Chapter 94. Insomnia: Assessment and Management of Sleep Disorders

1. Why is it important to understand the regulation of normal sleep?

2. What are the most common causes of disrupted sleep in hospitalized patients?

3. What are the consequences of sleep deprivation?

4. What are the key questions that an examiner should ask when approaching a patient with impaired sleep?

5. What are nonpharmacologic and pharmacologic modalities for preventing and treating sleep problems in hospitalized patients?

Sleep disruption is a common problem among hospitalized patients. Patients frequently report disturbed sleep not only during their hospital stay but also prior to and after discharge. 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 clinicians to incorporate the evaluation and treatment of sleep problems as part of routine hospital care. In order to effectively treat sleep complaints, one has to understand the regulation of normal sleep and how various disorders may influence or impair this process. Early recognition and treatment of sleep complaints can improve recovery among hospitalized patients.

Even in healthy individuals, partial and total sleep deprivation significantly impacts sleep architecture and sleep quality. Evidence supports that persistent lack of sleep can impair physiologic processes and could potentially affect recovery from acute illness or injury. Sleep duration, architecture, and the sleep–wake cycle are closely associated with many metabolic and regulatory processes. Sleep deprivation can result in detrimental physiologic and psychological sequelae. Sleep deprivation has been associated with insulin resistance, impaired postural control, decreased ventilatory drive, increased sympathetic cardiovascular activation, blunted hypothalamic–pituitary–adrenal axis responsiveness, and impaired host defenses. The lack of restorative sleep increases the risk of developing anxiety, mood disorders, and delirium, especially in acutely ill older patients. In the presence of acute physical infirmity, inadequate sleep may further compound illness and recovery.

Sleep architecture refers to a characteristic pattern of sleep and includes two major stages: non–rapid eye movement (NREM) and rapid eye movement (REM) sleep. Normal sleep latency, or time to fall asleep, is usually 10 to 20 minutes, and total sleep time ranges from 6 to 9 hours per 24 hours. NREM sleep consists of three stages (S1–S3), with each stage leading to a progressively deeper level of sleep. S3 is known as deep sleep or slow-wave sleep (SWS), is predominant during the first third of the sleep period, and is believed to be necessary for physiologic restoration. SWS is associated with a decrease in metabolic rate, heart rate, and oxygen consumption and is anabolic in protein and hormone synthesis. REM sleep follows SWS and is characterized by an activated brainwave pattern seen with electroencephalography (EEG), muscle paralysis (atonia), and periodic bursts of rapid eye movements. Dreaming occurs during REM sleep and is hypothesized to be essential for emotional and cognitive well-being. REM sleep is a catabolic phase and can be associated with cardiovascular and respiratory instability. REM sleep occurs predominantly in the later period of sleep. Additionally, the ability to consolidate sleep declines with age, requiring most elderly persons to nap during the day in order to achieve a normal total amount of sleep.

Sleep disruption may also occur when regulatory processes are impaired or altered. Sleep regulation is a balance between a homeostatic or biologic need for sleep or “sleep debt” and the intrinsic body clock, or circadian pacemaker. Homeostatic mechanisms are regulated in the preoptic area in the brain, while circadian systems are governed by the suprachiasmatic nucleus (SCN) of the hypothalamus. Melatonin, a hormone produced by the pineal gland, is associated with sleep induction. It builds up as darkness increases and is inhibited by ambient light. The adrenal secretion of cortisol follows a circadian pattern and peaks in the early morning hours in preparation for the increased metabolic demands during wakefulness. Neurotransmitters are intrinsically involved in sleep regulation and include gamma-aminobutyric acid (GABA), serotonin, histamine, norepinephrine, acetylcholine, hypocretin, glutamate, and glycine. REM sleep is promoted by acetylcholine. SWS is induced primarily by GABA. Neurotransmitters that promote wakefulness include acetylcholine, histamine, noradrenaline (norepinephrine), serotonin, dopamine, and hypocretin (orexin). Many of the drugs that are commonly prescribed in hospitalized patients affect one or more of these neurotransmitters, thus promoting sedation (antihistamine) or activating effects (dopamine) such as wakefulness, and, in vulnerable patients, delirium.

There are numerous factors that may contribute to disturbed sleep in hospitalized patients, including primary sleep disorders, medical illnesses, psychiatric illness, drugs, and the hospital environment. Additionally, the manifestations of sleep disruption and/or sleep deprivation will vary depending on the individual.

