Delirium
This article is about the mental state and medical condi-
tion. For other uses, see Delirium (disambiguation).
“Cognitive impairments” redirects here. For other forms
of cognitive impairment, see Cognitive impairment.
Delirium, or acute confusional state, is an organically-
caused decline from a previously attained baseline level
of cognitive function. It is typified by fluctuating course,
attentional deficits and generalized severe disorganization
of behavior. It typically involves other cognitive deficits,
changes in arousal (hyperactive, hypoactive, or mixed),
perceptual deficits, altered sleep-wake cycle, and psy-
chotic features such as hallucinations and delusions.
Delirium itself is not a disease, but rather a clinical
syndrome (a set of symptoms). It may result from an un-
derlying disease, from drugs administered during treat-
ment of that disease in a critical phase, withdrawal from
drugs, from a new problem with mentation, or from vary-
ing combinations of two or more of these factors. It is
a corollary of the criteria that a diagnosis of delirium
usually cannot be made without a previous assessment,
or knowledge, of the affected person’s baseline level of
cognitive function. In other words, a mentally disabled
or person who is suffering who from this will be oper-
ating at their own baseline level of mental ability would
be expected to appear delirious without a baseline mental
functional status against which to compare.
Delirium may be caused by a disease process outside
the brain that nonetheless affects the brain, such as
infection (urinary tract infection, pneumonia) or drug
effects, particularly anticholinergics or other CNS de-
pressants (benzodiazepines and opioids).[1] Although
hallucinations and delusions are sometimes present in
delirium, these are not required for the diagnosis, and the
symptoms of delirium are clinically distinct from those
induced by psychosis or hallucinogens (with the excep-
tion of deliriants.) Delirium must by definition be caused
by an organic process, i.e., a physically identifiable struc-
tural, functional, or chemical problem in the brain (see
organic brain syndrome), and thus, fluctuations of men-
tation due to changes in purely psychiatric processes or
diseases, such as sudden psychosis from schizophrenia or
bipolar disorder, are (by definition) not termed delirium.
Like its components (inability to focus attention, mental
The core features are:
confusion and various impairments in awareness and tem-
poral and spatial orientation), delirium is the common
manifestation of new organic brain dysfunction (for any
reason). Delirium requires both a sudden change in men-
tation, and an organic cause for this. Thus, without care-
ful assessment and history, delirium can easily be con-
fused with a number of psychiatric disorders or long
term organic brain syndromes, because many of the signs
and symptoms of delirium are conditions also present
in dementia, depression, and psychosis.[2] Delirium may
newly appear on a background of mental illness, baseline
intellectual disability, or dementia, without being due to
any of these problems.
Treatment of delirium requires treating the underlying
cause. In some cases, temporary or palliative or symp-
tomatic treatments are used to comfort patients or to
allow better patient management (for example, a pa-
tient who, without understanding, is trying to pull out
a ventilation tube that is required for survival). Delir-
ium is probably the single most common acute disorder
affecting adults in general hospitals. It affects 10-20%
of all hospitalized adults, and 30-40% of elderly hos-
pitalized patients and up to 80% of ICU patients. In
ICU patients or in other patients requiring critical care,
delirium is not simply an acute brain disorder but in
fact is a harbinger of much greater likelihood of death
within the 12 months which follow the ICU patient’s
hospital discharge.[3] Antipsychotics are generally a first-
line treatment for delirium; however, when delirium
is caused by alcohol or sedative hypnotic withdrawal,
benzodiazepines are a first-line treatment.[4]
1 Definition
In common usage, delirium is often used to refer to
drowsiness, disorientation, and hallucination. In medical
terminology, however, a number of different symptoms,
including temporary disturbance in consciousness, with
reduced ability to focus attention and solve problems, are
the core features of delirium. Occasionally sleeplessness
and severe agitation and irritability are part of “delirium.”
Hallucination, drowsiness, and disorientation are not re-
quired, but may be contribute to the diagnosis.
There are several medical definitions of delirium (includ-
ing those in the DSM-IV and ICD-10). However, all in-
clude some core features.
