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Anesthesia > Pain Lecture > Flashcards

Pain Lecture Flashcards

1
Q

What is pain?

A

A sensation
Unpleasant, aversive
Complex, multifactorial
Emotional, subjective, individual
Associated to damages/possibility of damages to body
Previous experiences: stress, fear, memory: modify pain perception
Subsequent painful episodes can be felt as more painful
Pain modifies the animal behavior and its expression

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2
Q

What is the pain pathway?

A

transduction, transmission,
modulation and perception

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3
Q

Describe the transduction pathway

A

the nociceptors, specialized
sensory receptors, are responsible for detecting the noxious stimulus and transforming it
into electric signal (action potential) that will be conducted to the central nervous system.

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4
Q

What are the free nerve endings involved in nociception?

A

primary afferent Aδ and C fibers
distributed
throughout the body, somatic and visceral (skin, viscera, muscles, joints, meninges)

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5
Q

WHat are types of noxious stimuli?

A

mechanical, thermal or chemical stimuli.

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6
Q

Describe transmission

A

transmit information from the periphery to the dorsal horn of the grey matter of
the spinal cord

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7
Q

What are A-beta fibers?

A

Primary afferent fibers that carry non-noxious stimuli

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8
Q

The primary afferent fibers involved in transmission are also known as? And what are these?

A

first order neurons
Aδ and C fibers, Aβ fibers

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9
Q

Aδ NT? and characteristics?

A

NT: glutamate

lightly myelinated and smaller diameter, and hence conduct more slowly than Aβ fibers

Strong, rapid, sharp, localized, acute pain (initial reflex response to acute pain)
Moderately rapid signal conduction: 5-30 meters/sec.
Neospinothalamic pathway

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10
Q

C NT? and characteristics?

A

Neurotransmitter :glutamate & substance P
Unmyelinated
Slow, burning, diffuse, dull pain
Slow conduction: 0.5-2 meters/sec.
Paleospinothalamic pathway
Polymodal: responding to thermal, chemical and chemical stimuli

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11
Q

Aβ Fibers NT & characteristics?

A

NT: GABA
Highly myelinated –> rapid signal transduction

Touch, vibration, pressure, non-noxious stimuli, position in space
Activated with inflammation
Allodynia and central/peripheral sensitization
Rapid signal conduction: 50-120 meters/sec.

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12
Q

Describe modulation.

A

Synapse in the dorsal horn of the spinal cord of A-delta and C fibers with secondary afferent neurons
Complex interactions occur
determine activity of the secondary afferent neurons

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13
Q

Modulation of pain will cause what via the release of NT?

A

The modulation implies the amplification or inhibition of the transmission of noxious signals via the release of many neurotransmitters.

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14
Q

Excitatory NT

A

Glutamate and substance P

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15
Q

Modulating NT

A

NE, opioids, and serotonin

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16
Q

Inhibitory NT

A

GABA and glycine

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17
Q

Describe perception

A

This is where the nociception is perceived as pain as the cortical interpretation of the
noxious stimulus happens in the cerebral cortex

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18
Q

T/F Pain cannot be perceived by animals
while they are unconscious.

A

True

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19
Q

Whats important about nociception and GA?

A

it is important to understand that the nociceptive
mechanisms that lead to its perception are still active unless they are specifically blocked at
least at one of the steps previously mentioned. Noxious stimuli during anesthesia can
dramatically increase the pain perceived when an animal regains consciousness

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20
Q

The cerebral cortex is also a

A

central analgesia system

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21
Q

The release of what during perception helps to decrease or abolish pain?

A

enkephalins, endorphins,
serotonin

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22
Q

What is nociceptive pain?

A
  • occurs when peripheral neural receptors are activated by noxious stimuli (trauma, surgical incision, infection, heat, or cold).
    -Physiological/adaptive/biological purpose: Alters animal’s behavior: Protection
  • Abrupt, temporary, predictable:
    Intensity/duration depends on insult’s severity
  • Associated to little or no tissue damage and does not always necessitate treatment
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23
Q

Nociceptive pain stops when?

A

External stimulus is removed Inflammation has resolved Healing is achieved

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24
Q

What is inflammatory pain?

A
  • results gradually from activation of the immune system in response to injury/infection.
  • Chemical changes in tissues around the nociceptors facilitate
    (lower threshold), or directly cause, nociceptor activation (adjacent nociceptors exposed to the same chemical changes)
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25
Q

Describe acute inflammatory pain.

