Pain and Sedation Assessment

Chapter 161 Pain and Sedation Assessment






DEFINITION OF PAIN


Pain has been defined by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”1 By definition, then, pain is a subjective event and cannot truly be measured by an objective observer.


The perception of pain and response to a noxious stimulus is determined not only by the degree of injury, but also the individual’s unique experience. Pain assessment becomes inherently more difficult in veterinary patients as a result of the obvious limitations of verbal communication, with attempts to anthropomorphize the animal’s behavior, which increase the degree of error in our assessment. As a result, a number of assessment techniques have been published in the veterinary literature over the past several years, some of which are undergoing validation using strict criteria.


In contrast, nociception involves the series of electrochemical events that start at the site of tissue injury and result in the perception of pain. These events can be monitored, measured, and quantified in an experimental setting. Nociception generally involves four distinct processes:






In addition, the processes involved in the perception of pain are no longer viewed as a static system. Long-term changes occur within the peripheral and central nervous systems following noxious stimulation, that then alter the body’s response to further sensory input.



PAIN VERSUS STRESS


In general, physiologic and behavioral responses to pain have been used to develop a number of assessment tools or rating scales to determine the level of pain and/or sedation in the veterinary patient. These scales may change depending on the circumstances under which they are used (e.g., acute pain following trauma or surgery versus chronic pain of orthopedic or neuropathic origin), the underlying disease process (e.g., cancer versus orthopedic disease), and the location (somatic versus visceral, deep versus superficial) or severity of the inciting stimulus.


It is important to recognize that these pain scoring systems have little value in optimizing our analgesic therapy unless the person implementing them has a basic understanding of pain physiology and pathways. Understanding mechanisms of pain transmission and antinociceptive mechanisms allows a logical choice in prescribing analgesics for our patients. Analgesia may be directed toward minimizing inflammatory changes at the site of injury, inhibiting transduction or transmission of the nociceptive signal (both at peripheral and spinal endings), or increasing the activity of descending inhibitory pathways acting at the central nervous system. For example, opioids have traditionally been viewed as centrally acting drugs and most frequently are given systemically. However, they may also be given epidurally or intrathecally, stimulating opioid receptors found at the level of the spinal cord to produce analgesia. In addition, there is now evidence for the action of endogenous opioids on peripheral sites following tissue damage.


Opioid receptors are manufactured in the cell body (dorsal root ganglion) and transported not only toward the central terminal in the dorsal horn, but also toward the periphery. These peripheral receptors then become active following tissue damage or chronic inflammation (e.g., within the joint capsule). This has led to an interest in the peripheral administration of opioids, such as intraarticular administration of morphine in dogs following cruciate ligament repair.


Another confounding factor in assessing pain in our veterinary patients is that it is frequently accompanied by stress and anxiety. The stress response may occur in the absence of injury and in response to any number of environmental factors, including restraint, new surroundings, the presence of other animals, or other perceived threat to the animal. As anxiety increases the stress response to a painful stimulus, the response itself begins to negatively affect the individual. Such responses include behavioral changes associated with “fight or flight”; neuroendocrine responses including cortisol release, hyperglycemia, and catecholamine release; and physiologic changes associated with sympathetic nervous system stimulation (e.g., tachycardia, hypertension, vasoconstriction), immunosuppression, and hypercoagulability.


In terms of pain assessment, many of the physiologic changes seen during the stress response are similar to those seen in the pain response. The patient may not eat nor sleep well and, in conjunction with the neurohormonal responses, this sets up an overall catabolic state. Although it is incumbent upon the medical provider to treat the animal on the assumption that it may be in pain, frequently it is not possible to quiet the animal using analgesics alone and a sedative agent such as diazepam, midazolam, acepromazine, or low-dose α2-agonist must be added to reduce the anxiety and allow the animal to rest and recuperate.

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Pain and Sedation Assessment

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