• Disturbance of consciousness (that is, reduced clar-
ity of awareness of the environment, with reduced
ability to focus, sustain, or shift attention)[5]
1
2 2 SIGNS AND SYMPTOMS

• Change in cognition (e.g., problem-solving impair- severe confusion and disorientation, developing with rel-
ment or memory impairment) or a perceptual dis- atively rapid onset and fluctuating in intensity. In its hy-
turbance (hallucination)[5] poactive form, it is manifested by an equally sudden with-
drawal from interaction with the outside world. Delirium
• Onset of hours to days, and tendency to fluctuate.[5] may occur in a mixed type where someone may fluctuate
between both hyper- and hypoactive periods. Delirium as
• Behaviour may be either overactive or underactive,
a syndrome is one which occurs more frequently in people
and sleep is often disturbed, with loss of the normal
in their later years. However, when it occurs in the course
Circadian rhythm.[5]
of a critical illness, delirium has been found to occur in
• Thinking is slow and muddled but the content is of- young and old patients at relatively even rates.
ten complex.[6]
2.1 Inattention and associated cognitive
Other clinical features include disorganized thinking, deficits
poor memory, delusions, and mood lability.[5]
Inattention is the cardinal and required symptom to
diagnose delirium and is noticeable on interview by
2 Signs and symptoms distractibility and inability to shift and / or sustain
attention.[9] More formal testing can include the months
Delirium is a syndrome encompassing an array of of the year backwards, serial sevens or digit span tests.
neuropsychiatric symptoms, including a disturbance Disorientation (another symptom of confusion, and usu-
in consciousness/attention and cognition that develops ally a more severe one) describes the loss of awareness
acutely and tends to fluctuate.[5] The change in cognition of the surroundings, environment and context in which
(memory deficit, disorientation, language disturbance) or the person exists. It may also appear with delirium, but
the development of a disturbance, must be one that is it is not required, as noted. Disorientation may occur in
not better accounted for by a pre-existing, established, time (not knowing what time of day, day of week, month,
or evolving dementia.[7] Other symptoms can include season or year it is), place (not knowing where one is) or
disorientation, thought disorder, memory problems, lan- person (not knowing who one is).
guage disorder, sleep disturbance, delusions, mood la- Memory impairment occurs[5] and is linked to inatten-
bility, psychomotor changes (changes in rate of activ- tion. Reduction in formation of new long-term memory
ity/movement), and hallucinations.[5] (which by definition survives withdrawal of attention), is
Delirium occurs as a stage of consciousness in the con- common in delirium, because initial formation of (new)
tinuum between normal awakeness/alertness and coma. long-term memories generally requires an even higher de-
During the 20th century, delirium was described as a gree of attention than do short-term memory tasks. Since
‘clouding of consciousness’ but this rather nebulous con- older memories are retained without need of concentra-
cept has been replaced by a better understanding of the tion, previously formed long-term memories (i.e., those
components of phenomenology that culminate in severely formed before the period of delirium) are usually pre-
impaired higher order brain functions. Lipowski de- served in all but the most severe cases of delirium.
scribed delirium as a disorder of attention, wakefulness,
cognition, and motor behaviour, while a disturbance in at-
2.2 Higher level thinking
tention is often considered the cardinal symptom.[5] Dis-
rupted sleep-wake cycles can result from a loss of normal Delirious patients have diminished comprehension as ev-
circadian rhythm.[5]
idenced by reduced ‘grasp’ of their surroundings and
Accumulating evidence indicates three core domains difficulties in connecting with their immediate environ-
of delirium phenomenology: “Cognition”, composed ment, executive dysfunction affecting abstraction, initia-
of inattention and other cognitive deficits; “Higher tion/perseveration, switching mental sets, working mem-
Level Thinking Processes” including impaired execu- ory, temporal sequencing and organization, insight and
tive function, semantic expression and comprehension; judgment. Though none of these cognitive deficits is spe-
and “Circadian Rhythm” including altered motor ac- cific to delirium, the array and pattern is highly suggestive.
