9 Lindsey C. Snyder1, Christopher Snyder1, and Donald Beebe2 1 School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA 2 Apex Dog and Cat Dentistry, Englewood, CO, USA It has been well documented that periodontal disease is extremely prevalent in the canine and feline populations (see Chapter 5 – Periodontology). The high prevalence of disease equates to a large number of small animal veterinary patients being anesthetized yearly for dental cleanings, diagnostics, and treatments. Since most patients will have justifiable reason to undergo general anesthesia multiple times in their lives for the purpose of maintaining a healthy and pain‐free oral cavity, considerations should be made to make general anesthesia as safe as possible. One study reported that the most common adverse events associated with general anesthesia (hypotension, cardiac dysrhythmias, blood loss, hypercapnea, or hypoxemia) occurred in as many as 12% of dogs and 10.5% of cats [1]. The use of pre‐anesthetics medications and regional anesthetic techniques with local anesthetics both offer the advantage that polypharmacy has to offer – a multimodal approach to delivering anesthesia and decreasing perception of noxious stimulation. Use of hydromorphone or oxymorphone as premedications have shown a reduction in minimum alveolar concentration (MAC) (hydromorphone decreased by 48% and oxymorphone by 43%) to respond to a noxious stimulus [2]. The administration of a local anesthetic alone has demonstrated a 23% reduction in MAC in dogs [3]. Pain, by definition, is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. In 1986, the International Association for the Study of Pain (IASP) defined pain as a sensory and emotional experience associated with real or potential injuries [4]. Pain begins at the site of tissue injury and is initiated by specialized nerve fibers called nociceptors. Nociceptors are free nerve ending receptors of sensory neurons responsible for sensing potentially damaging stimuli in response to tissue injury and are found throughout the tissues of the body. Nociceptors can be activated by mechanical, thermal, or chemical stimuli through the process of transduction. High threshold nociceptors are stimulated at the site of injury. With a high degree of mechanical stimulation induced by surgical trauma, mechanical, polymodal, and mechanothermal nociceptors would all be stimulated. The stimulus would then be transduced into electrical impulses that would be transmitted to the dorsal horn of the spinal cord via fast, myelinated A‐delta fibers and slower, unmyelinated C‐fibers. The afferent nerve, either A‐delta or C‐fibers, enters the spinal cord via the dorsal nerve root and terminates on the cells in the dorsal horn of the gray matter. Nerves may then ascend or descend one or two segments in Lissauer’s tract. The majority of A‐delta fibers terminate in the most superficial layer of the spinal cord, lamina I, or the marginal zone. Most C‐fibers also terminate in the superficial horn, lamina II, or the substantia gelatinosa. It is in the dorsal horn that modulation of nociceptive input occurs. The impulse is then projected to the cortex via the ascending spinal tracts. The spinothalamic tract is the most prominent nociceptive pathway. Originating in the dorsal horn, it crosses midline and courses cranially until it terminates in the thalamus. The spinoreticular tract also carries impulses to several midbrain sites. At supraspinal levels, nociceptive neurons have been identified in portions of the pons, midbrain, thalamus, hypothalamus, and cerebral cortex. The cortex modulates both the cognitive and aversive aspects of pain sensation and mediates complex behavior patterns through the perception of pain. Opioid, gamma aminobutyric acid (GABA), serotonin, and norepinephrine receptors are present in supraspinal centers. Descending pathways include motor pathways to alleviate pain as well as inhibitory pathways responsible for release of endogenous opioids affecting the dorsal horn. Peripherally, tissue damage by injury, disease, or inflammation releases endogenous algogenic substances into the extracellular fluid surrounding nociceptors. The substances (H+, K+, serotonin, histamine, prostaglandins, bradykinin, substance P) are directly excitatory to the nociceptor membrane, as well as indirectly through their effects on microcirculation (peripheral sensitization). In the dorsal horn of the spinal cord, glutamate, the major excitatory neurotransmitter in the nervous system found in almost every pain fiber [1], and aspartate act at excitatory N‐methyl‐D‐aspartate (NMDA) receptors (central sensitization). Activation of the NMDA receptor for glutamate leads to wind‐up pain, a state where a constant stimulus elicits responses that are 4–5 times increased despite the peripheral input remaining the same [5]. Substance P, a pain neuropeptide, is released in the spinal cord. Spinal neurons that become hyperexcitable have been shown to demonstrate reduced thresholds to stimulus, an increase in receptive field sizes, and ongoing activity despite the stimulus. These are the mechanisms that are likely to be the basis for allodynia, hyperalgesia, and spontaneous pain states [5]. Unlike inflammatory hyperalgesia that has a