PAIN & ANALGESIA
Download
Report
Transcript PAIN & ANALGESIA
PRINCIPLES OF PAIN
MANAGEMENT & ANALGESIA
“THERE IS NO COMING TO
CONSCIOUSNESS WITHOUT PAIN.”
-CARL JUNG
PRINCIPLES OF PAIN & ANALGESIA
WHAT IS PAIN?
An unpleasant sensory or emotional experience associated with
actual or potential tissue damage
Pain results when nerve cells in the skin or deep tissues, called
nociceptors, detect a noxious stimulus
2 types of sensory neurons that detect and transmit pain
A
delta fibers (large, myelinated)
Transmit sharp, discrete pain signals that allow the patient
to localize the source of pain.
transmits somatic pain
C fibers (small, nonmyelinated)
Transmit dull, aching, throbbing pain that cannot be easily
localized
transmits somatic & visceral pain (visceral pain is only
transmitted by C fibers)
PRINCIPLES OF PAIN & ANALGESIA
THE PAIN PATHWAY
TRANSDUCTION: transformation of noxious thermal,
chemical, or mechanical stimuli into electrical signals
called action potentials by A-delta & C fibers
TRANSMISSION: these sensory impulses are then
conducted to the spinal cord
MODULATION: in the spinal cord where the A-delta &
C fibers terminate, the impulses can be altered by other
neurons, which either amplify or suppress them.
PERCEPTION: the impulses are transmitted to the
brain, where they are processed and recognized.
THE PHYSIOLOGY OF PAIN
PRINCIPLES OF PAIN & ANALGESIA
WHAT IS PAIN?
Somatic pain arises from the skin, soft tissues, muscles,
bones, or joints
Easily localized through stabbing, throbbing, or
aching
Visceral pain arises from internal organs
not easily localized and is characterized by cramping
or burning
Referred pain term used to describe the pain that is felt
in a body part other than where the actual pain
stimulus is coming from
PRINCIPLES OF PAIN & ANALGESIA
WHAT IS PAIN?
Hyperalgesia
is increased sensitivity to a stimulus
Neuropathic pain arises from direct damage to peripheral
nerves or the spinal cord.
May be shooting, sharp, or tingling
Phantom limb or stump pain is sensation or pain arising
from the missing body part
Pain can also be classified according to onset and duration
Acute pain has an abrupt onset and a relatively short
duration of action. *Effectively treated with analgesic drugs
Chronic pain has a slow onset, and duration of several
months to years. *May be unresponsive to drug therapy
PRINCIPLES OF PAIN & ANALGESIA
MYTHS ABOUT PAIN IN ANIMALS
Consider how some people without medical backgrounds may
view the animal’s response to pain
PRINCIPLES OF PAIN & ANALGESIA
THE 5 FREEDOMS OF ACCEPTABLE ANIMAL
WELFARE
Freedom from hunger
Freedom from physical and thermal discomfort
Freedom from pain, injury, & disease
Freedom to express normal behavior
Freedom from fear and distress
PRINCIPLES OF PAIN & ANALGESIA
WHAT ABOUT OUR ANIMAL PATIENTS AND/OR
OUR JOBS COULD MAKE MONITORING FOR
PAIN OR USING ANALGESICS DIFFICULT?
PRINCIPLES OF PAIN & ANALGESIA
MONITORING SIGNS OF PAIN
Consider how we as humans display pain vs. how our animal
patients display pain. Write some ways you can monitor for
pain in animals.
3 TYPES OF BEHAVIORS ASSOCIATED W/PAIN IN
ANIMALS
PRINCIPLES OF PAIN & ANALGESIA
PAIN ASSESSMENT
The measurement of pain is important to:
Pain scales
Based on observer’s assessment of patient’s spontaneous
behaviors, and behaviors on handling, interaction, and
manipulation, & maybe physiologic parameters.
