TOPICAL REVIEW

Analgesia for Anesthetized Patients

Kip A. Lemke, DVM, MSc, Dipl. ACVA, and Catherine M. Creighton, DVM
Many perioperative pain management protocols for cats and dogs are overly complex, some are ineffective, and
still others expose patients to unnecessary risk. The purpose of this article is to provide clinicians with a basic
understanding of the pathophysiology of perioperative pain and a working knowledge of the principles of
effective therapy. First, the concept of multimodal analgesic therapy is discussed. Next, the pathophysiology of
perioperative pain and the clinical pharmacology of the major classes of analgesic drugs are reviewed. And last,
a simplified approach to managing perioperative pain in cats and dogs is presented.
2010 Elsevier Inc. All rights reserved.
Keywords: analgesia, anesthesia, pain, dogs, cats

ultimodal analgesic therapy has gained widespread

acceptance in the management of perioperative pain
in both dogs and cats.1-3 In recent years, a clearer understanding of the pathophysiology of perioperative pain has provided the conceptual framework for a more rational use of
analgesic drugs and techniques. Surgical trauma and inflammation produce sensitization of the peripheral nervous system, and the subsequent barrage of nociceptive input produces sensitization of neurons in the dorsal horn of the spinal
cord. Blockade or attenuation of ascending nociceptive pathways or activation of descending antinociceptive pathways
by different classes of analgesic drugs usually provides better
analgesia with fewer side effects than unimodal therapy with
a single class of analgesic drugs. Because peripheral and central neural blockade with local anesthetics are the only analgesic techniques that can produce complete blockade of peripheral nociceptive input, these techniques are the most
effective way to attenuate sensitization of the central nervous
system and the development of pathological pain.4,5 Clinicians should also remember that atraumatic surgical technique is always the most effective method to prevent peripheral and central sensitization and the development of pain
postoperatively.
The neuroendocrine or stress response to surgical trauma
compromises hemostatic, metabolic, and immunological
function, which increases perioperative morbidity and mortality.6,7 Early studies in human infants undergoing cardiac
surgery demonstrated that the neuroendocrine response was
significantly reduced by intraoperative administration of
halothane and fentanyl when compared with administration
of halothane alone.8 In a subsequent clinical study, the morFrom the Atlantic Veterinary College, University of Prince Edward Island,
Charlottetown, Prince Edward Island, Canada.
Address reprint requests to: Kip A. Lemke, DVM, MSc, Dipl. ACVA, Atlantic Veterinary College, University of Prince Edward Island, 550 University Ave, Charlottetown, PE, Canada, C1A 4P3. E-mail: klemke@upei.ca.
2010 Elsevier Inc. All rights reserved.
1527-3369/06/0604-0171\.00/0
doi:10.1053/j.tcam.2009.12.003

70

tality rate dropped from 25% to 0% in a similar group of

infants when sufentanil was given intraoperatively and additional opioids were given postoperatively.9 Perioperative use
of neural blockade, in particular central neural blockade,
also attenuates the neuroendocrine response and dramatically reduces mortality and the incidence of major complications in human patients undergoing a wide variety of surgical
procedures.10 In this analysis of 141 clinical trials, patients
with central neural blockade had a 30% reduction in mortality and a 40% to 60% reduction in major complications
(thromboembolism, hemorrhage, respiratory depression,
pneumonia) when compared with those without central neural blockade. Intraoperative use of multimodal analgesic
therapy also reduces inhalation anesthetic requirements and
autonomic responses to noxious surgical stimuli. These reductions improve cardiopulmonary function intraoperatively and facilitate a rapid, smooth recovery from anesthesia
postoperatively.
Alpha-2 agonists, opioids, N-methyl-D-aspartate (NMDA) antagonists, cyclooxygenase (COX) inhibitors, and neural
blockade with local anesthetics are often used perioperatively
as part of a multimodal strategy to manage pain.1-3 These
classes of analgesic drugs can be incorporated easily into
anesthetic and pain management plans for cats and dogs
undergoing most types of surgical procedures. Alpha-2 agonists can be used preoperatively and postoperatively to provide sedation and analgesia. Opioids can be used throughout
the perioperative period to reduce anesthetic requirements
and to manage pain. NMDA antagonists (ketamine) can be
used throughout the perioperative period to manage pain in
patients with significant central sensitization and pathological pain. COX inhibitors can be used postoperatively to reduce opioid requirements and provide more effective analgesia with fewer side effects. Peripheral and central neural
blockade with local anesthetics can be used intraoperatively
to reduce anesthetic requirements and attenuate the development of central sensitization. Neural blockade can also be
used postoperatively to manage pain in selected patients. A
clear understanding of the pathophysiology of pain and the

Volume 25, Number 2, May 2010

71

clinical pharmacology of the major classes of analgesic drugs

is required to use multimodal analgesic therapy safely and
effectively in anesthetized patients.

Pathophysiology
The terminology used to describe the pathophysiology of
pain is confusing, so defining a few terms relevant to the
management of perioperative pain is important. Nociception
is defined as the neural response to a noxious stimulus. Specifically, nociception includes signal transduction and nerve
conduction in the peripheral nervous system, and synaptic
transmission, projection, and modulation of nociceptive input in the central nervous system (Fig 1). Pain, on the other
hand, is a complex sensation that requires integration of
nociceptive and other sensory input at the cortical level. Pain
is defined as an unpleasant sensory or emotional experience
that is associated with actual or potential tissue damage. Pain
can be further classified anatomically as somatic or visceral
pain, or temporally as acute or chronic pain. Recent neuroanatomical and functional imaging studies suggest that pain
is one component of an interoceptive system that is primarily
responsible for maintaining internal homeostasis, and that
there are significant differences among species in the neural
components that make up this system.11
Most perioperative pain is due to surgical trauma and inflammation. Some patients may have preexisting tissue
trauma and inflammation, and others may have pain associated with nerve injury. Although a small number of surgical
patients may experience both inflammatory and neuropathic
pain, inflammatory pain is by far the most common type of
perioperative pain. The mechanisms of inflammatory pain
are reasonably well understood and form the basis for rational, effective, multimodal analgesic therapy. Neuropathic
pain is relatively uncommon in surgical patients, and the
mechanisms of neuropathic pain are similar to those of inflammatory pain.12,13 Consequently, clinicians should focus
on understanding the pathophysiology and management of
inflammatory pain.