protective role, allodynia has no obvious biological utility to the organism [6]. Inhibitory receptors are also present in the dorsal horn, and include GABA, opioid, alpha‐2, and adenosine receptors. Within the supraspinal centers, release of endogenous opioids is connected to the periaquaductal gray area. The periaquaductal gray area is a major source of descending pathways responsible for modulatory control of spinal nociceptors [7]. Pain can be separated into inflammatory pain, where pain is induced by direct stimulation of nociceptors by inflammatory mediators released by damaged tissue (surgical or otherwise) and neuropathic pain, where pain is caused by a direct disease or trauma to a sensory nerve. Inflammatory pain is induced by chemical mediators, whereas neuropathic pain is induced by altered electrical signaling secondary to changes in the ion channels that produce action potentials within the nerves [5]. Pain can be further divided into visceral and somatic in origin. With the different types of pain, their management is different as well. For example, neuropathic pain is notoriously more difficult to treat than inflammatory pain. Cancer pain in the bone, either a primary tumor or via metastasis, is a severe type of pain that will become chronic if not treated appropriately [5]. Even small areas of pain can have enhancing effects on overall pain sensitivity. The chronic pain from myofascial temporomandibular joint (TMJ) disease can profoundly increase pain sensitivity of remote areas [8]. Non‐odontogenic sources of dental pain are reported in humans but have yet to be proven in veterinary patients [9]. Analgesics work at several sites along the pain pathway. Transmission can be inhibited by the use of local anesthetics at the site of injury as well as alpha‐2 agonist drugs. Transduction may be inhibited by administration of non‐steroidal anti‐inflammatory drug Due to the complexity of the pain pathway, the management of pain is complex as well. As a painful impulse passes through the many parts of the brain, the pathways become increasingly complex. At each level, the impulse is subject to enhancement and modulation [5], making management challenging. The intensity of the pain experience is variable in individuals, adding another layer to the challenge of treating pain. Pain is a multifaceted sensation involving the entire nervous system [5], thus using drugs that affect the various levels of the pain pathway, in combination, can be more effective than using one analgesic alone. This multimodal approach to pain management is now widely used in veterinary medicine to decrease the dose of individual analgesic drugs, thereby decreasing the side effects of individual drugs. The chronicity associated with many commonly presenting dental and oral conditions emphasize the need for multimodal techniques in the approach to pain management. A common method of pain management is to approach the pain pathway itself. By affecting the many steps in the pathway, pain can be minimized most effectively by utilizing multiple mechanisms. For example, using hydromorphone and dexmedetomidine as premedications for a younger dog, then inducing with propofol and maintaining anesthesia with isoflurane and supplementing with local anesthetic dental blocks, an NSAID and a fentanyl constant rate infusion, combined, would affect transduction, transmission, modulation, and perception. This would be an ideal plan, as all of the steps in the pain pathway are affected (Table 9.1). Table 9.1 Various steps of the pain pathway with associated medications providing anesthetic and analgesic activities. Individual drug pharmacology dictates the dosing and dosing intervals. For drugs with short half‐lives, a constant rate of infusion might be necessary for administration. Often, if using a longer acting drug, re‐dosing may be necessary mid‐procedure for surgeries lasting longer than the half‐life of the drug. Additionally, the chronicity of most dental conditions and wind‐up associated with chronic pain, pain management should not end with the completion of the procedure. Instead, pain management may require days to weeks of treatment for success. The authors refer the reader to other texts for pharmacokinetic and pharmacodynamic information of various analgesics in veterinary species, as that is beyond the scope of this chapter. Dental cleanings and oral treatment procedures both require access to the oral cavity while maintaining the patient under general anesthesia. Palatal surgeries involving the caudal oral cavity, caudal maxillectomy or mandibulectomy and maxillomandibular trauma reconstruction are all procedures in which the endotracheal tube may be a hindrance to surgical exposure or monitoring occlusion. Alternatives to conventional orotracheal intubation in various species include: pharyngostomy [10, 11], temporary tracheostomy [12], transmylohyoid intubation [13], and nasotracheal intubation [14, 15]. Alternatives to orotracheal intubation should be considered to improve visualization and surgical exposure, especially if a symphysiotomy approach is deemed necessary. Modifications to create a shortened endotracheal tube have been proposed as an alternative to repeatedly extubating the patient when verifying