tivity and fragmented sleep-wake cycle.[8] Phenomenol- Language disturbances in delirium include anomic apha-
ogy studies suggest that “core” symptoms occur with sia, paraphasias, impaired comprehension, agraphia, and
greater frequency while other less consistent “associated” word-finding difficulties. Incoherent or illogical / ram-
symptoms may reflect the biochemical influence of par- bling conversation is reported commonly. Disorgan-
ticular aetiologies or genetic, neuronal or physiological ised thinking includes tangentiality, circumstantiality and
vulnerabilities.[8] a proneness to loose associations between elements of
Delirium may present in hyperactive, hypoactive, or thought which results in speech that often makes limited
mixed forms. In its hyperactive form, it is manifested as sense with multiple apparent irrelevancies. This aspect
2.5 Dementia in ICU survivors 3

of delirium is common but often difficult for non-experts hourly basis. Interestingly, Barrough noted in 1583 that
to assess reliably. if delirium resolves, it may be followed by a “loss of
memory and reasoning power.” Recent long-term studies
bear this out, showing that many patients end up meet-
2.3 Sleep changes ing criteria for delirium for an alarmingly long time.[13]
For example, in ICU cohorts, it is common to find that
Disruption of sleep-wake cycle is almost invariably 10% of patients still have delirium at the time of hospital
present in delirium and often predates the appearance discharge.[14]
of a full-blown episode. Minor disturbances with in-
somnia or excessive daytime somnolence may be hard
to distinguish from other medically ill patients without 2.5 Dementia in ICU survivors
delirium, but delirium typically involves more substan-
tial alterations with sleep fragmentation or even complete Dementia is supposed to be an entity that continues to de-
sleep-wake cycle reversal that reflect disturbed circadian cline, such as Alzheimer’s disease. Another way of look-
rhythm regulation. The relationship of circadian distur- ing at dementia, however, is not strictly based on the de-
bances to the characteristic fluctuating severity of delir- cline component but on the degree of memory and execu-
ium symptoms over a 24-hour period or to motor distur- tive function problems. It is now known, for example, that
bance is unknown. between 50% and 70% of ICU patients have tremendous
Motor activity alterations are very common in delirium. problems with ongoing brain dysfunction that looks a lot
They have been used to define clinical subtypes (hypoac- like the degree of problems experienced by Alzheimer’s
tive, hyperactive, mixed) though studies are inconsistent or TBI (traumatic brain injury) patients and which leaves
as to the prevalence of these subtypes.[10] Cognitive im- too many ICU survivors disabled and unable to go back to
pairments and EEG slowing are comparable in hyperac- work and unable to serve effectively [15]
as the matriarchs and
tive and hypoactive patients though other symptoms may patriarchs of their families. This is a distressing per-
vary. Psychotic symptoms occur in both although the pre- sonal and public health problem that is getting an increas-
vailing stereotype suggests that they only occur in hyper- ing amount of scrutiny in ongoing investigations. The
active cases. Hypoactive cases are prone to non detection implications of such an “acquired dementia-like illness”
or misdiagnosis as depression. A range of studies suggest (note: the term here is being used in a circumstance in
that motor subtypes differ regarding underlying patho- which not all patients continue to decline as some have
physiology, treatment needs, and prognosis for function persistent yet stable brain dysfunction and others with
and mortality though inconsistent subtype definitions and newly acquired brain problems can recover fully) are pro-
poorer detection of hypoactives impacts interpretation of found at the private level, dismantling the person’s life in
these findings.[11] very practical ways such as inability to find a car in a park-
ing lot or even complete shopping lists or job-related tasks
Psychotic symptoms occur in up to 50% of patients with done previously for years. The societal relevance is also
delirium. While the common non-medical view of a huge when one considers work-force issues related to the
delirious patient is one who is hallucinating, most people inability of a young wage earner being unable to work be-
who are medically delirious do not have either hallucina- cause of either being a newly disabled ICU survivor them-
tions or delusions. Thought content abnormalities include selves or because they now have to care for their family
suspiciousness, overvalued ideation and frank delusions. member who is now suffering this “dementia-like” illness
Delusions are typically poorly formed and less stereo- following ICU care.
typed than in schizophrenia or Alzheimer’s disease. They
usually relate to persecutory themes of impending dan-
ger or threat in the immediate environment (e.g. being
poisoned by nurses). Misperceptions include deperson-
3 Causes
alisation, delusional misidentifications, illusions and hal-
lucinations. Hallucinations and illusions are frequently Delirium arises through the interaction of a number of
visual though can be tactile and auditory. Abnormali- predisposing and precipitating factors. A predisposing
ties of affect which may attend the state of delirium may factor might be any biological, psychological or social
include many distortions to perceived or communicated factor that increases an individual’s susceptibility to delir-
emotional states. Emotional states may also fluctuate, so ium. An individual with multiple predisposing factors
that a delirious person may rapidly change between, for is said to have ‘high baseline vulnerability’, and this is
example, terror, sadness and jocularity.[12] closely associated with frailty (see below). A precipitat-
ing factor is any biological, psychological or social fac-
tor that can trigger delirium. The division of causes into
2.4 Persistent delirium ‘predisposing’ and ‘precipitating’ is useful in order to as-
sess an individual’s risk of suffering from delirium, and
It was thought for many years that all delirium was a in guiding the management of delirium – however there
transient state of brain dysfunction that fluctuated on an may be a significant degree of overlap between the two
4 4 PATHOPHYSIOLOGY
categories.
Delirium most commonly affects the frail and infirm.