A

Rapid onset, severity of injury dictate intensity/length of painful process
Generally reversible if proper healing occurs

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26
Q

Examples of acute inflammatory pain?

A

Postoperative pain (surgical wound/surrounding tissues until healed)

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27
Q

Describe chronic inflammatory pain

A
  • Beyond expected duration of disease process/injury healing (severe/non-healing/non-treated condition)
  • Has no biological purpose, no clear end-point
  • Potentially resistance to conventional analgesic therapy
  • Affects physical/emotional wellbeing & can lead to/be maladaptive
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28
Q

Example of chronic inflammatory pain?

A

Arthritis, chronic otitis, gingivitis, chronic pancreatitis, long-term dermatologic conditions, etc.

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29
Q

Neuropathic pain is due to:

A

is initiated or caused by an important primary lesion or
dysfunction within the nervous system (peripheral (nerve root injury, plexus avulsion) or
central), and accompanied by persistent painful stimuli

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30
Q

Describe how chronic pain can lead to neuropathic pain.

A
  • if after the initial injury or disease, there is continual nociceptive activation
    and eventually changes in the functioning nervous system, leading to the development of a
    neuropathic component.
  • Ex: Repetitive chewing, biting, licking, scratching, spontaneous crying, adverse reaction to touch, no visible pathology
  • Ex: Diabetic neuropathy, nerve transection (post amputation pain), nerve root tumor, brachial plexus avulsion, spinal cord injury, meningitis, polyneuropathy
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31
Q

Neuropathic pain and underlying conditions must be..?

A

treated

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32
Q

What is dysfunctional (functional) pain?

A
  • develops when the tissue damages produce a severe
    inflammation and highly activates the nociceptors, inducing an excitement of the neurons.
  • Present beyond expected time of inflammation/healing
  • Radiates beyond original injury boundaries
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33
Q

Why is dysfunctional pain hard to treat?

A

Does not respond well to NSAID/opioids

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34
Q

What causes amplification of dysfuctional pain?

A

Changes at molecular/cellular level amplify pain
Increased sensibility of pain pathway

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35
Q

Dysfunctional pain is characterized by:

A

central hyperalgesia and allodynia

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36
Q

What is causes peripheral sensitization?

A

Tissue damage
- Inflammatory mediators
- Stimulate nociceptors

Inflammation
- Reduce the activation threshold of nociceptors
- Primary hyperalgesia
a. Secondary hyperalgesia
b. Allodynia

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37
Q

Increased sensitivity around a lesion site will lead to:

A

hyperalgesia and allodynia

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38
Q

What causes central sensitization?

A

AKA dorsal horn windup

Pre-synaptically
- Increased transmitter release

Post-synaptically
- Increased response to transmitter

A-β fibers
- Modification/recruitment to transmit painful influx

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39
Q

Central Sensitization is due to:

A

Constant noxious input from periphery to spinal cord and it leads to increased pain facilitation/decreased pain inhbition

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40
Q

What is hyperalgesia?

A

exaggerated response to a noxious stimulus.

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41
Q

Examples of hyperalgesia?

A
  • The inflammation post-injury decreases the pain threshold.
  • An example of hyperalgesia is
    exaggerated pain in response to a slightly painful procedure such as a skin pinch.
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42
Q

What is primary hyperalgesia?

A

Pain felt following surgery in the area of the incision and in the surrounding swelling/bruising

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43
Q

What is secondary hyperalgesia?

A

Increased sensitivity to claw trimming in the hind limb of a dog with hip osteoarthritis

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44
Q

What is allodynia?

A

Pain caused by a non-painful stimulus (touch, vibration, pressure,
proprioception).

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45
Q

Allodynia is caused by the recruitment of?

A

the recruitment of Aβ nerve fibers
(touch, vibration, pressure)

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46
Q

Examples of allodynia?

A

pain in response to light touch, as demonstrated by the decreased tactile threshold observed in approximately 30% of cats with.

Severe sunburn

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47
Q

Why is pain assessment hard in Vetmed?

A

Non-verbal patients

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48
Q

Should you assess pain everytime? WHy?

