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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
70
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. Spe-
cifically, nociception includes signal transduction and nerve
conduction in the peripheral nervous system, and synaptic
transmission, projection, and modulation of nociceptive in-
put 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 neuro-
anatomical 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 in-
flammation. Some patients may have preexisting tissue
trauma and inflammation, and others may have pain associ-
ated 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 ratio-
nal, effective, multimodal analgesic therapy. Neuropathic
pain is relatively uncommon in surgical patients, and the
mechanisms of neuropathic pain are similar to those of in-
flammatory 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 Figure 1. Overview of nociceptive and antinociceptive path-
tissues and project to the dorsal horn of the spinal cord, brain ways. Surgical trauma activates mechanical, chemical, and
stem, thalamus, and cerebral cortex (Fig 1). The nociceptive thermal nociceptors. Action potentials are conducted to the
pathways are composed of 3 general types of neurons. The dorsal horn of the spinal cord by primary afferent nerve
first-order neurons are primary afferent neurons, and these fibers. Second-order projection neurons encode and relay sig-
neurons are responsible for transduction of noxious stimuli nals to the brainstem and thalamus. Third-order neurons in
and conduction of electrical signals to the dorsal horn of the the thalamus project to the limbic system and somatosensory
spinal cord. The second-order neurons are projection neu- cortex where pain is perceived. Descending antinociceptive
rons, and these neurons receive input from the primary affer- pathways modulate nociceptive processing at the level of the
ent neurons and project to the medulla, pons, midbrain, thal- thalamus, brainstem, and spinal cord. Different classes of
amus, and hypothalamus. Third-order supraspinal neurons analgesic drugs act at different sites in the nociceptive and
integrate input from spinal neurons and project to subcorti- antinociceptive pathways. Multimodal analgesic therapy in-
cal and cortical areas where pain is finally perceived. Su- hibits processing of nociceptive input at 2 or more sites. PAG,
praspinal processing of afferent nociceptive input is also periaqueductal gray; RVM, rostroventral medulla.
72 Topics in Companion Animal Medicine
closely integrated with regulation of the autonomic nervous defined. Noxious mechanical stimuli may activate a mechan-
system. ically gated ion channel directly, or shearing forces may re-
Primary afferent neurons are bipolar neurons. The cell lease adenosine triphosphate, which acts on purine receptors
bodies of these bipolar neurons are located in the trigeminal (P2X). Noxious chemical stimuli (H⫹) activate acid-sensing
and dorsal root ganglia, and their axons project peripherally ion channels and transient receptor potential vanilloid
to somatic and visceral tissues and centrally to the dorsal (TRPV1) channels. Noxious heat also activates TRPV1 chan-
horn of the spinal cord. Some primary afferent neurons re- nels as well as related channels (TRPV2), and noxious cold
spond to noxious or high-threshold stimuli, and others re- activates transient receptor potential menthol (TRPM8)
spond to non-noxious or low-threshold stimuli (touch). Af- channels.
ferent nociceptive neurons have free nerve endings that Nociceptive afferent neurons synapse with second-order
change or “transduce” noxious mechanical, thermal, or neurons in the dorsal horn of the spinal cord. Projection
chemical stimuli into electrical signals. Somatic tissues have a neurons and interneurons are the 2 major types of nocicep-
higher density of nociceptive nerve fibers and smaller recep- tive neurons in the dorsal horn, and these neurons are orga-
tive fields, whereas visceral tissues have a lower density of nized in layers or laminae. Neurons that mediate nociception
nociceptive nerve fibers and larger receptive fields. These an- are located in laminae I, II, and V. Projection neurons are
atomical differences may account for some of the qualitative located in laminae I and V, and they have axons that cross
differences between somatic (discrete) and visceral (diffuse) midline and project to third-order supraspinal neurons. Pro-
pain. jection neurons located in lamina I receive input directly from
Primary afferent neurons are classified by axon diameter, A␦ and C nociceptive fibers and are classified as nociceptive-
the presence or absence of myelination, and their response to specific and polymodal nociceptive neurons, respectively.