Common Sleep Disorders

By far, insomnia is the most common sleep complaint among patients in both ambulatory and hospital settings. The prevalence of chronic insomnia is high, with approximately 20–30% of the general population reporting ongoing symptoms. Chronic insomnia is associated with decreased quality of life, daytime functional limitations, chronic pain, increased risk of medical and psychiatric illnesses, substance abuse, increased utilization of health services, and increased risk of death.

Insomnia can manifest in several ways. The International Classification of Sleep Disorders (ICSD-2) published by the American Academy of Sleep Medicine (AASM) defines insomnia as difficulty initiating or maintaining sleep, waking up too early, or sleep that is chronically nonrestorative or perceived to be poor in quality. To meet diagnostic criteria for insomnia, these symptoms must be associated with daytime mental or physical sequelae that impair the functional status of the individual. Insomnia may be a primary disorder or may be comorbid with another physical or mental illness.

In the landmark Sleep Heart Health Study, population subgroups were identified who were at increased risk for poor sleep. Older individuals (> 60 years old) were shown to have a lower arousal threshold associated with increased awakenings at night, decreased sleep efficiency, and decreased REM quantity. Each of these changes contributes to poor sleep quality and can result in poor daytime functioning, excessive sleepiness, or cognitive changes, which are commonly noted in the elderly. Although women demonstrated increased SWS compared to men, they had more complaints of poor sleep quality associated with worsening daytime functioning. The precise reason for this is unknown but is speculated to involve hormonal influence as well as greater prevalence of comorbid conditions associated with insomnia, such as depression.

Other common primary sleep disorders that frequently coexist with medical illnesses include obstructive sleep apnea (OSA), restless leg syndrome (RLS), and periodic limb movement disorder (PLMD). Table 94-1 describes these common sleep disorders and provides differential diagnoses to consider. These disorders may present with a variety of symptoms.

OSA affects approximately 24% of men and 9% of women in the United States and is associated with substantial mental and physical morbidity. Untreated OSA likely contributes to a significant proportion of acute hospital admissions, particularly for heart or respiratory failure. OSA may go unrecognized until a patient is incidentally hospitalized and observed to have difficulty breathing, paradoxical breathing, or oxygen desaturation. Risk factors for OSA include obesity, hypothyroidism, male gender, family history, African American race, and certain craniofacial characteristics: acromegaly, micrognathia or retrognathia, large tongue, or Mallampati class 3–4. OSA is characterized by episodes of complete or partial pharyngeal obstruction during sleep that cause snoring, apneic episodes, choking, dyspnea, and restlessness. These episodes are associated with intermittent nocturnal sympathetic activation leading to nocturnal awakenings and cortical arousals, all of which lead to daytime symptoms of fatigue, sleepiness, and cognitive impairment. Chronic sympathetic activation and intermittent hypoxemia are associated with increased vascular injury and inflammation that are known to occur in cardiovascular disease. Treatment of OSA with positive airway pressure (PAP) is shown to improve control of hypertension, diabetes, pulmonary hypertension, atrial fibrillation, and mortality.

Approximately 20% of patients with OSA will have concomitant RLS or PLMS/D, which are distinct problems and need to be differentiated from peripheral neuropathy and positional or nocturnal leg cramps. RLS is thought to affect as much as 40% of the population and is characterized by an unpleasant crampy, “creeping” or “crawling” sensation in the lower extremities that is relieved by persistently moving the legs. RLS frequently starts in the late evening or before bedtime, and often is a major cause of sleep-onset insomnia. The requisite bed rest during hospitalization can worsen RLS, further exacerbating sleep problems. It is also associated with many metabolic disorders, particularly renal disease, iron deficiency, and diabetes. Other conditions associated with RLS include pregnancy, rheumatoid arthritis, fibromyalgia, multiple sclerosis, and Parkinson disease. The etiology of RLS is not completely understood, but it may relate to inadequate generation or transport of dopamine due to iron deficiency or other metabolic disturbances. Serum iron and ferritin levels should be evaluated and treated if ferritin levels are < 75 μg. Aggressive treatment of other underlying diseases should be considered as first-line therapy. Selective serotonin uptake inhibitors (SSRIs) and alcohol may exacerbate RLS and should be avoided. Additional treatment includes the use of a dopaminergic agent at bedtime, such as ropinirole (Requip). Other agents that are effective, particularly in individuals with neuropathy, are gabapentin, narcotics, and benzodiazepines.