A

Daily assessment of the level of pain in any patient
Including a pain score on every physical exam sheet/procedure

Pain must be assessed in every patient, because when recognized and successfully treated, it lowers the incidence of chronic refractory pain, accelerate the recovery, reduce the incidence of patient readmission, and improves the owner satisfaction.

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49
Q

T/f Pain is a vital sign like temperature, heart rate, respiratory rate and blood pressure

A

True!!

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50
Q

How do you objectively measure pain?

A
  • Quantify pain
    a. Specific numbers obtained to compare pain presence/level
    b. Decrease impact of evaluator’s emotion/experience/knowledge
  • Physiological indicators
  • Biochemical markers
  • Measurement of the animal’s activity
  • Nociceptive thresholds determination
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51
Q

What are some physiologic indicators of pain?

A
  • heart rate, respiratory rate and arterial blood
    pressure.
  • BUT these are non-specific to pain:
    a. Stress, anxiety, fear, comorbidity, hypotension (i.e. reflex tachycardia), hypovolemia, drugs given
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52
Q

Physiologic indicators of pain are complementary of other methods like?

A

Follow trend on the patient
Identify an acute painful stimulus
Evaluate the response to analgesic treatment

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53
Q

What are some biologic markers of pain?

A

Epinephrine, norepinephrine, endorphins, cortisol
In relation with Pain scoring system/markers
Expensive assays, invasive methods, no rapid results
Application are actually restrained to research use

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54
Q

Biologic markers of pain cannot differentiate between what?

A

Cannot differentiate pain from stress:
- In relation with Pain scoring system/markers
- Expensive assays, invasive methods, no rapid results
- Application are actually restrained to research use

55
Q

What is the pain pressure threshold (Algometry)?

A

are highly variable between animals (remember pain is individual) but they are usually consistent within the same individual.

  • Algometry have the advantage of providing a number (quantitative, objective) and being applicable to many location on the body but the animal can develop a tolerance to the applied pressure each time it is used and therefore result in a falsely increased threshold overtime
56
Q

Pain pressure thresholds are used in what animals and what kind of stimuli can they test?

A

Horses, rodents, cats, dogs, cows, pigs, etc.
Hand-held devices: clinical use
Mechanical
Thermal

57
Q

What are activity monitors?

A
  • Collar w/AM: accelerometer chips record daily activity (Heyrex® collar technology)
    a. Effective outcome measure of ortho pain
  • Studies in healthy dogs & dogs suffering from OA
    a. Normal ranges: distance travelled/study period
  • Recent studies suggest AM can be an effective outcome measure in cats with osteoarthritis as well
58
Q

What is the subjective measure of pain? Is this more reliable?

A
  • Can be affected by interindividual variability from evaluator’s side if the method is not specific, sensitive and reliable/repeatable from one individual to another
  • Most relevant methods use specific pain behavior
    a. Facial expression (seem to be the most reliable and practical tools for pain assessment)
59
Q

Pain related behavior is variable due to what specific factors?

A
  • Vary among species, breeds, sex, age
  • Depend on type of injury/type of pain
  • Social animals (dogs): show pain clearly, seek human attention
  • Predators : less shy to show their pain
  • Prey-type (ruminants/rodents): hide pain, difficult for the veterinarian, caretaker, owner to identify pain
  • Social organization
60
Q

What subjective assessment is the key in pain assessment in animals?

A
  • Behavior assessment
  • What’s patient’s normal behavior? Maintaining normal/usual behavior? Developed new/unusual behavior?
61
Q

Behavior assessment is first:

A

observational

62
Q

What are you assessing in observational behavior assessments?

A

Appearance, Appetite
Blepharospasm with ocular pain
Change in posture and positioning: pray position in dogs (pancreatitis), cats, horses (pelvic flexure impaction)
Activity, attitude, restlessness, sleepiness, comfort, lameness
Abnormal biting/licking, kicking abdomen: (horse/cow)
Disappearance of the normal behaviors

63
Q

2nd part of behavior assessment is:

A

Interactive (contact with patient)

64
Q

What are you assessing in interactive behavior assessments?