mechanical, thermal, and chemical stimuli. A afferent neu- Projection neurons in lamina V receive input from both no-
rons have large, myelinated axons that conduct impulses at a ciceptive and non-nociceptive (A) fibers and are classified as
velocity of greater than 30 m/sec. The free nerve endings of wide, dynamic-range neurons. Interneurons are located in
these fibers respond to non-noxious mechanical stimuli lamina II and also receive input from nociceptive and non-
(touch) but do not respond to noxious stimuli directly. A␦ nociceptive (A) fibers. Inhibitory and excitatory interneu-
nociceptive neurons have small, myelinated axons that con- rons play a central role in gating and modulating nociceptive
duct impulses at a velocity of 3 to 30 m/sec. The free nerve input. Propriospinal neurons that project across several der-
endings of these fibers contain membrane-bound receptors matomes are also present in the dorsal horn and are respon-
that respond primarily to intense mechanical and thermal sible for segmental reflexes associated with nociception.
stimuli and are called mechanothermal nociceptors. C noci- Glutamate is the primary excitatory neurotransmitter in
ceptive neurons have small, unmyelinated axons that con- the dorsal horn of the spinal cord. Nociceptive as well as
duct nerve impulses at a velocity of less than 3 m/sec. The free non-nociceptive fibers co-release glutamate and neuropep-
nerve endings of these fibers contain membrane-bound recep- tides (substance P, neurokinin A, calcitonin gene–related
tors that respond to chemical as well as thermal and mechan- peptide). With normal afferent input, glutamate binds
ical stimuli and are called polymodal nociceptors. Small, my- to ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionoic acid
elinated A␦ fibers carry the nociceptive input responsible for (AMPA) receptors located on the postsynaptic membrane of
the fast, sharp pain that occurs immediately after injury. The projection neurons. Neuropeptides bind to several types of
nociceptive input responsible for the prolonged dull pain that receptors on the postsynaptic membrane. With intensive af-
occurs several seconds later is carried by small, unmyelinated ferent input, prolonged activation of AMPA and neuropep-
C fibers. Silent nociceptive neurons are also present in so- tide receptors leads to progressive depolarization of the
matic tissues. The free nerve endings of these neurons only postsynaptic membrane and activation of additional types of
respond to mechanical and thermal stimuli after they are glutamate receptors. Activation of a specific type of gluta-
activated by chemical (inflammatory) mediators. This classi- mate receptor, the NMDA receptor, plays a key role in the
fication scheme is derived from analysis of fibers that inner- development of central sensitization.
vate the somatic tissues (skin). Visceral pain is qualitatively The spinothalamic tract (STT) is the major ascending no-
different from somatic pain and is typically dull and poorly ciceptive pathway in carnivores and primates.11,16 Lamina
localized. Visceral pain also lacks the fast and slow compo- I, nociceptive (nociceptive-specific, polymodal nociceptive)
nents that are characteristic of somatic pain. neurons are somatotopically organized, modality-selective
Transduction of mechanical, thermal, and chemical stim- neurons with small receptive fields that convey discrete nox-
uli by the free nerve endings of A␦ and C nociceptive fibers is ious mechanical, thermal, and chemical afferent input. These
mediated by membrane-bound receptors.13-15 Most of these neurons project to the ventromedial nucleus of the lateral
receptors are nonselective cation channels that are gated thalamus, which projects to the insular cortex and the sec-
by temperature, chemical ligands, or mechanical shearing ondary somatosensory cortex. These neurons also project to
forces. Activation of these channels increases inward conduc- the mediodorsal nucleus of the medial thalamus, which
tion of Na⫹ and Ca⫹2 ions, which ultimately depolarizes the projects to the anterior cingulate cortex. Like the dorsal
membrane and generates a burst of action potentials. The horn, glutamate is an important excitatory neurotransmitter
mechanisms of mechanical signal transduction are not well within the thalamic nuclei. Lamina V, wide, dynamic-range
Volume 25, Number 2, May 2010 73
neurons have large receptive fields, are not somatotopically GABA by local interneurons, inhibit presynaptic calcium
organized or modality selective, and are responsible for inte- channels that modulate neurotransmitter release. This inhi-
gration of all afferent input to the dorsal horn. These neurons bition, mediated by presynaptic noradrenergic (␣2), opioid
project to the motor thalamus (ventrodorsal and ventrolat- (), and GABAB receptors, limits release of glutamate and
eral nuclei), which projects to the basal ganglia and the pri- neuropeptides from primary afferent neurons, which inhibits
mary somatosensory cortex. Axons from lamina I are con- nociceptive transmission. Release of norepinephrine, en-
centrated in the lateral STT, and axons from lamina V are kephalins, and GABA in the dorsal horn hyperpolarizes pro-
concentrated in the ventral STT. The thalamus relays afferent jection neurons, which also inhibits nociceptive trans-
input from the STT and integrates this information with af- mission. This inhibition is mediated by postsynaptic
ferent input from the autonomic nervous system. Projection noradrenergic (␣2) and opioid () receptors that activate
