Delaney et al.

Annals of Intensive Care (2015) 5:3

DOI 10.1186/s13613-015-0043-2

REVIEW Open Access

Sleeping on a problem: the impact of sleep

disturbance on intensive care patients - a clinical
review
Lori J Delaney1,2*, Frank Van Haren3,4 and Violeta Lopez4,5

Abstract
Sleep disturbance is commonly encountered amongst intensive care patients and has significant psychophysiological
effects, which protract recovery and increases mortality. Bio-physiological monitoring of intensive care patients reveal
alterations in sleep architecture, with reduced sleep quality and continuity. The etiological causes of sleep disturbance
are considered to be multifactorial, although environmental stressors namely, noise, light and clinical care interactions
have been frequently cited in both subjective and objective studies. As a result, interventions are targeted towards
modifiable factors to ameliorate their impact. This paper reviews normal sleep physiology and the impact that
sleep disturbance has on patient psychophysiological recovery, and the contribution that the clinical environment
has on intensive care patients’ sleep.
Keywords: Clinical care; Environment; Intensive care; Light; Sleep; Sleep deprivation; Sleep fragmentation; Noise

Review and rapid eye movement (REM) sleep. NREM consists

Introduction of three stages which constitutes between 75% to 80% of
Sleep is considered to be an essential biological function the total sleep time (TST) [3] with the first stage (N1)
to maintain physiological and emotional wellbeing. How- acting as a transition between wakefulness and deep
ever, sleep in the intensive care unit (ICU) has been re- sleep. N1 is characterised by physical drowsiness, com-
ported by survivors of critical illness to be of a poor bined with decreased ocular movements and a reduction
quality and a major stressor associated with their admis- in muscle activity [3,4]. This is followed by N2, in which
sion [1]. The proclivity for sleep and circadian disturbance the individual becomes decreasingly unaware of their
amongst ICU patients has been attributed to the intrusive surroundings, yet remains easily roused by noise [5]. As
clinical care and clinical environment, with environmental sleep progresses, N2 becomes the predominant stage
factors inclusive of noise, and light as etiological causes. making up 45% to 55% of the NREM phase.
As a result, patients exhibit symptoms consistent with Stage N3 consists mostly of slow wave activity and is
dyssomnia, such as difficulty with sleep initiation and frag- considered to be an anabolic and physically restorative
mentation, and early morning awakenings [2]. This paper stage [6]. This stage is prominent in the first third of the
discusses the impact of environmental factors: noise, light night’s sleep and is deemed to be the deepest and most
and clinical care interactions on patient sleep and the psy- restful stage of the sleep cycle. During slow wave sleep
chophysiological consequences of sleep disturbance. (SWS), metabolic activity is at its lowest leading to a
reduction in oxygen consumption. Growth hormone is
secreted during this stage which promotes protein syn-
Normal sleep architecture thesis, tissue healing and physical recovery [7]. In con-
Sleep involves a number of sequential stages, with two trast, the proceeding REM phase features increased
predominate phases: non-rapid eye movement (NREM) cerebral and physiological activity, whereby the brain’s
* Correspondence: [email protected] metabolic rate reflects that of a wakeful state with bursts
1
Clinical Nursing, University of Canberra, Canberra, Australia of REM, coupled with skeletal muscle atonia [3,8-10].
2
Australian National University, Canberra, Australia The time spent in REM sleep increases over the length
Full list of author information is available at the end of the article

