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Featured Articles: Narrative Review Article

Perioperative Management of Insomnia, Restless Legs, Narcolepsy, and Parasomnias

Hershner, Shelley MD*; Auckley, Dennis MD

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doi: 10.1213/ANE.0000000000005439
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The perioperative time period is highlighted by mental, emotional, and physiologic stress imparted by the anxiety of having surgery and undergoing anesthesia coupled with the physical alterations resulting from the surgical intervention, anesthesia, pain, introduction of new medications, and changes in underlying physiologic functions. As a result, underlying medical conditions, including sleep disorders, can worsen in the perioperative environment. This has been well documented for sleep-disordered breathing, which worsens postoperatively and has been associated with adverse outcomes following surgery.1,2 Recently, attention has focused on other sleep disorders that may be aggravated in the perioperative setting and thus contribute to postoperative morbidity. This review will provide updates on other significant sleep disorders and how they may be impacted by the perioperative milieu and thus potentially influence clinical outcomes. The authors will focus on insomnia, restless legs syndrome (RLS), narcolepsy, and parasomnias.


Insomnia can be divided into short-term (<3 months duration) and chronic (>3 months duration) insomnia. The diagnosis of insomnia requires a history of difficulty falling asleep, difficulty staying asleep, and/or awakening earlier than desired, and this must be accompanied by daytime symptoms.3 This section will review patients with a known diagnosis of short-term or chronic insomnia undergoing surgery. Sleep disruption in the inpatient setting is covered in a separate review in this special edition.

Roughly, a third of the population will suffer from short-term insomnia at any given time, whereas about 10% of the population manifests symptoms of chronic insomnia.3 However, in some populations, the prevalence of insomnia is considerably higher, including the elderly, those with underlying psychiatric (ie, depression and anxiety), and/or certain medical conditions (ie, pulmonary disorders, heart failure, diabetes, cancer, chronic pain, obstructive sleep apnea [OSA] and RLS).4,5 As a result, patients admitted to the hospital may have high rate of preadmission insomnia.6,7

Insomnia is associated with physiological activation, including increases in measures of cardiovascular, metabolic, hormonal, and electroencephalographic activity.8 The enhanced sympathetic nervous system activation is thought to influence not only daytime function and quality of life but may adversely impact cardiovascular risk and mortality, particularly for the development of hypertension and myocardial infarction.8,9 Insomnia associated with short nocturnal sleep duration has also been associated with risk for diabetes.10

Surprisingly, there is little literature assessing the consequences of preexisting insomnia on postoperative outcomes. One small study used actigraphy to assess sleep in the 6 nights preceding surgery and found that more time spent awake in the 2 nights before surgery correlated with postoperative delirium,11 suggesting short-term insomnia may affect postoperative neurocognitive function. A more recent cohort study examined 1870 patients undergoing hip arthroplasty at US military hospitals and reported 8.8% carried a diagnosis of insomnia preoperatively, and that this predicted higher rates of opioid prescriptions (at least 3 or more) after surgery (odds ratio [OR] = 1.97 [95% confidence interval {CI}, 1.39-2.79]), as well as more medical visits and health care costs in the 2 years following surgery.12 As insomnia and chronic pain are reciprocally linked,13 and poor sleep enhances pain sensitivity, this finding is not unexpected. However, there are no data examining the impact of preexisting insomnia on other psychiatric, cardiovascular, or metabolic outcomes after surgery.

