Pain was adopted as the fifth vital sign in human medicine in 1996 following the objective pulse, blood pressure, respiration and temperature. In veterinary medicine we are following suit as identification and treatment of pain in our patients has become an integral part of practicing better medicine. Despite the fact that the majority of us probably prescribe some level of pain reducing medication every day of practice, pain management in veterinary medicine is still in its infancy. Until recently, pain management was an elective in veterinary school rather than a requirement. The various classes of analgesics from opioids to NMDA antagonists to alpha-2 agonists were taught in the context of anesthesia – what would lead to MAC (minimum alveolar concentration) sparing effects, side effects etc.
Treating pain appropriately and effectively is dependent on an understanding of the underlying pathophysiology. An extensive detailed review is beyond the scope of this article and the reader is referred to the attached references to gain a more in depth understanding. The basic pain pathway begins with a noxious stimulus that is transduced by a nociceptor into an action potential that is then transmitted via an afferent neuron to the dorsal horn of the spinal cord. In the dorsal horn of the spinal cord, the action potential is received, modulated and projected to the brain where perception occurs.
Over the years, I have adopted certain axioms that guide my own pain management techniques and protocols which I hope in sharing will help others:
- Multimodal analgesia is best. As evidenced by looking at the pain pathway in the most basic way, there are multiple levels where we may decrease or inhibit pain in our patients. At the level of the nociceptor (transduction/transmission) local anesthetics are our most potent analgesic, although opioids and non-steroidal anti-inflammatories can provide analgesia on this level. When looking at the level of the spinal cord (modulation/projection), it is here where the majority of analgesics can exert an effect – the aforementioned ones in addition to alpha2 agonists, NMDA antagonists, SSRIs, and anticonvulsants. Finally, we can change the perception of pain by using anesthetics, benzodiazepines, and phenothiazines in addition to opioids and alpha2 agonists.
An applied example of multimodal analgesia is a vehicular trauma dog that presents with evidence of a pelvic fracture, degloving over the right rear distal limb, and pulmonary contusions. On admit this dog would benefit from a full mu-agonist, lidocaine splash block over the degloving site post initial lavage and rough debridement and placement of a wet to dry bandage. Ongoing in hospital care may include an opioid CRI paired with a ketamine CRI with an indwelling epidural catheter for local anesthetic infusion. Post surgical repair, a possible multimodal analgesic discharge plan may include a fentanyl patch with ongoing administration of gabapentin and a NSAID with tramadol as needed.
- Look for evidence of pain in a behavior change – especially in cats. Signs of pain are not always as obvious as when a pet attempts to bite with manipulation of a limb or palpation of the abdomen. Pain may be more subtle such as in an older cat who does not vocalize with palpation, but who the owner reports is sleeping in unusual areas or defecating outside of the litterbox. Undiagnosed chronic pain associated with osteoarthritis or chronic pancreatitis may present in this fashion.
- Do not fear using full mu-agonists. In my experience, the one analgesic in our arsenal that should be used in the majority of situations is a full mu-agonist. There is a fear of using these analgesics with pets that may present in shock due to concern for cardiorespiratory depression. Cardiac depression is a more human specific phenomenon, while respiratory depression can occur in our veterinary patients – but tends to be minimal until the opioid is combined with an inhalant anesthetic. The advantage of using full mu agonist over buprenorphine or butorphanol is not only an increased level of analgesia, but the ability to reverse the effects if undesirable. One of the worst initial analgesics to administer a trauma patient or acute abdomen is buprenorphine as it may not be sufficient for the animal’s analgesic needs, it cannot be readily reversed, and due to its strong affinity to the mu-receptor it may decrease the efficacy of any full mu-agonist that is subsequently administered.
- Always err on the side of treating for pain. As veterinarians, we are all amateur behaviorists and can pick up clinical signs of pain in our patients that a layperson may overlook. Where we may fall short in our assessment is in an obtunded patient or a patient in shock. Even in a pet that may be too metabolically or hemodynamically compromised to demonstrate signs of pain, the pain pathway may still be active and ongoing. The cost of not treating pain is far greater in most situations than the risks of using analgesia in a compromised patient. Untreated pain can result in ileus, immunosuppression, decreased tissue healing, significant loss of quality of life and in its most severe manifestation – maladaptive pain. The single best rule of thumb is that if the pet has a condition that you believe would be painful to you, analgesia should be provided.
