Chapter 19 The Prevention and Management of Pain in Canine Patients 493Chronic pain
Osteoarthritis
The most common chronic pain condition rec-
ognized in dogs, OA, also presents one of the
greatest challenges to treatment because of its
progressive pathology and difficulty in early
recognition. Indeed, in contradistinction to
humans, canine OA is largely conformational
in origin, meaning the inflammatory and
degenerative process begins at a very early
age—as young as puppies. We must begin to
conceive of canine OA as a lifetime disease,
subtly symptomatic in patients long before
they are obviously symptomatic to us, and
initiate preventative and therapeutic meas-
ures far earlier in life than we are usually
accustomed. Furthermore, OA is increas-
ingly recognized as a maladaptive if not
abjectly neuropathic pain state (present in
25% of human knee OA patients) (Hochman
et al., 2011).
The pain of OA is felt less at the damaged
articular surfaces than in the periarticular struc-
tures: an inflamed synovium, tension on a
fibrotic joint capsule, and exertion on weak-
ened ligaments, tendons, and muscle. OA is a
disease of the entire joint organ, and indeed of
the entire musculoskeletal system as the patient
shifts weight to other limbs, and treatment has
to be targeted accordingly.
Given the variable biological nature of OA,
paucity of properly designed multimodal
treatment studies in dogs, and widely diver-
gent client and veterinarian values, difficulty
exists in formulating a standard approach. Yet
it is possible to point out where the evidence is
strongest and the neurophysiological/phar-
macological rationale the most compelling.
Note that of the top five modalities from an
evidence‐based perspective, at least three of
them are non‐pharmacological in nature. It is
not all about drugs!
(1) NSAIDs: An abundance of literature in
humans and dogs, as well as two system-
atic reviews of treatments for canine OA,
reveal this class of drug to be, by far, the
most predictably effective therapy. The
new piprant class of anti‐inflammatory,
analgesic drugs are included here. The
new EP‐4 receptor antagonist Galliprant®
may be alternatively used.
(2) PSGAGs (Adequan®, CartrophenVet®)
and/or nutraceuticals (see Chapter 4).
(3) Weight optimization: This is the primary
preventative method to slow the develop-
ment of OA in dogs (Smith et al., 2006),
and is imperative if the patient is already
overweight. The role of adipose tissue as
a mediator of systemic inflammation, the
contribution of central obesity to chronic
pain in humans (doubling the risk for it;
Ray et al., 2011), and the primacy of
weight loss (just 6% in dogs) to diminish
OA pain is established (Marshall et al.,
2010). With an overweight patient, both
the clinician and client are wasting time,
energy, and money on other interventions
until and unless weight optimization is
achieved.
(4) Eicosapentaenoic acid‐rich diet (Mehler
et al., 2016): These formulations have been
demonstrated in several studies to elicit
improved gait, mobility, and an NSAID‐
sparing effect.
(5) Physical rehabilitation, one cornerstone of
which is therapeutic exercise. Controlled
exercise elicits hypoalgesia through a
variety of mechanisms: gate theory (spi-
nal‐level blockade of nociceptive signal-
ing in favor of touch, pressure, and
proprioception); activation of the endoge-
nous cannabinoid system; increased
strength and microstability of joint soft
tissue structures; and promoting weight
optimization.
(6) Pain‐modifying analgesic drugs: One or
more of the following:
(a) Amantadine
(b) Gabapentin or pregabelin
(c) ± Tramadol.
(7) New drugs to consider:
(a) Duloxetine or venlafaxine
(b) Tapentadol
(c) Acetaminophen + hydrocodone or
codeine (breakthrough pain only)
(d) Biological therapies (intra‐articular
PRP, stem cell transplantation, stro-
mal vascular fraction, autologous
conditioned serum).