1. To understand the function of dexmedetomidine as an analgesic
2. To understand proper patient selection with dexmedetomidine
3. To understand the different routes of administration of dexmedetomidine
Many clinics throughout the world use dexmedetomidine for sedation. But, did you know that dexmedetomidine is also labeled as an analgesic a fact that often gets overlooked in practice. Dexmedetomidine is the active S-enantiomer of the alpha-2 agonist medetomidine. Removal of the inactive molecule, levomedetomide results in dexmedetomidine being a “purified” product with increased potency and decreased stress on the liver. Many practices are familiar with dexmedetomidine as an alpha-2 agonist sedative that is reliable, fast-acting, and reversible with atipamezole.
Dexmedetomidine and medetomidine’s main effects are to produce sedation with both somatic and visceral analgesia. Analgesic effects of dexmedetomidine are principally due to spinal anti-nociception via binding to non-noradrenergic receptors (heteroreceptors) located on the dorsal horn neurons of the spinal cord (Stein 2013). This mechanism of action inhibits the release of norepinephrine (a catecholamine released by the adrenal gland and part of the fight-or-flight response) and therefore prevents transmission of further nerve impulses. This provides both sedation and analgesia.
Dexmedetomidine is also being used frequently as an in hospital constant rate infusion for rough recoveries and breakthrough analgesia. Constant rate infusion of low dose dexmedetomidine (1 to 2 mcg/kg/h); can be used in severely painful or anxious patients to provide sedation and analgesia. Dexmedetomidine can also be added to a preexisting opioid infusion for increased sedation and analgesia. Because dexmedetomidine has the potential to cause severe bradycardia and hypotension, these patients should be monitored very closely by a dedicated recovery technician. A loading dose of at least 0.5 µg/kg (0.0005 mg/kg) dexmedetomidine IV should precede the initiation of the dexmedetomidine CRI (Zeltman 2013).
Epidural use of dexmedetomidine can enhance the analgesic effects of other agents given epidurally. Besides the previously mentioned action at heterotropic spinal receptors, dexmedetomidine also produces analgesia by stimulation of cholinergic interneurons when given epidurally (Gaynor, Muir 2009). It acts synergistically with epidural opioids, improving the quality and duration of analgesia, and recent human studies have shown that the addition of 2 µg/kg dexmedetomidine epidurally to 2.5 ml of intrathecal bupivacaine prolongs the duration of analgesia, and decreases the requirement of rescue analgesics in patients undergoing lower-limb orthopedic surgery (Jain 2012). It should be noted that, dexmedetomidine is highly lipophilic, and is rapidly absorbed from the epidural space, which can lead to systemic levels of the drug.
Dexmedetomidine is gaining some ground recently as more practices are experimenting with using it transmucosally in felines, in addition to the intramuscular and intravenous routes. Transmucosal dosing allows even fractious cats to receive sedation and analgesia. Often cats given transmucosal dexmedetomidine are not at a surgical plane of anesthesia but are sedate enough to allow physical exams, blood draws, and IV catheter placement. Dexmedetomidine can also be combined with buprenorphine and given via the oral-transmucosal route (Santos 2010). Oral dosing can range from 20–40 mcg/kg.
It should be noted that dexmedetomidine has serious cardiac side effects and seriously effects cardiac output. Dexmedetomidine and medetomidine should be reserved for patients that are heart healthy and have no exercise intolerance. alpha-2 agonists are not intended for animals with respiratory or cardiovascular compromise.
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