Table 1. - Common Medications Used in the Treatment of Insomnia
Class Example medications Half-life Potential side effects Withdrawal
Benzodiazepines Temazepam 8–15 h Daytime sleepiness, cognitive impairment, motor incoordination, worsen OSA, respiratory depression Rebound insomnia, confusion, agitation
Triazolam 2–5 h
Benzodiazepine receptor agonists Zaleplon 1 h Daytime sleepiness, cognitive impairment, motor incoordination, risk of fall, complex sleep-related behaviors Rebound insomnia
Zolpidem 1.5–4.5 h
Eszopiclone 6–9 h
Orexin receptor antagonist Suvorexant 12 h Daytime sleepiness, headaches, narcolepsy-like symptoms, worsen OSA Rebound insomnia
Lemborexant 17–19 h
Antidepressants Doxepin 15 h Daytime sleepiness, headaches, nausea confusion (T), orthostatic hypotension (T), arrhythmias (T) Rebound insomnia, withdrawal syndrome (may be severe with trazodone)
Trazodone 7–10 h
Melatonin active agents Melatonin (OTC) <1 h Daytime sleepiness, headaches (R), dizziness (R) None
Ramelteon 1.5–3 h
Over-the-counter Diphenhydramine 8.5 h Daytime sleepiness, cognitive impairment (Di, D), delirium (Di, D), anticholinergic effects (Di, D) None
Doxylamine 10–13 h
Valerian Unknown
Abbreviations: D, doxylamine; Di, diphenhydramine; OSA, obstructive sleep apnea; OTC, over-the-counter; R, ramelteon, T, trazodone.

The medications used in the treatment of insomnia are varied and range from over-the-counter medications to powerful sedatives. A detailed review of these medications is not feasible here, though many of the more common ones used in practice are listed in Table 1. Insomnia medications run the risk of potentially interacting with anesthetics, opioids, and the changing physiology that could alter metabolism (most all of these drugs are hepatically metabolized), consequently raising the risk of adverse outcomes. Specific theoretical concerns include their effects on cognition, delirium, fall risks, respiratory depression, and cardiovascular outcomes. The use of sedative-hypnotics in the general population has been growing,17 and it is increasingly recognized that their preoperative use is associated with higher rate of postoperative complications,18 particularly when combined with opioids before surgery.19 In certain populations, such as those with OSA, a condition that frequently coexists with insomnia, the combination of sedatives and opioids postoperatively can lead to respiratory depression with catastrophic outcomes.2 Conversely, abruptly discontinuing some insomnia medications may run the risk of withdrawal syndromes, which could complicate postoperative care.


The management of patients with insomnia undergoing surgery should take into account a number of factors, many of which need to be considered on a case-by-case basis. General guidelines are listed in Table 2. For patients with severe insomnia and/or on chronic sedative-hypnotic medication, consultation with the patient’s primary care or sleep medicine provider can help develop a plan for perioperative care, particularly concerning the cessation, dose adjustment, or continued use of sleep-related sedatives perioperatively. Some patients, such as those over the age of 65 years old, those with a significant postoperative pain medication requirement, and/or those with major cardiopulmonary comorbidities should be considered for enhanced monitoring postoperatively. It is also important for perioperative providers to recognize that insomnia often coexists with OSA,20 and that OSA is frequently undiagnosed preoperatively but associated with worse postoperative outcomes.1,2 And finally, some patients may self-treat insomnia with alcohol, and thus the risk of alcohol withdrawal may need to be considered when planning perioperative care.21

Table 2. - Perioperative Management of Insomnia
Encourage Avoid
• Quiet hospital environment between 2200 and 0600
• Use of ear plugs and eye masks
• White noise at night
• Education of healthy sleep habits and relaxation techniques
• Monitor for coexisting OSA and ETOH withdrawal
• Continue home prescribed hypnotics only if deemed safe based on clinical status
• Use of melatonin rather than a hypnotic if introducing a new sleep aid
• Discontinue hypnotic agents at discharge if started during hospitalization
• Sleep disruption by careful timing of:
 ˚ Vitals
 ˚ Blood draw
 ˚ Rounds
• Inadequate pain control
• Inadequately treated nausea and cough
• Caffeine and other stimulants
• Fall risk by monitoring patients on hypnotics
Abbreviations: ETOH, alcohol; OSA, obstructive sleep apnea.

It is reasonable to hypothesize that insomnia, both chronic and short-term, could lead to higher rates of adverse postoperative outcomes based on the underlying pathophysiology of insomnia, the medications used to treat insomnia, and the interactions between these factors with anesthesia and surgical recovery. As noted earlier, insomnia is associated with sympathetic overactivity,8,9 and much like patients with OSA, insomnia patients lose the normal sleep-related nocturnal dip in blood pressure.14 These factors could potentially interact with the stress of surgery and anesthesia and place patients at increased risk for cardiovascular events postoperatively. Likewise, it has been recognized that insomnia with short sleep duration can affect glycemic control,15 and that hyperglycemia following surgery is associated with worse outcomes.16 However, whether insomnia directly contributes to these outcomes has not been studied.