from neurons in the lateral thalamus to neurons in the insular potassium channels, which leads to an outward flux of
and secondary somatosensory cortex appears to be responsi- potassium ions and hyperpolarization of the postsynaptic
ble for the sensory-discriminative aspects of pain. Projection membrane. This inhibition is also mediated by postsynap-
from neurons in the medial thalamus to neurons in the ante- tic GABAA receptors that activate chloride channels,
rior cingulate cortex appears to be responsible for the moti- which leads to an inward flux of chloride ions and hyper-
vational-affective aspects of pain. Projection from neurons in polarization of the postsynaptic membrane. In summary,
the motor thalamus to neurons in the primary somatosensory release of norepinephrine, endogenous opioids, and GABA
cortex appears to be responsible for sensory and motor inte- inhibits synaptic transmission between primary afferent
gration. Direct connections between the lateral thalamus and neurons and projection neurons by inhibiting neurotrans-
the dorsal margin of the insular cortex (interoceptive cortex) mitter release and hyperpolarizing the postsynaptic mem-
are more developed in primates than in carnivores. brane, which effectively shuts down the key synapse in the
dorsal horn.
Antinociceptive Pathways
Peripheral and Central Sensitization
Mammals also have descending antinociceptive pathways
Neural plasticity is defined as the ability of the nervous
that modulate nociceptive input at spinal and supraspinal
system to modify its function in response to different envi-
levels (Fig 1). The antinociceptive pathways begin at the su-
ronmental stimuli. Surgical trauma and inflammation pro-
praspinal level and project to neurons in the dorsal horn of
duce sensitization of the peripheral nervous system, and the
the spinal cord. The periaqueductal gray matter (midbrain),
subsequent barrage of nociceptive input produces sensitiza-
locus ceruleus (pons), and nucleus raphe magnus (medulla)
tion of neurons in the dorsal horn of the spinal cord. Periph-
are all important structures in the modulation of nociceptive
eral and central sensitization of nociceptive pathways plays a
input. The periaqueductal gray matter receives direct input
central role in the development of pathological pain.17 Pa-
from the thalamus and the hypothalamus, and indirect input
tients with no preexisting tissue trauma and inflammation
from the insular cortex and the anterior cingulate cortex.
experience pain that is physiological or protective in nature
These neurons in the periaqueductal gray matter send projec-
(Table 1). This type of inflammatory pain is well localized,
tions to neurons in the nucleus raphe magnus, which project
proportionate to the peripheral stimulus, and subsides once
to the dorsal horn of the spinal cord. Neurons in the locus
the inflammatory process resolves. Patients with significant
ceruleus project directly to the dorsal horn, and they may also
tissue trauma and inflammation experience pain that is
receive input from the periaqueductal gray matter.
pathological or debilitating in nature (Table 2). This type of
Endogenous opioids (endorphins, enkephalins, dynor-
inflammatory pain is diffuse, disproportionate to the periph-
phins), serotonin, and norepinephrine are the primary neu-
eral stimulus, and continues beyond resolution of the inflam-
rotransmitters in the descending antinociceptive pathways.
matory process. A key concept that is often lost when trying
Axons that originate in the nucleus raphe magnus release
to understand the clinical relevance of neural plasticity is that
serotonin in the dorsal horn of the spinal cord and are called
central sensitization occurs secondary to surgical trauma,
“serotonergic” neurons. Similarly, neurons that originate in
inflammation, and the development of peripheral sensitiza-
the locus ceruleus release norepinephrine in the dorsal horn
and are called “noradrenergic” neurons. Supraspinal release
of endogenous opioid peptides activates both types of neu-
rons, whereas supraspinal release of release of ␥-aminobu- Table 1. Characteristics of Physiological Pain
tyric acid (GABA) inhibits both types of neurons. Supraspinal ● Protective
inhibition of descending antinociceptive pathways is medi- ● Discrete or well localized
ated by GABAA receptors. At the supraspinal level, endoge- ● No peripheral or central sensitization
nous opioids not only activate descending antinociceptive ● Proportionate to the peripheral stimulus
pathways, but inhibit GABA-mediated inhibition of these ● Subsides once the inflammatory response resolves
same pathways, which is called “disinhibition.” ● Pain can be differentiated from touch
Release of norepinephrine and serotonin in the dorsal horn ● Responds well to conventional analgesic therapy
of the spinal cord, and subsequent release of enkephalins and
74 Topics in Companion Animal Medicine
tilation may be required to prevent significant hypoventila- amine for the NMDA receptor and has a shorter duration of
tion (PaCO2 ⬍ 60 mm Hg). Intraoperatively, the dose range action. The clinical analgesic potency of S(⫹) ketamine is
for fentanyl in dogs is 0.005 to 0.01 mg/kg/h. Fentanyl can approximately twice that of the racemic mixture. Nonrace-
also be given postoperatively as an intravenous constant-rate mic mixtures of ketamine may be available for use in small
infusion at a dose range of 0.001 to 0.005 mg/kg/h. Objective animals in the near future.