Frailty is usually the result of multiple physical and social
causes, and is often viewed as a symptom of old age or
ill health. Health can be described as a balance between
fitness and frailty, in which fitness results from physical
and socioeconomic assets, and frailty results from phys-
ical and socioeconomic deficits. Frail individuals (i.e.
those with significant predisposing factors) demonstrate
an inability to compensate for additional physical or so-
cial stressors (‘precipitating factors’). In a frail individual,
a single or mild precipitating factor could be sufficient to
trigger an episode of delirium. Conversely, delirium may
only result in a fit individual if they suffer serious or mul-
tiple precipitating factors. It is important to note that the
factors affecting the fitness or frailty of an individual can
change over time, thus an individual’s risk of delirium is
in a state of flux.
3.1 Predisposing factors
The most important predisposing factors are listed below:
• Older age
• Cognitive impairment / dementia
• Physical comorbidity (biventricular failure, cancer,
cerebrovascular disease)
• Psychiatric comorbidity (e.g., depression)
• Sensory impairment (vision, hearing)
• Functional dependence (e.g., requiring assistance
for self-care and/or mobility)
• Dehydration / malnutrition
• Drugs and drug-dependence.
• Alcohol dependence
3.2 Precipitating factors
Any acute factors that affect neurotransmitter, neuroen-
docrine or neuroinflammatory pathways can precipitate
an episode of delirium in a vulnerable brain. Clinical
environments can also precipitate delirium, and optimal
nursing and medical care is a key component of delirium
prevention.[16] Some of the most common precipitating
factors are listed below:
• Metabolic
• Malnutrition
• Dehydration, electrolyte imbalance
• Anaemia
• Hypoxia
• Hypercapnoea
• Hypoglycaemia
• Endocrine disorders (e.g., SIADH, Addison’s
disease, hyperthyroidism, hypercalcaemia)
• Infection
• Especially respiratory and urinary tract infec-
tions
• Medication
• Anticholinergics, dopaminergics, opioids,
steroids, recent polypharmacy
• Vascular
• Stroke/Transient ischaemic attack
• Myocardial infarction, arrhythmias, decom-
pensated heart failure
• Physical/psychological stress
• Pain
• Iatrogenic event, esp. post-operative, mechan-
ical ventilation in ICU
• Chronic/terminal illness, esp. cancer
• Post-traumatic event (e.g., fall, fracture)
• Immobilisation/restraint
• Severe constipation/fecal impaction
• Urinary retention
• Other
• Substance withdrawal (esp. alcohol, benzodi-
azepines)
• Substance intoxication
• Traumatic head injury
4 Pathophysiology
4.1 Animal models
The pathophysiology of delirium is not well understood
and a lack of animal models that are relevant to the syn-
drome has left many key questions in delirium pathophys-
iology unanswered. Earliest rodent models of delirium
used an antagonist of the muscarinic acetylcholine re-
ceptors, atropine, to induce cognitive and EEG changes
similar to delirium. Similar anticholinergic drugs such as
biperiden and scopolamine have also produced delirium-
like effects. These models, along with clinical studies of
drugs with ‘anticholinergic activity’ have contributed to a
hypocholinergic theory of delirium.[17]
4.3 Neuroimaging 5

Profound systemic inflammation occurring during bac- the review focused on a narrow range of biomarkers with
teraemia/sepsis is also known to cause delirium (of- no overlap between studies. Studies were generally small,
ten termed septic encephalopathy). Modeling this in studying heterogeneous populations with different times
mice also causes robust brain dysfunction and probably of CSF sampling in relation to delirium, and no clear con-
a delirium-like state, although these animals are typically clusions could be drawn. Broadly, delirium may be asso-
too sick to assess cognitively and measures such as EEG ciated with: increased serotoninergic and dopamine sig-
and magnetic resonance imaging/spectroscopy are neces- nalling; reversible fall in somatostatin; increased cortisol;
sary to demonstrate dysfunction. and increase in some inflammatory cytokines (IL-8, IL-
1β), but possibly not others (TNF-α).
Animal models that interrogate interactions between
prior degenerative pathology and superimposed systemic One additional study has since been published.[20] Post-
inflammation have been developed more recently and operative delirium was strongly associated with pre-
these demonstrate that even mild systemic inflammation, operative cognitive decline. However, CSF Aβ1-42, tau,
a frequent trigger for clinical delirium, induces acute and and phosphorylated-tau levels were not associated with
transient attentional/working memory deficits, but only delirium status, nor did they correlate significantly with
in animals with prior pathology.[18] Prior dementia or cognitive function before the onset of delirium. The two
age-associated cognitive impairment is the primary pre- main explanations for these findings are either: (1) the
disposing factor for clinical delirium and ‘prior pathol- study was underpowered to detect mediating pathways
ogy’ as defined by these new animal models may con- between premorbid cognitive impairment, Alzheimer’s
sist of synaptic loss, network disconnectivity, and primed pathology biomarkers and subsequent delirium; or (2)
microglia (brain macrophages that are ‘primed’ by the pri- postoperative delirium arises through pathophysiological
mary pathology to produce exaggerated responses to sub- pathways that are distinct from Alzheimer’s disease.
sequent inflammatory insults).