Restless Legs Syndrome

RLS is a sensory-motor sleep-related movement disorder that occurs during wakefulness. The diagnosis is made by history and requires 4 specific criteria be met: (1) an urge to move the legs, usually associated with an uncomfortable and unpleasant sensation in the legs, (2) that begin or worsen during periods of rest or inactivity, (3) are partially or totally relieved by movement, such as walking or stretching, and (4) occur exclusively or predominantly in the evening or night rather than during the daytime.3 The sensations described by patients take on a variety of terms, including “creeping,” “crawling,” “pulling,” “aching,” “water flowing,” “electrical current,” etc. About 50% of RLS sufferers describe the sensations as painful.3

RLS affects about 5%–10% of the population, though the prevalence varies depending on criteria used for frequency of symptoms.3 RLS is more common in women,22 and increases in prevalence with age.23 RLS can be an isolated condition or occur in the setting of a number of accompanying disorders, including iron deficiency, chronic renal failure, pregnancy, neuropathy (especially related to diabetes), and spinal stenosis.24 In addition, RLS can be worsened or precipitated by immobility,25 sleep deprivation,26 and the use of several medications (most notably first-generation antihistamines, some antidepressants, and medications that block dopamine),27 and potentially the excessive intake of caffeine, alcohol, and tobacco. The pathophysiology of RLS appears to be related to underlying genetics and brain iron deficiency, which negatively impacts central nervous system dopamine pathways.28

RLS has been associated with poor sleep (longer sleep latency, shorter sleep duration), impaired quality of life, worsened daytime function, and hypertension.29,30 Controversy exists about whether RLS is associated with other cardiovascular diseases, though patients with RLS lose the normal sleep-related nocturnal dip in blood pressure, possibly resulting from sleep fragmentation and sympathetic activation.30,31 Treatment of RLS can be highly effective and improves not only RLS symptoms but sleep and quality of life.28,32 A number of behavioral and life style changes (ie, stretching, mental alertness activities, reducing caffeine and tobacco) can be helpful, though there are limited data on these strategies. Food and Drug Administration (FDA) approved treatments for RLS include dopaminergic agonists (ie, pramipexole, ropinirole, and rotigotine), alpha-2-delta calcium channel ligands (ie, gabapentin enacarbil—a prodrug of gabapentin), and a vibratory counter stimulus device.32 The dopaminergic agonists are highly effective, though patients can develop rebound (increased symptoms as the blood drug levels decrease) and augmentation (earlier onset, changing location, and/or increased severity of symptoms) that may limit their use in some cases. Alpha-2-ligands, including pregabalin, appear to work as well as dopaminergic agonists, and are particularly effective for painful variants of RLS.28,32 Their mechanism of action is not fully understood. Iron supplementation for iron deficiency, as determined by serum ferritin levels used as a surrogate for brain iron stores, is typically addressed during treatment (note, a ferritin level <75 μg/L is considered low for patients with RLS, though this is well within the normal range of ferritin levels). In more difficult cases, opioids appear to reduce symptoms for some patients, and occasionally sedative-hypnotic agents are used to help with RLS-related insomnia. Both classes of medications carry potential long-term side effects and caution is advised.24,32