Pain scores should be reassessed regularly and preferably by
the same person to minimize observer variation.
PRINCIPLES OF PAIN & ANALGESIA
PAIN ASSESSMENT TOOLS: Simple descriptive
scale
PRINCIPLES OF PAIN & ANALGESIA
PAIN ASSESSMENT TOOLS: Numeric rating scales
PRINCIPLES OF PAIN & ANALGESIA
PAIN ASSESSMENT TOOLS: Visual analogue scale
PAIN ASSESSMENT TOOLS: Comprehensive scales
PRINCIPLES OF PAIN & ANALGESIA
CONSEQUENCES OF UNTREATED PAIN
Consider the long term effects of untreated pain
PRINCIPLES OF PAIN & ANALGESIA
PHYSIOLOGICAL SIGNS OF PAIN
PRINCIPLES OF PAIN & ANALGESIA
WHAT IS ANALGESIA?
Analgesia is the absence of the awareness of pain, achieved through
the use of drugs or other modes of therapy. It applies to the relief of
pain without the loss of consciousness.
WHAT ARE THE GOALS FOR PAIN CONTROL?
Control pain at every stage of treatment
to administer analgesics before the patient has an awareness of pain.
This is known as preemptive analgesia.
Decreases the analgesic requirements
Decreases CNS sensitization
To prevent windup, an event caused by a buildup of chemical
mediators that intensify the pain response
PRINCIPLES OF PAIN & ANALGESIA
METHODS OF PAIN CONTROL WITHOUT MEDS
Endorphins are endogenous compounds produced by the
pituitary gland and the hypothalamus that bind to opioid
receptors during situations of trauma or stress. They resemble
opiates in their ability to provide pain relief and a feeling of wellbeing. “natural pain reliever”
Nursing care:
Other therapies to control pain:
PRINCIPLES OF PAIN & ANALGESIA
METHODS OF PAIN CONTROL USING MEDS
OPIOIDS
NSAIDS
OTHERS: alpha-2 agonists, ketamine, steroids
LOCAL ANESTHETICS
METHODS OF PAIN
CONTROL USING MEDS
OPIOIDS
OPIOIDS
MODE OF ACTION:
Acts on 4 different receptors in the brain and spinal cord
Mu
Kappa
Delta
Sigma(only cause hallucination, euphoria/dysphoria)
An opioid agent may act as an agonist (stimulating agent) or antagonist
(blocking agent) at each receptor
Some opioid agents are considered mixed agonist/antagonists in that they
block one type of receptor and stimulate another or partial agonists in that
they only partially stimulate some opioid receptors
Binding to these receptors can result in a number of effects:
ANALGESIA
Respiratory depression
Sedation
Dysphoria
And others,…
OPIOIDS
REVERSIBILITY
One major advantage of opioids is their reversibility with pure
antagonists such as NALOXONE, which is the most effective
Naloxone competitively binds to opioid receptors
It is also possible to use a mixed agonist/antagonist such as
BUTORPHANOL or a partial agonist such as BUPRENORPHINE
to reverse the effects of the pure agonists
CONTROLLED
OPIOIDS
MORPHINE: a FULL AGONIST (stimulates all 4
receptors)
Great for moderate to severe pain
Produces significant sedation
cardiovascular & respiratory depression
SIDE EFFECT/CAUTIONS:
Can cause excitement in cats (use lower doses)
Often results in VOMITING due to its effects on the CRTZ
Give slowly IV otherwise severe histamine release can lead to hypotension and
pruritis
Other FULL AGONISTS include oxymorphone,
hydromorphone, and fentanyl
OPIOIDS
FENTANYL: a FULL AGONIST
(stimulates all 4 receptors)
the injectable has a rapid onset of action
and short duration of action. Onset of
action: 2 min; duration of effect: 20-30 min
commonly used as a transdermal skin patch
Fentanyl is slowly absorbed through the
skin and may take 4-12 hrs in cats, and 1224 hrs in dogs to reach therapeutic levels
See pg 230 in your book, Procedure 7-1 for
instructions on placing a fentanyl patch.