While it is difficult to state with confidence whether delir-
4.3 Neuroimaging
ium is occurring in a non-verbal animal, comparisons
with human DSM-IV criteria remain useful. According
The neuroimaging correlates of delirium are very difficult
to DSM-IV, demonstration of acute onset impairments
to establish. Many attempts to image people with concur-
in attention and some other cognitive domain, that cannot
rent delirium will be unsuccessful. In addition, there is a
be better explained by existing dementia and that are trig-
more general bias selecting younger and fitter participants
gered by physiological disturbances resulting from some
amenable to scanning, especially if using intensive proto-
general medical condition should be present in order to
cols such as MRI.
reach a ‘diagnosis’ of delirium. Recent animal models ful-
fill these criteria reasonably well.[18] Whether the deficit is Most of the literature has been summarised by a sys-
one of attention or short-term memory is difficult to dis- tematic review.[21] This found 12 articles for inclusion,
sect, but it is undeniably distinct from long-term mem- most with small sample sizes (total number of cases
ory, consistent with observations in patients with delir- 127). There was substantial heterogeneity in populations,
ium. There is an urgent need to understand more about study design, and imaging modalities such that no firm
the mechanisms of dysfunction underpinning delirium conclusions were made. Generally, structural imaging
and data arising from these and other animal models must suggested that diffuse brain abnormalities such as atro-
form part of the discussion on delirium pathophysiology. phy and leukoaraiosis might be associated with delirium,
though few studies could account for differences in key
variables such as age, sex, education or underlying cogni-
4.2 Cerebrospinal fluid biomarkers tive function and education.
Since publication of the systematic review, five further
Studies of cerebrospinal fluid (CSF) in delirium are dif- studies have been published. The largest-scale report was
ficult to perform. Apart from the general difficulty of re- VISIONS.[22][23] This prospectively examined the neu-
cruiting participants who are often unable to give consent,
roimaging correlates of delirium in 47 participants after
the inherently invasive nature of CSF sampling makes critical illness. Delirium duration was related to measures
such research particularly challenging. However, a few of white matter tract integrity and this in turn was re-
studies have exploited the opportunity to sample CSF lated to poorer cognitive outcomes at 3 and 12 months.
from persons undergoing spinal anaesthesia for elective In addition, brain volumes were also assessed and related
or emergency surgery. Indeed, spinal anaesthesia may in to cognitive outcomes in the same manner. Overall, the
fact be the anaesthetic modality of choice for frail older
study found that longer duration of delirium was associ-
patients, so these studies are often undertaken in highlyated with smaller brain volume and more white matter
relevant populations. disruption, and both these correlated with worse cogni-
A systematic review identified 8 studies involving 235 tive scores 12 months later.
patients (142 with delirium).[19] Overall, 17 different Two studies examined delirium risk as a post-operative
biomarkers were considered and each article identified in complication after elective cardiac surgery. These
6 5 DIAGNOSIS

both showed that white matter damage predicted post-
operative delirium.[24][25] One functional MRI study re-
ported a reversible reduction in activity in brain areas lo-
calising with cognition and attention function.[26]
• Delirium may be distinguished from psychosis, in
which consciousness and cognition may not be im-
paired (however, there may be overlap, as some
acute psychosis, especially with mania, is capable of
producing delirium-like states).

• Delirium is distinguished from dementia (chronic

4.4 Neurophysiology
organic brain syndrome) which describes an “ac-
quired” (non-congenital) and usually irreversible
Electroencephalography (EEG) is an attractive mode of
cognitive and psychosocial decline in function. De-
study in delirium as it is able to capture measures of
mentia usually results from an identifiable degenera-
global brain function. There are also opportunities to
tive brain disease (for example Alzheimer disease or
summarise temporal fluctuations as continuous record-
Huntington’s disease). Dementia is usually not asso-
ings, compressed into power spectra (quantitative EEG,
ciated with a change in level of consciousness, and
qEEG). Since the work of Engel and Romano in the
a diagnosis of dementia requires a chronic impair-
1950s, delirium has been known to be associated with
ment.