© 2015 Delaney et al.; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction
in any medium, provided the original work is properly credited.
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 2 of 10

of the night and makes up 20% to 25% of TST [6]. Problematic to the investigation of severity of illness on
Whilst REM sleep contributes to a restful night sleep, sleep is the numerous contributing factors such as mech-
this phase has a lower threshold for awakening than anical ventilation, pain, pharmacological agents and the
SWS. greater need for clinical interventions, which confound
The onset of oneiric phenomena has traditionally been the ability to determine causality.
associated with REM sleep; however neurophysiological
research indicates that dreaming occurs in both REM Physiological effects of sleep disturbance
and NREM phases [11,12]. The occurrence of oneiric ac- Physiologically, sleep deprivation has a myriad of nega-
tivity between the phases have some qualitative variances tive cognitive, autonomic [23], metabolic [24,25] and
with dream activity during NREM sleep being associated hormonal [7,26,27] effects on the body that may contrib-
with memory processing and recall of experiences, ute to prolonged ICU admission and in turn may con-
whilst in REM sleep it is characterised by visuohallucina- tribute to an increase in patient morbidity. Findings
tory and unusual content [13]. The role of dreaming is derived from animal-based studies reveals that sleep
thought to have importance for cognition, associated deprivation is associated with increased mortality; the
with mental processing and memory consolidation. implications of such findings within the ICU setting have
the capacity to be profound as sleep disturbance is com-
Sleep disturbance in ICU monly experience by this patient cohort [27,28].
The sleep physiology of ICU patients indicates that
whilst their TST is often normal (7 to 9 h) [2,14-17], Effects on the respiratory system
sleep is highly fragmented with patients experiencing 6.2 The chemosensitivity of the brain’s respiratory centre is
awakenings per hour [2]. Sleep quality is further com- reduced amongst sleep-deprived patients, with White
promised as the majority of sleep is spent in stages N1 et al. [29] reporting a decrease in intrinsic ventilatory re-
and N2 which is perceived to be ‘light sleep’ with limited sponse to hypoxic and hypercapnic states. Further, stud-
restorative benefits. Subsequently, the characteristics of ies have reiterated varying adverse effects of sleep
non-consolidated light sleep have resulted in ICU pa- deprivation on respiratory muscle function including
tients being sleep deprived. This has been attributed to a Phillip et al. [30] who demonstrated a significant reduc-
reduction in the duration of REM sleep and SWS, the tion in FEV1 (mean decline of 6%) and FVC (mean de-
supposition is that these phases support restorative pro- cline of 5%) in sleep-deprived patients with underlying
cesses and are important for recovery [16,18]. Due to a chronic obstructive pulmonary disease (COPD) com-
lack of quality sleep, patients experience daytime somno- pared to non-sleep-deprived COPD patients. Further-
lence, with as much as 50% of patient TST occurring more, maximal inspiratory pressure (MIP) was found to
during daylight hours [15,16,19,20]. Sleep cycles which decrease from 81.5 ± 8.8 cmH2O in rested individuals to
traverse both day and night perpetuate the phase shifting 75.9 ± 7.6 cmH2O in those who were sleep deprived
of circadian rhythms with sleep disturbance persisting [30]. Issues associated with inspiratory muscle endur-
months after discharge from ICU [21]. ance has also been reported by Cheng and Tang [31],
The impact of severity of illness on sleep architecture who found that sleep deprivation amongst healthy indi-
and sleep disturbance has been widely considered; how- viduals resulted in a significant decline in respiratory
ever, there are limited studies explicitly investigating this muscle strength. Findings such as these suggest that sleep-
factor. There exists some clinical indication that higher deprived states may contribute to patient hypoventilation,
acuity scores are associated with greater sleep disturb- adversely effecting pulmonary reserves and overall readi-
ance, specifically increased fragmentation and number of ness and ability to expedite weaning from mechanical
awakenings [22]. Gabor et al. [15] reported that healthy ventilation.
participants exposed to the ICU environment compared
to ICU patients did not demonstrate the same level of Effects on the cardiovascular system
sleep disturbance and reduction in SWS, suggesting that The manifestation of cardiovascular effects of sleep
critical illness may be a contributing factor to the abnor- deprivation emanates from the stimulation of the sym-
malities seen in the sleep architecture of ICU patients. pathetic nervous system (SNS) and the release of the
However, in this study, the healthy participants were catecholamines adrenaline and noradrenaline. As a re-
only exposed to the noise within the environment and sult, increases in blood pressure and heart rate are re-
not to the full sensory experience of ICU such as frequent ported due to changes in baroreflex sensitivity [32-34].
clinical interactions and invasive monitoring. Further, pa- Ogawa et al. [33] reported that increased baroreflex
tients with higher acuity score also demonstrate consider- results in a 12 mmHg elevation in blood pressure as a
able reduction in the EEG activity, which confounds the result of a single night’s sleep deprivation amongst
ability to accurately interpret polysomnographical data. healthy individuals.
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 3 of 10