PLMD occurs in about 80% of those with RLS and is characterized by stereotyped involuntary limb movements that occur every 20 to 40 seconds during sleep. These can result in frequent cortical arousals, daytime somnolence, and fatigue. PLMS are found at higher frequency in several medical conditions, including hypertension, renal disease, and alcohol dependence. PLMS can be treated with longer-acting benzodiazepines such as clonazepam, and with dopaminergic agents.

General Medical Disorders

Numerous medical illnesses can directly impair sleep physiology, leading to a cyclical interaction in which impaired sleep impedes recovery (Figure 94-1). Table 94-2 lists selected medical and neurologic conditions, their associated sleep-related problems, and suggestions on how to alleviate these problems.

A recent study examined risk factors for sleep disturbance during hospitalization and found that the severity of comorbid conditions and poor performance of activities of daily living (ADL) predicted sleep complaints during admission. Physician awareness of the impact of sleep disturbance in hospitalized patients is vital since about half of patients admitted on general medical wards will complain of sleep disruption.

Patients with pulmonary disorders and OSA can be profoundly affected by the normal physiologic changes that occur during sleep, particularly in REM sleep. REM sleep is associated with increased upper airway collapsibility and accessory muscle atonia (causing decreased muscle strength), which can result in episodes of marked oxygen desaturation. Patients with chronic obstructive pulmonary disease (COPD) demonstrate decreased total sleep time (TST), SWS, and REM sleep due to shortness of breath, nocturnal cough, and wheezing that impair sleep quality and duration. Sleep deprivation then further negatively impacts the work of breathing, creating a vicious cycle. Noninvasive positive pressure ventilation (NPPV) improves sleep efficiency, total sleep time, and quality of life in patients with hypercapnic COPD without significantly improving gas exchange and should be considered as an adjunctive therapy for improving sleep and quality of life in these patients.

Endocrine and metabolic disorders have also been associated with sleep disruption. Patients with diabetes mellitus have decreased total sleep time and impaired sleep quality due to nocturia and neuropathic pain. Inadequate sleep may also affect glucose control. Inadequate quality or quantity of sleep has been shown to be a risk factor for developing type 2 diabetes mellitus in large prospective studies and is associated with increased levels of glycosylated hemoglobin (HbA1c) in patients with type 2 diabetes mellitus. Both hypo- and hyperthyroidism have been associated with sleep disruption. Hypothyroidism is associated with daytime somnolence, fatigue due to reduced SWS and often coexists with OSA. Hyperthyroid patients often complain of insomnia, which has been attributed to a hypermetabolic state.

Neurologic and Psychiatric Conditions

Since the brain and its various neurotransmitter systems are critical in regulating sleep and wakefulness, patients with neurologic disorders have an increased risk of developing sleep disorders. Common problems include increased sleep fragmentation and wakefulness, with increases of stage 1 sleep and reductions of SWS and REM. Patients with neurodegenerative disorders have an increased risk of REM sleep behavior disorder characterized by vivid and unusual dreams with physically vigorous, violent-type behaviors that may appear as acute delirium and result in patient injury. About half of hospitalized patients with traumatic brain injury report insomnia and may develop circadian rhythm disturbances. Poststroke patients can develop insomnia or hypersomnia and are at higher risk for developing OSA in the first several months.

Fifty-seven percent of patients with chronic pain also complain of impaired sleep. Sleep disruption is so common in fibromyalgia (75%) that it is considered to be a key diagnostic symptom. Poor nighttime sleep is associated with decreased pain tolerance and greater pain intensity the following day. Pain causes sleep fragmentation by increasing cortical arousals; in turn, sleep deprivation may increase pain sensitivity by inhibiting opioid protein synthesis or reducing opioid receptor affinity.

Sleep disturbance is a diagnostic criterion for mood, anxiety, substance abuse, and psychotic disorders. Thus, comorbid psychiatric disorders must be considered in hospitalized patients with sleep complaints, even if not previously diagnosed. Major depression is particularly common in hospitalized patients with early morning insomnia. Longitudinal studies have found that prior insomnia was associated with two- to fivefold increase in the odds of mood and anxiety disorders and suicide. Often, sleep disorders precede the onset of clinical depression, supporting the importance of assessing patient sleep quality during hospitalization.