Due to a number of changes that can occur in the perioperative environment, there have long been concerns about RLS worsening during surgery and/or postoperatively and that this may impact postoperative outcomes.27,33 Sleep disruption and sleep loss are common preceding and following surgery,11 and this can aggravate RLS.26,27 Forced immobility, either via bedrest or casting/splinting, is often required following surgery and can worsen RLS symptoms.25,27 Anemia occurs in up to 40% of hospitalized patients,34 and the development of iron deficiency will exacerbate RLS.27,35 In some patients, medications used to treat RLS are withheld perioperatively due to either medication errors, nothing through the mouth (NPO) status or worry about the use of the medication in the postoperative setting. Abrupt cessation of these medications can lead to significant rebound RLS symptoms.27 The perioperative addition of medications known to aggravate RLS can precipitate RLS in patients previously under control.27,36 Finally, there is controversy about whether or not the use of spinal anesthesia can promote RLS or not.37,38 An early study found 9% of patients undergoing spinal anesthesia developed new-onset “transient RLS;37” however, a follow-up study did not find any new cases of RLS following spinal anesthesia.38 The mechanism by which this would occur is uncertain, though some authors have postulated that it may be related to deficits in spinal sensorimotor integration.37

Despite these concerns, the literature on RLS in the perioperative setting consists primarily of case reports, and there are limited controlled data. Case reports have detailed intraoperative and postoperative agitation, wound breakdown, hyperadrenergic states, and sleep deprivation, all resulting from uncontrolled RLS during or following surgery.27,33,39–41 The reports describe return trips to the operating room, worsened postoperative quality of life and pain control, and delayed recovery from surgery including a prolonged inpatient length of stay.27,33,39–41 In a survey study of 45 patients with RLS who recently had surgery, 9% felt their RLS symptoms had worsened though details were not provided on other outcomes.42 Interestingly, 16% felt their RLS symptoms had improved following surgery, which could reflect postoperative opioid use.42


Management of RLS patients undergoing surgery should include attention to their current RLS symptoms and treatment, with an understanding of alternative management options when needed. These recommendations are based on known management strategies for outpatient RLS, extrapolation of data, and common-sense postoperative care,27 and general recommendations are provided in Table 3. Ambulating patients as soon as able postoperatively may help to prevent nocturnal worsening of symptoms. Simple and safe maneuvers to improve sleep and reduce sleep fragmentation/deprivation postoperatively should be implemented (these are addressed elsewhere in this issue of Anesthesia & Analgesia). Limiting blood loss through conservative use of phlebotomy, and treatment of any developing iron deficiency are also advised. As much as possible, continued use of the patient’s home RLS medications is recommended, unless otherwise contraindicated by the clinical situation. It is important to administer these at the correct time and avoid skipping doses to prevent the emergence of RLS or potential withdrawal symptoms. For most RLS treatments, there are intravenous (IV) and/or transdermal alternatives, but if the medications must be withheld, then slow tapering per pharmacy/manufacturer guidelines is recommended for the dopaminergic agonists (neuroleptic malignant syndrome can occur with abrupt withdrawal), gabapentin enacarbil (withdrawal seizures can occur with abrupt withdrawal of more than 600 mg per day dosing), and opioids (opioid withdrawal syndrome).

Table 3. - Perioperative Management of RLS
Encourage Avoid
• Early ambulation
• Continuation of RLS medications
• Options for nonoral medications
 ˚ Rotigotine transdermal patch
 ˚ IV opioid medications
• Oral iron if needed/tolerated
• Stretching
• Use of sequential compression devices
• Mental alertness activities
• Reduce caffeine
• Immobility
• Sleep disruption/deprivation
• Blood loss
• RLS precipitating medications:
 ˚ First-generation antihistamines
 ˚ Metoclopramide and prochlorperazine
 ˚ Dopamine antagonists
 ˚ Haloperidol
 ˚ Selective serotonin reuptake inhibitors
• Inadequate pain control
Abbreviations: IV, intravenous; RLS, restless legs syndrome.

In patients who are prohibited from oral intake (made NPO), rotigotine comes as a transdermal patch and may substitute for oral dopaminergic agonists. IV opioid therapy can also be effective at controlling RLS symptoms in patients who are NPO. Another option would be to apply counter stimulation via sequential compression devices (SCDs). SCDs are often used for prophylaxis against deep vein thrombosis but may be an effective strategy to control RLS symptoms following surgery. And finally, avoiding the use of medications known to precipitate or aggravate RLS (eg, first-generation antihistamines, metoclopramide, haloperidol, selective serotonin reuptake inhibitors) is likely to be beneficial. If medications in these classes are needed, alternatives that will not worsen RLS should be sought (eg, second-generation antihistamines). For patients who are complicated, such as those on more than 1 RLS medication or those experiencing severe symptoms postoperatively, consultation with a sleep medicine provider is advised.


