Pain management for oral surgery in dogs and cats
Aug 01, 2007
Understanding the terminology and physiology and managing oral pain in our patients is the focus of this series.
This month, the concepts of nociception, peripheral sensitization and central sensitization will be discussed as they relate to patient management.
The second part of the series will provide a detailed description of regional nerve blocks for oral surgery. The third will describe agents commonly used for analgesia. A discussion of chronic-and cancer-pain management and clinical use of constant-rate infusions will conclude the series.
The conversion of a noxious stimulus (mechanical, chemical or thermal) into electrical energy by a peripheral nociceptor or free afferent nerve ending is termed transduction. The propagation of the impulse from the site of oral injury through primarily trigeminal afferents is referred to as transmission. The nerve fibers responsible for sharp pain are the fast A-delta fibers. Dull, throbbing pain is caused by stimulation of slow C fibers. A-beta nerve fibers are tactile and consequently have a much lower threshold. Neurons from these fibers synapse with nociceptive-specific and wide-dynamic-range neurons in the medulla's nucleus caudalis, resulting in modulation. Nucleus caudalis tissue is very similar to that of the spinal cord dorsal horn that modulates pain from areas other than the oral cavity. Exitory neuropeptides, like glutamate and substance P, are active in the synapse and facilitate the pain signals by binding to their receptors on these neurons. Concurrently, endogenous (opioid, serotonergic and noradrenergic), descending analgesic systems serve to decrease the nociceptive response.
Following surgical manipulation of the oral cavity we can expect a greatly enhanced postoperative nociceptor response to any additional stimulation. The resulting enhanced response is termed peripheral sensitization (hyperalgesia).
Primary hyperalgesia is the term for peripheral hyperalgesia at the actual site of the injury. The damaged tissue releases a number of compounds, including ATP, potassium ions, hydrogen ions, prostaglandins, bradykinin and nerve growth-factors. Lymphocytes, monocytes, macrophages and mast cells are attracted to the site. These inflammatory cells then release cytokines that amplify and potentiate inflammation. Histamine is among the list of cytokines released that enhance vasodilation, causing plasma extravasation into surrounding tissues. As a result this "sensitizing soup" of substances extends beyond the actual site of tissue injury into the surrounding normal tissue, producing secondary hyperalgesia. Now even non-noxious stimuli, such as touch, can produce pain at and around the site of injury (allodynia).
Left untreated, peripheral sensitization produces similar changes in the wide dynamic range neurons of the nucleus caudalis producing a state called central sensitization or "windup."