Substance abuse disorders are also associated with sleep problems. Over half of patients undergoing alcohol rehabilitation exhibit symptoms of insomnia, such as increased sleep latency during the six months prior to entering treatment, and many report using alcohol for the purpose of initiating sleep. Indeed, untreated insomnia and other sleep problems may increase the risk of developing substance abuse problems due to “self-medicating” with alcohol and other substances to help with sleep. While alcohol and illicit substance intoxication and withdrawal are known to disrupt sleep directly, sleep disturbances may persist long after withdrawal symptoms have abated, sometimes years later.

Drugs that Affect Sleep

Many drugs used during hospitalization, such as antidepressants, anxiolytics, and narcotics, are well known to affect sleep. Table 94-3 depicts commonly used drugs and their effect on sleep architecture.

A common misperception is that sedatives promote quality sleep. Sedatives may initially help with sleep onset, but they actually diminish SWS and enhance stage 2 sleep, causing nonrestorative sleep. This may manifest as next day “hangover,” fatigue, irritability, and poor function. Additionally, routine medications used to treat medical illnesses also disrupt sleep. The most common agents that impair sleep include antiepileptic drugs (AEDs), tricyclic antidepressants (TCAs), antihypertensives, antihistamines, and corticosteroids. Lipophilic beta-antagonists such as propranolol and timolol can increase total wake time, decrease REM sleep, and increase the incidence of nightmares and insomnia. Hydrophilic beta-antagonists such as atenolol and sotalol do not have these effects. Anabolic steroids and beta-agonist bronchodilator therapy can cause severe anxiety, sleeplessness, and even psychosis. Vasopressor agents such as dopamine can cause cortical activation, leading to increased arousal and reduced SWS.

Medication dosing regimens used in the hospital can also impact sleep. For example, giving diuretics in the evening will result in nighttime polyuria, and dosing activating antidepressants in the late afternoon or evening can result in sleep-onset insomnia. Withdrawal from narcotics or alcohol or use of venlafaxine may cause severe REM intrusion associated with vivid dreams, nightmares, and exacerbation of underlying stress disorders. Careful evaluation and selection of all medications, interactions between agents, and paradoxical reactions to medications in the elderly must be considered if the patient is experiencing increased sleep disturbance and sleep disruption during hospitalization since these patients are especially vulnerable to drug-drug interactions, and paradoxical drug effects.

Hospital Environment

Sleeping in an unfamiliar environment is likely to negatively impact sleep, but the hospital environment has many additional disruptions, particularly in high-acuity settings. Environmental noise and patient care activities account for about 30% of patient awakenings in intensive care unit (ICU) patients. Peak noise levels in the ICU have average sound peaks of over 150 dB and often exceed 80 dB between midnight and 6 am. By comparison, a lawn mower or truck traffic has a sound level of 90 dB. The high noise level in hospitals has long been implicated as the major sleep disruptor, but studies in the past decade have found that patient care activities also cause a substantial disruption in sleep. This is in part due to routine activities, such as bathing, vital sign monitoring, radiologic studies, and phlebotomy that are conducted at night or early morning due to scheduling constraints.

Understanding that numerous factors may impair sleep during hospitalization allows clinicians to systemically evaluate and treat sleep problems. More than just prescribing sedative/hypnotic agents, the treatment for sleep disruption includes addressing multiple medical, behavioral, and environmental factors.

Assessment and evaluation of any sleep problem begins with an initial interview of the patient and family, as well as a review of the medical record for documentation of preexisting primary sleep disorders and any factor that could exacerbate or contribute to the current situation. Obtain a focused history by using questions listed in Table 94-4 to characterize the onset, duration, frequency, and specific characteristics of the patient's current sleep patterns. Next, establish whether the onset of the patient's sleep complaint began at the time of hospitalization. If the sleep disruption began with hospitalization, subsequent questions can then focus on hospital factors that may be impairing sleep, such as altered sleep hygiene behaviors. Inquire about the use or abuse of substances such as sedatives, antidepressants, AEDs, and opioids. Ask questions about the presence of pain syndromes, nocturnal gastroesophageal reflux, and other symptoms that often impact sleep.

