Clinical application, the use of dexmedetomidine in intensive care sedation

Optimal sedation strategy in the critically ill should achieve effective analgesia, targeted sedation and reduced risk of delirium and agitation. Whilst there is no single agent that can achieve these goals for all patients, a multimodal approach may optimise the use of different agents through multiple modes of action and reduce possible adverse events. This practice review provides an evidence based and expert opinion on the practical aspects of dexmedetomidine use as part of multimodal ICU sedation. Dexmedetomidine, when compared to conventional sedatives and opiates, has been demonstrated to be associated with both sedative and analgesic sparing effects, reduced delirium and agitation, minimal respiratory depression and predictable and desirable cardiovascular effects. In the intensive care setting, dexmedetomidine has been effectively used in post operative analgesia and sedation of high risk and complex surgical patients, and during transition from other conventional sedatives. Critically ill patients requiring ventilation for more than 24 hours and patients who experienced emergent agitation and or delirium have also been successfully managed with a dexmedetomidine regimen. Supplementary sedation and analgesia in addition to dexmedetomidine may be required to optimise comfort and safety in critically ill patients. Dexmedetomidine cannot be used to achieve deep sedation or to control acutely agitated or combative patients; therefore additional and rescue conventional sedatives may be required in some patients. A loading dose is unnecessary in most patients and if given, may increase the risk of hypotension and bradycardia. Although the current licensed dose is 1 μg/kg/hr, the maximum dose of dexmedetomidine used in ICU sedation clinical trials is 1.5 μg/kg/hr. Dexmedetomidine must not be given as a bolus at any time to avoid exaggerated cardiac depression. Dexmedetomidine infusion has dose dependent central nervous system and cardiovascular system effects with bradycardia and hypotension as the commonest side effects. It produces a state of sympatholysis, central sedation with significant synergy with other sedatives and analgesics. A starting dose in most patients is 0.4 μg/ kg/hr with hourly titration to achieve desired sedation. Withdrawal or addition of conventional sedatives and analgesics can be used to fine tune the desired sedation target and achieve optimal analgesia. There is no need to stop dexmedetomidine infusion prior to extubation. Withdrawal of dexmedetomidine was not associated with any nervous or cardiac manifestations of withdrawal. Dexmedetomidine is relatively contraindicated in patients with recent free microvascular flap surgical procedures, cerebrovascular surgery or with a risk of vasospasm or severe liver dysfunction and its safety has not been established in pregnancy. From Prince of Wales Hospital, Randwick, NSW, Australia (Yahya Shehabi), Frankston Hospital, Frankston, VIC, Australia (John A. Botha), Box Hill Hospital, VIC, Australia (David Ernest), Hawke’s Bay Hospital, Hastings, New Zealand (Ross C. Freebairn), Austin & Northern Hospitals, University of Melbourne, VIC, Australia (Michael Reade), Sir Charles Gairdner Hospital, Perth, WA, Australia (Brigit L. Roberts), University of Sydney, Nepean Hospital, Penrith, NSW, Australia (Ian Seppelt and Leonie Weisbrodt). Address for correspondence: Associate Professor Yahya Shehabi Medical Director, Acute Care Program, Intensive Care Services, Prince of