486 Canine Sports Medicine and Rehabilitation
Commercial 5% lidocaine patches (Lidoderm®)
are labeled for humans with postherpetic neural-
gia (shingles), but have been described for
postoperative paraincisional analgesia in dogs
(Weil et al., 2007), with minimal systemic absorp-
tion noted (Weiland et al., 2006). The adhesive
patches can be cut to the desired size and shape.
One cautionary note is that an entire patch
contains 700 mg of lidocaine, a toxic dose if
ingested; therefore, adequate precautions must
be taken.
Intravenous lidocaine
There is evidence in humans for intravenous
lidocaine’s (IVL) anesthetic‐sparing effect, and
its ability to speed the return of bowel function,
decrease postoperative pain, minimize opioid
consumption, and shorten the hospital stay
after abdominal surgery (Groudine et al., 1998).
Evidence in dogs is somewhat weaker at this
point (MacDougall et al., 2009), although there
may be a synergistic effect with other drugs.
Formulas for a combination morphine, lido-
caine, and ketamine i.v. CRI have been described
for dogs (Muir et al., 2003). The combination is
profoundly analgesic, fairly sedating, and is
superior for the most painful postoperative
states. IVL has also been shown to elicit a sus-
tained effect on neuropathic pain in humans
(Cahana et al., 1998).
Other drugs in class
● Mexilitine is an oral sodium‐channel
blocker, often called oral lidocaine and
labeled for use as a cardiac antiarrhythmic.
It has also been used to treat chemotherapy‐
induced neuropathic pain states in humans
(Egashira et al., 2010). Its utility for chronic
pain conditions in dogs is unestablished.
Subanesthetic ketamine constant rate
infusion
NMDA receptor antagonism remains a research
focus for pain in humans (Fisher et al., 2000).
Ketamine is a dissociative anesthetic that binds
to a phencyclidine receptor inside the NMDA
receptor (i.e., the calcium channel would
already have to be open and active for ketamine
to exert its effect). Once bound, it decreases the
channel’s opening time and frequency, thus
reducing Ca+ ion influx and dampening sec-
ondary intracellular signaling cascades. It
appears to be protective against hyperalgesia
and central hypersensitization in the postoper-
ative setting (Hocking et al., 2007), including in
the dog (Slingsby & Waterman‐Pearson, 2000),
and the evidence in humans is strong for its
pain‐preventive effects when given intrave-
nously as a CRI at subanesthetic doses. Ideal
subanesthetic ketamine plasma concentrations
in the dog have been reported at 2–3 μg/mL,
which can be achieved by administering keta-
mine i.v. CRI at 10 μg/kg/min (Boscan et al.,
2005). The 2015 AAHA/AAFP Pain Management
Guidelines state that clinicians should consider
the modality as part of a multimodal approach
to transoperative pain management, especially
in patients at risk for maladaptive pain (Epstein
et al., 2015). Such patient populations include,
but are not limited to, those with nerve injury
(including iatrogenic, e.g., amputation), severe
tissue trauma (surgical or otherwise), and
with long‐standing inflammation (e.g., OA) or
pre‐existing chronic pain condition.Tips for use
The recommended intraoperative rate can be
accomplished by placing 60 mg (0.6 mL of 100
mg/mL stock) ketamine in 1 L of fluids admin-
istered at intraoperative rates of 10 mL/kg/h.
Postoperatively, the rate can be reduced to
maintenance rates of 2 mL/kg/h, which admin-
isters the ketamine CRI at 2 μg/kg/min. A
loading dose of 0.25–0.5 mg/kg ketamine i.v. is
recommended prior to the initiation of the CRI
in order to rapidly achieve plasma levels.Alpha‐2 agonistMedetomidine and dexmedetomidine bind to
opioid‐like receptors on C‐ and A‐delta fibers,
especially in the central nervous system.
Binding presynaptically, norepinephrine pro-
duction is reduced and sedation occurs; bind-
ing postsynaptically, analgesia is produced,
and is profoundly synergistic with opioids. It