Delirium in the adult intensive care unit: does the chosen drug play a significant role?

Abstract

Characteristics of sedation and analgesia have moved from deep toward lightened and cooperative sedation and analgesia with control of delirium. Although sedative drugs potently modulate neurotransmission in the central nervous system (CNS) to provide their sedative effects, a body of recent work suggests that some of these properties may contribute to delirium and in turn to the long-term impairment of cognitive recovery after intensive care unit (ICU) stay. Delirium has been shown to predict both long-term mortality and severe cognitive sequelae after ICU stay. Classical sedatives (propofol, benzodiazepines) and analgesics are causative factors for delirium. Recently, dexmedetomidine, a potent, and short acting agonist of the alpha2-adrenergic receptors, has been developed as a primary sedative for ICU mechanically ventilated patients. This agent exerts its effects via a unique mechanism (agonist of the alpha2-adrenoceptors) which confers some favorable properties with respect to the goals to be achieved in a sedated, mechanically ventilated patient (cooperative sedation). This agent has been shown to reduce the prevalence of delirium and days with coma in comparison with a benzodiazepine-based sedation regimen. Its sedation profile preserves arousability and its mechanism of action preserves non rapid eye movement sleep, which may contribute to its delirium-sparing effects as well. The need for CNS acting drugs, such as sedatives and analgesics, has to be carefully evaluated on a daily basis at the bedside to limit the potential detrimental effects associated with oversedation in critically ills.