 Once
we accept the fact
that animals feel
pain in a manner very similar to the way we feel pain,
the question immediately arises as to what can we do
about that pain. The short answer is, "Lots." There
are a variety of drugs and techniques available to help
ease the pain our furry companions feel.
Some of this is pretty technical. Every practitioner
has certain "hobbies" within the scope of their
practice. These are areas that the practitioner finds
particularly interesting, and about which he or she
develops a high degree of skill and expertise. I
personally (Dr. Nield, that is), find pain management
very interesting, and have over the years spent a lot of
time studying and researching this fascinating field.
While I can't claim to be a specialist in pain
management (it is not ethical to claim to be a
specialist in something umless you are board certified
in thast field), I do believe that we do an excellent
job of managing pain at Sunnyside Veterinary Clinic, and
that we have some things to offer that you may not find
just anywhere else.
Pain is a sensation we feel when our body is
damaged.
That is how nature
lets us know that there is a problem. In this respect,
pain has a physiologic function, because it leads us to
avoid the thi ng
thsat caused the pain (pulling away from a hot stove),
to protect the injured part while it heals (not walking
on a broken leg), and to even begin treatment of a wound
(in the case of dogs, licking a wound).
Pain
starts with receptors
at the ends of
nerves called nociceptors.
The word itself comes from the same roots as the words
noxious and
receptor. Nociceptors
are activated by bad things, like
 burns,
cuts, blunt trauma, stretching, chemical reactions etc.
They are also activated by pressure, touch, and other
normal stimuli. Some areas, like the skin, are
well-supplied with nociceptors. Other areas, like the
liver, have very few nociceptors. There are separate
nociceptors for heat, stretching, touch, and trauma. Here,
mechanical, chemical, and thermal energy causes the
nociceptors to be activated. The chemical stimuli can
come from either outside sources, such as an acid burn,
or internal sources. When tissues are injured, say by a
bruise or a cut, they release a number of substances.
Histamine, prostaglandins, bradykinins, and other
compounds associated with inflammation are released
which act directly on the nociceptors.
A
particularly interesting aspect
of
nociceptor function is
peripheral
sensitization. Sensory endings
in inflamed tissue display
 enhanced
sensitivity to stimulation so that ususally non-painful
stimuli become painful (allodynia) and the perception of
painful stimuli becomes more intense (hyperalgesia).
Various inflammatory mediators like histamine,
bradykinins, and prostaglandins have been shown to cause
sensitization in this way. Thus, the sensory endings of
nociceptors are modulated and, through them, the
perception of pain.
Once
nociceptors are activated,
they
send signals up the nerves towards the brain. There are
different kinds of nerves. There are
fast "A-delta" nerves, which rapidly carry the initial
sensation sharp pain, slow "C" nerves which carry
the secondary dull, throbbing pain sensations, and very
sensitive "A-beta," or tactile nerves , which have a
lower threshold of stimulation and which are responsible
for our sense of touch.
The first stop is the spinal cord.
Here, a complex process of switching, routing, and modul ation
occurs. The spinal cord is the first place the body
tries to make sense out of all the varied and assorted
signals the injured area sends it. All the different
signals from all the different types of nociceptors and
all the different types of nerve fibers converge for the
first time in the spinal cord.
S ometimes
good things happen
to the pain signal in
the spinal cord, sometimes bad things happen to the pain
signal. In a certain region of the spinal cord, called
the dorsal horn, a lot of bad things can happen to a
pain signal. Through a process called "dorsal
horn wind-up," a form of
central sensitization,
a relatively mild pain stimulus can be amplified and
modulated such that it becomes exagerated. Long after
the initial cause of the pain has subsided, dorsal horn
wind-up can result in prolonged and exaggerated pain.
The
next stop for the pain signal is the brain.
Once the modified
pain signal reaches the brain
it is processed further. Things like fear and anxiety
are allowed to modify the pain sensation. All of the
pre-processed signals from all of the various nerves are
processed into the
perception of pain. This final result
is the sum of all the pre-processing that goes on in the
nociceptors, nerves and spinal cord combined with a lot
of post-processing that occurs in the brain itself. In
some cases, all the pain signals bouncing around can
lead to a generalized hyperexcitiablity called central sensitization,
which can lead to excessive pain.