- Be always on the lookout for maladaptive pain and neuropathic pain. As alluded to above, maladaptive pain is essentially pain without purpose and is a direct result of untreated acute pain or ongoing pain that persists after the inciting insult has been resolved. Neuropathic pain can be viewed as a subset of maladaptive pain as it is due to pain as a result of damage to a part of the nervous system (most commonly peripheral nerves). This damage to the nervous system can manifest as allodynia (pain associated with a non-painful stimulus) and hyperalgesia (exaggerated pain response to a painful stimulus) due to up regulation of pain facilitating receptors in the spinal cord and recruitment of sensory receptors as nociceptors. In our patients, this type of pain may be present as behavioral (tail chasing, loss of interest in normal activity), dermatologic (self trauma) or any other number of conditions (feline interstitial cystitis, Chiari malformation…). We need to be aware of this type of pain as it is typically refractory to analgesics such as opioids, and it is not the same as chronic pain. Neuropathic and maladaptive pain has been documented to develop within hours of an insult. These patients may require ketamine to reduce the wind up or ongoing therapy with gabapentin or amantadine to regain quality of life.
- Anxiety is pain. When an animal is anxious, the increased level of circulating catecholamines and cortisol potentiates and exaggerates the pain response. Combining analgesia with anxiolytic therapy is ideal to treat pain effectively and prevent maladaptive pain. Commonly used medications in our ICU setting for anxiety are trazodone and midazolam and at times the use of sedatives such as phenothiazines or alpha2 agonists are warranted to allow a patient to rest. It is important to remember that out of the above listed drugs only the alpha 2 agonists have analgesic effects. The most effective way to treat anxiety in the clinical setting is in combination of an analgesic (e.g. opioids) with a sedative or anxiolytic.
- Always elect for reversible medications if able. Choosing your analgesics by ease of reversal can be essential when performing an analgesic trial or treating a depressed patient. Full mu-agonists remain my first choice as one can fully reverse their effects with naloxone or provide partial reversal with butorphanol (mu antagonist, kappa agonist). When using naloxone, one must remember the duration of action is only 30 to 60 minutes and a patient can become renarcotized if not observed. I prefer using butorphanol at 0.1 mg/kg as it has been observed to reverse more of the depressive effects of full mu-agonists while leaving and potentially potentiating the analgesic effects.
- The analgesic protocol should always be adapted to the individual patient. There is no “one size fits all” dosing for pain medications. For geriatric or neonatal patients, I tend to administer a smaller dose as their volume of distribution and ability to metabolize is different than an adult animal. For conditions which have the potential for intense pain such as feline urethral obstruction, thromboembolism, gastric dilation volvulus or comminuted open fractures, I will use the higher end of the dose range.
- Don’t forget to utilize loco-regional analgesia. Local anesthetics such as lidocaine and bupivacaine are the most potent analgesic in our arsenal as they can physically stop pain at the level of transduction by inhibiting sodium channels and by extension inhibiting action potentials. Numerous techniques exist for blocking peripheral nerves whether an intercostal block for rib fractures or a sacrococcygeal block for feline urethral obstruction. The caveat with local anesthetics is that as potent as they are for providing analgesia, they are largely non-specific in their action. These drugs can block sodium channels indiscriminately resulting in profound CNS or cardiac complications. In addition, cats are markedly more sensitive to the side effects of lidocaine.
- Complementary therapies and continuing your education! All of this talk of pharmacology is only a singular part of the pain management world. Here in emergency and ICU we tend to use mainly pharmacologic analgesics, but do explore other modalities such as acupuncture. Besides acupuncture, the availability of therapeutic laser and targeted pulse electromagnetic therapy in practice along with rehabilitation techniques and facilities give us more means in which to provide effective pain management. Complementary therapies also include basic nursing care: hot and cold compresses, splinting/casting for stabilization, increasing patient comfort.
I believe that one of the most crucial steps in pain management is remaining current on the literature and new developments as this field remains rapidly changing.In the next decade, we may be seeing the advent of stem cell therapy and cannibinoid based medications for our pets.In addition, certain pain medications such as tramadol may be falling out of favor in dogs.With oral administration in dogs, tramadol produced minimal levels of M1 metabolite.The M1 metabolite is the active one that carries all of the opioid-like effects.Recent studies have demonstrated that tramadol may not be an effective pain medication administered alone to a dog, especially in the case of orthopedic pain and we may be giving tramadol for the benefit of the serotonin uptake inhibiting effects in dogs – not the mu-agonist effects we were hoping to produce.
In conclusion, the days where animals were assumed to not feel pain are long past. Besides the inherent better medicine and better business aspects, pain management remains one of the moral imperatives that we have as practicing veterinarians. To ignore pain or minimize it is to do a disservice to our patients and to the oath we took as veterinarians to relieve animal suffering.
Handbook of Veterinary Pain Management. Gaynor/Muir. 2014
Essentials of Small Animal Anesthesia and Analgesia. Grimm, Tranquill, Lamont. 2011
AAHA/AAFP Pain Management Guidelines for Dogs and Cats.