Effects on the immunological system Effects on the metabolic system

Neuro-immunological research asserts that there exists a During nocturnal sleep, downregulation occurs in the
bidirectional relationship between sleep deprivation and hypothalamus-pituitary-adrenal (HPA) axis and the SNS,
the immune system. Although the vast majority of stud- which both have important roles in stress responses.
ies conducted are animal based, the reported changes Ensuing is a decrease in noradrenaline, adrenaline and
identified in the immunological system in response to cortisol levels which suppresses the immune systems
sleep deprivation can have significant implications for anti-inflammatory cytokines [43]. During sleep, particu-
critically ill patients. larly SWS, growth hormone is released in combination
The adaptive immune response and the functioning of with prolactin and leptin which provide pro-inflammatory
the T cells have been reported to be vulnerable to sleep signals which triggers the immune system activation [44].
disturbance, as studies have identified that sleep plays an The HPA axis plays an integral role in the body’s response
important role in the extravasation of the T cells [35,36]. to stress, primarily via the release of cortisol. Abnormal
The resulting increase in the propensity for sleep during cortisol levels in ICU patients contribute to further distur-
illness may play an important role in promoting the bances with circadian rhythms, as cortisol release is
function of the immune response and overall recovery. normally increased prior to waking to stimulate the in-
Previous animal studies have identified that interleukin dividual into a state ready to be active. An increase in
(IL)-1 and tumour necrosis factor (TNF) contribute to cortisol levels and suppression of melatonin produces
an increase in non-REM sleep and sleep fragmentation a propensity for patients to be in a wakeful state which
[37]. This occurs as immunoreactive neurons of the cy- may further exacerbate catabolic activity and increases
tokines which are located in regions of the brain that oxygen consumption.
play a role in the sleep-wake cycle. Although the re- Sleep disturbance adversely effects carbohydrate metab-
ported propensity for sleep during critical illness remains olism resulting in insulin resistance and glucose clearance.
unknown, it is hypothesised that the role of IL-1 and its Whereby, the increase in SNS activity and the ensuing
interaction with 5-hydrotryptamine (5-HT) may proffer stress response suppresses the release of insulin from pan-
an explanation. The onset of fever in response to creatic beta cells [45,46]. The impact of this on healthy in-
invading pathogens potentiates the immune response dividuals is an increased susceptibility to chronic health
and promotes survival. The resulting increase in pro- conditions such as coronary artery disease and diabetes.
inflammatory cytokines such as IL-1 impacts on the Within the ICU patient population, this can exacerbate
sleep architecture through increasing the NREM phase underlying co-morbidities, putting them at risk for add-
with greater fragmentation and reducing REM sleep; itional secondary complications. For example, instability
these effects, however, allow for an enhanced inflamma- in blood glucose levels has been associated with increased
tory response [38-40]. The increased NREM sleep is patient mortality [47]. The immunological effects of sleep
thought to be an important aspect that supports the on- disturbance also have a concomitant effect on metabolic
set of fever; as during this phase the brain and body functions with pro-inflammatory cytokines increasing in
temperature is reduced, along with metabolic activity activity with moderate total sleep loss, which contributes
[37]. These features of the NREM stage allow for en- to insulin resistance [44].
hance heat dissipation with the corresponding increase
in sleep fragmentation further facilitates heat loss [37]. Effects on the neurocognitive system
Furthermore, the function of natural killer (NK) cells The onset of delirium amongst ICU patient ranges be-
has been shown to be adversely effected in sleep- tween 60% to 80% for mechanically ventilated patients
deprived states, although research findings have not al- and 20% to 50% for non-mechanically ventilated patients
ways been consistent. Irwin et al. [41] found that the [48,49]. Delirium has been identified as an independent
functionality of NK cells was reduced by 30% in sleep- predictor for adverse patient outcomes including increased
deprived states in healthy subjects. This was further reit- hospital length of stay, a persistent decline in cognitive
erated in their 1996 study which demonstrated that status and increased patient mortality [48-50].
whilst NK cell activity initially declined, it did improve A number of factors have been purported to contribute
after sleep recovery. In contrast, Dinges et al. [42] re- to the development of delirium, with sleep deprivation
ported that NK cell activity was increased in healthy thought to be a contributing factor. However, the rela-
adults who were sleep deprived; however, leukocyte tionship is not clearly understood in regard to whether
function was suppressed. Although much of the research sleep deprivation leads to delirium or if the onset of de-
investigating the relationship between immune function lirium contributes to sleep deprivation. Nonetheless,
and sleep deprivation has been conducted on healthy in- sleep deprivation and delirium share a number of similar
dividuals, it is apparent that sleep provides an important features namely a decline in cognitive function inclusive
role in the effective functioning of the immune system. of psychomotor vigilance, memory and disturbances in
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 4 of 10