The next step is to assess for preexisting mood, anxiety, psychotic, and substance use disorders, all of which may be exacerbated in the midst of an acute hospitalization. It is also important to rule out delirium. The nighttime awakenings and behavioral disturbances associated with delirium should not be mistaken for “insomnia.” This mistake can lead to delirious patients being treated with medications such as benzodiazepines or antihistamines, which can worsen the delirium. Before prescribing a sleep agent, assess for the presence of suboptimally treated medical, neurologic, psychiatric condition, or a primary sleep disorder (see Tables 94-1 and 94-2). Care should be taken to rely only on sound, documented evidence or a confirmatory medical history when formulating the diagnosis. For example, a patient may state that he has “apnea” because his wife speculates this, but he has never had a formal evaluation for OSA.

Last, but not least, evaluate the extent to which environmental factors such as noise level, various therapies, and hospital routines may be impairing sleep. Discuss the importance of maintaining a quieter environment with key staff members. When available, relaxation tapes, massage, and warm (noncaffeinated) beverages are preferable to pharmacologic strategies, as shown in Table 94-5.

In addition, limit potential iatrogenic causes of disrupted sleep by using alternative drugs or drug regimens, and consider altering evaluation and treatment interventions to promote uninterrupted sleep at night. Carefully review the medication list and consider whether the drugs themselves, the dosing regimens, or the methods of administration are disrupting sleep. If possible consider changing drugs or altering the timing of administration. An algorithm for diagnosing and treating sleep problems in hospitalized patients is outlined in Figure 94-2. By following these steps, the provider can develop a treatment plan that addresses primary sleep disorders, untreated comorbidities, and iatrogenic causes of poor sleep.

Although nonpharmacologic therapies are ideal, it may be difficult to provide these in the hospital setting, or they may be only partially effective in resolving the sleep problem. In these instances, pharmacologic strategies may be needed. Care must be taken in choosing the appropriate drug due to increased risk of side effects and drug–drug interactions in sick patients. To choose an appropriate sleep agent, evaluate the drug's efficacy, mechanism of action, and side-effect profile. Then match these characteristics with the patient's clinical condition(s). In patients with comorbid sleep and psychiatric problems, consider using a sedating psychotropic at bedtime to promote sleep.

The U.S. Food and Drug Administration (FDA) has approved three classes of medications for the treatment of insomnia: benzodiazepine GABAA receptor agonists, nonbenzodiazepine GABAA receptor agonists (non-BzRAs), and melatonin-receptor agonists (Table 94-6). Benzodiazepines include estazolam (ProSom), flurazepam (Dalmane), quazepam (Doral), temazepam (Restoril), and triazolam (Halcion). Flurazepam and quazepam have long half-lives, increasing the risks of side effects and drug interactions, and should generally be avoided in hospitalized patients. For similar reasons, it is prudent to avoid use of other long-acting benzodiazepines such as clonazepam (Klonopin) and diazepam (Valium), unless there is a specific indication such as RLS. All benzodiazepines except lorazepam, oxazepam, and temazepam have significant hepatic metabolism and should be used with caution in patients with liver disease.

Although non-BzRAs are structurally unrelated to benzodiazepines, they also act at the GABAA receptor, and have many similar characteristics and risks. These agents include eszopiclone (Lunesta), zaleplon (Sonata), zolpidem (Ambien), and zolpidem extended-release (Ambien CR). Both benzodiazepines and non-BzRAs have a risk for abuse and dependence. Although there is much less risk of dependence with the nonbenzodiazepines, it appears prudent to avoid using all of these agents to treat insomnia in patients with a prior history of sedative-hypnotic or alcohol dependence.

Side effects of benzodiazepines include daytime sedation, anterograde amnesia, cognitive impairment, incoordination, dependence, tolerance, rebound insomnia, and, importantly, respiratory depression. The side-effect profile of non-BzRAs is generally similar but appears to be less severe. Additionally, zolpidem and eszopiclone have been associated with delirium-like episodes, hallucinations, and sleepwalking, which can be exacerbated in the hospital setting. Long-acting agents should not be used in the elderly due to increased risk of falls, daytime sedation, and adverse cognitive effect. Ideally, both classes of drugs should be completely avoided in the elderly, but if absolutely needed, the lowest possible dose should be used.

Ramelteon (Rozerem) is a synthetic melatonin analogue with a longer half-life than natural melatonin. Ramelteon has demonstrated efficacy in decreasing sleep latency, as well as increasing total sleep time, but does not cause drowsiness the next day. Because ramelteon is not a general central nervous system (CNS) depressant, it would not be expected to decrease respiratory drive, and it appears safe in patients with COPD. Furthermore ramelteon has been shown to lack abuse potential. Interestingly, despite facilitating sleep, ramelteon does not make patients feel sedated, and some patients who expect to feel sedated prior to sleep (based on experience with other drugs) may believe that ramelteon is not working. Patient education may help ameliorate this problem.