Narcolepsy is a central hypersomnolence disorder characterized by excessive daytime sleepiness along with hypnagogic hallucinations, sleep paralysis, disturbed nighttime sleep, and in some cases, cataplexy.3 Cataplexy occurs when an emotion, most often laughter, causes the sudden loss of muscle tone and control without loss of consciousness.43 This may manifest as knees buckling, a head or jaw drop, or loss of the ability to speak; these episodes are relatively brief and last a few minutes. Diagnostic criteria differentiate between 2 narcolepsy subtypes: narcolepsy type I (NT1, associated with cataplexy or a proven hypocretin/orexin deficiency) and narcolepsy type 2 (NT2, without cataplexy and normal hypocretin/orexin level if measured).3 NT1 is due to the loss of hypocretin/orexin producing cells in the lateral hypothalamus.44 The etiology of NT2 is not known.

Treatment of narcolepsy consists of symptomatic management.45 Stimulant medications can improve excessive daytime sleepiness. Antidepressant medications treat cataplexy and may improve hypnagogic hallucinations and sleep paralysis. Sodium oxybate can treat both excessive daytime sleepiness, cataplexy, and sleep fragmentation. It is a central nervous system depressant and can also suppress respiration.46,47 It likely works through gamma-aminobutyric acid B receptors. It has an effect on dopaminergic, serotonergic, and noradrenergic neurons.46,48 Recently, 2 new wake-promoting medications for narcolepsy have become available: pitolosant, a histamine inverse agonist and solriamfetol, a dopamine, and norepinephrine reuptake inhibitor.49,50

Patients with narcolepsy may experience several types of perioperative complications: worsening of baseline narcolepsy symptoms, anesthesia, and narcolepsy-related medication effects, and cardiopulmonary complications (Table 4).51,52 Available literature is sparse and consists primarily of case reports, case series, and an isolated systematic review.52 Not all studies have shown an increase in perioperative complications.53,54 In a survey study, 55% of narcoleptic patients self-reported adverse events and perioperative complications.51 These included surgical complications, difficulty waking postanesthesia, increased cataplexy, inadequate pain relief, and increased symptoms related to narcolepsy-related medication discontinuation. In a systematic review of the literature, the majority of perioperative complications reported were cardiopulmonary.52 Of note, in pregnant patients with narcolepsy, narcolepsy or its treatment were often felt to be the reason for a cesarean delivery, for example, fetal distress or status cataplecticus.55

Table 4. - Potential Narcolepsy-Related Perioperative Complications
Narcolepsy-related symptoms Obstetric-related Anesthetic-related Cardiopulmonary
• Increased cataplexy
 ˚ Status cataplecticus
• Hypnagogic hallucinations
• Sleep paralysis
• Hypersomnolence
• Stimulant withdrawal
• Antidepressant withdrawal
Indications for cesarean delivery:
• Fetal distress
• Worsening narcolepsy symptoms
• Cataplexy
• Intraoperative awareness
• Sensitivity to anesthetic agents
• Delayed emergence
• Inadequate pain control
• Postoperative nausea and vomiting
• Respiratory depression
• Hypotension
• Hypertension
• ST depression
• Arrhythmia
 ˚ Bradycardia
 ˚ Tachycardia
• Pulmonary embolism
• Emergency response team activations

There are several potential mechanisms by which narcolepsy and/or its treatment could increase perioperative complications. These include intrinsic features of narcolepsy, medications used for treatment, and comorbid sleep disorders. Autonomic control may be impaired in patients with narcolepsy, especially control of heart rate and body temperature,56 and this could potentially be aggravated following surgery. A reduction in heart rate in association with periodic limb movements, which are commonly seen during sleep in patients with narcolepsy, is noted for patients with NT1. Loss of nocturnal blood pressure dipping has been observed in animal models and NT1 subjects.57 In animal studies, the administration of hypocretin/orexin elevates arterial blood pressure, heart rate, oxygen consumption, body temperature, and plasma catecholamine levels. The increased blood pressure and heart rate are mediated mainly by sympathetic activation.58–60 Taken together, these studies suggest that hypocretin/orexin modulates autonomic responses with a resultant potential for increased cardiovascular risk. Hypocretin/orexin system may impact emergence, but not induction, from anesthetic agents.61,62 In a rat model, intracerebral injection of orexin-A decreased the time to emergence from propofol anesthesia. Since NT1 patients have lower levels of hypocretin/orexin theoretically, they may have a longer emergence from propofol.