occlusion during fracture repair and placing orthodontic or prosthodontics devices [16]. Feline oral pain syndrome (FOPS) refers on a disorder affecting cats, resulting in an exaggerated response to a painful or non‐painful stimuli resulting in discomfort and mutilation [17]. The condition is believed to be a result of a nervous system dysfunction that either centrally or peripherally affects the ganglion of the trigeminal nerve. Burmese cats were overrepresented in one study (88%), which suggests a heritability component of the condition [17]. The condition may be analogous with other allodynic conditions and similarly responds to distracting the patient or use of anticonvulsants. Bimodal age distribution of cats (<12 months of age and 7 years of age) demonstrated that young and middle‐aged cats are predisposed. No specific sex predilection has been reported. Some cats have been shown to demonstrate clinical signs during permanent tooth eruption and pain subsides following eruption of the canine teeth, while others commonly demonstrate signs following triggers such as eating, drinking or grooming. Most cats demonstrate unilateral discomfort affecting one side of the face. All patients should be closely evaluated for signs of oral lesions or pathology. While the specific trigger or etiology of the condition may not be specifically known, some cats show improvement of signs following dental treatments suggesting that other sources of oral pain may contribute to this behavioral disorder. Response to therapy seems individual and variable regarding which medications may be most helpful at managing the condition. Medications reported as being helpful have included: NSAIDs, corticosteroids, antibiotics, phenobarbital, diazepam, amitriptyline, and opioids. Reported successful treatment of FOPS cases treated with phenobarbital and diazepam support the belief that this is a manifestation of neuropathic pain. Local anesthetic agents should be considered as part of the overall analgesic management of the dental patient. These agents decrease transmission of nociception to the central nervous system (CNS) by selectively binding ion‐selective Na+ channels, thereby preventing nerve impulse transmission. This results in a preemptive analgesic effect. Removal of noxious stimulation should also result in a decreased need for general anesthetics, and potentially promote a faster smoother recovery from general anesthesia. Longer‐acting local anesthetic medications may help attain a smoother transition from the peri‐operative period to the post‐operative period. Incorporation of local and regional anesthesia will decrease requirements for other analgesic agents, allowing for formulation of a more balanced multimodal approach to pain control. Pain perception occurs via simulation of A‐delta and C nerve fibers in the dental pulp. Acute pain is perceived by stimulation of A‐delta fibers while C‐fibers are associated with chronic, dull discomfort and chronic stimulation. Stimulation of nerve fibers occurs by transduction of stimuli into the nerve terminus and propagation of the signal through nerve fibers (transmission) and opening and closing of sodium channels. Pain is modulated at the level of the central nervous system after propagation of the signal through the pre‐ganglionic trunk. Sensitization is the phenomenon by which the threshold of nerve stimulation is lowered. Sensitization can also occur centrally, resulting in an exaggerated perception of pain for stimuli that would normally be perceived as non‐painful. Considering the prevalence of periodontal disease, conditions of hyperalgesia (increased response to a normally painful stimulus) and allodynia (perceived pain resulting from a non‐painful stimulus) are likely to impact many veterinary patients. Regional anesthetic alone has demonstrated a reduction in minimum alveolar concentration by 23% in one study [3]. Lidocaine is labeled for veterinary use, but benefits of longer acting local anesthetics are used off‐label for the benefits of increased duration of action. While other local anesthetics are recognized to demonstrate prolonged effects, one study has questioned the efficacy of the local anesthetic in the porcine model evaluating a palatal nerve block [18]. Anatomic landmarks for the local anesthetics are listed below; however, it remains difficult to accurately assess the successful placement of the drug when performing either the caudal maxillary nerve block [19] as well as potential unreliable effects when performing the middle mental nerve block [20]. The proper placement of local and regional nerve blocks requires comprehensive knowledge of neuroanatomy and relevant anatomical landmarks. Sensory innervation to the oral cavity is primarily from two branches of the trigeminal nerve (cranial nerve V), the maxillary nerve, and the mandibular nerve and their branches. The maxillary nerve originates from the round foramen and courses rostrally along the dorsal margin of the medial pterygoid muscle to the pterygopalatine fossa. At this location the maxillary nerve branches, giving rise to the zygomatic and pterygopalatine nerves and continues as the infraorbital nerve as it passes through the maxillary foramen into the infraorbital canal. The