Limited data exist on the efficacy of non-FDA-approved medications for insomnia, such as antihistamines, antidepressants, and conventional and atypical antipsychotics, examples of which are listed in Table 94-7.

The administration of antihistamines, barbiturates, chloral hydrate, and alternative/herbal therapies has been discouraged because the benefits rarely outweigh the risks associated with their use. Antihistamines are the most commonly used over-the-counter agents for chronic insomnia. Diphenhydramine (Benadryl) has been shown to be better than placebo to treat insomnia, but data are lacking to definitively endorse its use to promote sleep. Selecting a non-FDA-approved medication with a sedative effect can be appropriate when the patient has a concomitant illness that also requires treatment, such as a sedating antihistamine (diphenhydramine) in an individual with asthma who is also experiencing insomnia. The anticholinergic action of antihistamines may lead to orthostatic hypotension, urinary retention, or delirium in vulnerable patients. Therefore, diphenhydramine should probably be avoided in hospitalized patients.

Trazodone is the most commonly prescribed antidepressant for the treatment of insomnia. Trazodone is popular among prescribers because, unlike most benzodiazepines, trazodone does not have a recommended limited duration of use and is perceived as being “safer.” However, with long-term use, the hypnotic effects of trazodone diminish. In addition, trazodone has been associated with arrhythmias in patients with preexisting cardiac conduction system disease. For this reason, we recommend that trazodone be used as a short-term alternative to benzodiazepines for patients with hypercapnia or hypoxemia, and in those with a history of drug abuse or dependence, but should not generally be prescribed for most patients with sleep disturbances who do not require treatment of depression. Mirtazapine, a newer antidepressant, which promotes both sleep and appetite, may be particularly helpful for patients with cancer, acquired immunodeficiency syndrome (AIDS), and other conditions in which the triad of poor sleep, anorexia, and depression is common. Mirtazapine is a noradrenergic and specific serotonergic agent that causes inverse, dose-dependent sedation (15 mg doses are less sedating). To target sleeplessness, start with a dose between 7.5 and 15 mg. If this dose is ineffective, it is unlikely that increasing the dose will be of benefit for sleep. Interestingly, some patients with OSA appear to exhibit a reduction in the apnea-hypopnea index with this drug, but mirtazapine's tendency to cause weight gain may limit its utility in this patient population.

TCAs are sedating and useful in a select population of patients who having underlying neuropathy or chronic pain syndromes. Otherwise, these should not be used as first-line agents to promote sleep in hospitalized patients. TCAs increase the risk of cardiac conduction abnormalities, decrease seizure threshold, and have significant anticholinergic and anti-alpha-adrenergic effects. In patients with dementia, the anticholinergic effect of TCAs may precipitate delirium. Also, conventional and atypical antipsychotics have a similar side-effect profile and should not be used routinely as first-line agents for insomnia, except in patients who have a psychiatric history where agitation may coexist or be precipitated by hospitalization, and in acute delirium. Atypical antipsychotics should be used cautiously in the elderly due to increased risk of death associated with them. Haloperidol, a conventional antipsychotic, may alternatively be given in a low dose. Electrocardiograms should be followed, particularly in patients with structural heart disease and those on medications that may prolong the QT interval. Lastly, chloral hydrate, the oldest hypnotic, has been displaced by barbiturates and subsequently benzodiazepines. However, it can still be useful in select circumstances. It comes in liquid or pill form and does not suppress epileptiform discharges; therefore, it is useful in patients where sedation may be masking seizure activity. Due to its high abuse potential, potential for lethal overdose, and hepatic and renal toxicity, it is essentially obsolete in the United States today.

Sleep disruption is extremely common among hospitalized medical patients, negatively impacting patient satisfaction and potentially delaying recovery. Sleep complaints can be addressed by identifying the cause or causes of poor sleep through a systematic evaluation. Treating the underlying factors first before prescribing sleeping aids is paramount and may include modifying treatment modalities and the hospital environment. Finally, pharmacologic sleep aids should be considered, but care needs to be taken to choose an appropriate drug based on the patient's age and medical comorbidities and the specific nature of their sleep problem.