A

Responds to petting
Seeks attention
Has no reaction, ignores the evaluator/becomes aggressive
Avoids evaluator, tries to hide
Displays vocalization

Reacts/not to manipulation of the painful zone

65
Q

Signs of pain in dogs

A

Whimpering/Howling/Growling
Decreased social interaction/playful behavior
Anxious expression, Submissive behavior
Guarding behavior, refusal to be touched/pet
Aggression, biting
Refusal to move/take stairs/jump
Decreased appetite, weight loss, sleeplessness
Self-mutilation (chewing), nails worn off
Changes in posture/weight bearing, stiffness
Change in urinary/defecating habits

66
Q

Signs of pain in cats

A

Reduced activity, quietness, loss of curiosity
Loss of appetite, weight loss
Changes in urinary/defecation habits
Hiding, guarding behavior
Hissing or spitting
Lack of agility/jumping, stiff posture/gait
Excessive licking/grooming
Stops grooming/matted fur
Tail flicking

67
Q

Signs of pain in horses

A

Immobility (in corner of its box stall)
Decreased interaction
Aggressive behavior
Decreased resting/eating time & exploring behavior
Non-weight bearing, lameness, weight shifting
Bruxism, muscle tremors, ears and head low, mydriasis, dilated nares, stiff jaw

68
Q

Signs of pain in ruminants

A

Lameness
Weight loss, decreased milk production
Vocalization, agitation, isolation (goat, sheep)
Bruxism (abdominal pain), decreased rumination
Kicking, abduction of pelvic limbs (inflammatory mastitis)
Avoiding reactions, rapid ear movement (post dehorning), flehming (sheep)
Arched, hunched back, reluctance to move, growling (reticulo-peritonitis)
Position changes (standing/decubitus), restlessness (castration sheep)

69
Q

What are some behavioral changes that you must consider with chronic pain?

A

More insidiously and gradual manifestation
Good knowledge of signs/symptoms of pain
Be ahead in detecting and treating pain
Consulting/involving the owner

70
Q

What are pain scales?

A
  • Most animal species
  • Include specific species behavior
    a. modified, absent or present painful state
  • Help integrate pain evaluation in physical exam
  • Can train students/staff
  • Evaluate efficacy of an analgesic treatment
  • In research, allows comparison of treatments
71
Q

The ideal pain scale is

A
  • multidimensional
  • Easy to use (utility)
  • Specific
  • Sensitive
  • Repeatable (reliability)
72
Q

What are the unidimensional pain scales used in Vetmed?

A

VAS: Visual Analog Scale
DIVAS: Dynamic and interactive VAS
NRS: Numerical Rating Scale
SDS: Simple Descriptive Scale

73
Q

What is VAS?

A

Straight line, 2 extremities: “no pain” & “worst pain possible”
In human medicine: easy, sensitive (continuous), effective
In animals, evaluation requires external observer (proxy assessment)

74
Q

VAS in animals is

A
  • poorly repeatable inter-observer
  • Requires knowledge of pain
  • but is easy to use for monitoring trends (i.e. whether pain is getting worse or improving) and is widely accepted as a sensitive instrument for behavioral pain assessment.
75
Q

What is DIVAS?

A

Adds interactive component to VAS
- Palpation of the painful zone or the
- Use of an algometry device (nociceptive threshold)

76
Q

DIVAS observations are performed in 2 phases:

A

; first from a distance (no interaction), secondly, after interaction with
the patient.

77
Q

What is NRS?

A

Semi-subjective scale
In human: more sensitive then SDS, more repetitive then VAS

Numerical rating scale is an ordinal scale where
there are numbers from 0-10 or 0 -100

78
Q

What is SDS?

A
  • Semi-subjective
  • Categories: no pain, mild pain, moderate, etc.
  • Simple to use but the least sensitive of the pain scale
  • Limited choices, does not allow detection of subtle changes
  • Lack specificity if descriptors not specific to pain
  • least sensitive of the pain scale
    because since the choices are limited to the one proposed in the scale, it does not allow for
    detection of subtle changes and can lack specificity if descriptors are not adequately linked
    to pain manifestations but more to stress.
79
Q

What pain scale is used to evaluate equine lameness?

A

SDS
Scale inspired of this model in vet medicine are the lameness score where a non-weight bearing lameness would be a 5/5.

80
Q

What is the multidimensional pain scale?