pterygopalatine nerve branches into the major and minor palatine nerves, which innervate the soft and hard palate. Immediately before entering the infraorbital canal, the infraorbital nerve gives rise to the caudal superior alveolar nerve, which innervates the first and second molars. Within the infraorbital canal the middle and rostral superior alveolar nerves branch from the infraorbital nerve, supplying sensory innervation to the premolars via small foramina at the floor of the canal, and to the canines and incisors via the incisivomaxillary canal. The infraorbital nerve exits at the infraorbital foramen branching into the external nasal, internal nasal, and superior labial nerves. At the level of the infraorbital foramen, sensory innervation to the dentition and its associated bone and soft tissue structures has already disseminated. Desensitization of these tissues requires deposition of local anesthetic caudal to the infraorbital foramen, either within the canal or at the pterygopalatine fossa. The mandibular nerve originates from the round foramen, courses rostrally along the medial side of the TMJ and gives rise to the buccal, the masseteric, and the auriculotemporal nerves. The buccal branch courses laterally and provides sensory innervation to vestibular mucosa and skin ventral to the zygomatic arch. The masseteric branch supplies motor innervation to the masseter muscle. The mandibular nerve continues rostrally to the medial surface of the caudal mandible. The mandibular nerve continues rostrally as the inferior alveolar nerve as it enters the mandibular canal via the mandibular foramen, where alveolar sensory branches are given off to the teeth. Just caudal to the mandibular canal entrance, two branches arise, the lingual and mylohyoid or inferior alveolar nerves. The lingual nerve provides sensory innervation to the rostral two‐thirds of the tongue and, via the sublingual branch, to the sublingual mucosa. The mylohyoid innervates the mylohyoid muscle and rostral belly of the digastricus muscle; it also provides sensory innervation to the caudal two‐thirds of the intermandibular mucosa. The inferior alveolar nerves course rostrally within the mandibular canal, providing sensory input to the mandibular teeth via foramina in the canal wall. The nerve branches rostrally into the caudal, middle, and rostral mental nerves, exiting at three corresponding mental foramina. The mental nerves provide sensory innervation to the lower lip and rostral one‐third of the intermandibular area. At the level of the middle mental foramen, the inferior alveolar nerve has already passed on sensory innervation to the teeth; to desensitize dentition and associated structures requires infiltration of local anesthetic caudal to foramen. Local anesthetic medication can be easily administered using a one milliliter syringe and small gauge needle. Size 25‐ to 30‐gauge needles are commonly used with needle lengths ranging from 5/8 to 1.5 inches. Regular needles for injection are frequently used for local block administration but short, atraumatic “b‐bevel” needles are also available and in unconfined spaces may be more efficient at displacing rather than penetrating the nerve [21]. Large or giant breed dogs using certain intraoral approaches to the caudal maxillary nerve block may require additional needle length and an over‐the‐needle catheter or spinal needle may be necessary. Glass cartridges preloaded with a local anesthetic agent may be used with a metal administration syringe. However, the availability of disposable syringes is commonplace in veterinary dentistry.
Anesthesia and Pain Management
9.1 Introduction
9.2 Pathophysiology of Pain
s( NSAIDs), opioids, local anesthetics, and corticosteroids. The modulation of the spinal pathways can be altered by the use of local anesthetics (epidural, spinal), opioids (epidural, spinal, systemic), NSAIDs, NMDA antagonists (systemically, epidurally, spinally), tricyclic antidepressants, and anticonvulsants. Perception at supraspinal levels can be inhibited by the administration of anesthetics, opioids, alpha‐2 agonists, benzodiazepines, and phenothiazines.
9.3 Management of Pain
Transduction
The process in which afferent nerve endings take part in translating noxious stimuli (e.g., a needle stick) into a nociceptive impulse
Local anesthetics
NSAIDs
Transmission
The process in which impulses are sent to the dorsal horn of the spinal cord
Local anesthetics
Modulation
The process of decreasing or amplifying the pain‐related neural signals, primarily in the dorsal horn of the spinal cord, with input from ascending and descending pathways
Local anesthetics
Opioids
Alpha‐2 agonists
NSAIDs
Projection
The process of sending the pain impulse from the dorsal horn of the spinal cord to the higher levels of conscious perception
Local anesthetics
Perception
The subjective experience of pain that results from the interaction of transduction, transmission, modulation, and awareness of nociception
Opioids
Alpha‐2 agonists
Centrally acting analgesics
NSAIDs
9.4 Airway Management
9.5 Feline Oral Pain Syndrome (FOPS)
9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
9.6.1 Intraoral Regional Nerve Blocks
9.6.2 Drugs and Materials
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