clinical data on the use of intraoperative and postoperative Ketamine can be used to manage pain throughout the peri-
fentanyl infusions in cats are limited. operative period at anesthetic and subanesthetic doses.46 In-
Fentanyl patches were designed to be applied to human travenous or intramuscular administration of anesthetic
skin. Even in healthy cats and dogs, systemic absorption of doses produces “dissociative” anesthesia with poor muscle
fentanyl from transdermal patches is erratic.43,44 In surgical relaxation in both cats and dogs. Cardiovascular effects are
patients, altered body temperature, peripheral circulation, limited, and ventilation is better maintained than with other
and hydration can all compromise transdermal absorption of anesthetic drugs. Dysphoria and seizures can also occur after
fentanyl. On the other hand, heating pads and forced-air administration of high doses of ketamine, but dysphoria is
warmers can dramatically increase fentanyl absorption intra- less severe or absent at low subanesthetic or analgesic doses.
operatively and postoperatively. Consequently, preoperative The anesthetic effects of ketamine last for approximately 30
and intraoperative use of fentanyl patches should be avoided. minutes, but motor effects can persist for several hours. In-
Once normal body temperature, peripheral circulation, and travenous administration of ketamine at an infusion rate of
hydration are restored, fentanyl patches can be used postop- 0.6 mg/kg/h decreases isoflurane requirements by 25%.37 In-
eratively with reasonable efficacy. Onset time is very slow, traoperative and postoperative administration of ketamine
and there is a 12- to 24-hour lag before effective plasma also reduces pain scores in dogs after forelimb amputation.47
concentrations are reached. If the patch stays properly ad- Because of the potential for dysphoria, opioid infusions are a
hered to on the patient, plasma fentanyl concentrations are better choice for most patients than opioid-ketamine infu-
maintained for 3 to 5 days. Transdermal fentanyl is dosed at sions or ketamine infusions alone. However, patients with
a rate of 0.003 to 0.005 mg/kg/h in cats and dogs. significant preexisting central sensitization or those undergo-
Opioid agonist-antagonists are also used to manage peri- ing major procedures with significant surgical trauma may
operative pain in cats and dogs. Butorphanol is the opioid benefit from intraoperative and postoperative opioid-ket-
agonist-antagonist used most commonly in small animals. amine infusions. Intraoperatively, the intravenous infusion
Butorphanol is an agonist at the OP2 () receptor and an dose range for cats and dogs is 0.4 to 0.6 mg/kg/h. Postoper-
antagonist or partial agonist at the OP3 () receptor. The atively, a lower intravenous infusion dose range of 0.2 to 0.3
analgesia produced by butorphanol is not as profound as that mg/kg/h is used to avoid dysphoria and motor effects. An
produced by opioid agonists, and its duration of action is intravenous bolus of 0.5 to 1.0 mg/kg can be given as a
relatively short (1-2 hours). However, side effects (vomiting, loading dose or to provide short-term analgesia.