A
  • Multiple parameters: physiologic, behavioral, interactive
  • Each parameter has its own SDS
  • Allows observer assigns number based on description
  • Total Pain Score (TPS): identification, severity of pain
  • Helps to determine need for rescue analgesia
81
Q

Pain scales in dogs:

A

Glasgow pain scale (short version) - orthopedic
Colorado State University (CSU) acute pain scale - DOGS

82
Q

The Glasgow pain scale is:

A

GLASGOW PAIN SCALE
SHORT FORM
Preference***
Scientifically validated
Simple to use

83
Q

The CSU pain scale is

A

Partially-validated
Clinical use
Simple to use

84
Q

The pain scales used in cats are:

A
  • Glasgow Feline Composite pain scale (CMPS-FELINE)
  • UNESP/BOTUCATU- feline pain scale
  • Colorado State University (CSU) acute pain scale – CATS
  • Feline Grimace pain scale
85
Q

The Glasgow CMPS in felines is:

A

VALIDATED
RELIABLE
REPRODUCTIBLE
SIMPLE

86
Q

The Sao Paulo Uni UNESP/BOTUCATU in felines is:

A

Scientifically validated
Validated translation
Preference
More complicated to use

87
Q

The CSU pain scale in felines is:

A

Non-validated
Used in clinic
Simple to use

88
Q

Why is facial expression used to evaluate pain?

A
  • Indicators of emotion in both human & animals
  • In pain, we demonstrates unconsciously Micro Facial Expressions
    a. Impossible to hide (unlike behavior)
  • Help identify pain in non verbal individuals/animals
    a. In children, facial expression is most consistent expression of pain
    b. Particularly useful in animal prey species
89
Q

What is the Grimace Scale?

A
  • Observation of presence/prominence of “Facial Action Units” (FAU)
    a. Orbital Tightening, Nose Bulge, Ear Position and Whisker Change, etc.
    b. Directly in real-time (clinical use)
    c. Post hoc from photographs or videos (research)
  • Facial expression = Pain face
90
Q

Grimace scale is used most often in what species?

A

Cats but also mice, horses, sheep, rabbits, rats

91
Q

WHat is an example schedule of Post-SX pain assessment?

A

Pre-op to 8 hrs afters then again 12 hr, 16 hr, 24 hr, 32 gr, 40 h, 48 h, 60 h, 72 h, 96 h

92
Q

What are some negative consequences of pain?

A
  • Pain is a disease, an illness

Pain left untreated can lead to:
- Decreased appetite
- Weight loss
- Lack of hydration
- Impaired intestinal and renal function
- Delayed wound healing
- High risk of infection, bad hygiene
- Disturbed sleep, aggressive/irritable behavior

93
Q

What are the advantages of treating pain?

A
  • Earlier return to eating avoiding weight loss
  • Less catabolism
  • More rapid recuperation
  • Better healing
  • Better intestinal and renal function
  • Acceptance of treatment and manipulation
94
Q

How do you provide pain management as an individual TX?

A
  • Analgesia is an individual prescription
  • Come up with analgesic protocol
95
Q

Describe factors to consider in an analgesic protocol.

A
  • Intensity of the anticipated pain
  • Age of the patient
  • Concomitant diseases (diabetes, cardiac valvular insufficiency, renal failure, etc.)
  • Breed and/or genetic predispositions, etc.
  • Availability of molecules/modality and cost associated
96
Q

What is the PLANNED/STRUCTURE approach to pain management?

A
  • Anticipate analgesic needs: preventive/early analgesia
  • Develop and individual pain assessment/treatment plan
  • Treat based on type, severity, duration of expected pain
  • Evaluate pain & treatment efficacy: scale/questionnaire
  • Continuous assessment vs one-time evaluation
    a. Maintain, modify or discontinue treatment
    b. Cycles: PLAN-TREAT-EVALUATE the patient
97
Q

What does the PLAN-ANTICIPATE-TX approach mean?

A

plan for pain, If pain is anticipated then administer analgesia

98
Q

After you TX you must..

A

Evaluate
- See if pain is controlled

99
Q

**

Pain is back (ie not controlled) so you should:

A

Administer analgesia
- Part of the RETURN-EVALUATE approach

100
Q

What is preventive analgesia?

A

Analgesics administration before the painful stimulus occurs

101
Q

Preemptive analgesia in a surgical context allows for:

A

allows to decrease/cut the intensity of the pain pre-, intra- and postoperatively

102
Q

T/F pain associated with SX is not predictable

A

False! its 100% predictable

103
Q

Trauma or surgery pain can be managed by:

A
  • Surgery: Prevent pain: protocol including analgesia before pain occurs
    a. Perioperative pain extends beyond 24 hours
  • Trauma : Treat pain as early as possible
104
Q

What are the traditional molecules used for analgesia?