OPIOIDS
BUPRENORPHINE: partial
agonist of the mu receptor(aka
bupi, buprenex)
Delayed onset of action, (40 min IM) but longer
duration of action than other opioids – 6-8 hrs
Best used for mild to moderate pain
The injectable product is effectively given to
cats transmucosally (applied to the gingiva,
under the tongue, in cheek pouch)
Can be used to reverse the effects of pure
agonists, while maintaining some analgesic
effect. Not as effective as naloxone
THIS DRUG IS PART OF THE VTI PROTOCOL
FOR DOGS & CATS*
OPIOIDS
BUTORPHANOL: mixed
agonist(kappa,sigma)/antagonist
(mu)(aka torb, torbugesic)
Best used for mild to moderate pain; and is
commonly used as a cough suppressant
Can be used to reverse the effects of pure
agonists. Not as effective as naloxone
Commonly combined with a sedative such as
dexmedetomidine or acepromazine
MIXING AN OPIOID & SEDATIVE IS
KNOWN AS NEUROLEPTANALGESIA
OPIOIDS
TRAMADOL: a non-opiate drug that has agonist
activity at the mu receptor
Oral tablets
Useful post-operative pain med in dogs and cats
Not currently controlled
METHODS OF PAIN
CONTROL USING MEDS
NSAIDS
NSAIDS
MECHANISM OF
ACTION:
Inhibits the synthesis of
prostaglandins by blocking
the enzyme cyclooxygenase
( aka COX-1 & COX-2)
COX-1 leads to the
production of beneficial
prostaglandins
COX -2 leads to the
production of harmful
prostaglandins that are
present during tissue damage
and inflammation.
NSAIDS
BENEFITS OF NSAIDS:
No strict record keeping
Little abuse potential
Effective when given orally
No sedative, cardiovascular, or respiratory effects
Antipyretic effects
SIDE EFFECTS/CAUTIONS:
GI upset/GI ulcers due to inhibition of prostacyclin
DO NOT USE CONCURRENTLY w/ STEROIDS
renal toxicity due to inhibition of PGE2
hepatic toxicity
Inhibits platelet aggregation due to blockage of thromboxane
NSAIDS
RIMADYL (carprofen)
Approved for use in DOGS ONLY!
Oral(chewable tablets) and injectable forms available
Less likely to cause side effects mentioned previously due to its
COX-2 selectivity
Common uses:
Post-operative pain relief
Pain relief from osteoarthritis and other musculoskeletal injuries
PART OF THE CANINE POST-OP PAIN CONTROL
PROTOCOL AT VTI
NSAIDS
METACAM (meloxicam)
Approved for use in dogs and cats
COX-2 selective
Oral and injectable formulations available
PART OF FELINE POST-OP PAIN CONTROL PROTOCOL AT
VTI
METHODS OF PAIN
CONTROL USING MEDS
OTHERS:
ALPHA-2 AGONISTS
KETAMINE
ALPHA-2 AGONISTS & KETAMINE
ALPHA-2 AGONISTS (ex: dexdomitor, xylazine)
Short duration of action (~90 minutes)
Also causes profound sedation, bradycardia
Commonly combined with butorphanol
Reversible (analgesic effects are reversed as well)
KETAMINE
Works by antagonizing NMDA receptors in the spinal cord
Blocking NMDA receptors prevents central sensitization & windup
Effective for somatic analgesia, but limited visceral
analgesia
Duration of action is short 30min
METHODS OF PAIN
CONTROL USING MEDS
LOCAL
ANESTHETICS
LOCAL ANESTHETICS
WHAT IS LOCAL
ANESTHESIA/ANALGESIA?