One
of the most important concepts to master
about pain
management is the idea that our nerves are not
just wires that carries pain signals from point A to the
computer-like brain, which then impartially processes
the pain signal. On the contrary, our nervous system
processes pain a lot like a community processes a
disaster. Several different people may see an accident
happen (the nociceptors), but each may report it in a
different way. Some people are more excitable than
others, and some may give an inflated report (peripheral
sensitization). They then pass the initial report along
to other people at the coffee shop (the spinal cord),
and there may be considerable discussion with some wild
speculation thrown in. Sometimes things get out of hand
(dorsal horn wind-up), and a exaggerated message
emerges. The coffee shop people pass their information
as they perceive it along to the newspaper (the brain),
where the editorial committe tries to process it. Like
most committees, sometimes excitable people can dominate
the process (central sensitization), leading to a
response that may or may not be appropriate for the
original accident.
Because of the complexities of the nervous system,
with all it's
nociceptors, nerve fibers, dorsal horns, and brain
synapses, there are a lot of points at which we can
control and modify the pain signals. Lets start at the
very beginning and evaluate how various drugs can modify
the pain process.
The nociceptors are where the pain response
begins.
Several classes of
drugs act directly on the nociceptors to modify the pain
response. Non-Steroidal Anti-Inflammatory Drugs, or
NSAID's
for short, are one such class. Aspirin, ibuprofen,
meloxicam, phenylbutazone, and Rimadyl are all NSAID's.
They act to reduce the amount of prostaglandins that are
released by injury, thus reducing their direct nociceptor
stimulation and their peripheral sensitization.
A second class of drugs that act directly on the
nociceptors are the local
anesthetics. These are drugs like
lidocaine, bupivicaine, and novocaine. They are
injected at the site of pain, and they totally block the
nociceptors temporarily, just like when we go to the
dentist's and he injects novocaine into our gums.
Blocking the pain, even temporarily, can have a great
effect even after the local anesthetics wear off because
that prevents the spinal cord and brain from getting
over-zealous in thier modification of the pain response.
A third class of drugs that can act on the nociceptor
level are the opioids.
They will be discussed in depth later, but there are
some opioid receptors present in the periphery, and they
can have a local effect there.
The next place we can influence the pain
response is at the spinal cord.
Here, drugs like
opioids
are very useful. Opioids are named after opium (opium-oid),
which as we all know is a very potent drug derived
 from
poppies that was commonly abused in the last few
centuries. There are many opioids, including heroin,
codeine, morphine, hydromorphone, fentanyl,
buprenorphine, nalbuphine, tramadol, and
a dozen others. Opioids act on
opioid receptors,
which are
specialize sites on nerves that bind the opioid molecule
and cause it to have an effect on the nerve.
This
effect is an actual blunting of the pain response.
There are lots of opioid receptors in the spinal cord,
and opioids act on them to decrease, often dramatically,
the pain response. Opioids turn the volume down, so to
speak. Way down. Anyone who has had an opioid before
will attest to their beneficial properties.
Other drugs can have an effect on the spinal cord.
NMDA antagonists are
one such class. Most people ar e
not familiar with NMDA antagonists. However, there are
NMDA receptors located in the spinal cord. These NMDA
receptors, when activated, produce a prolonged and
excessive pain response, even to injuries which should
not be all that painful. This is called
dorsal horn wind-up,
a form of central
sensistization. NMDA antagonists block
the NMDA receptors, preventing them from being
activated. A perplexing assortment of drugs have NMDA
antagonistic properties:
ketamine (an anesthetic),
dextromethorphan
( the cough suppressant in Robitussin), and
amantidine
(an anti-viral agent, also used to treat Parkinson's
Disease) are the most commonly used.
Other drugs called Alpha-2
agonists also work to reduce pain at the
level of the spinal cord. These drugs also have strong
sedative effects
The final place we can influence the pain
response is the brain.
Fortunately, there are lots of opioid receptors in the
brain. Here, these drugs can have a profound effect on
how much things hurt. Opioid receptors in the brain
also produce some fairly profund behavioral changes as
well. This would explain the popularity of such drugs
of abuse as opium and hashish. Many opioids produce a
sense of immense well-being, euphoria, or being high.