Nociceptive Pathways
Ascending nociceptive pathways begin in the peripheral
tissues and project to the dorsal horn of the spinal cord, brain
stem, thalamus, and cerebral cortex (Fig 1). The nociceptive
pathways are composed of 3 general types of neurons. The
first-order neurons are primary afferent neurons, and these
neurons are responsible for transduction of noxious stimuli
and conduction of electrical signals to the dorsal horn of the
spinal cord. The second-order neurons are projection neurons, and these neurons receive input from the primary afferent neurons and project to the medulla, pons, midbrain, thalamus, and hypothalamus. Third-order supraspinal neurons
integrate input from spinal neurons and project to subcortical and cortical areas where pain is finally perceived. Supraspinal processing of afferent nociceptive input is also

Figure 1. Overview of nociceptive and antinociceptive pathways. Surgical trauma activates mechanical, chemical, and
thermal nociceptors. Action potentials are conducted to the
dorsal horn of the spinal cord by primary afferent nerve
fibers. Second-order projection neurons encode and relay signals to the brainstem and thalamus. Third-order neurons in
the thalamus project to the limbic system and somatosensory
cortex where pain is perceived. Descending antinociceptive
pathways modulate nociceptive processing at the level of the
thalamus, brainstem, and spinal cord. Different classes of
analgesic drugs act at different sites in the nociceptive and
antinociceptive pathways. Multimodal analgesic therapy inhibits processing of nociceptive input at 2 or more sites. PAG,
periaqueductal gray; RVM, rostroventral medulla.

72
closely integrated with regulation of the autonomic nervous
system.
Primary afferent neurons are bipolar neurons. The cell
bodies of these bipolar neurons are located in the trigeminal
and dorsal root ganglia, and their axons project peripherally
to somatic and visceral tissues and centrally to the dorsal
horn of the spinal cord. Some primary afferent neurons respond to noxious or high-threshold stimuli, and others respond to non-noxious or low-threshold stimuli (touch). Afferent nociceptive neurons have free nerve endings that
change or transduce noxious mechanical, thermal, or
chemical stimuli into electrical signals. Somatic tissues have a
higher density of nociceptive nerve fibers and smaller receptive fields, whereas visceral tissues have a lower density of
nociceptive nerve fibers and larger receptive fields. These anatomical differences may account for some of the qualitative
differences between somatic (discrete) and visceral (diffuse)
pain.
Primary afferent neurons are classified by axon diameter,
the presence or absence of myelination, and their response to
mechanical, thermal, and chemical stimuli. A afferent neurons have large, myelinated axons that conduct impulses at a
velocity of greater than 30 m/sec. The free nerve endings of
these fibers respond to non-noxious mechanical stimuli
(touch) but do not respond to noxious stimuli directly. A
nociceptive neurons have small, myelinated axons that conduct impulses at a velocity of 3 to 30 m/sec. The free nerve
endings of these fibers contain membrane-bound receptors
that respond primarily to intense mechanical and thermal
stimuli and are called mechanothermal nociceptors. C nociceptive neurons have small, unmyelinated axons that conduct nerve impulses at a velocity of less than 3 m/sec. The free
nerve endings of these fibers contain membrane-bound receptors that respond to chemical as well as thermal and mechanical stimuli and are called polymodal nociceptors. Small, myelinated A fibers carry the nociceptive input responsible for
the fast, sharp pain that occurs immediately after injury. The
nociceptive input responsible for the prolonged dull pain that
occurs several seconds later is carried by small, unmyelinated
C fibers. Silent nociceptive neurons are also present in somatic tissues. The free nerve endings of these neurons only
respond to mechanical and thermal stimuli after they are
activated by chemical (inflammatory) mediators. This classification scheme is derived from analysis of fibers that innervate the somatic tissues (skin). Visceral pain is qualitatively
different from somatic pain and is typically dull and poorly
localized. Visceral pain also lacks the fast and slow components that are characteristic of somatic pain.
Transduction of mechanical, thermal, and chemical stimuli by the free nerve endings of A and C nociceptive fibers is
mediated by membrane-bound receptors.13-15 Most of these
receptors are nonselective cation channels that are gated
by temperature, chemical ligands, or mechanical shearing
forces. Activation of these channels increases inward conduction of Na and Ca2 ions, which ultimately depolarizes the
membrane and generates a burst of action potentials. The
mechanisms of mechanical signal transduction are not well

Topics in Companion Animal Medicine

defined. Noxious mechanical stimuli may activate a mechanically gated ion channel directly, or shearing forces may release adenosine triphosphate, which acts on purine receptors
(P2X). Noxious chemical stimuli (H) activate acid-sensing
ion channels and transient receptor potential vanilloid
(TRPV1) channels. Noxious heat also activates TRPV1 channels as well as related channels (TRPV2), and noxious cold
activates transient receptor potential menthol (TRPM8)
channels.
Nociceptive afferent neurons synapse with second-order
neurons in the dorsal horn of the spinal cord. Projection
neurons and interneurons are the 2 major types of nociceptive neurons in the dorsal horn, and these neurons are organized in layers or laminae. Neurons that mediate nociception
are located in laminae I, II, and V. Projection neurons are
located in laminae I and V, and they have axons that cross
midline and project to third-order supraspinal neurons. Projection neurons located in lamina I receive input directly from
A and C nociceptive fibers and are classified as nociceptivespecific and polymodal nociceptive neurons, respectively.
Projection neurons in lamina V receive input from both nociceptive and non-nociceptive (A) fibers and are classified as
wide, dynamic-range neurons. Interneurons are located in
lamina II and also receive input from nociceptive and nonnociceptive (A) fibers. Inhibitory and excitatory interneurons play a central role in gating and modulating nociceptive
input. Propriospinal neurons that project across several dermatomes are also present in the dorsal horn and are responsible for segmental reflexes associated with nociception.
Glutamate is the primary excitatory neurotransmitter in
the dorsal horn of the spinal cord. Nociceptive as well as
non-nociceptive fibers co-release glutamate and neuropeptides (substance P, neurokinin A, calcitonin generelated
peptide). With normal afferent input, glutamate binds
to -amino-3-hydroxy-5-methyl-4-isoxazolepropionoic acid
(AMPA) receptors located on the postsynaptic membrane of
projection neurons. Neuropeptides bind to several types of
receptors on the postsynaptic membrane. With intensive afferent input, prolonged activation of AMPA and neuropeptide receptors leads to progressive depolarization of the
postsynaptic membrane and activation of additional types of
glutamate receptors. Activation of a specific type of glutamate receptor, the NMDA receptor, plays a key role in the
development of central sensitization.
The spinothalamic tract (STT) is the major ascending nociceptive pathway in carnivores and primates.11,16 Lamina
I, nociceptive (nociceptive-specific, polymodal nociceptive)
neurons are somatotopically organized, modality-selective
neurons with small receptive fields that convey discrete noxious mechanical, thermal, and chemical afferent input. These
neurons project to the ventromedial nucleus of the lateral
thalamus, which projects to the insular cortex and the secondary somatosensory cortex. These neurons also project to
the mediodorsal nucleus of the medial thalamus, which
projects to the anterior cingulate cortex. Like the dorsal
horn, glutamate is an important excitatory neurotransmitter
within the thalamic nuclei. Lamina V, wide, dynamic-range