respiratory depression, bradycardia) are less likely to occur
after administration of butorphanol than after administra-
Local Anesthetics
tion of morphine, hydromorphone, or fentanyl. Intraopera-
tive administration of butorphanol also reduces isoflurane Local anesthetics have the unique ability to produce com-
requirements by 10% to 20% in cats and dogs.36,45 Butor- plete blockade of sensory nerve fibers and prevent the devel-
phanol can be used perioperatively to manage mild to mod- opment of central sensitization. Consequently, peripheral
erate pain. The preanesthetic intramuscular dose range for and central neural blockade are often used in combination
butorphanol in cats and dogs is 0.2 to 0.4 mg/kg. Approxi- with other analgesic and anesthetic drugs to manage periop-
mately half of the preanesthetic dose can be given intraoper- erative pain. Local anesthetics block the generation and con-
atively or postoperatively. Butorphanol can be given postop- duction of nerve impulses by inhibiting voltage-gated sodium
eratively as an intravenous constant-rate infusion at a dose channels in nerve fibers. Lidocaine is also given systemically
range of 0.1 to 0.2 mg/kg/h. Small intravenous doses of bu- to manage pain and to reduce ileus after abdominal surgery.
torphanol (0.1 mg/kg) can also be given postoperatively to The mechanism of action of systemic administration of lido-
reverse sedation and respiratory depression caused by admin- caine is unclear, but peripheral, central, and antiinflamma-
istration of excessive doses of opioid agonists. tory mechanisms have been proposed.48
Lidocaine, mepivacaine, and bupivacaine are the local an-
esthetics used most commonly in cats and dogs. Lidocaine
NMDA Antagonists
has a fast onset (10 minutes) and a short duration of action
Glutamate is the endogenous agonist for spinal and su- (1-2 hours) and is used for short diagnostic and surgical
praspinal NMDA receptors. Blockade of NMDA receptors in procedures. Mepivacaine is similar to lidocaine in potency
the dorsal horn of the spinal cord prevents windup and the and onset, but has a longer duration of action (2-3 hours),
development of central sensitization. Ketamine is the most causes less tissue irritation, and has a higher therapeutic in-
widely used NMDA antagonist in veterinary medicine. Ket- dex. Bupivacaine is approximately 4 times the potency of
amine is supplied as a racemic mixture of 2 optical enanti- lidocaine and mepivacaine, has a slow onset (20 minutes),
omers. S(⫹) ketamine has 4 times the affinity of L(⫺) ket- and a long duration of action (4-6 hours) and is used for most
Volume 25, Number 2, May 2010 77
surgical procedures. Aminoamide local anesthetics are highly given subcutaneously to cats and dogs immediately after sur-
protein-bound and are metabolized primarily by the liver. gery at a dose of 2 mg/kg. Therapy with ketoprofen can be
Consequently, anemic and hypoproteinemic patients are continued at a dose of 0.5 mg/kg twice daily for 3 to 5 days.
more susceptible to local anesthetic toxicity. In most patients, Meloxicam and carprofen have a slow onset time (1-2 hours)
the clearance of lidocaine is dependent on blood flow rather and a long duration of action (24 hours). These drugs do not
than hepatic metabolism. As a result, the clearance of lido- appear to inhibit platelet function and do not prolong bleed-
caine is significantly reduced in patients with low cardiac ing time in healthy animals. Meloxicam can be given subcu-
output. Local anesthetics are relatively safe if they are used taneously to dogs immediately after surgery at a dose of 0.2
correctly. Administration of an excessive dose and accidental mg/kg. Therapy with meloxicam can be continued at a dose
intravenous administration are the most common causes of of 0.1 mg/kg once daily for 3 to 5 days. Carprofen can be
systemic toxicity in small animals. As a general rule, the total given subcutaneously to dogs immediately after surgery at a
dose of lidocaine or bupivacaine should not exceed 8 mg/kg dose of 4 mg/kg. Therapy with carprofen can be continued at
or 2 mg/kg, respectively. Clinicians should always consider a dose of 4 mg/kg once daily for 3 to 5 days. Deracoxib is also
including peripheral or central neural blockade in their peri- labeled for perioperative use in dogs, but no parenteral for-
operative pain management plans. These techniques reduce mulation is available. Side effects are not usually a problem in
inhalation anesthetic requirements, attenuate the neuroendo- healthy animals with normal platelet, gastrointestinal, and
crine response to surgical trauma, and improve outcome. renal function. There is little benefit to preoperative admin-
Local anesthetic techniques for cats and dogs are described in istration of COX inhibitors, and there is significant risk for
detail in several recent articles.4,49,50 patients with compromised platelet and renal function.
Systemic administration of lidocaine can be used periop-
eratively 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 require-
ments 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.
