pain

what is pain?

* complex experience
* dynamic interactions between physical, cognitive, spiritual, emotional, and environmental factors
* not just a response to injury

why is acute pain protective?

* it promotes withdrawal from painful stimuli
* allows injured parts to heal
* teaches avoidance

what 3 parts of the nervous system are involved in sensation, perception & response to pain?

1. afferent pathways
2. interpretive centers
3. efferent pathways

nociception

perception of pain

nociceptors

* Pain receptors
* free nerve endings in the afferent peripheral nervous system

nociceptive stimuli

stimuli of a certain intensity that cause, or are close to causing tissue injury

what do nociceptors respond to?

• sharp objects
• electric currents
• application to heat & cold to skin
• chemical stimuli

when are nociceptors not activated?

with low intensity

where are noiceptors widely distributed?

• skin
• dental pulp
• meninges

where are there no nociceptors?

brain

what are the 4 phases of nociception?

1. Transduction
2. Transmission
3. Perception
4. Modulation

transduction

* begins when nociceptors are activated by noxious stimuli
* painful stimuli converted to action potentials at the sensory receptor
* substances/chemical mediators released as a result of direct injury & inflammation

where does transduction occur?

at the ends of A-delta fibers & C fibers

prostaglandin

* important chemical mediator that creates the reactions that cause pain, fever, & inflammation
* target of some pharmacologic treatments

transmission

action potential is generated & transmitted along nerve fibers

what are the nerve fibers involved in transmission?

• A-delta
• C fibers

A-delta nerve fibers

* small diameter
* myelinated- rapid transmission of acute pain
* pain is sharp, stinging, cutting, & pinching
* well localized

C nerve fibers

• small diameter
• unmyelinated- slow transmission of chronic pain
• pain is dull, burning, aching
• poorly localized

A-alpha & B-beta nerve fibers

* large diameter
* do NOT transmit pain signals

perception

• conscious awareness of painful sensation
• brain receives signals & interpret them as painful

What is pain perception influenced by?

• attention
• distraction
• anxiety
• fear
• fatigue
• previous painful experiences/expectations

pain tolerance

• greatest intensity of pain a person can handle
• varies greatly over time

pain threshold

• lowest intensity of pain that a person can recognize
• perceptual dominance occurs

opioid tolerance

Requires larger amounts for same effect

modulation of pain

process by which the sensation of pain is inhibited or modified

modulation physiology

• synaptic transmission of pain signals is altered
• can be amplified or dampened
• neurotransmitters: encephalons & endorphins
• opioids such as endorphins mediate pre-synaptic
• morphine mimics effect of endorphins

gate control theory

• theory that if we can block the pain before it gets to the brain we can stop or lower pain perception
• touch, rubbing skin, massage, distraction, acupuncture, getting active, TENS unit

Neurotransmitters

• modulate control related to transmission of pain impulse
• excitatory or inhibitory : can enhance or inhibit pain
• over 50: norepinephrine, acetylcholine, dopamine, serotonin, GABA

endorphins

natural neurochemicals or endogenous opioids that aid in inhibiting the pain response

acute pain

• nociceptive
• normal protective mechanism to tissue injury
• transient, can last seconds to months but no longer than 3 months
• often stimulates the ANS to produce physical response to pain
• ↑ HR, ↑ BP, diaphoresis, dilated pupils

chronic pain

• lasting for more than 3-6 months (well beyond the expected healing time)
• serves no purpose, often seems out of proportion to observable tissue damage
• can be ongoing or intermittent
• changes in PNS & CNS cause disregulation of nociception & pain modulation
• often no ANS response

neuropathic pain

• chronic pain involving nerves
• caused by a primary lesion or dysfunction in nervous system
• leads to long-term changes in pain pathway structures & abnormal processing of sensory information