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Volume 25, Number 2, May 2010

neurons have large receptive fields, are not somatotopically
organized or modality selective, and are responsible for integration of all afferent input to the dorsal horn. These neurons
project to the motor thalamus (ventrodorsal and ventrolateral nuclei), which projects to the basal ganglia and the primary somatosensory cortex. Axons from lamina I are concentrated in the lateral STT, and axons from lamina V are
concentrated in the ventral STT. The thalamus relays afferent
input from the STT and integrates this information with afferent input from the autonomic nervous system. Projection
from neurons in the lateral thalamus to neurons in the insular
and secondary somatosensory cortex appears to be responsible for the sensory-discriminative aspects of pain. Projection
from neurons in the medial thalamus to neurons in the anterior cingulate cortex appears to be responsible for the motivational-affective aspects of pain. Projection from neurons in
the motor thalamus to neurons in the primary somatosensory
cortex appears to be responsible for sensory and motor integration. Direct connections between the lateral thalamus and
the dorsal margin of the insular cortex (interoceptive cortex)
are more developed in primates than in carnivores.

Antinociceptive Pathways
Mammals also have descending antinociceptive pathways
that modulate nociceptive input at spinal and supraspinal
levels (Fig 1). The antinociceptive pathways begin at the supraspinal level and project to neurons in the dorsal horn of
the spinal cord. The periaqueductal gray matter (midbrain),
locus ceruleus (pons), and nucleus raphe magnus (medulla)
are all important structures in the modulation of nociceptive
input. The periaqueductal gray matter receives direct input
from the thalamus and the hypothalamus, and indirect input
from the insular cortex and the anterior cingulate cortex.
These neurons in the periaqueductal gray matter send projections to neurons in the nucleus raphe magnus, which project
to the dorsal horn of the spinal cord. Neurons in the locus
ceruleus project directly to the dorsal horn, and they may also
receive input from the periaqueductal gray matter.
Endogenous opioids (endorphins, enkephalins, dynorphins), serotonin, and norepinephrine are the primary neurotransmitters in the descending antinociceptive pathways.
Axons that originate in the nucleus raphe magnus release
serotonin in the dorsal horn of the spinal cord and are called
serotonergic neurons. Similarly, neurons that originate in
the locus ceruleus release norepinephrine in the dorsal horn
and are called noradrenergic neurons. Supraspinal release
of endogenous opioid peptides activates both types of neurons, whereas supraspinal release of release of -aminobutyric acid (GABA) inhibits both types of neurons. Supraspinal
inhibition of descending antinociceptive pathways is mediated by GABAA receptors. At the supraspinal level, endogenous opioids not only activate descending antinociceptive
pathways, but inhibit GABA-mediated inhibition of these
same pathways, which is called disinhibition.
Release of norepinephrine and serotonin in the dorsal horn
of the spinal cord, and subsequent release of enkephalins and

GABA by local interneurons, inhibit presynaptic calcium

channels that modulate neurotransmitter release. This inhibition, mediated by presynaptic noradrenergic (2), opioid
(), and GABAB receptors, limits release of glutamate and
neuropeptides from primary afferent neurons, which inhibits
nociceptive transmission. Release of norepinephrine, enkephalins, and GABA in the dorsal horn hyperpolarizes projection neurons, which also inhibits nociceptive transmission. This inhibition is mediated by postsynaptic
noradrenergic (2) and opioid () receptors that activate
potassium channels, which leads to an outward flux of
potassium ions and hyperpolarization of the postsynaptic
membrane. This inhibition is also mediated by postsynaptic GABAA receptors that activate chloride channels,
which leads to an inward flux of chloride ions and hyperpolarization of the postsynaptic membrane. In summary,
release of norepinephrine, endogenous opioids, and GABA
inhibits synaptic transmission between primary afferent
neurons and projection neurons by inhibiting neurotransmitter release and hyperpolarizing the postsynaptic membrane, which effectively shuts down the key synapse in the
dorsal horn.

Peripheral and Central Sensitization

Neural plasticity is defined as the ability of the nervous
system to modify its function in response to different environmental stimuli. Surgical trauma and inflammation produce sensitization of the peripheral nervous system, and the
subsequent barrage of nociceptive input produces sensitization of neurons in the dorsal horn of the spinal cord. Peripheral and central sensitization of nociceptive pathways plays a
central role in the development of pathological pain.17 Patients with no preexisting tissue trauma and inflammation
experience pain that is physiological or protective in nature
(Table 1). This type of inflammatory pain is well localized,
proportionate to the peripheral stimulus, and subsides once
the inflammatory process resolves. Patients with significant
tissue trauma and inflammation experience pain that is
pathological or debilitating in nature (Table 2). This type of
inflammatory pain is diffuse, disproportionate to the peripheral stimulus, and continues beyond resolution of the inflammatory process. A key concept that is often lost when trying
to understand the clinical relevance of neural plasticity is that
central sensitization occurs secondary to surgical trauma,
inflammation, and the development of peripheral sensitiza-

Table 1. Characteristics of Physiological Pain

Protective
Discrete or well localized
No peripheral or central sensitization
Proportionate to the peripheral stimulus
Subsides once the inflammatory response resolves
Pain can be differentiated from touch
Responds well to conventional analgesic therapy

