Correspondence  |   August 2017
Nocturnal Dexmedetomidine in Nonintubated, Critically Ill Patients: Sleep or Sedation?
Author Notes
  • Kansas University Medical Center, Kansas City, Kansas (H.G.M.).
  • (Accepted for publication May 8, 2017.)
    (Accepted for publication May 8, 2017.)×
Article Information
Correspondence   |   August 2017
Nocturnal Dexmedetomidine in Nonintubated, Critically Ill Patients: Sleep or Sedation?
Anesthesiology 8 2017, Vol.127, 397-398. doi:10.1097/ALN.0000000000001721
Anesthesiology 8 2017, Vol.127, 397-398. doi:10.1097/ALN.0000000000001721
In November 2016’s issue of Anesthesiology, Wu et al., in their article “Low-dose Dexmedetomidine Improves Sleep Quality Pattern in Elderly Patients after Noncardiac Surgery in the Intensive Care Unit: A Pilot Randomized Controlled Trial,”1  demonstrated polysomnographic improvement in sleep in patients treated with low-dose (0.1 µg kg−1 h−1) prophylactic dexmedetomidine. Although many nonpharmacologic strategies have been proposed to improve sleep quality in the intensive care unit (ICU), nocturnal infusions of the α-2 agonist and sedative dexmedetomidine have been increasingly utilized in nonintubated ICU patients in efforts to reduce the incidence or duration of delirium, which affects 20 to 80% of ICU patients and is associated with prolonged lengths of stay and possibility increased mortality.2  Because the efficacy of the treatments of delirium have been disappointingly limited, increasing enthusiasm has been placed on preventative techniques, such as ensuring that ICU patients achieve adequate durations of sleep.3  A pathophysiologic rationale for this therapy comes from observational polysomnographic studies that demonstrated a dramatic reduction in both restorative rapid eye movement (REM) and slow-wave (stages 3 and 4) sleep in ICU patients.4,5  Dexmedetomidine infusions generate an electroencephalogram pattern that resembles stage 2 non-REM sleep in treated patients, which is the basis of its usage in the ICU to promote sleep.4,5  However, in these polysomnographic studies, treated subjects also demonstrated severely disrupted overall sleep architecture, with few achieving slow-wave sleep or REM sleep of any significant duration.4,5  In addition, an animal study demonstrated a complete loss of REM sleep with dexmedetomidine infusions, with treated rats requiring significant posttreatment rebound in both non-REM and REM sleep need.6  In the study by Wu et al.,1  there was no significant difference in the occurrence of stage 3 non-REM sleep, and REM sleep remained absent in the two groups. Although they demonstrated an improvement in sleep efficiency or the ratio of total sleep time to total monitoring time, this metric does not account for sleep architecture. Importantly, there was also no observed difference in delirium, a predefined secondary outcome. In addition, the authors noted a decreased ICU length of stay but an increased hospital length of stay in dexmedetomidine patients.
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