Sleep and circadian rhythms are essential regulators of physiological homeostasis, influencing immune, metabolic, cardiovascular, and neurocognitive functions. In critically ill patients, these systems are frequently disrupted by the intensive care unit (ICU) environment, therapeutic interventions, and underlying illness. Increasing evidence suggests that sleep and circadian dyssrhythmias are associated with clinical outcomes during and after critical illness. This narrative review summarizes current knowledge on sleep and circadian rhythm alterations in adult ICU patients and examines their associations with short and long-term outcomes. We review studies using a wide range of assessment tools, including polysomnography, electroencephalography, actigraphy, cardiopulmonary coupling, hormonal profiling (melatonin and cortisol), temperature rhythms and clock gene expression. The relationship between these alterations and outcomes such as respiratory recovery, delirium, inflammation, illness severity, mortality, and post-intensive care syndrome is discussed. Across multiple studies, disrupted sleep architecture, characterized by reduced total sleep time, loss of rapid eye movement sleep, and atypical electroencephalographic patterns, has been associated with prolonged mechanical ventilation, weaning failure, and noninvasive ventilation failure. Alterations in sleep and circadian rhythmicity are also linked to delirium and markers of acute brain dysfunction. Circadian rhythm disruption, reflected by blunted or phase-shifted hormonal rhythms and altered clock gene expression, correlates with systemic inflammation, disease severity, and adverse prognosis. Emerging data further indicate that sleep and circadian disturbances may persist long after ICU discharge and contribute to cognitive impairment, psychological distress, fatigue, and reduced quality of life. Although methodological limits remain, the available evidence supports sleep and circadian rhythms as clinically relevant biomarkers of critical illness severity and brain dysfunction. Whether these represent modifiable therapeutic targets that can improve prognosis requires confirmation through rigorous interventional trials designed to account for the substantial confounding inherent in this population.