language and perception which is characterised by halluci- combined with increased intra-cranial pressure can se-
nations and delusions [51,52]. Although recommendations verely affect cerebral functioning and neurotransmitter
aimed at minimising the likely onset and complications activity resulting in decreased EEG activity. Sleep dis-
associated with delirium include reducing sleep disturb- turbance within this patient cohort may have significant
ance, one of the major challenges is associated with the implications for recovery outcomes, with previous re-
pharmacological agents used to treat symptoms associated search indicating that the presence of SWS and REM
with delirium. Many of the pharmacological agents such sleep, along with sleep efficiency correlated to improved
as haloperidol and benzodiazepines used can potentially cognitive outcomes [60]. The negative effects that TBI
exacerbate sleep disturbance, due their inhibitory effect on has on sleep can persist for months after ICU discharge
SWS and REM sleep [52]. and are predominantly associated with sleep initiation
Commonly used GABA agonists such as propofol and and maintenance and sleep architecture which can ad-
benzodiazepines (Table 1) increase total sleep time and versely affect cognition and behaviour [61,62].
decrease sleep latency; however, these decrease N3 and
REM sleep stages [53,54]. The pharmacokinetics of these Environmental factors impacting of ICU patients sleep
medications suppresses cerebral function which pro- The importance of sleep in patient recovery can be
duces changes in EEG activity such as a reduction in deprioritized in ICU due to the need to meet increas-
delta activity [55]. Similarly, commonly used opioids, ingly complex care requirements. Sleep disturbance has
morphine and fentanyl, increase total sleep time, they emerged as an indicator for adverse clinical outcomes
adversely impact N3 and inhibit REM sleep [56]. Al- [52,63] and in turn should not be viewed as a passive
though sedation and analgesia is commonly required to physical state but rather acknowledged as an important
support therapies such as mechanical ventilation and bio-physiological process. The impact of the ICU environ-
promote patient comfort, understanding the cumulative ment on patient sleep has been frequently reported on
effects of commonly used pharmacological agents and and investigated as a primary etiological cause of sleep dis-
identifying newer emerging medications that may reduce turbance. Factors such as light, noise, clinical care-related
the negative effects on sleep is an area for further re- interactions, combined with medications and acute illness
search. Preliminary animal-based research regarding the have all been hypothesised as causal factors for sleep
effective of dexmedetomidine indicates that it increases deprivation [1,2,7,15,16,19,64,65] (Table 2).
N3 sleep, whilst ICU-based research suggests that inci-
dences of delirium onset maybe reduced [57]. These Effects of noise levels
preliminary findings suggest the dexmedetomidine Noise levels in ICU have been presumed to be the most
may have an important role in the management of crit- disruptive environmental stressor that patients are sub-
ically ill patients, which may reduce the incidences of jected to and are a relentless feature due the cacophony
delirium and the degree of sleep disturbance experi- of clinical activity and technological monitoring. Noise is
ence by patients. defined in terms of mechanical energy and is commonly
The impact that traumatic brain jury (TBI) has on
sleep can be profound. The prevalence of TBI ranges be- Table 2 Factors impacting on sleep architecture
tween 30% and 84% and makes up a large percentage of
Factor Example
critical care admissions [58,59]. In the acute phase of
Environmental noise Staff conversations and monitoring
presentations, the impact that pharmacological agents alarms