2 types of nociceptive pain

somatic and visceral

somatic pain

involves musculoskeletal system

somatic pain complaints

constant, achy

location of somatic pain

• well-localized in skin & subcutaneous tissues
• bone
• muscle
• blood vessels
• connective tissue

examples of somatic pain

• incision pain
• bone fractures
• osteoarthritis
• peripheral vascular disease

visceral pain

involves organs, inflammation sometimes present

visceral pain complaints

cramping, splitting, N/V, diaphoresis

visceral pain location

• originates in internal organs or body cavity linings
• poorly localized
• diffuse
• deep

visceral pain examples

• kidney stones
• appendicitis
• bladder spasms
• constipation
• organ metastases
• spastic bowel
• inflammatory bowel disease
• heart attack
• chronic hepatitis

neuropathic pain complaints

• shooting
• burning
• electric-shock
• sharp
• numb
• motor weakness

neuropathic pain location

• originates in injury to peripheral nerve
• spinal cord
• brain
• poorly localized

neuropathic pain examples

• diabetic neuropathy
• postherpetic neuralgia
• tumor-related nerve compression
• phantom limb pain
• trigeminal neuralgia
• central post-stroke pain

referred pain

• pain is felt at a distance from actual pathology
• common in visceral pain
• example: MI pain felt in chest, jaw, left arm

phantom pain

• sensations of pain that originates from an amputated part
• constant
• most intense right after amputation
• generally resolves over time

Non-Opioids and adjuvants

medication that relieve pain without causing loss of consciousness

opioid analgesics

• manage moderate to severe pain
• mild or strong agonist

most widely used non-opioid analgesic

Tylenol (acetaminophen)

Tramadol (Ultram)

centrally acting nonopioid analgesic

Tramadol MOA

• Binds to mu receptors, weakly
• inhibits norepinephrine/serotonin reuptake

tramadol indication

treat moderate to severe pain, PO

Tramadol adverse effects

• drowsy
• dizzy
• headache
• nausea
• constipation
• respiratory depression
• rare : seizures when combined with other CNS depressants

Gabapentin (Neurontin)

Anticonvulsant

gabapentin MOA

thought to spontaneously suppress neuronal firing

gabapentin indications

• to complement effects to opioids
• used specifically for neuropathic pain

Gabapentin adverse effects

• drowsy, dizzy, visual problems
• can only be partially reversed with naloxone

Non-opioid analgesics

* NSAIDs and acetaminophen
* used to treat mild to moderate pain

NSAIDS

• analgesic, antipyretic, anti-inflammatory
• nonselective COX inhibitors
• selective COX-2 inhibitors
• mild-moderate pain

acetminophen (tylenol)

• analgesic & antipyretic
• no anti-inflammatory properties
• mild-moderate pain

types of NSAIDs

• aspirin, ibuprofen, naproxen, ketorolac (nonselective COX inhibitor)
• celecoxib (COX-2 selective)

NSAIDs indications

• treat mild to moderate pain
• inflammation
• fever

NSAIDS MOA

• anti-prostaglandins
• decreases prostaglandins by blocking a key enzyme: cyclooxygenase (COX) which is crucial to production of prostaglandins

COX-1

• enzyme that protects the gastric mucosa and needed for thromboxane synthesis
• aspirin only **thromboxane activates platelets**

COX-2

• responsible for inflammation & fever
• promotes synthesis of prostaglandins involved in inflammatory processes

Non-selective COX inhibitors

• aspirin, ibuprofen, naproxen
• both COX-1 & COX-2 inhibited → prostaglandins & thromboxane synthesis
• aspirin is more anti-thrombotic than ibuprofen & naproxen

common side effects of NSAIDs

• GI upset, stomach ulcers, GI bleeding

• rash

• edema

• kidney failure

• increases in BP

• inhibits platelet aggregation

• SOA in asthma patients

Selective COX-2 inhibitors

• Celecoxib (Celebrex)
• only COX-2 blocked
• GI mucosa still protected & platelet function not impacted
• serious cardiovascular thrombotic events

black box warnings with NSAIDS

• cardiovascular risk
• gastrointestinal risk

NSAIDS black box warning: cardiovascular risk

* may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, & stroke, which can be fatal
* risk may increase with duration of use
* patients with CVD or risk factors for CVD may be at greater risk