74
Table 2. Characteristics of Pathological Pain

Debilitating
Diffuse or poorly localized
Significant peripheral and central sensitization
Disproportionate or exaggerated response to the peripheral stimulus
Continues beyond resolution of the inflammatory response
Pain cannot be differentiated from touch
Does not respond well to conventional analgesic therapy

tion. Consequently, atraumatic surgical technique and neural

blockade are far more effective than other types of analgesic
therapy in limiting the development of pathological pain,
blunting the stress response, preventing major complications,
and reducing mortality.18,19
Peripheral sensitization occurs as a direct consequence of
tissue trauma and inflammation. Tissue trauma leads to the
release of inflammatory mediators from damaged cells (H,
K, prostaglandins), plasma (bradykinin), platelets (serotonin), mast cells (histamine), and macrophages (cytokines).
Some inflammatory mediators activate nociceptors directly
(bradykinin), whereas others sensitize nociceptors (prostaglandins). Activation of nociceptors also leads to antidromal
or retrograde activation of nociceptive nerve fibers and release of substance P and other neuropeptides. Release of
these neuropeptides leads to mast cell degranulation, vasodilation, edema, and further activation and sensitization of
nociceptors. Peripheral sympathetic nerve terminals also
contribute to activation and sensitization of nerve terminals
by releasing norepinephrine and prostaglandins. Ultimately,
tissue trauma and inflammation produce a sensitizing soup
of chemical mediators that convert high-threshold nociceptors to low-threshold nociceptors. In other words, peripheral
sensitization is characterized by a reduction in the activation
threshold of peripheral nociceptors.
Central sensitization occurs as an indirect consequence of
tissue trauma and inflammation and is contingent to a large
degree on the development of peripheral sensitization. Constant activation of sensitized peripheral nociceptors leads to
sustained release of glutamate and neuropeptides from afferent fibers. Constant activation of AMPA and neuropeptide
receptors on dorsal horn projection neurons leads to progressive cellular depolarization and activation of additional types
of glutamate receptors (NMDA, metabotropic). Normally,
the channel of NMDA receptor complex is blocked by a
magnesium plug. Progressive depolarization of the postsynaptic membrane releases this plug, activates the receptor
complex, and increases inward conduction of Ca2 ions. This
influx of calcium, along with activation of other types of
receptors, leads to activation of phospholipases, polyphosphoinosites, kinases, and other intracellular messengers.
These activity-dependent changes lead to an increase in the
excitability of dorsal horn projection neurons. This initial

Topics in Companion Animal Medicine

phase of central sensitization is called short-term sensitization. If the inflammatory process continues for several days,
gene regulatory proteins are activated, new types receptors
are expressed, and dorsal horn projection neurons become
even more reactive to subsequent nociceptive input. This
phase of central sensitization is called long-term sensitization. Activation of NMDA receptors and the subsequent influx of Ca2 also leads to the release of arachidonic acid,
which is converted to prostaglandins by COX. Prostaglandins act presynaptically and postsynaptically to facilitate the
development of central sensitization. Glial cells also appear
to facilitate the development of central sensitization. Microglia and astrocytes normally play a supportive role in neurotransmission, but they are also activated by glutamate and
neuropeptides released from primary afferent fibers. Activated glial cells release adenosine triphosphate, glutamate,
nitric oxide, and cytokines, which facilitate release of neurotransmitters from afferent fibers and further sensitization of
projection neurons.

Clinical Pharmacology
The primary goal of perioperative multimodal analgesic therapy is to limit the development of peripheral and central
sensitization, and prevent the development of pathological
pain. Effective analgesic therapy also blunts the neuroendocrine response, reduces major complications, and improves
outcome. There are 5 major classes of analgesic drugs, and
each class blocks or modulates nociceptive input at one or
more sites of action (Fig 1). Alpha-2 agonists and opioids
alter the central perception of pain. Activation of supraspinal
and spinal alpha-2 receptors and opioid receptors also inhibits synaptic transmission in the dorsal horn of the spinal cord.
Dissociative anesthetics (ketamine) block NMDA receptors
on projection neurons, which inhibit the development of central sensitization. Peripheral and central neural blockade
with local anesthetics also inhibits the development of central
sensitization. COX inhibitors reduce inflammation, which
limits the development of peripheral sensitization. COX inhibitors also reduce the synthesis of prostaglandins in the
dorsal horn of the spinal cord, which limits the development
of central sensitization.

Selective Alpha-2 Agonists

Norepinephrine is the endogenous ligand for spinal and
supraspinal alpha-2 adrenergic receptors. Medetomidine and
dexmedetomidine are the selective alpha-2 agonists currently
available in North America. Medetomidine is supplied as a
racemic mixture of 2 optical enantiomers. Dexmedetomidine
is the active enantiomer, whereas levomedetomidine has no
apparent pharmacological activity. As a result, dexmedetomidine is approximately twice as potent as medetomidine.
The clinical effects of medetomidine and dexmedetomidine
are comparable when equivalent sedative doses are administered to cats and dogs. Medetomidine has a rapid onset after
parenteral injection, and the drug has a duration of action of

Volume 25, Number 2, May 2010

approximately 1 hour in dogs. The alpha-2 to alpha-1 adrenergic receptor selectively ratios for medetomidine and xylazine are 1620:1 and 160:1, respectively.20 Medetomidine and
dexmedetomidine are approved for use in dogs in Canada
and the United States, and studies evaluating the use of these
drugs in cats have been completed.21-24
Selective alpha-2 agonists induce reliable dose-dependent
sedation, analgesia, and muscle relaxation in cats and
dogs.25,26 The sedative and analgesic effects of selective alpha-2 agonists are mediated by activation of alpha-2 adrenergic receptors located in the pons (locus ceruleus) and the
dorsal horn of the spinal cord, respectively. In addition to
providing sedation and analgesia, preoperative administration of medetomidine reduces the amount of intravenous and
inhalation anesthetic required to induce and maintain anesthesia.27-29 Perioperative administration of selective alpha-2
agonists also blunts the neuroendocrine response and reduces
catecholamine and cortisol levels.30,31 Blood pressure increases, and heart rate and cardiac output decrease after medetomidine administration. Bradycardia and atrioventricular
blockade are potential complications, and heart rate and
rhythm should be monitored closely. Medetomidine does not
sensitize the myocardium to catecholamines or facilitate development of ventricular arrhythmias in patients anesthetized with isoflurane.32,33 Respiratory rate and minute
ventilation are well maintained after administration of
medetomidine or dexmedetomidine in conscious and anesthetized dogs.34,35 Blood glucose and urine production increase significantly after administration of medetomidine.
Selective alpha-2 agonists are used perioperatively to sedate and calm patients, provide muscle relaxation, and potentiate the analgesic and anesthetic effects of other drugs.
Medetomidine and dexmedetomidine are administered at
relatively low doses, and the use of these drugs is usually
limited to healthy, hemodynamically stable patients. Preoperatively, selective alpha-2 agonists are often given in combination with opioids. The preanesthetic intramuscular dose
ranges for medetomidine in healthy dogs and cats are 0.005
to 0.01 mg/kg and 0.01 to 0.02 mg/kg, respectively. Ultralow doses of medetomidine can be given postoperatively to
provide sedation. The postanesthetic intramuscular dose
ranges for medetomidine in healthy for healthy dogs and cats
are 0.001 to 0.002 mg/kg and 0.002 to 0.004 mg/kg, respectively. Dexmedetomidine can be given at approximately half
of the medetomidine dose. Atropine or glycopyrrolate can be
used to manage bradycardia associated with administration
of low and ultra-low doses of selective alpha-2 agonists.

