reinforcement

pain gate theory

• explains why rubbing an injured area can help reduce pain

• Non-painful stimuli(holding/rubbing a throbbing finger) can block pain signals in the spinal cord, reducing pain perception.

• Pain signals travel through small A-delta and C fibers into the dorsal horn of the spinal cord.

• In the substantia gelatinosa, which acts as a "gate," these pain signals can be interrupted.

• Larger A-beta fibers (touch, pressure, vibration) activate inhibitory neurons, closing the gate and preventing pain transmission.

A-delta fibers

• Small, thinly myelinated fibers

• Faster conduction than C-fibers.

• Carry sharp, localized, acute pain (e.g., pinprick, cut).

• Involved in the first response to painful stimuli.

A-beta fibers

• Larger, myelinated fibers

• Very fast conduction

• Detect light touch, pressure, vibration, and proprioception

• Inhibit pain signals by closing the gate in the substantia gelatinosa (Gate Control Theory)

parietal lobe

primary somatosensory cortex is located here

involved:

• in awareness of somatic sensations

• touch, pain, temperature

A-alpha fibers

• Largest, heavily myelinated fibers with the fastest conduction

• Carry proprioceptive and motor information from muscles and joints.

• Not directly involved in pain but essential for body awareness and movement coordination.

ADME connection to opioids

• Absorption→ depends on the route of administration

• Distribution→ distributes to skeletal muscle, liver, kidneys, lungs, intestinal tract, spleen, brain

  • adults have 20% to 35% protein binding

  • peak plasma concentration: oral- 1 hr, IV-20 mins

• metabolism→ hepatic via conjugation

• elimination→ via urine and feces

  • metabolites might cause toxicity with renal insufficiency

ADME- Distribution and opioids

• distributes to skeletal muscle, liver, kidneys, lungs, intestinal tract, spleen, brain

  • adults have 20% to 35% protein binding

  • peak plasma concentration: oral- 1 hr, IV-20 mins

Mu1 receptor

effects:

• analgesia

• euphoria

• confusion, dizziness

• nausea

• sedation

• involved in histamine and dopamine release

mu 2 receptor

effects:

• respiration depression

• cardiovascular effects(hypotension)

• GI effects(slow motility)

• urinary retention

• miosis(pupil constriction)

• histamine and dopamine release

delta receptor

effects:

• analgesia

• cardiovascular effects

• respiratory depression

kappa receptor

effects:

• analgesia

• psychomimetic effects(nightmares)

hydromorphone(dilaudid)

opioid with high efficacy

• 5x stronger than morphine

• given post-operation

morphine definiton

opioid with high efficacy

• gold standard of opioid

• causes the release of histamine(itching/pruritis can follow)

fentanyl

opioid with high efficacy

• 80-100 times more potent than morphine(highly potent)

• used for post op pain management

• dosage= mcg not mg

methadone(metadol)

opioid with high efficacy

• used in opioid addiction

• has a different mechanism of action than other opioids

opioids based on efficacy

• fentanyl

• morphine

• meperidine

• methadone(metadol)

• hydromorphone(dilaudid)

Fast-Acting Medicine Makes Might Healers

combination drugs

opioids + non narcotic analgesic = synergistic effect

• benefit→ dependence on drug can be reduced

• e.g. Percocet(oxycodone + acetaminophen)

• e.g. percodan(oxycodone + ASA)

• e.g. Vicodin(hydrocodone + acetaminophen)

• Tylenol #1-#4→ numbers= how much codeine is present, 1 being the lowest and 4 being the highest

morphine mechanism of action

class→ opioid analgesic/opiate receptor agonist

dose forms: tablets, parenteral

opioids bind to opiates receptors(mu, kappa, delta) in the CNS

• act as agonists of endogenously occurring opioids(enkephalins, endorphins, and dynorphins)

• reduce perception of and response to pain

morphine indication, side effects, assessment

• indication→ management of moderate to severe pain

• contraindications→ hypersensitivity, severe respiratory distress, head injury

• adverse and common side effects→ severe respiratory/ CNS depression(most common in those who are opioid naive)

  • urinary retention

  • pruritis

• Assess→ type, location and intensity of pain prior and at peak following administration

• use equianalgesic chart when changing routes, or from one opioid to another

• education for patient→ instruct patient on how and when to ask for pain medication

  • may cause dizziness or drowsiness

  • avoid concurrent use of alcohol

naloxone/Narcan

mechanism of action:

• blocks mu and kappa receptors

class: opioid antidote(agonist)

administration:

• should be given carefully and slowly just until client start to respond with increased respiratory rate and a clearing mental status

• parenteral, intranasal

onset→ 2-4 minutes

duration of action→ 45 mins

• if given to chronic opioid-user the client eill also wake up in aggressive behaviours(euphoria is disrupted)

narcan/naloxone indication, side effects, assessment

• indications→ reversal of CNS depression and respiratory depression due to suspected opioid overdose

• contraindication→ hypersensitivity

• adverse/side effects→ ventricular arrhythmia

  assessment:

• monitor respiratory rate, rhythm and depth

• pulse, ECG, BP, and LOC frequently for 3-4 hrs after expected peak

• dilute and administer in slow increments for sensitive patients(< 1 week opioid use)

• assess for signs of opioid withdrawal

• education for patient→ explain purpose and effects for patient

pressure sensitive sensors

• Ruffini’s endings

• Pacinian corpuscles

• Krause’ end bulbs

Fine touch sensors

• messiner’s corpuscle

• Merkel discs

• root hair plexus

temperature and pain sensors

• free nerve endings

• nociceptors→ important in experiencing pain

dermatome

area of skin supplied by sensory nerve fibers from a single spinal nerve root

• each spinal nerve carries sensory signals (such as touch, pain, and temperature) from a specific strip of skin to the spinal cord and brain

side effects of opioids

central nervous system→ cause CNS depression- drowsiness, dizziness, confusion, or mental clouding

• respiratory system→ respiratory depression(slow, shallow breathing) and apnea in severe cases

• cardiovascular→ bradycardia in most cases, tachycardia during compensation and hypotension or palpations

• gastrointestinal→ constipation due to slowed intestinal motility and nausea, vomiting, or reduced appetite

• genitourinary system→ urinary retention

• integumentary system→ pruritis

how to respond to opioid side effects

• nausea and vomiting→ usually resolves in few days, antiemetics can be used or switch the opioid

• sedation→ decrease dose

• constipation→ (most common) stool softeners, osmotic stimulants

  • peripherally-acting opioid antagonists, switch opioids or avoid bulking agents

• pruritis→ switch opioids or antihistamines

• urinary retention→ switch opioids

If pain is <4/10 you should

use non-opioid medications

• less invasive route e.g. PO

• NSAIDs, tylenol(or both)

If pain is 4-6/10 you should…

use opioids

• use a less invasive route e.g. PO

• synergy, combination drugs, Morphine

If pain is >6/10 you should

higher potency opioids

• consider IV route

• consider PCA(patient controlled analgesia) → a computerized machine that gives you medicine for pain when you press a button

Patient controlled analgesia(PCA)

device is programmed syringe pump which delivers the opioid infusions according to individualized settings

• Bolus dose= initial dose to get pain under control

• Lockout time= how many minutes are needed until patient gets other dose

• Dose duration- can set the duration for how long the infusion lasts before it can be administered again

• Background infusion= critically assess