NSAIDS black box warning: gastrointestinal risk

* cause an increased risk of serious gastrointestinal adverse effects including bleeding, ulceration, & perforation of the stomach, which can be fatal
* events can occur at any time with use & without warning symptoms
* elderly patients are at greater risk

aspirin MOA

prevents platelet activation/aggregation (by inhibiting COX)

Acute aspirin poisoning

• nausea/vomiting
• seizures
• cerebral edema

chronic aspirin poisoning

• nausea/vomiting
• tinnitus- ringing in the ears
• heading loss

who should you not give aspirin to?

children under 15 years → risk of reye's syndrome (swelling of brain & liver)

what is the most potent NSAID?

ketorolac

Ketorolac (Toradol) specific considerations

• most potent NSAID
• given IV or IM (PO less common)

ketorolac indications

• used to treat acute/short-term moderate to severe pain

• primarily used in post-op setting

• reduced pain & inflammation

• analgesic effect similar to morphine but without respiratory depression

how long can ketorolac be used?

5 days or less

ketorolac side effects

• GI ulcers & higher risk of renal dysfunction (especially if patients has decreased renal function at baseline or are dehydrated)

Acetaminophen (Tylenol) MOA

• unknown
• possibly decreases prostaglandin synthesis in CNS

Acetaminophen indications

mild to moderate pain, fever (antipyretic)

acetaminophen limitation

• no anti-inflammatory properties
• ceiling effect

acetaminophen adverse effects

• large amounts → acute hepatic necrosis, liver failure with chronic long term use & mild nephropathy
• look for jaundice, elevated LFTs, & creatinine levels

acetaminophen adult dose restriction

• 4 grams/24 hours
• must count tylenol & other medication combinations with tylenol

percocet

oxycodone with acetaminophen

Lortab, Vicodin, Norco

hydrocodone with acetaminophen

Acetylcysteine (Mucomyst)

acute ingestion antidote for acetaminophen

Tylenol and alcohol

• BAD MIXTURE
• chronic alcohol users should limit use (

Pearls for Practice → Non-opioid analgesics

• can alternate true NSAIDs with acetaminophen
• good to give in conjunction with opioids for moderate to severe pain
• choose true NSAIDs (not Tylenol) if inflammation is causative factor

opioids

moderate to severe pain

opioids for pain relief

• Morphine
• Hydromorphone (Dilaudid)
• Fentanyl (Duragesic)
• Codeine
• Oxycodone
• Hydrocodone
• Narcan/naloxone (antidote for opioids)

general considerations for all opioids

* all are high-alert drugs
* asses LOC, BP, pulse, & respirations before & periodically during administration
* if respiratory rate is < 10/min, assess level of sedation
* physical stimulation may be sufficient to prevent significant hypoventilation
* subsequent doses may need to be decreased by 25-50%
* initial drowsiness will diminish with continued use

what do you need to assess before & periodically during administration of opioids?

* LOC
* BP
* Pulse
* Respirations

All opioids are what kind of drugs?

High alert drugs

morphine

• schedule II → high abuse potential
• given oral, liquid or parenteral
• interacts with alcohol & CNS depressants
• moderate to severe pain (5-8)

morphine MOA

• mu agonist → mimics action of endogenous opioids at mu receptors
• binds to mu receptor & creates response

morphine serious adverse effects

• respiratory depression
• CNS depression

morphine common adverse effects

• constipation
• drowsiness/fatigue
• confusion, dry mouth, itching

morphine nursing considerations

as will all opioids → may impair the mental/physical abilities required for operating machinery or car