Opioids
Endorphins, enkephalins, and dynorphins are the endogenous ligands for spinal and supraspinal opioid receptors.
Currently, 3 major classes of opioid receptors have been
cloned: OP1 (), OP2 () and OP3 (). OP1, OP2, and OP3
receptors modulate supraspinal and spinal analgesia, as well
as sedation, bradycardia, respiratory depression, and gastrointestinal motility. Receptor subtypes of each of these classes

75
have been identified, and expression of these subtypes varies
among tissues. There are also significant differences in the
expression of opioid receptors among species. Parenteral administration of opioids usually causes sedation in dogs,
whereas administration of high doses of opioids can cause
excitation and dysphoria in cats. Respiratory depression is a
significant side effect in human patients, but ventilation is
better maintained in cats and dogs. Butorphanol, morphine,
hydromorphone, and fentanyl are the opioids used most
commonly in small animals. Buprenorphine and tramadol
have also been used perioperatively to a limited extent.
Opioid agonists are the safest and most effective class of
analgesic drugs used for the management of perioperative
pain in cats and dogs. Morphine, hydromorphone, and fentanyl are the opioid agonists used most commonly in small
animals. These analgesic drugs are agonists at all 3 types of
opioid receptors. Opioid agonists are equally efficacious in
treating moderate to severe pain, but differ in potency and
duration of action. Intraoperative administration of morphine, hydromorphone, or fentanyl reduces isoflurane requirements by 30% to 50% in cats and dogs.36-39 Significant
respiratory depression can occur intraoperatively and postoperatively if the additive effects of opioid agonists and general anesthetics are not considered. Morphine and hydromorphone are often administered as preanesthetics, and
vomiting can occur with either drug. High doses of hydromorphone ( 0.1 mg/kg) can also cause significant postoperative hyperthermia in cats.40-42 Morphine and hydromorphone have an intermediate duration of action (2-4 hours)
after parenteral administration. The preanesthetic intramuscular dose range for morphine in cats and dogs is 0.2 to 0.4
mg/kg. Hydromorphone is approximately 5 times more potent than morphine, and the preanesthetic intramuscular
dose range for hydromorphone in cats and dogs is 0.05 to 0.1
mg/kg. Approximately half of the preanesthetic dose of morphine or hydromorphone can be given intraoperatively or
postoperatively. Morphine can also be given epidurally alone
or in combination with local anesthetics. The dose range for
preoperative or postoperative epidural administration of
morphine is 0.1-0.3 mg/kg. At this dose range, the onset time
is slow (1-2 h), but the duration of action in long (12-24 h).
Morphine can also be given postoperatively as an intravenous constant-rate infusion at a dose range of 0.1 to 0.2
mg/kg/h. Morphine has a relatively long duration of action
and the drug will accumulate over time. As a result, patients
should be monitored closely, and the infusion rate should be
reduced as needed. Fentanyl can also be given intravenously
as a preanesthetic. The drug is approximately 100 times more
potent than morphine and has a relatively short duration of
action (0.5 hour). The preanesthetic intravenous dose range
for fentanyl in cats and dogs is 0.001 to 0.005 mg/kg. Fentanyl is less likely to accumulate over time, and the drug is
often given intraoperatively to dogs as an intravenous constant rate infusion. The amount of inhalation anesthetic required to maintain adequate anesthetic depth is reduced by
30% to 50%, which improves cardiovascular function.
Minute ventilation may decrease, and positive-pressure ven-

76
tilation may be required to prevent significant hypoventilation (PaCO2 60 mm Hg). Intraoperatively, the dose range
for fentanyl in dogs is 0.005 to 0.01 mg/kg/h. Fentanyl can
also be given postoperatively as an intravenous constant-rate
infusion at a dose range of 0.001 to 0.005 mg/kg/h. Objective
clinical data on the use of intraoperative and postoperative
fentanyl infusions in cats are limited.
Fentanyl patches were designed to be applied to human
skin. Even in healthy cats and dogs, systemic absorption of
fentanyl from transdermal patches is erratic.43,44 In surgical
patients, altered body temperature, peripheral circulation,
and hydration can all compromise transdermal absorption of
fentanyl. On the other hand, heating pads and forced-air
warmers can dramatically increase fentanyl absorption intraoperatively and postoperatively. Consequently, preoperative
and intraoperative use of fentanyl patches should be avoided.
Once normal body temperature, peripheral circulation, and
hydration are restored, fentanyl patches can be used postoperatively with reasonable efficacy. Onset time is very slow,
and there is a 12- to 24-hour lag before effective plasma
concentrations are reached. If the patch stays properly adhered to on the patient, plasma fentanyl concentrations are
maintained for 3 to 5 days. Transdermal fentanyl is dosed at
a rate of 0.003 to 0.005 mg/kg/h in cats and dogs.
Opioid agonist-antagonists are also used to manage perioperative pain in cats and dogs. Butorphanol is the opioid
agonist-antagonist used most commonly in small animals.
Butorphanol is an agonist at the OP2 () receptor and an
antagonist or partial agonist at the OP3 () receptor. The
analgesia produced by butorphanol is not as profound as that
produced by opioid agonists, and its duration of action is
relatively short (1-2 hours). However, side effects (vomiting,
respiratory depression, bradycardia) are less likely to occur
after administration of butorphanol than after administration of morphine, hydromorphone, or fentanyl. Intraoperative administration of butorphanol also reduces isoflurane
requirements by 10% to 20% in cats and dogs.36,45 Butorphanol can be used perioperatively to manage mild to moderate pain. The preanesthetic intramuscular dose range for
butorphanol in cats and dogs is 0.2 to 0.4 mg/kg. Approximately half of the preanesthetic dose can be given intraoperatively or postoperatively. Butorphanol can be given postoperatively as an intravenous constant-rate infusion at a dose
range of 0.1 to 0.2 mg/kg/h. Small intravenous doses of butorphanol (0.1 mg/kg) can also be given postoperatively to
reverse sedation and respiratory depression caused by administration of excessive doses of opioid agonists.