a generalised slowing of background activity.[27]
A systematic review identified 14 studies for inclusion, • Delirium is distinguished from depression.
representing a range of different populations: 6 in older
• Delirium is distinguished by time-course from the
populations, 3 in ICU, sample sizes between 10 and
confusion and lack of attention which result from
50).[28] For most studies, the outcome of interest was the
long term learning disorders and varieties of con-
relative power measures, in order: alpha, theta, delta fre-
genital brain dysfunction. Delirium has also been
quencies. The relative power of the theta frequency was
referred to as 'acute confusional state' or 'acute brain
consistently different between delirium and non-delirium
syndrome'. The key word in both of these descrip-
patients. Similar findings were reported for alpha fre-
tions is “acute” (meaning: of recent onset), since
quencies. In two studies, the relative power of all these
delirium may share many of the clinical (i.e., symp-
bands was different within patients before and after delir-
tomatic) features of dementia or developmental dis-
ium.
abilities including attention deficit hyperactivity dis-
order, with the important exception of symptom du-
ration.
4.5 Neuropathology
Delirium represents an organically caused decline from a
Only a handful of studies exist where there has been an
previously attained level of cognitive functioning. It is a
attempt to correlate delirium with pathological findings
corollary of these differential criteria that a diagnosis of
at autopsy. A case series has been reported on 7 patients
delirium cannot be made without a previous assessment,
who died during ICU admission.[29] Each case was ad-
or knowledge, of the affected person’s baseline level of
mitted with a range of primary pathologies, but all had
cognitive function. In other words, a mentally disabled or
acute respiratory distress syndrome and/or septic shock
demented person who is operating at their own baseline
contributing to the delirium. 6/7 had evidence of hypop-
level of mental ability might appear to be delirious with-
erfusion and diffuse vascular injury, with consistent in-
out a baseline functional status against which to compare.
volvement of the hippocampus in 5/7.
A case-control study examined 9 delirium cases with
6 age-matched controls, investigating inflammatory cy- 5.1 Mental illness
tokines and their role in delirium.[30] Persons with
delirum had higher scores for HLA-DR and CD68 Some mental illnesses, such as a manic episode of bipolar
(markers of microglial activation), IL-6 (cytokines disorder, or some types of acute psychosis, may cause a
pro-inflammatory and anti-inflammatory activities) and rapidly fluctuating impairment of cognitive function and
GFAP (marker of astrocyte activity). These results might
ability to focus. Outwardly this appears similar to a con-
suggest a neuroinflammatory substrate to delirium, but fused state caused by inadequate brain metabolism but it
the conclusions are limited by biases from selection of
actually comes from problems in functioning. However,
controls. they are not technically causes of delirium, since any fluc-
tuating cognitive symptoms that occur as a result of these
mental disorders are considered by definition to be due to
the mental disorder itself, and to be a part of it. Thus,
5 Diagnosis physical disorders can be said to produce delirium as a
mental side-effect or symptom, although primary mental
Differential points from other processes and syndromes disorders which produce the symptom cannot be put into
that cause cognitive dysfunction: this category once identified. However, such symptoms

may be impossible to distinguish clinically from delirium 6 Prevention
resulting from physical disorders, if a diagnosis of an un-
derlying mental disorder is yet to be made.
5.2 Diagnosis in general settings
Multiple guidelines recommend that delirium should
be diagnosed when it presents to healthcare services.
Much evidence suggest, however, that delirium is greatly
underdiagnosed.[31] Higher rates of detection of delirium
in general settings (for the ICU see below) can be as-
sisted by the use of validated delirium screening tools.
Many such tools have been published. They differ in
duration, complexity, need for training, and so on. Ex-
amples of tools in use in clinical practice are: Delirium
Observation Screening Scale,[32] the Nursing Delirium
Screening Scale (Nu-DESC),[33] the Confusion Assess-
ment Method,[34] the Recognizing Acute Delirium As
part of your Routine (RADAR) tool [35] and the 4 “A"s
Test or 4AT.[36]
5.3 Diagnosis in ICU
In the ICU, international guidelines recommend that ev-
ery patient gets checked for delirium every day (usually
twice or more a day) using a validated clinical tool.[37]
The two most widely used are the Confusion Assessment
Method for the ICU (CAM-ICU)[38] and the Intensive
Care Delirium Screening Checklist (ICDSC).[39] There
are translations of these tools in over 20 languages and
they are used globally in many thousands of ICUs, and
instructional videos and myriad implementation tips are
available.[40] It is not as important which tool is used as
that the patient gets monitored. Without using one of
these tools, 75% of ICU delirium is missed by the prac-
ticing team, which leaves the patient without any likely
active interventions to help reduce the duration of his/her
delirium.[41]
The most salient component of the definition of delirium
that nurses and other healthcare professionals use at the
bedside is whether or not the patient can pay attention and
follow simple commands (see videos and literature[40] ).