COX Inhibitors
Prostaglandins play a central role in inflammation and the
development of peripheral sensitization. Production of pros-
taglandins in the dorsal horn of the spinal cord also contrib-
utes to the development of central sensitization. Inhibition of
constitutive (COX-1) and inducible (COX-2) cyclooxygen-
ase inhibits the conversion of arachadonic acid to prostaglan-
dins and thromboxanes and produces a peripheral antiin-
flammatory 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 Figure 2. Components of balanced anesthesia. General an-
effects.52,53 esthetics (propofol, isoflurane) are used to induce hypnosis or
Several COX inhibitors are approved for perioperative use a loss of consciousness, but these drugs have very low thera-
in cats and dogs. COX inhibitors are usually given postoper- peutic indices and produce significant cardiopulmonary de-
atively alone or in combination with opioids. Parenteral for- pression at clinically relevant doses. Concurrent administra-
mulations of ketoprofen, meloxicam, and carprofen are tion of analgesic drugs not only attenuates autonomic
available in Canada and the United States and are better responses (increased heart rate and arterial pressure, in-
suited for perioperative administration. Ketoprofen has a creased respiratory rate) to surgical trauma, but reduces the
rapid onset (0.5 hour), a short half-life, and an intermediate amount of intravenous and inhalation anesthetics required to
duration of action (12 hours). The drug inhibits platelet func- induce and maintain anesthesia. Administration of alpha-2
tion but does not appear to prolong bleeding time in healthy agonists and local anesthetics can also improve muscle relax-
animals undergoing elective surgery.54 Ketoprofen can be ation.
78
Table 3. Examples of Anesthetic and Pain Management Protocols for Healthy Cats*
Surgical Procedure Preoperative Management Intraoperative Management Postoperative Management Comments
Castration Premedication Induction and maintenance Ketoprofen: 2.0 mg/kg, SC Mild pain
(Protocol 1) Acepromazine: 0.1-0.2 Ketamine: 10-15 mg/kg, IM immediately after recovery from
mg/kg, IM anesthesia
Butorphanol: 0.2-0.4
mg/kg, IM
Castration Premedication Induction and maintenance Ketoprofen: 2.0 mg/kg, SC Mild pain
(Protocol 2) Medetomidine: 0.01-0.02 Ketamine: 5-10 mg/kg, IM immediately after recovery from
mg/kg, IM† anesthesia
Butorphanol: 0.2-0.4
mg/kg, IM
Ovariohysterectomy Premedication Induction Ketoprofen: 2.0 mg/kg, SC Moderate pain
(Protocol 1) Acepromazine: 0.1-0.2 Thiopental: 8-12 mg/kg, IV to immediately after recovery from Some patients may require
mg/kg, IM effect anesthesia additional hydromorphone
Hydromorphone: 0.05-0.1 Isoflurane: 3% Ketoprofen: 1.0 mg/kg, PO postoperatively.
mg/kg, IM Maintenance once daily for 2-3 days
Isoflurane: 1.5%-2.5%
Ovariohysterectomy Premedication Induction Ketoprofen: 2.0 mg/kg, SC Moderate pain
(Protocol 2) Medetomidine: 0.01-0.02 Thiopental: 4-6 mg/kg, IV to immediately after recovery from Some patients may require
mg/kg, IM† effect anesthesia additional hydromorphone
Hydromorphone: 0.05-0.1 Isoflurane: 3% Ketoprofen: 1.0 mg/kg, PO postoperatively.
mg/kg, IM Maintenance once daily for 2-3 days
⫾ Glycopyrrolate: 0.01 mg/ Isoflurane: 1.0%-2.0%
kg, IM
Onychectomy Premedication Induction Ketoprofen: 2.0 mg/kg, SC Moderate pain
(Protocol 1) Acepromazine: 0.1-0.2 Propofol: 4-6 mg/kg, IV to immediately after recovery from Digital nerve block reduces
mg/kg, IM effect anesthesia anesthetic requirements
Hydromorphone: 0.05-0.1 Isoflurane: 3% Ketoprofen: 1.0 mg/kg, PO and improves analgesia
mg/kg, IM Maintenance once daily for 2-3 days postoperatively.
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
Volume 25, Number 2, May 2010 79
ratory rate, heart rate, and blood pressure) that occur during
surgery as a result of noxious stimulation usually reflect inade-
Ketoprofen: 1.0 mg/kg, PO
Postoperative Management
Ketoprofen: 2.0 mg/kg, SC
*Some of these drugs are not approved for use in cats in Canada or the United States.
2 mg/kg.
Medetomidine: 0.01-0.02
mg/kg, IM
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