NMDA Antagonists
Glutamate is the endogenous agonist for spinal and supraspinal NMDA receptors. Blockade of NMDA receptors in
the dorsal horn of the spinal cord prevents windup and the
development of central sensitization. Ketamine is the most
widely used NMDA antagonist in veterinary medicine. Ketamine is supplied as a racemic mixture of 2 optical enantiomers. S() ketamine has 4 times the affinity of L() ket-

Topics in Companion Animal Medicine

amine for the NMDA receptor and has a shorter duration of
action. The clinical analgesic potency of S() ketamine is
approximately twice that of the racemic mixture. Nonracemic mixtures of ketamine may be available for use in small
animals in the near future.
Ketamine can be used to manage pain throughout the perioperative period at anesthetic and subanesthetic doses.46 Intravenous or intramuscular administration of anesthetic
doses produces dissociative anesthesia with poor muscle
relaxation in both cats and dogs. Cardiovascular effects are
limited, and ventilation is better maintained than with other
anesthetic drugs. Dysphoria and seizures can also occur after
administration of high doses of ketamine, but dysphoria is
less severe or absent at low subanesthetic or analgesic doses.
The anesthetic effects of ketamine last for approximately 30
minutes, but motor effects can persist for several hours. Intravenous administration of ketamine at an infusion rate of
0.6 mg/kg/h decreases isoflurane requirements by 25%.37 Intraoperative and postoperative administration of ketamine
also reduces pain scores in dogs after forelimb amputation.47
Because of the potential for dysphoria, opioid infusions are a
better choice for most patients than opioid-ketamine infusions or ketamine infusions alone. However, patients with
significant preexisting central sensitization or those undergoing major procedures with significant surgical trauma may
benefit from intraoperative and postoperative opioid-ketamine infusions. Intraoperatively, the intravenous infusion
dose range for cats and dogs is 0.4 to 0.6 mg/kg/h. Postoperatively, a lower intravenous infusion dose range of 0.2 to 0.3
mg/kg/h is used to avoid dysphoria and motor effects. An
intravenous bolus of 0.5 to 1.0 mg/kg can be given as a
loading dose or to provide short-term analgesia.

Local Anesthetics
Local anesthetics have the unique ability to produce complete blockade of sensory nerve fibers and prevent the development of central sensitization. Consequently, peripheral
and central neural blockade are often used in combination
with other analgesic and anesthetic drugs to manage perioperative pain. Local anesthetics block the generation and conduction of nerve impulses by inhibiting voltage-gated sodium
channels in nerve fibers. Lidocaine is also given systemically
to manage pain and to reduce ileus after abdominal surgery.
The mechanism of action of systemic administration of lidocaine is unclear, but peripheral, central, and antiinflammatory mechanisms have been proposed.48
Lidocaine, mepivacaine, and bupivacaine are the local anesthetics used most commonly in cats and dogs. Lidocaine
has a fast onset (10 minutes) and a short duration of action
(1-2 hours) and is used for short diagnostic and surgical
procedures. Mepivacaine is similar to lidocaine in potency
and onset, but has a longer duration of action (2-3 hours),
causes less tissue irritation, and has a higher therapeutic index. Bupivacaine is approximately 4 times the potency of
lidocaine and mepivacaine, has a slow onset (20 minutes),
and a long duration of action (4-6 hours) and is used for most

Volume 25, Number 2, May 2010

surgical procedures. Aminoamide local anesthetics are highly
protein-bound and are metabolized primarily by the liver.
Consequently, anemic and hypoproteinemic patients are
more susceptible to local anesthetic toxicity. In most patients,
the clearance of lidocaine is dependent on blood flow rather
than hepatic metabolism. As a result, the clearance of lidocaine is significantly reduced in patients with low cardiac
output. Local anesthetics are relatively safe if they are used
correctly. Administration of an excessive dose and accidental
intravenous administration are the most common causes of
systemic toxicity in small animals. As a general rule, the total
dose of lidocaine or bupivacaine should not exceed 8 mg/kg
or 2 mg/kg, respectively. Clinicians should always consider
including peripheral or central neural blockade in their perioperative pain management plans. These techniques reduce
inhalation anesthetic requirements, attenuate the neuroendocrine response to surgical trauma, and improve outcome.
Local anesthetic techniques for cats and dogs are described in
detail in several recent articles.4,49,50
Systemic administration of lidocaine can be used perioperatively to reduce inhalation anesthetic requirements, to
provide analgesia, to control ventricular arrhythmias, and to
manage postoperative ileus. Intravenous administration of
lidocaine at a rate of 3 mg/kg/h reduces isoflurane requirements by 20% to 30%.37,51 Intravenous loading doses of 1 to
2 mg/kg are appropriate for most dogs. Intraoperatively, the
intravenous infusion dose range for dogs is 4 to 6 mg/kg/h.
Postoperatively, a lower intravenous infusion dose range of 2
to 3 mg/kg/h is used to provide analgesia and to improve
gastrointestinal motility. Objective clinical data on the use of
intraoperative and postoperative lidocaine infusions in cats
are limited.

77
given subcutaneously to cats and dogs immediately after surgery at a dose of 2 mg/kg. Therapy with ketoprofen can be
continued at a dose of 0.5 mg/kg twice daily for 3 to 5 days.
Meloxicam and carprofen have a slow onset time (1-2 hours)
and a long duration of action (24 hours). These drugs do not
appear to inhibit platelet function and do not prolong bleeding time in healthy animals. Meloxicam can be given subcutaneously to dogs immediately after surgery at a dose of 0.2
mg/kg. Therapy with meloxicam can be continued at a dose
of 0.1 mg/kg once daily for 3 to 5 days. Carprofen can be
given subcutaneously to dogs immediately after surgery at a
dose of 4 mg/kg. Therapy with carprofen can be continued at
a dose of 4 mg/kg once daily for 3 to 5 days. Deracoxib is also
labeled for perioperative use in dogs, but no parenteral formulation is available. Side effects are not usually a problem in
healthy animals with normal platelet, gastrointestinal, and
renal function. There is little benefit to preoperative administration of COX inhibitors, and there is significant risk for
patients with compromised platelet and renal function.