The advent of daily monitoring for delirium, made easy
by the CAM-ICU[42] and other assessment tools, as well
as proper documentation, had led to important changes in
the culture of ICUs and rounds in that the entire team can
now discuss the brain and how it is doing in terms of being
“on” (not delirious) or “off” (delirious) and then focus on
the several most likely causes of delirium in any specific
patient. Thus, it is not the monitoring itself that changes
the patient’s clinical course, but rather it is this combi-
nation of monitoring and then relaying the information
on rounds in the ICU that makes such a huge difference
in awareness of this form of organ dysfunction and then
enables a difference to be made in clinical outcomes.
7
Episodes of delirium can be prevented by identifying hos-
pitalized people at risk of the condition: those over 65,
those with a known cognitive impairment, those with hip
fracture, those with severe illness.[43] Close observation
for the early signs is recommended in those people.
Systematically addressing the common contributing fac-
tors (such as constipation, dehydration and polyphar-
macy), as well as providing a therapeutic environment
(such as adequate lighting, minimizing noise, clear com-
munication, minimizing relocation, signage, ways to tell
the time, and helping the person to walk and be mobile)
may prevent delirium.[43][44][45] Rates with a number of
interventions together decrease rates to 0.72 from base-
line in the elderly.[46]
It is thought that 30–40% of all cases of delirium could
be prevented, and that high rates of delirium reflect nega-
tively on the quality of care.[44] Melatonin and other phar-
macological agents have been studied for prevention of
postoperative delirium, but evidence is not clear.[47]
7 Treatment
Treatment of delirium involves two main strategies: first,
treatment of the underlying presumed acute cause or
causes; secondly, optimising conditions for the brain.
This involves ensuring that the patient with delirium has
adequate oxygenation, hydration, nutrition, and normal
levels of metabolites, that drug effects are minimised,
constipation treated, pain treated, and so on. Detection
and management of mental stress is also very impor-
tant. Therefore, the traditional concept that the treatment
of delirium is 'treat the cause' is not adequate; patients
with delirium actually require a highly detailed and ex-
pert analysis of all the factors which might be disrupting
brain function.
Non-pharmacological treatments are the first measure in
delirium, unless there is severe agitation that places the
person at risk of harming oneself or others. Avoiding un-
necessary movement, involving family members, having
recognizable faces at the bedside, having means of orien-
tation available (such as a clock and a calendar) may be
sufficient in stabilizing the situation.[43][44] If this is in-
sufficient, verbal and non-verbal de-escalation techniques
may be required to offer reassurances and calm the per-
son experiencing delirium.[43] Only if this fails, or if de-
escalation techniques are inappropriate, is pharmacolog-
ical treatment indicated.[43][44]
“The T-A-DA method (tolerate, anticipate, don't
agitate)”[48] is an effective management technique for
people with delirium. All unnecessary attachments are
removed (IVs, catheters, NG tubes) which allows for
greater mobility.[48] Patient behavior is tolerated even
if it is not considered normal as long as it does not put
8 9
the patient or other people in danger.[48] This technique
requires that patients have close supervision to ensure
that they remain safe.[48] Patient behavior is anticipated
so care givers can plan required care. Patients are treated
to reduce agitation.[48] Reducing agitation may mean
that patients are not reoriented if reorientation causes
agitation.[48]
Physical restraints are occasionally used as a last resort
with patients in a severe delirium. Restraint use should be
avoided as it can increase agitation and risk of injury.[49]
In order to avoid the use of restraints some patients may
require constant supervision.
The pharmacological treatment for delirium depends
on its cause. Antipsychotics, particularly haloperidol,
are the most commonly used drugs for delirium and
the most studied.[43][44] Evidence is weaker for the
atypical antipsychotics, such as risperidone, olanzapine
and quetiapine.[44][50] British professional guidelines by
the National Institute for Health and Clinical Excellence
advise haloperidol or olanzapine.[43]
Benzodiazepines themselves can cause delirium or
worsen it,[44] and lack a reliable evidence base.[51]
However, if delirium is due to alcohol withdrawal
or benzodiazepine withdrawal or if antipsychotics
are contraindicated (e.g. in Parkinson’s disease or
neuroleptic malignant syndrome), then benzodiazepines
are recommended.[44] Similarly, people with dementia
with Lewy bodies may have significant side-effects to an-
tipsychotics, and should either be treated with a small
dose or not at all.[43]
The antidepressant trazodone is occasionally used in the
treatment of delirium, but it carries a risk of oversedation,
and its use has not been well studied.[44]
8 Prognosis
There is substantial evidence that delirium results in
long-term poor outcomes in older persons admitted to
hospital.[52] This systematic review only included studies
that looked for an independent effect of delirium (i.e., af-
ter accounting for other associations with poor outcomes,
for example co-morbidity or illness severity).