Table 1 The effect of pharmacological agents on sleep Prolonged exposure to low

levels of artificial light
Pharmacological agent TST SWS REM
Inflammatory mediators
Propofol ↑ ↓ ↓
Pain
Lorazepam ↑ ↓ ↓
Pharmacological agents Sedative, opioids, benzodiazepines
Alprazolam ↑ ↓ ↓ and inotropes
Diazepam ↑ ↓ ↓ Mechanical ventilation
Haloperidol ↑ ↑ ↓ Increased cortisol release
Morphine ↓ ↓ ↓ Decreased endogenous
Fentanyl ↑ ↓ ↓ melatonin levels
Midazolam ↑ ↓ ↓ Critical illness
Dexmedetomidine ↑ ↑ ↓ Clinical interactions Vital sign monitoring, pathological
investigations and medication
TST, total sleep time; SWS, slow wave sleep; REM, rapid eye movement; administration
↑, increase; ↓, decrease.
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 5 of 10

reported in the A weighted decibel (dB) scale as it most have primarily involved an educational approach to en-
accurately attenuates the noise levels heard by the hu- hance staff awareness of the impact their behaviours
man ear [66]. The measure of decibels is logarithmic, have in contributing to noise levels and promoting re-
and as a result, a 10-dB increase in noise constitutes a ductions in alarm volume settings to promote a diur-
doubling of the noise level [67]. nally appropriate environment. However, these studies
The World Health Organisation (WHO) recommends have employed subjective assessments of the impact of
that noise levels within hospital wards should not exceed behaviour modification, such as clinical staff perception
30 dB(A) at night in order to reduce sleep disturbance of nocturnal noise, as opposed to using an objective en-
[68]. The ability for ICUs to meet the WHO recommen- vironmental measure of noise. This has been problem-
dations is improbable and is further reiterated within the atic as studies that have employed environmental noise
literature whereby ICUs worldwide repeatedly cite noise monitoring to determine the effect of behaviour modifica-
levels in excess of 50 dB [2,64,65,69-71]. Moreover, noise tion on noise have been unable to achieve a measurable
levels in ICUs have steadily increased over the past de- reduction in noise levels [81]. Furthermore, achieving sus-
cades, with a study conducted by Busch-Vishnich [72] tainable change in the clinical environment has not been
quantifying this at a rate of 0.38 dB(A) per day and 0.42 extensively investigated as behaviour modification studies
dB(A) per night, per year. The evolving advances in have been undertaken over short durations, with follow-
medical care, technology and increasing patient acuity up assessments conducted after the immediate interven-
are contributing factors to the acoustical changes within tion period.
the clinical environment. The noise generated from alarms Studies employing objective measures of sleep have re-
associated with the intensive monitoring of patients fre- ported varying results. Aaron et al. [75] investigated the
quently exceeds 70 dB(A), which is reflective of the noise impact of noise on sleep via polysomnography (PSG)
generated by traffic [73]. Further, with the increasing am- and reported that noise sources exceeding 50 dB(A) re-
bient noise level, the impact of the Lombard effect can be sulted in electroencephalographic changes indicative of
compounded. This communication phenomenon results arousal in 25% of cases. However, this finding has not