Medications used to treat narcolepsy can increase perioperative risk.63 Stimulant medications can increase perioperative risk through vasospasm due to increased catecholamines, elevated blood pressure and heart rate, and prolonged QT interval.64 In a systematic review on nonnarcoleptic patients, 2 of 3 studies on adults showed an association with stimulant use and adverse cardiovascular outcomes, while 6 of 7 studies on children and adolescents did not show an increased cardiovascular risk.64 Discontinuation of narcolepsy medications can exacerbate narcolepsy symptoms as well as anesthesia-associated symptoms.52 The abrupt discontinuation of antidepressants may result in status cataplecticus.65 Discontinuation of stimulant medications can worsen baseline sleepiness.

Stimulant medications may also affect anesthesia. In an animal study, IV methylphenidate shortened emergence from isoflurane.66 Blood gas experiments demonstrate that methylphenidate increases minute ventilation which increases anesthetic elimination from the brain. Dextroamphetamine had similar results.67 Modafinil decreases fatigue, sleepiness and increases alertness postoperatively among nonnarcoleptic patients due to its wake-promoting mechanisms.68 These studies support that discontinuation of narcolepsy-related medications before surgery could worsen narcolepsy symptoms, particularly hypersomnolence, and thus potentially delay emergence from anesthesia.

Narcolepsy patients are at increased risk of comorbid sleep disorders. In a surgical cohort, 40.8% of narcolepsy patients also had OSA versus 19.1% of control subjects (P ≤ .001).53 The etiology of this increased risk is not known, but may relate to the influence of hypocretin/orexin on upper airway muscle tone.69 REM behavior disorder (RBD) is more prevalent in narcolepsy.70 Untreated OSA increases perioperative risk, while parasomnias may theoretically result in adverse events.


Table 5. - Perioperative Management of Narcolepsy
Encourage Avoid
• Counseling on worsening of narcolepsy symptoms
• Counseling when to resume driving
• Continuation of narcolepsy medications
• Obstetric-related
 ˚ Consider continuation of cataplexy medications
• Utilization of short-acting agents, for example, propofol and remifentanil
• Bispectral index monitoring for anesthesia depth
• Multimodal analgesia and regional anesthesia when possible
• Resuming stimulant medications early in the postoperative period
• Drug-drug interactions
• Inadequate pain control
• Abrupt discontinuation of cataplexy medications (SSRI, TCA, SNRI)
• Unstable cardiopulmonary status
• Unstable body temperature
• Emotional circumstances which may trigger cataplexy
• Fall risks from cataplexy
Abbreviations: SNRI, serotonin and norepinephrine reuptake inhibitors; SSRI, selective serotonin reuptake inhibitors; TCA, tricyclic antidepressants.

At this time, there is inadequate literature on the perioperative complications of narcolepsy patients for the development of practice guidelines. That said, the literature does offer support for the management recommendations in Table 5, and perioperative providers should consider these recommendations when caring for patients with narcolepsy.


Parasomnias are abnormal behaviors that arise during sleep.3 Parasomnias are classified by the sleep stage in which the parasomnia occurs: nonrapid eye movement sleep (NREM) sleep or REM sleep. Examples of NREM parasomnias include sleep walking and night terrors.3,71 These automatic sleep-related behaviors can consist of quite complex activities such as eating, opening doors, and in rare cases, driving. NREM parasomnias are more prevalent in children and young adults. Mechanistically, NREM parasomnias occurs as the result of a partial arousal out of sleep. Triggers for NREM parasomnia are sleep deprivation, alcohol consumption, febrile illness, stress, untreated OSA, febrile illness, and hypnotic use.3,71 Typically, NREM parasomnia does not require medication treatment, but rather management is via the avoidance of triggers.71 If medication is used, a low-dose benzodiazepine is often effective.

