Key Clinical Questions
What are common causes of sleep disturbance in hospitalized patients?
How do you approach the patient complaining of sleep disturbance?
Which inpatient populations are at high risk of sleep disturbance, and what are the corresponding common primary or secondary sleep problems?
How do you choose a hypnotic agent based on etiology of insomnia and medical comorbidities?
What are the nonpharmacologic behavioral alternatives in cases of insomnia, hypersomnia, or sleep disturbance secondary to circadian mismatch?
Sleep remains one of the least understood physiological processes, despite the significant percentage of our lives spent in the sleep state. As such, it is at the modern day frontier of not only scientific inquiry but also clinical knowledge and practice. Perhaps nowhere is this better illustrated than in the inpatient setting where, despite our increasing understanding of the wide-ranging role of sleep on a spectrum ranging from mood and attentiveness to metabolic physiology to molecular signaling in the healthy state, little effort is expanded to optimize sleep quantity and quality during acute illness and recovery. In fact, little is known about sleep architecture, duration, and disturbance in the inpatient setting, and correlates of sleep variables with clinical outcomes. However, it is estimated that approximately one-third of hospitalized patients have insomnia at the time of admission. Additionally, up to 69% of postsurgical patients continue to complain of prolonged sleep problems after hospital discharge. The high prevalence of sleep disturbance among this population warrants the evaluation and treatment of sleep problems as part of routine hospital care. Early recognition and treatment of sleep complaints may improve recovery among hospitalized patients.
Sleep disturbance in the outpatient population, primarily as investigated in the context of obstructive sleep apnea (OSA) associated both with recurrent hypoxemia but also recurrent arousals resulting in sleep fragmentation and sympathetic overactivation, has been implicated in increased morbidity and mortality in a variety of cardiovascular (refractory hypertension, congestive heart failure [CHF], atrial fibrillation, stroke), metabolic (insulin resistance, diabetes, obesity), and psychiatric (mood disorders, anxiety) phenotypes. Outside of OSA, self-reported, and therefore subjective, short (<6 hours) and long (>10 hours) overnight sleep duration have both been associated with increased cardiometabolic morbidity and mortality in large epidemiological studies. This, at first glance contradictory, proposed inverted U shape relationship of sleep duration and mortality may be due to two aspects of sleep. The first refers to the current leading hypothesis as to the primary purpose of sleep, namely a “restorative” anabolic function, perhaps especially of slow-wave or “deep” sleep, the latter necessary for growth hormone secretion. The hypothesis is that persistently shortened sleep duration, either due to overall shortened sleep zone or recurrent sleep interruption, may curtail the organism’s chance of physiological restoration.
Indeed, studies of chronic partial sleep deprivation in humans demonstrate metabolic disturbance with decreased leptin (satiety hormone) and increased ghrelin (appetite stimulating hormone) secretion, hypothermia due to impaired temperature regulation, acute insulin resistance equivalent to ...