in individuals increasing their speech amplitude in order been consistently reported in proceeding studies; further,
to enhance the intelligibility of their speech within noisy there is a discrepancy between self-reported sleep quality
environments and contributes to a rapid escalation in and the biophysiological data obtained regarding sleep.
environmental noise. This creates an environment that Studies employing time synchronised monitoring of
is detrimental to patients’ sleep as noise levels fre- sleep via polysomnography and environmental noise
quently undulate between low levels, with frequent monitoring, such as Freedman et al. [16] identified that
short, sharp and unpredictable escalations in noise [74]. only 11.5% of arousals and 17% of awakenings could be
Both subjective and objective studies have reported attributed to noise. Likewise, in a similar study, Gabor
noise as a primary source of sleep disturbance, with staff et al. [15] identified that 20% of awakenings were the
being the primary source of the generated noise [15,16,75]. direct result of environmental noise. Neither study was
Subjective studies investigating the impact of noise on sleep able to account for the cause of the remaining 75% to
indicate that ICU patients identify the exposure to noise 80% of arousals but postulated that clinical interactions
and inability to sleep as a major stressor recounted by may account for much of these. However, this was not
patients. Further, objective studies indicate that the supported by Gabor et al.’s [15] findings, whereby only
noise generated with within the environment is not con- 7% of awakenings could be associated with clinical inter-
ducive to the ability to sleep. The primary source of actions. Subsequently, the degree to which noise acts as
noise within the clinical environment has been attrib- the pathogenesis of sleep disturbance in ICU remains
uted to staff behaviours, which Kahn et al. [76] reported unclear, although it is commonly reported as an issue by
accounted for greater than 50% of noise sources with an survivors of critical illness.
average noise level of 84 dB. Previous studies have sug-
gested that the disruptive nature of staff behaviours Effects of clinical interactions
evolve from the propensity of staff to deprioritized The need for clinical interventions increases exponen-
sleep, due to patients being intubated and sedated, and tially in ICU as many assessments are scheduled on an
lacked knowledge regarding the psychophysiological ef- hourly basis such as vital sign monitoring, fluid balance
fects of sleep deprivation [70,77]. As a result of subject- assessments and pharmacological administration. These
ive studies, behaviour modification strategies have been interventions in combination with basic care needs es-
widely investigated as a means to curtail the impact of tablish an environment in which sleep is easily depriori-
noise generated by staff on patient sleep and have been tized and disrupted. Furthermore, the design of ICU can
cited as being successful in reducing noise levels by 6% compound issues, as the clinical area is frequently open
to 20% [78-80]. These behaviour modification activities planned with patients segregated from each other by
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 6 of 10

