We found substantial agreement among a large, interdisciplinary cohort of international experts regarding evidence supporting recommendations, and the remaining literature gaps in the assessment, prevention, and treatment of Pain, Agitation/sedation, Delirium, Immobility (mobilization/rehabilitation), and Sleep (disruption) in critically ill adults. Highlighting this evidence and the research needs will improve Pain, Agitation/sedation, Delirium, Immobility (mobilization/rehabilitation), and Sleep (disruption) management and provide the foundation for improved outcomes and science in this vulnerable population.

Delirium occurs frequently in critically ill patients and has been associated with both short-term and long-term consequences. Efforts to decrease delirium prevalence have been directed at identifying and modifying its risk factors. One potentially modifiable risk factor is sleep deprivation. Critically ill patients are known to experience poor sleep quality with severe sleep fragmentation and disruption of sleep architecture. Poor sleep while in the intensive care unit is one of the most common complaints of patients who survive critical illness. The relationship between delirium and sleep deprivation remains controversial. However, studies have demonstrated many similarities between the clinical and physiologic profiles of patients with delirium and sleep deprivation. This article aims to review the literature, the clinical and neurobiologic consequences of sleep deprivation, and the potential relationship between sleep deprivation and delirium in intensive care unit patients. Sleep deprivation may prove to be a modifiable risk factor for the development of delirium with important implications for the acute and long-term outcome of critically ill patients.

Objectives This study investigates the possibility of a relationship between oversedation and mortality in mechanically ventilated patients. The presence of burst suppression, a pattern of severely decreased brain wave activity on the electroencephalogram, may be unintentionally induced by heavy doses of sedatives. Burst suppression has never been studied as a potential risk factor for death in patients without a known neurologic disorder or injury. Design: Post hoc analysis of a prospectively observational cohort study. Setting Medical intensive care units of a tertiary care, university-based medical center. Patients A total of 125 mechanically ventilated, adult, critically ill patients. Measurements and Main Results A validated arousal scale (Richmond Agitation-Sedation Scale) was used to measure sedation level, and the bispectral index monitor was used to capture electroencephalogram data. Burst suppression occurred in 49 of 125 patients (39%). For analysis, the patients were divided into those with burst suppression (49 of 125, 39%) and those without burst suppression (76 of 125, 61%). All baseline variables were similar between the two groups, with the overall cohort demonstrating a high severity of illness (Acute Physiology and Chronic Health Evaluation II scores of 27.4 ± 8.2) and 98% receiving sedation. Of those with burst suppression, 29 of 49 (59%) died within 6 months compared with 25 of 76 (33%) who did not demonstrate burst suppression. Using time-dependent Cox regression to adjust for clinically important covariates (age, Charlson comorbidity score, baseline dementia, Acute Physiology and Chronic Health Evaluation II, Sequential Organ Failure Assessment, coma, and delirium), patients who experienced burst suppression were found to have a statistically significant higher 6-month mortality [Hazard’s ratio = 2.04, 95% confidence interval, 1.12–3.70, p = 0.02]. Conclusion The presence of burst suppression, which was unexpectedly high in this medical intensive care unit population, was an independent predictor of increased risk of death at 6 months. This association should be studied prospectively on a larger scale in mechanically ventilated, critically ill patients.