The pathognomonic REM parasomnia is RBD.3 RBD is seen in older individuals, often those with Parkinson disease, dementia with Lewy body disease, or multiple system atrophy.70 The sleep-related behaviors of RBD consist of abrupt violent movements such as punching and kicking usually in association with negative and/or violent dream content. Patients with RBD can hurt themselves or their bed partner. Clinically, these patients may have a history of “falling out of bed,” vivid dream content, and loud vocalizations. RBD results from the loss of the muscle paralysis that occurs during normal REM sleep.72 Triggers are less well defined but stress and sleeping in a different environment may worsen RBD, and some medications have been associated with RBD (ie, serotonin-specific reuptake inhibitors, tricyclic antidepressants).72 Treatment consists of low-dose benzodiazepines or melatonin 10–12 mg.73

Safety counseling is vital in both NREM and REM parasomnias. Currently, there is little literature on perioperative complications of parasomnias. In 1 case report, a patient with Parkinson disease had a severe episode of RBD following electrode placement for left subthalamic stimulation.74 Mechanistically, both surgery and the postoperative period could trigger either parasomnia type, but especially a NREM parasomnia. This may be due to the sleep deprivation and fragmentation that can occur in the hospital setting. Withholding a benzodiazepine postoperatively could trigger a parasomnia if a patient’s benzodiazepine is withheld postoperatively to limit sedation and respiratory depression. Chronic use of benzodiazepines is a risk factor for intraoperative awareness.75 The increased prevalence of RBD among Parkinson disease, dementia with Lewy body disease, multiple system atrophy is important because this population is at an increased risk of delirium.76 These patient’s risk of delirium would be further compounded by the surgery, hospitalization, and pain medications. RBD behaviors could also be mistaken for delirium.


Table 6. - Perioperative Management of Parasomnias
Encourage Avoid
• Continue benzodiazepines postoperatively when safe
• For REM parasomnias, use melatonin 10 mg when a benzodiazepine cannot be continued postoperatively
• Continue positive airway pressure for patients with a parasmonia and obstructive sleep apnea
• Adequate sleep duration
• Sleep disruption
• Abrupt discontinuation of benzodiazepines
• Identifying sleep-related parasomnias behaviors as delirium
• Elevated temperature
• Fall risk from sleep-related behaviors
Abbreviation: REM, rapid eye movement sleep.

At this time, the primary recommendation for the management of parasomnias in the perioperative environment is awareness that the surgery, the hospital setting, and discontinuation of treatment-related benzodiazepines could all potentially exacerbate parasomnias (Table 6). If this were to occur, consultation with a sleep medicine provider is recommended.


In summary, although the literature clearly supports that OSA is associated with perioperative complications, growing data suggest that other sleep disorders possibly may increase the risk for postoperative adverse events, or at least mechanistically have the potential to contribute to worse outcomes. Further research is needed to better delineate the prevalence and mechanisms of perioperative complications related to sleep disorders beyond OSA, as well as the best management strategies for patients with sleep disorders subjected to the perioperative environment. There is growing interest in addressing sleep and insomnia in the hospital, as sleep deprivation has been associated with numerous poor outcomes that potentially could be magnified following surgery. Another area ripe for investigation is the role of stimulants in anesthetic and postoperative care. A growing portion of the population is being prescribed stimulants for conditions other than just narcolepsy, and a better understanding of how to manage these medications during hospitalization is vital. Until such a time as more data and guidelines are available, it behooves surgeons, anesthesiologists, perioperative providers, and sleep medicine providers to be aware of these other sleep disorders, the medications used to treat them, and their potential for perioperative complications.


Name: Shelley Hershner, MD.

Contribution: This author helped write and edit the manuscript.

Name: Dennis Auckley, MD.

Contribution: This author helped write and edit the manuscript.

This manuscript was handled by: Toby N. Weingarten, MD.


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