curtains, which achieves little in quashing the impact of melatonin secretion [89-92]. Melatonin is an important
the clinical environment on patients’ senses. regulator hormone of the circadian rhythm. Melatonin
Early observational studies conducted by Walker [82] levels increase during the early hours of the night to fa-
and Woods [83] reported that patients were disturbed cilitate the onset of sleep and decrease during the morn-
between 1 and 14 times per hour, and given that a single ing when cortisol levels increase. Whilst there is a focus
sleep cycle requires 90 to 110 min to complete, patients on the potential role of melatonin in promoting sleep in
cared for in the ICU have little ability to achieve quality this patient population, subjective studies have reported
sleep. In more contemporary studies such as Lee et al.’s that ICU survivors perceived light exposure to be min-
[84], 50% of subjects reported being woken 2 to 5 times imally disruptive to their ability to sleep [93]. Hu et al.
throughout the night, which contributed to difficulties [94] investigated the effect of non-invasive, non-
falling back to sleep once woken. This finding has been pharmacological interventions of ear plugs and eye
corroborated by previous studies conducted by Redeker masks on ICU patients (n = 14) who underwent PSG
and Hedges [85] and Tranmer et al. [1]. In contrast, sleep monitoring. The study found that these interven-
studies conducted by Tamburri et al. [86] and Celik tions resulted in an increase in recorded REM sleep, a
et al. [87] report much higher patient to staff interac- reduction in REM latency with less arousals (p < 0.05)
tions with both studies reporting between 40 and 60 in- and an elevation in melatonin levels (p =0.002). Suggesting
teractions per night. Comparatively, the frequency of that although patients may not perceive exposure to light
disruptions for mechanically ventilated patients was a major cause of sleep disturbance, it appears to have a
found to be substantially higher, with Le et al. [88] detrimental effect of sleep wake patterns, and simple inter-
reporting that patients experienced 20 to 60 disruptions ventions may be able to minimise its effects.
per hour. A considerable body of research focuses on how light
The intensive monitoring that patients are subjected exposure affects endogenous melatonin secretion and
to is detrimental to the intrinsic sleep cycle, suggesting the potential efficacy of supplemental melatonin as a
that under these conditions ICU patients will experience means to entrain the circadian rhythm and overcome
sleep deprivation. Further, in an observational study by the lack of light variation to maintain the external zeit-
Le et al. [88], nursing staff reported that 13.9% of noc- geber. Munigler [95] reported that melatonin secretion
turnal interactions could be safely omitted and, in turn, was suppressed in patient with sepsis compared to non-
reduce the disturbance to patients. This suggests that a septic ICU patients who demonstrated normalised circa-
number of nursing-based activities are performed as a dian patterns similar to healthy individuals. In a double
routine rather than based on clinical evidence and ne- blind placebo controlled study (n = 8), patients receiving
cessity. This highlights the need for clinical staff to crit- supplemental melatonin demonstrated an improvement
ically evaluate the necessity for some of the care in sleep duration and sleep quality [96]. In contrast, a
provided and to consider making adjustments to work- study conducted by Egi et al. [97] involving 32 tracheos-
flow in order to promote nocturnal sleep. tomised ICU patients was inconclusive regarding the
benefits of melatonin in promoting sleep, finding that al-
Effects of light though melatonin levels increased in the treatment
Regulation of the circadian rhythm is influenced by so- group it did not result in improved observable nocturnal
called zeitgebers (environmental cues) to remain entrained sleep (240 min versus 243.4 min in the placebo group).
to the typical day/night routine. Prominent zeitgebers in- A similar study undertaken by Bourne et al. [98] also
clude meal times and exposure to daylight, both of which studied the effect of supplemental nocturnal (21:00 h)
can be suppressed amongst critically ill patients. Nutrition melatonin administration of 10 mg in 27 ICU patients
is frequently provided enterally on a 24-h continuum, who had undergone trachesotomy insertion to promote
whilst ICU design and critical illness does not permit pa- ventilator weaning. The reported outcome of this study
tient exposure to adequate natural light. Subsequently, the was that sleep in the treatment group increased by 1 h
outcome of inappropriately timed zeitgebers in combin- (sleep efficiency index difference = 0.12, 95% CI −0.02 to
ation with prolonged exposure to low levels of artificial 0.27, p = 0.04) compared to the placebo group, along
lighting can impact on the circadian pacemaker leading to with an objective improvement in sleep quality as evalu-
circadian disturbance. ated by bispectral index (BIS).
The protracted exposure to artificial lighting obfus- Melatonin has emerged as a possible treatment to
cates the normal circadian rhythms, with light levels maintain the circadian rhythm with oral administration
within ICUs being highly variable, ranging between a having good bioavailability, with minimal negative effects
mean of 5 and 1,400 Lux. Exposure to low levels of arti- on respiration despite its hypnotic effects [99]. To date,
ficial light less than 500 Lux and for as little as 20 min the studies conducted have involved small participant
has been identified as sufficient to suppress nocturnal numbers and variances in sleep assessment. Future studies
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 7 of 10