COX Inhibitors
Prostaglandins play a central role in inflammation and the
development of peripheral sensitization. Production of prostaglandins in the dorsal horn of the spinal cord also contributes to the development of central sensitization. Inhibition of
constitutive (COX-1) and inducible (COX-2) cyclooxygenase inhibits the conversion of arachadonic acid to prostaglandins and thromboxanes and produces a peripheral antiinflammatory effect. In the dorsal horn, inhibition of COX
produces a central analgesic effect. COX inhibitors vary in
their selectivity for the different isoenzymes, as well as their
ability to produce central analgesic and antiinflammatory
effects.52,53
Several COX inhibitors are approved for perioperative use
in cats and dogs. COX inhibitors are usually given postoperatively alone or in combination with opioids. Parenteral formulations of ketoprofen, meloxicam, and carprofen are
available in Canada and the United States and are better
suited for perioperative administration. Ketoprofen has a
rapid onset (0.5 hour), a short half-life, and an intermediate
duration of action (12 hours). The drug inhibits platelet function but does not appear to prolong bleeding time in healthy
animals undergoing elective surgery.54 Ketoprofen can be

Figure 2. Components of balanced anesthesia. General anesthetics (propofol, isoflurane) are used to induce hypnosis or
a loss of consciousness, but these drugs have very low therapeutic indices and produce significant cardiopulmonary depression at clinically relevant doses. Concurrent administration of analgesic drugs not only attenuates autonomic
responses (increased heart rate and arterial pressure, increased respiratory rate) to surgical trauma, but reduces the
amount of intravenous and inhalation anesthetics required to
induce and maintain anesthesia. Administration of alpha-2
agonists and local anesthetics can also improve muscle relaxation.

78

Table 3. Examples of Anesthetic and Pain Management Protocols for Healthy Cats*
Preoperative Management

Intraoperative Management

Postoperative Management

Comments

Castration
(Protocol 1)

Premedication
Acepromazine: 0.1-0.2
mg/kg, IM
Butorphanol: 0.2-0.4
mg/kg, IM
Premedication
Medetomidine: 0.01-0.02
mg/kg, IM
Butorphanol: 0.2-0.4
mg/kg, IM
Premedication
Acepromazine: 0.1-0.2
mg/kg, IM
Hydromorphone: 0.05-0.1
mg/kg, IM

Induction and maintenance

Ketamine: 10-15 mg/kg, IM

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia

Mild pain

Induction and maintenance

Ketamine: 5-10 mg/kg, IM

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia

Mild pain

Induction
Thiopental: 8-12 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.5%-2.5%
Induction
Thiopental: 4-6 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.0%-2.0%

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia
Ketoprofen: 1.0 mg/kg, PO
once daily for 2-3 days

Moderate pain
Some patients may require
additional hydromorphone
postoperatively.

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia
Ketoprofen: 1.0 mg/kg, PO
once daily for 2-3 days

Moderate pain
Some patients may require
additional hydromorphone
postoperatively.

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia
Ketoprofen: 1.0 mg/kg, PO
once daily for 2-3 days

Moderate pain
Digital nerve block reduces
anesthetic requirements
and improves analgesia
postoperatively.

Castration
(Protocol 2)

Ovariohysterectomy
(Protocol 1)

Ovariohysterectomy
(Protocol 2)

Onychectomy
(Protocol 1)

Premedication
Medetomidine: 0.01-0.02
mg/kg, IM
Hydromorphone: 0.05-0.1
mg/kg, IM
Glycopyrrolate: 0.01 mg/
kg, IM
Premedication
Acepromazine: 0.1-0.2
mg/kg, IM
Hydromorphone: 0.05-0.1
mg/kg, IM

Induction
Propofol: 4-6 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.5%-2.5%
Digital nerve block
0.5% bupivacaine:
0.5-1.0 mL
Do not exceed a total dose of
2 mg/kg.

Topics in Companion Animal Medicine

Surgical Procedure

79

Dexmedetomidine can be substituted at approximately half the medetomidine dose.

*Some of these drugs are not approved for use in cats in Canada or the United States.

Clinical Management

Abbreviations: IM, Intramuscularly; IV, intravenously; SC, subcutaneously; PO, by mouth.

Moderate pain
Digital nerve block reduces
anesthetic requirements
and improves analgesia
postoperatively.
Ketoprofen: 2.0 mg/kg, SC
immediately after recovery from
anesthesia
Ketoprofen: 1.0 mg/kg, PO
once daily for 2-3 days
Premedication
Medetomidine: 0.01-0.02
mg/kg, IM
Hydromorphone: 0.05-0.1
mg/kg, IM
Glycopyrrolate: 0.01 mg/
kg, IM
Onychectomy
(Protocol 2)

Induction
Propofol: 2-3 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.0%-2.0%
Digital nerve block
0.5% Bupivacaine:
0.5-1.0 mL
Do not exceed a total dose of
2 mg/kg.