A
  • Local anesthetics and loco-regional analgesia
  • Opioids
  • NSAIDs
  • Dexmedetomidine and other alpha-2 agonists
  • Ketamine, Amantadine
  • Tramadol
  • Gabapentin
  • Maropitant
105
Q

How do local anesthetics and loco-regional anesthesia help manage pain?

A

Complete analgesia and total blocking of the transmission of the noxious stimulus
Pre, per post-op analgesia

106
Q

What are some local anesthetics and loco-regional anesthesia drugs?

A
  • Lidocaine, bupivacaine and prilocaine (EMLA cream), liposomal bupivacaine
  • Combined to other analgesic molecules like alpha-2 agonists and opioids to increase analgesic potency and length of action
107
Q

Opioids are used to treat?

A
  • Very efficient molecules to treat acute pain
    a. Part of premedication for painful procedure generally
  • Also have a small role to play in treating chronic pain
108
Q

The use of opioids for analgesia is most important through activation of what receptors?

A

MU opioid receptors

109
Q

Why are opioids good for pain management? and when do you use them?

A

Reversible
Period
Pre-op, Per-op, Post-op
Intensive and continuous care

110
Q

What are NSAIDs in terms of there use in pain management?

A
  • popular to control inflammatory pain in animals
  • Block COX –> fewer prostaglandins produced –> pain, inflammation, and fever reduced

They are not reversible and their therapeutic index is low

111
Q

What are some advantages of NSAIDs over opioids?

A
  • Longer length of action
  • Anti-inflammatory & Antipyretic
  • No modification/depression of behavior, cardiorespiratory function
  • No a controlled molecules (regulation)
112
Q

Grapiprant (Piprant) is used for only what spp? and whats it used for?

A
  • Dogs
  • Blocks PGE2 which is a Primary mediator of osteoarthritic pain and inflammation
113
Q

What are some things to consider for long term use of NSAIDs?

A
  • Requires a very frequent follow up of the patient
  • Biochemistry and urinalysis at beginning of the treatment
    a. Every 6 months in low-risk patients
    b. Every 2-4 months in high-risks patients
  • Pauses of 5 to 10 days without NSAIDs administration can decrease risks when switching from one NSAID to another
114
Q

How is Dexmedetomidine and other alpha-2 agonists used to main pain?

A
  • Potent analgesics acting on alpha-2 receptors
    a. Periphery of the body: nociception (transduction)
    b. Dorsal horn of the spinal cord (modulation)
  • Combination with other agents like opioids
  • Bolus and CRI during the surgery (important MAC reduction) and post-op period (multimodal analgesia and sedatives)

Good at visceral organs

115
Q

What is Anti-NGF monoclonal antibody TX?

A

Nerve growth factor (NGF) is an important driver of pain in osteoarthritis (OA)

116
Q

Whats an anti-NGF in cats?

A

Felinized anti-NGF mAb: Frunevetmab (Solensia)
Recently approved for use in cats in the USA

117
Q

Whats an anti-NGF in dogs?

A

Fully canine anti-NGF mAb (Bedinvetmab)
Recently approved for use in dogs in USA

118
Q

What are ketamine and amantadine used for in pain management?

A
  • NMDA-receptor antagonist
    a. Reduces central sensitization/anti-hyperalgesia (modulation)
    b. Immunomodulatory effects, directly suppress proinflammatory cytokine production
  • Prevent/treat central sensitization, hyperalgesia, allodynia, present in inflammatory & neuropathic pain
  • Ketamine: CRI: part of multimodal analgesia
  • Amantadine: Dosages of 3-5 mg/kg PO SID (less hallucinogen)
119
Q

When do you use Lidocaine IV?

A

Abdominal & neuropathic pain
Analgesia & MAC reduction: inhibition nociceptive processing (modulation)
Used as CRI alone or combined (MLK), pre, per, post-op

120
Q

Who can you give Lidocaine IV to?

A

Safe at recommended dosage on many species (dogs, horses, cows, ruminants, pigs)
In cats, not recommended as benefits (mild/no increase in nociceptive threshold) do not outweigh risks (hypotension)

121
Q

How is Gabapentin used in pain management?

