Pain
Management





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 thing 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 modulation 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.

Sometimes 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 are 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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