Comments
Preoperative Management
Surgical Procedure

Table 3. Continued

Intraoperative Management

Postoperative Management

Volume 25, Number 2, May 2010

Multimodal analgesia is not a difficult concept to understand,

nor is it a difficult concept to put into practice. In the perioperative setting, a multimodal analgesic protocol is simply a balanced anesthetic and pain management protocol (Fig 2). At first
glance, the notion that analgesic drugs should be given to anesthetized patients that are unable to consciously perceive pain
seems irrational. However, most intravenous (propofol) and
inhalation (isoflurane, sevoflurane) anesthetics simply produce
unconsciousness and do not substantially alter nociceptive processing. In fact, autonomic responses (sudden changes in respiratory rate, heart rate, and blood pressure) that occur during
surgery as a result of noxious stimulation usually reflect inadequate analgesia rather than insufficient anesthetic depth. The
safest approach for most patients is to limit the amount of inhalation anesthetic required by providing supplemental intraoperative analgesic therapy with opioids and local anesthetic
techniques.
After initial assessment of analgesic requirements and
identification of major anesthetic risk factors, drugs are selected to minimize risk and to provide optimal anesthetic and
pain management throughout the perioperative period. Patient monitoring and supportive care are also selected to optimize cardiopulmonary function and to minimize anesthetic
risk. Hypoventilation (PaCO2 60 mm Hg), hypotension
(mean arterial pressure 60 mm Hg), and bradycardia are
common perioperative complications. Care should be taken
to avoid or reduce doses of anesthetic and analgesic drugs
that have similar side effects. Opioids and inhalation anesthetics can induce significant respiratory depression. Acepromazine, inhalation anesthetics, and epidural anesthesia
can cause significant hypotension. Alpha-2 agonists and opioids can cause bradycardia and enhance oculovagal and viscerovagal reflexes triggered by surgical manipulation. Given
the potential for significant intraoperative complications,
there is no substitute for diligent patient monitoring by a
qualified, experienced anesthetist.
The type of surgery (invasive vs minimally invasive) and
the surgical site (somatic vs visceral) should also be considered when developing anesthetic and pain management
plans. Pain must be managed aggressively throughout the
perioperative period in patients scheduled for invasive surgical procedures, whereas postoperative administration of
COX inhibitors may be appropriate for patients scheduled
for minimally invasive procedures. Peripheral or central neural blockade is appropriate for most patients scheduled for
surgical procedures of the front or hind limbs and for those
scheduled for dental procedures. Conversely, complete
blockade of nociceptive input from somatic and visceral afferents may be impossible to achieve in patients scheduled for
thoracic or abdominal surgical procedures.
Perioperative use of analgesic drugs and techniques reduces the doses of intravenous and inhalation anesthetics
required to induce and maintain anesthesia, improves cardiopulmonary function during surgery, and promotes a smooth
recovery from anesthesia after surgery. These analgesic drugs

80

Table 4. Examples of Anesthetic and Pain Management Protocols for Healthy Dogs*
Surgical Procedure

Postoperative Management

Comments

Induction
Propofol: 4-6 mg/kg, IV to effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.5%-2.5%
Induction
Propofol: 2-3 mg/kg, IV to effect
Isoflurane: 3%
Maintenance:
Isoflurane: 1.0%-2.0%

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia

Mild pain

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia

Mild pain

Induction
Thiopental: 8-12 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.5%-2.5%
Induction
Ovariohysterectomy Premedication
(Protocol 2)
Medetomidine: 0.005-0.01 mg/ Thiopental: 4-6 mg/kg, IV to
kg, IM
effect
Hydromorphone: 0.05-0.1 mg/ Isoflurane: 3%
kg, IM
Isoflurane: 3%
Glycopyrrolate: 0.005-0.01
Maintenance
mg/kg, IM
Isoflurane: 1.0%-2.0%
Dentistry with an
Premedication
Induction
upper canine
Midazolam: 0.1-0.2 mg/kg, IM Propofol: 4-6 mg/kg, IV to effect
extraction
Hydromorphone: 0.05-0.1 mg/ Isoflurane: 3%
kg, IM
Maintenance
Isoflurane: 1.0%-2.0%
Infraorbital nerve block
0.5% Bupivacaine: 0.5-1.0 mL

Meloxicam: 0.2 mg/kg, SC

immediately after recovery from
anesthesia
Meloxicam: 0.1 mg/kg, PO
once daily for 2-3 days

Moderate pain
Some patients may require
additional hydromorphone
postoperatively.

Meloxicam: 0.2 mg/kg, SC

immediately after recovery from
anesthesia
Meloxicam: 0.1 mg/kg, PO
once daily for 2-3 days

Moderate pain
Some patients may require
additional hydromorphone
postoperatively.

Ketoprofen: 2.0 mg/kg, SC

immediately after recovery from
anesthesia
Ketoprofen: 1.0 mg/kg, PO
once daily for 2-3 days

Moderate pain
Infraorbital nerve block
reduces anesthetic
requirements and improves
analgesia postoperatively.

Premedication
Acepromazine: 0.05-0.1 mg/kg,
IM
Butorphanol: 0.2-0.4 mg/kg,
IM
Castration
Premedication
(Protocol 2)
Medetomidine: 0.005-0.01 mg/
kg, IM
Butorphanol: 0.2-0.4 mg/kg,
IM
Glycopyrrolate: 0.005-0.01
mg/kg, IM
Ovariohysterectomy Premedication
(Protocol 1)
Acepromazine: 0.05-0.1 mg/kg,
IM
Hydromorphone: 0.05-0.1 mg/
kg, IM

Topics in Companion Animal Medicine

Intraoperative Management

Castration
(Protocol 1)

Preoperative Management

81
and techniques also have the potential to reduce major complications and improve outcome. In a busy practice setting,
simple, straightforward anesthetic and pain management
protocols are the best choice for most patients. Pain can be
managed safely and effectively in the vast majority of surgical
patients with opioids, COX inhibitors, and peripheral or
central neural blockade. Alpha-2 agonists, NMDA antagonists, and other adjunctive drugs are helpful in patients with
significant short-term or long-term central sensitization. And
last, atraumatic surgical technique is the first, and most important, step in the prevention of peripheral and central sensitization and the development of pathological pain. Examples of balanced anesthetic and pain management protocols
for routine surgical procedures in healthy cats and dogs are
outlined in Tables 3 and 4, respectively.

Dexmedetomidine can be substituted at approximately half the medetomidine dose.

*Some of these drugs are not approved for use in dogs in Canada or the United States.

References

Abbreviations: IM, Intramuscularly; IV, intravenously; SC, subcutaneously; PO, by mouth.

Moderate pain
Epidural anesthesia reduces
anesthetic requirements and
improves analgesia
postoperatively.
Meloxicam: 0.2 mg/kg, SC
immediately after recovery from
anesthesia
Meloxicam: 0.1 mg/kg, PO
once daily for 4-6 days
Premedication
Midazolam: 0.1-0.2 mg/kg, IM
Hydromorphone: 0.05-0.1 mg/
kg, IM
Cruciate repair

Induction
Thiopental: 8-12 mg/kg, IV to
effect
Isoflurane: 3%
Maintenance
Isoflurane: 1.0%-2.0%
Epidural anesthesia (lumbosacral)
0.5% Bupivacaine: 1.0 mL/5 kg
2.5% Morphine: 0.2 mg/kg

Comments
Preoperative Management
Surgical Procedure

Table 4. Continued

Intraoperative Management

Postoperative Management

Volume 25, Number 2, May 2010

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