A
  • May modulate pain by altering calcium channels and suppressing glutamate and substance P release in the dorsal horn of the spinal cord
  • Potential analgesia for chronic neuropathic pain
  • No supporting data currently for analgesia in acute/chronic inflammatory pain
  • Main side effect: sedation: stress reducer in cats (adjunct)
    a. 10-30 mg/kg PO: transport/stressful event/vet clinic/echography
122
Q

Tramadol in pain management?

A
  • Only oral form available in the USA
    a. Bioavailability of tramadol : 65% in dogs, 93% in cats
  • Analgesia via serotoninergic, noradrenergic &, if metabolized, via opioid pathway (weak opioid)
    a. Dogs, goats, horses, camels: no-opioid as active metabolite, O-Desmethyltramadol (M1), is marginally produced
    b. Cats: metabolized in M1: efficient, but very bitter taste, causes hypersalivation and vomiting
  • Still under study
123
Q

How is Maropitant (Cerenia) used to manage pain?

A
  • Antiemetic with central and peripheral effect
  • Potent selective antagonist of neurokinin-1 receptors (NK1) where it blocks binding of substance P
    a. Analgesia?: No
  • Include in protocol if using MU agonists opioids, general anesthesia, alpha-2 agonists or if patient has other conditions that apply to use of antiemetic
  • Improves the patient’s comfort
  • Injection can be painful (dilute or cool)
124
Q

What are some non-pharmacologic things used to manage pain?

A

Cold Therapy, Acupuncture, Physiotherapy
Complement to analgesia
Multimodal approach

125
Q

Example of cold therapy

A
  • Topical: ice/frozen substrate (paper cups, buckets and bags) or cold compression devices/circulation sleeves
126
Q

How does cold therapy work for pain management?

A

Decreases the temperature of underlying tissues (2-4 cm)
- Decreased activation of tissue nociceptors, slower conduction velocity along peripheral axons (cold-induced neuropraxia)
- Specific peripheral cold-sensitive ion channels: decreases nociceptive signalling & activates inhibitory interneurons
- Decreases oedema: sympathetically mediated vasoconstriction
- Reduces muscle spasm (major cause of discomfort)

127
Q

Other factors of cold therapy protocol?

A
  • Any surgical incision: part of the analgesic protocol
  • 15 to 20 minutes every 6 to 8 hours: immediately after surgery, for several days after
  • Continued after discharge by caregivers
  • Also valuable in chronic pain with an inflammatory component or muscle spasm
  • Dose-related, time-related and disease-related effects that vary on a patient basis
128
Q

How does accupuncture manage pain?

A

Analgesic:
- Release of endogenous opioids
- Blocks/controls ascending pain pathway

Non-invasive, very little risk, even comfortable!

Reduces nausea, analgesia for inflammatory, neuropathic, surgical pain, DJD pain

129
Q

Multimodal analgesia is

A

Combination of analgesics acting at different sites in the pain pathway, but in synergy
Improves the analgesic potency of protocol
Minimize side effects of each molecule

130
Q

What can we do to prevent/limit nociception?

A

o NSAID- metacam
o Opioids - hydromorphine
o Corticosteroids- pred
o Local anesthetic- lido or bupiv
o Alpha-2 agonists- dex

131
Q

What can we do to inhibit impulse aka transmission?

A

o Opioids - hydromorphine
o Local anesthetic- lido or bupiv
o Alpha-2 agonists- dex

132
Q

What can we do to prevent central sensitization?

A

o Opioids - hydromorphine
o Local anesthetic- lido or bupiv
o Alpha-2 agonists- dex
o NMDA-antagonists- ketamine
o Touch (acupressure, massage): Stimulation of Aβ fibers causes inhibition of the
transmission of Aδ and C fibers by inhibitory interneurons
o Tricyclic antidepressants (serotonin, norepinephrine)
o NSAIDs (C and Aδ fibers)

133
Q

What can we do to prevent/limit conscious perception?

A

o Alpha-2 agonist
o Opioids
o Benzodiazepines
o Volatiles anesthetics
o Phenothiazine
o Tender loving care (TLC)

134
Q

To treat surgical plan there must be 3 ? to ask when planning analgesia?

A

Is there a loco-regional block that can be done?
What is the best opioid in this case?
Are there any contraindication to NSAIDS administration?

IF POSSIBLE, INCLUDE ALL 3 IN THE ANALGESIA PROTOCOL

Anesthesia (7 decks)

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