involving larger participant numbers and standardised Table 3 Interventions to reduce sleep disturbance
sleep monitoring via PSG are required to ascertain the Intervention Example
potential of melatonin as a standard therapy, along with Establish a nocturnal environment By reducing volumes of
the effect of concurrent interventions such as eye masks alarms and phones.
and ear plugs to negate some of the sensory experience Enhance staff awareness of noise Soundear
of the ICU environment. produced by conversations
Employ the use of night settings in
Sleep monitoring techniques monitoring equipment with backlighting
to reduce exposure to light.
Sleep-related research conducted amongst ICU patients
clearly identifies significant sleep disturbances, which Judicious use of pharmacological agents
can have deleterious implications on their psycho- Monitor, assess and treat pain
physiological condition which protract recovery. Des- Devise individualised sleep hygiene routines
pite these findings, there remains no method that is Employ relaxation techniques in Music therapy and massage
feasible for widespread implementation that accurately preparation for sleep
monitors patients’ sleep within the ICU environment. Decrease environmental stimulus Via the use of eye masks and
Although PSG provides considerable benefits over ear plugs
other strategies in being able to provide details of sleep Reduce nocturnal clinical interactions Cluster clinical care and
physiology, it is not a strategy that is feasible to be im- scheduling of procedures
plemented widely as it is expensive, labour intensive Ventilator support to promote rest
and technically difficult. In comparison, simple cost- overnight
effective methods involving clinical observations are Reduce daytime napping in order to
reduce circadian dys-synchrony
questionable regarding their accuracy as studies have
indicated that these result in an overestimation of sleep Promote daytime activity Such as sitting out of bed
and mobilisation
time and quality [17,65,100]. This was demonstrated by
Nicolas and colleagues’ [8] quantitative single blinded
descriptive study, investigating nursing-based assess- mechanical ventilation can be utilised to facilitate nocturnal
ment and patient perception of sleep which found that rest, and identification of pharmacological agents and
these correlated only 50% of the time, with nursing staff regimes that do not interfere with the intrinsic sleep
overestimating patients’ quality of sleep. Adjunct cycle. Further, identifying strategies that can be readily
methods such as actigraphy (ACTG) have been consid- implemented that endeavour to minimise the impact of
ered, although studies involving the ICU are few and complications associated with sleep deprivation. How-
participant numbers are small. There are, however, beit, research investigating sleep promotion strategies
some favourable attributes associated with ACTG use have lacked clinical efficacy [17,92,100], as PSG is not
in comparison to PSG in that it is cost effective, is easy viable for widespread implementation, behavioural assess-
to interpret and is able to collect data over an extended ments such as ACTG have not been able to accurately
period. The limitations of ACTG need to be acknowl- assess sleep in critically ill patients, and subjective assess-
edged in that it will provide no information regarding ments such as nursing-based observation frequently over-
the sleep architecture of patients and may be suitable estimate sleep. Adjunct interventions such as behaviour
only for a limited cohort of ICU patients. However, it modification of staff through education have only been
may be potentially useful in monitoring circadian dis- subjectively evaluated and their impact on the long term is
turbance and sleep fragmentation, both of which are not evaluated. Emerging benefit of eye masks and ear
major issues associated with ICU patients. Potentially, plugs may have some benefit in quashing the effect of the
further advancements in monitoring techniques and ICU environment on patients but do improve the sleep
the development of advanced monitoring algorithms architecture of patients. Similarly, melatonin administra-
may provide clinicians with a viable method. tion reports some promising benefits; however, larger
As a result there is a need to develop accurate and ef- studies are required. A primary issue confronting clinicians
fective clinical monitoring methods of sleep, to facilitate regarding sleep in ICU is the development of a method
the early recognition of sleep disturbance. Interventions that allows for sleep monitoring to be implemented as a
need to be implemented that aim to provide an environ- standard of clinical care, which provides accurate informa-
ment that supports sleep and recognises its role in pa- tion regarding the sleep of this patient cohort.
tient recovery (Table 3). Additional research needs to be
undertaken in order to understand the physiological im- Conclusions
pact of critical illness on patient sleep, the relationship Despite decades of research identifying the impact of
between delirium and sleep disturbance, along with how the clinical environment on ICU patients’ sleep, little
Delaney et al. Annals of Intensive Care (2015) 5:3 Page 8 of 10

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TNF: tumour necrosis factor; TST: total sleep time.
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