The use of a chemical agent on sensory neurons to produce a
disruption of nerve impulse transmission, leading to
temporary loss of sensation
LOCAL ANESTHETICS
CHARACTERISTICS OF LOCAL
ANESTHETICS
Exert their effects on neurons in the peripheral nervous system
and spinal cord that control pain, heat, cold, & pressure
Relatively few effects of the cardiovascular and respiratory
systems
Exert their effects in the area closest to the site of injection
Not normally transferred across the placenta
Safe for c-sections
LOCAL ANESTHETICS
ROUTES OF ADMINISTRATION
TOPICAL: must penetrate the epidermis to reach the dermis
where the peripheral nerves are located
Sprayed on intact skin for superficial procedures such as skin
biopsies (ex: ethyl chloride)
Creams can also be applied to desensitize skin for superficial
minor procedures (ex: lidocaine/prilocaine)
Splash blocks refer to the use of sprays or anesthetic soaked gauze
sponges on open wounds or surgical sites
Applied through a chest tube in patients having thoracic surgery
Should be done when patient is awake
Absorbed through the mucous membranes (larynx, eye, urethra)
Short duration of action and less pain relief when compared to
other routes of administration of local anesthetics
LOCAL ANESTHETICS
ROUTES OF ADMINISTRATION:
INFILTRATION(injection):
Local anesthetic can be injected subcutaneously, intradermally, or
between muscle planes
Ideally the site of injection is clipped and cleaned
Small needle (23-25 gauge) used to prevent tissue damage
Test efficacy by pricking the site with a needle
Do not inject into infected or inflamed tissues
Some local anesthetic drugs are combined with epinephrine
Epinephrine causes vasoconstriction which decreases rate of
absorption and prolonging effect
It also decreases the amount of drug entering the circulation,
decreasing chances of toxicity.
CAUTION AROUND AN INCISION OR ON EXTREMITIES AND
WITH PATIENTS WITH CV ABNORMALITIES
LOCAL ANESTHETICS
ROUTES OF ADMINISTRATION
NERVE BLOCKS: Injection of a local anesthetic in the
proximity of a specific nerve to desensitize a specific anatomic
location. Location of target nerve must be known and palpated
if possible.
Lameness exams in horses
Cornual blocks for dehorning cattle
Dental blocks in dogs and cats
Infiltration of nerves during amputation of a limb
Declawing cats
May take 15-20 minutes for absorption
Nerve blocks include line blocks and ring blocks
Cornual blocks for dehorning cattle
THIS NERVE BLOCK
IS ALSO A RING BLOCK
Dental blocks for tooth extractions
Maxillary Nerve block via
The infraorbital foramen
NERVE BLOCKS
Nerve blocks help pinpoint areas of pain
Paravertebral block
THESE ARE EXAMPLES OF LINE
BLOCKS
NERVE BLOCKS
THIS NERVE
BLOCK IS ALSO
A RING BLOCK
LOCAL ANESTHETICS
ROUTES OF ADMINISTRATION
NERVE BLOCKS
LINE BLOCKS: continuous line of local anesthetics placed SQ in
an area served by numerous small nerves
The needle is inserted along the line of infiltration and the
anesthetic is injected as the needle is withdrawn
If placed encircling an anatomic part, it is called a RING
BLOCK
INTRAARTICULAR: injecting local anesthetics directly into
a joint usually after surgery of the joint, immediately after
closure of the joint capsule
LOCAL ANESTHETICS
ROUTES OF ADMINISTRATION
EPIDURAL: blockage of sensory and motor nerves in the
rear, abdomen, pelvis, tail, hind limbs, and perineum
Anesthetist must be familiar with the anatomy of the terminal
spinal cord and lumbosacral vertebrae
Epidural space
Dura mater
arachnoid
Subarachnoid space w/CSF
Pia mater
Spinal cord
LOCAL ANESTHETICS
EPIDURALS
http://www.youtube.com/watch?v=zmwv
MHZG_5g
SIDE EFFECTS OF LOCAL ANESTHETICS
Allergy
Rash or hives in the area
Systemic toxicity
Sedation, nausea, restlessness, hyperexcitability, seizures,
respiratory suppression, coma
Infection (esp. w/epidurals)
Cranial infiltration of an epidural may cause serious
toxicity, respiratory suppression
death
METHODS OF PAIN CONTROL
Combining drugs from different categories (multimodal therapy, balanced analgesia) is more
beneficial than using high doses of one medication.
