Dexmedetomidine Administration in the Post-Anesthesia Care Unit

Introduction:

Dexmedetomidine is an alpha-2 adrenergic agonist, similar to Clonidine. The alpha-2 agonists have both analgesic and sedative effects. It is not used as an anesthetic in humans as such but in combination with other drugs. It is used for purposes like sedation (calm or sleeping state), analgesia (painless state), and anxiolysis (anxiety-free state). It has been used along with regional blocks to prolong the duration of anesthesia. In awake craniotomy procedures and fiberoptic intubation Dexmedetomidine has been used for procedural sedation. It is also used for ICU (intensive care unit) sedation in ventilated patients and those recovering from cardiac surgery. In children, it has also been used as an adjuvant to general anesthesia to minimize the incidence of delirium post-inhalational anesthesia. It has other uses, like treatments for alcohol withdrawal. It is considered to be superior in control approach in surgeries like bariatric and gynecological surgeries, laparoscopic procedures, major spine surgeries, and colorectal and hysterectomy surgeries. It is also the sedative of choice in patients with acute lung injury.

What Are the Properties of Dexmedetomidine?

• This drug is approved only for intravenous injections.

• Intravenous sedation in awake adults is started with a one microgram per kilogram loading dose that is administered for five to ten minutes, followed by a maintenance infusion of 0.2 to 1.4 microgram per kilogram per hour.

• It is also used as nasal and oral premedication.

• Dexmedetomidine has a short elimination half-life of fewer than three hours and rapid redistribution in minutes.

• It is metabolized in the liver, and cautious usage is to be followed in patients with liver disease.

• All the Dexmedetomidine metabolites are excreted in the urine.

What Are Dexmedetomidine’s Effects on Different Organ Systems?

1. Cardiovascular: According to research studies, a loading dose of Dexmedetomidine produces a small, transient rise in blood pressure along with reflex bradycardia (decrease in heart rate). Depending on the dose and rate of administration, Dexmedetomidine may produce bradycardia, hypotension, or hypertension in the patients. These side effects can be minimized by avoiding rapid bolus dosing.
2. Cerebral: Dexmedetomidine produces dose-dependent sedation. Since it is an opioid-sparing agent, it can significantly reduce general anesthesia requirements. Dexmedetomidine is the choice of agent for patients who are undergoing awake craniotomies.
3. Respiratory: Dexmedetomidine can be ideal for patients who are accustomed to mechanical ventilation as it does not produce any respiratory depression. It is also used for sedation in patients undergoing awake tracheal intubation.
4. Drug Interactions: In patients receiving beta-blockers, Dexmedetomidine can cause exaggerated bradycardia. So careful dosing is necessary.

How Is Dexmedetomidine Administered in a Post-anesthesia Care Unit?

Intraoperative usage of Dexmedetomidine can reduce the usage of intravenous and volatile anesthetics. In the perioperative period, Dexmedetomidine usage can blunt many of the cardiovascular responses due to its sedative, analgesia, and sympatholytic effects. Dexmedetomidine, when used post-operatively, especially in PACU (post-anesthesia care unit), helps prevent ventilatory depression. Some researchers have suggested Dexmedetomidine has neuroprotective effects, and some have suggested it has renoprotective effects. Supplemental administration of Dexmedetomidine will help decrease delirium following cardiac surgery. It will help protect the brain from the toxic effects of the anesthetic agents.

It is common for an opioid like Morphine or Hydromorphone, along with either Propofol or Dexmedetomidine, to provide analgesia and sedation during ICU transfers. Postoperative sedation can be maintained with Dexmedetomidine infusion.

Dexmedetomidine, given at the dosage of 0.5 micrograms per kilogram slowly with constant heart rate monitoring over 15 to 20 minutes before the end of tracheal intubation, will help reduce the emergence of delirium and agitation if the procedure is likely to produce postoperative pain. For postoperative pain management, a multimodal technique incorporating Ketorolac and intravenous Dexmedetomidine will reduce opioid dependency in pain patients.

What Are the Effects of Dexmedetomidine Usage in the PACU?

Postoperative hyperthermia (core temperature of lower than 36 degrees celsius) is an unpleasant and detrimental condition that occurs after general and neuraxial anesthesia. Postoperative shortening is also often seen after general and neuraxial anesthesia. According to ASA (American society of anesthesiologists), a patient's temperature should be measured within 15 minutes after surgery, and it should ideally be at least 36 degrees Celsius. Intraoperative infusion of Dexmedetomidine has been shown to be an effective prophylactic against complications. Along with local anesthesia (LA), additives like Clonidine, Dexamethasone, and Dexmedetomidine have been used to increase the duration of action of LA. In the PACU, bradycardia is usually iatrogenic and is due to drug-related causes that include beta-blocker therapy, anticholinesterase reversal of neuromuscular blockade, opioid administration, and treatment with Clonidine or Dexmedetomidine.

For postoperative pain, non-opioids like Dexmedetomidine can be used to prevent opioid dependency. It will also help in reducing the incidence of respiratory-related events like respiratory depression and post-operative arrest. In both cardiac and non-cardiac patients use of Dexmedetomidine in place of Propofol has reduced the incidence of PND (perioperative neurocognitive disorders) like delirium. Dexmedetomidine has been increasingly used in the ICU compared to benzodiazepines, as it reduces the incidence of postoperative delirium (POD).

It is also used in painful patients with extreme tolerance to Morphine. For patients with burn injuries, Dexmedetomidine has been used for providing sedation analgesia so as to decrease opioid requirements. In patients with hepatic impairments, Dexmedetomidine will be slowly eliminated; hence there is a necessity for dose reduction in such patients. Heart rate and cardiac output show a concentration-dependent decrease. Dexmedetomidine is used during a procedure to provide better hemodynamic stability for the patients and improved pain response compared to Ropivacaine. It has been used in the PACU for enhanced recovery after surgery (ERAS) and has given rise to improved postoperative outcomes and early discharge from PACU.

Conclusion:

Dexmedetomidine is the most recently released intravenous anesthetic. It is a highly selective alpha-2 adrenergic agonist that produces sympatholytic, hypnosis, sedation, and analgesia. Its usage is approved for ICU sedation of mechanically ventilated and intubated (initially) patients for up to 24 hours. It is also used in procedural sedation of non-intubated patients. With increasing frequency, Dexmedetomidine is also used as a sedative during invasive or radiological procedures and as an adjuvant for central or peripheral neneural blocks. It has minimal effect on respiration.