The concept of Pre-emptive Pain Medication is
very important.
Simply put, if
pain medications are given before the painful stimulus,
the over-all pain response is greatly reduced. The
nervous system will amplify and distort pain signals
that are received suddenly. The initial rush of pain
signals overwhelms the system, and nociceptors are
up-regulated, dorsal horn wind-up occurs, central
sensitization happens, and we consciously perceive the
pain to be greater than it really needs to
be. Pre-emptive pain management is giving pain control
medication before the pain even starts, thus damping
down the pain response mechanisms, preparing the nervous
system to handle the up-coming painful stimulus in the
most favorable way.
Multi-modal Pain Management is
another important concept.
This involves using different drugs from each class.
Say we give a normal dose of drug X, but the patient is
still painful. If we give more drug X, the comfort
level may increase, but we will also start to get bad
side-effects too and the levels of drug X climb. For
example, too much morphine is not a good thing because
of the severe respiratory depression it can cause.
However, if instead of giving the patient more drug X we
give a normal dose of drug Y, which acts in a different
way (or mode) than drug X, the patient will likely be
much more comfortable without experiencing any adverse
side effects. Th effects of drug X and drug Y will be
additive if not synergistic. If we add a dose of drug Z
to boot, the patient will experience great pain relief
while still not experiencing bad side-effects.
This is where the field of pain management overlaps with
the field of anesthesia. It is possible to design a
pre-op and inter-op anesthesia plan that will synergize
and compliment the post-op pain control plan. It is
also possible to design an anesthesia plan that will
provide absolutely zero pain relief (besides
unconsciousness). This is where anesthesiology becomes
both a science and an art, choosing medications that
will provide maximal benefit to each individual patient.
An example of Multi-modal, Pre-emptive Pain
Management
Let's consider a surgery for a ruptured ACL in a dog.
This is a major orthopedic surgery, and is known to be
quite painful. The patient is three years old, and
otherwise healthy. An ideal plan might start with a
pre-anesthetic injection of
hydromorphone, a potent
opioid,
combined with a low
 dose
of an alpha 2 agonist
such as medetomidine.
This combination provides a double-dose of pain relief
plus anxiety relief, a good thing when you are going in
to surgery. (2 modes so far)
The next step in a multi-modal approach would be to give
a little more hydromorphone as an epidural incection.
This route applies the potent opioid directly to the
spinal cord. At the same time it is often beneficial to
add bupivicaine
and lidocaine,
both local anesthetics,
to the epidural. (Now we are up to 3 modes)
When inducing anesthesia, it is a good idea to use a
protocol that involves
ketamine, an
NMDA antagonist
(mode 4) that doubles as an anesthetic.
This sets the stage to run a constant rate infusion
containing both ketamine
and lidocaine
and maybe more
hydromorphone. During
surgery, it is helpful to apply a low dose of
bupivicaine
directly inside the joint. (mode 5)
Post-op, a
constant rate infusion of
hydromorphone, ketamine and lidocaine
does wonders for the immediate post-op period.
(a continuation of modes 1 and 4)
For the next week or so, oral doses of
Rimadyl, a
powerful NASID
makes the recovery period comfortable. (mode
6)
By using
many different drugs, all at lower doses than would be
required were only one drug given, we can blunt the pain
response in many additive and synergistic ways.
Veterinarians, being both anesthesiologist and
surgeon and follow-up care provider
to their
patients, are in a much better position to administer
excellent pain control protocols to their patients than
many humans get when they have surgery. The
anesthesiologist never sees the patient after they roll
out of ther OR, the surgeon isn't in a position to tell
the anesthesiologist what to do, and neither are around
to help the patient cope with post-op discomfort.
Pain control
is both an art and a science.
Anmials
feel pain just like humans do, although they may not
show their pain in obvious ways. At Sunnyside
Veterinary Clinic, we feel an obligation to treat pain
in our animal patients as if it were our own pain. We
use pre-emptive, multi-modal anesthesia and pain control
plans, sometime simple, sometimes complex, but always
tailored to each individual patient's needs.
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