Pain is alleviated via different pathways
SPECIAL TECHNIQUES
NEUROMUSCULAR BLOCKING AGENTS
MECHANICAL VENTILATION
NEUROMUSCULAR BLOCKING AGENTS
Aka muscle-paralyzing
agents
These agents act by
interrupting normal
transmission of impulses
from motor neurons to the
muscle synapse
Site of action: neuromuscular
junction, where acetylcholine is
released by the neurons to attach
to muscle end plates.
NEUROMUSCULAR BLOCKING AGENTS
Two ways for these agents to disrupt the nervous transmission
Depolarizing agents – cause a single surge of activity at the neuromuscular junction,
followed by a refractory period. (Ex: succinylcholine)
Animals may show spontaneous muscle twitching followed by paralysis
Reversal agents are not effective
Non-depolarizing agents- block the receptors and the end plate. (ex: pancuronium,
atracurium)
No initial surge of activity at the neuromuscular junction, no spontaneous muscle
movements.
These agents can be reversed with neostigmine or edrophonium
Not commonly used in vet med, but can be useful in the following
situations.
Thoracic or diaphragmatic surgery
Orthopedic surgery
Ophthalmic surgery
C-sections
Facilitating difficult intubation
“balanced anesthesia” techniques
NEUROMUSCULAR BLOCKING AGENTS
Neuromuscular blocking agents allow relaxation of voluntary
muscles only. Skeletal muscles are affected in a predictable order
1st- Facial, neck paralysis
2nd- Tail, limb, abdominal muscles
Last- intercostal muscles, diaphragm
ADMINISTRATION
Normally given slowly IV
Onset of action: 2 minutes
Duration: 10-30 minutes
Animals on these drugs will require manual or mechanical
ventilation
ADVERSE EFFECTS
Hypothermia
Respiratory failure
Cardiac arrhythmias
MECHANICAL VENTILATION
Patient’s breathing is controlled by a ventilator rather than
compression of a reservoir bag
The ventilator automatically compresses a bellows, which forces
oxygen and anesthetic gas into the patient’s airways
The bellows is compressed at a specified rate and a specified volume
USES: not normally used in healthy anesthetized
patients, but can be helpful in:
Patient’s with compromised respiratory system
Thoracotomy surgery
Lengthy operations
MECHANICAL VENTILATION
MECHANICAL VENTILATION
Depending on the type of ventilator, the anesthetist
can deliver gases according to a pressure cycle, a
volume cycle, or a time cycle.
Pressure cycle – supplies air until the pressure reaches a preset
level. This is generally 12 cm to 20 cm.
Timed cycle – supplies air according to a set inspiratory time.
This is generally 1 to 1.5 seconds.
I:E ratio is 1:2 to 1:3
Volume cycle – delivers a preset tidal volume regardless of the
pressure required. This is generally 10-15 mL/kg
MECHANICAL VENTILATION
RISKS OF CONTROLLED VENTILATION
Excessive airway pressure may rupture alveoli
Cardiac output may be decreased if positive pressure is
maintained throughout inspiration and expiration
If ventilation rate is too high, excessive carbon dioxide may be
exhaled leading to respiratory alkalosis
Controlled ventilation is generally more efficient at delivering
anesthetic gas which may lead to exacerbation of side effects
such as hypotension and CNS depression.
Anesthetist may be tempted to relax on the monitoring