In older persons admitted to hospital, individuals expe-
riencing delirium are twice as likely to die than those
who do not (meta-analysis of 12 studies).[52] In the only
prospective study conducted in the general population,
older persons reporting delirium also showed higher mor-
tality (60% increase).[53]
Institutionalisation was also twice as likely after an ad-
mission with delirium (meta-analysis of 7 studies).[52] In
a community-based population examining individuals af-
ter an episode of severe infection (though not specifi-
cally delirium), these persons acquired more functional
limitations (i.e. required more assistance with their care
EPIDEMIOLOGY
needs) than those not experiencing infection.[54] After an
episode of delirium in the general population, functional
dependence increased threefold.[53]
The association between delirium and dementia is com-
plex. The systematic review estimated a 13-fold in-
crease in dementia after delirium (meta-analysis of 2
studies).[52] However, it is difficult to be certain that this
is accurate because the population admitted to hospital
includes persons with undiagnosed dementia (i.e. the
dementia was present before the delirium, rather than
caused by it). In prospective studies, people hospitalised
from any cause appear to be at greater risk of dementia[55]
and faster trajectories of cognitive decline,[55][56] but
these studies did not specifically look at delirium. In
the only population-based prospective study of delirium,
older persons had an eight-fold increase in dementia and
faster cognitive decline.[53] The same association is also
evident in persons already diagnosed with Alzheimer’s
dementia.[57]
9 Epidemiology
The highest prevalence of delirium (often 50% to 75% of
patients) is generally seen in critically ill patients in the
intensive care unit or ICU (which used to be referred to
by the misnomers “ICU psychosis” or “ICU syndrome”,
terms largely abandoned for the more widely accepted
and scientifically supported term ICU Delirium.[40] Since
the advent of validated and easy-to-implement delir-
ium instruments for ICU patients such as the Confu-
sion Assessment Method for the ICU (CAM-ICU)[38] and
the Intensive Care Delirium Screening Checkllist (IC-
DSC).,[39] of the hundreds of thousands of ICU patients
who develop delirium in ICUs every year, it has been rec-
ognized that most of them belong to the hypoactive vari-
ety, which is easily missed and invisible to the managing
teams unless actively monitored using such instruments.
The causes of delirium in such patients depend on the un-
derlying illnesses, new problems like sepsis and low oxy-
gen levels, and the sedative and pain medicines that are
nearly universally given to all ICU patients. Outside the
ICU, on hospital wards and in nursing homes, the prob-
lem of delirium is also a very important medical problem,
especially for older patients.
The most recent area of the hospital in which delirium
is just beginning to be monitored routinely in many cen-
ters is the Emergency Department, where the prevalence
of delirium among older adults is about 10%.[58] A sys-
tematic review of delirium in general medical inpatients
showed that estimates of delirium prevalence on admis-
sion ranged from 10 to 31%.[59] About 5% to 10% of
older adults who are admitted to hospital develop a new
episode of delirium while in hospital.[58] Estimates of
the prevalence of delirium in nursing homes are between
10% [58] to 45%.[60]

10 Society and culture
Delirium is one of the oldest forms of mental disorder
known in medical history.[61]
Sims (1995, p. 31) points out a “superb detailed and [10] de Rooij, SE; Schuurmans, MJ; van der Mast, RC; Levi,
lengthy description” of delirium in The Stroller’s Tale M (July 2005). “Clinical subtypes of delirium and their
[62][63] relevance for daily clinical practice: a systematic review.”.
from Charles Dickens' The Pickwick Papers.
10.1 Costs
In the USA, the cost of a patient admission with delirium
is estimated at between $16k and $64k, suggesting the
national burden of delirium may range from $38 bn to
[12] Leentjens, AF; Rundell, J; Rummans, T; Shim, JJ;
$150 bn per year (2008 estimate).[64] In the UK, the cost
[65]
is estimated as £13k per admission.
11 See also
• Deliriant
• Organic brain syndrome
12 References
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12 14 EXTERNAL LINKS

doi:10.1212/WNL.0b013e3181a4129a. PMC 2677515. 14 External links

PMID 19414723.
• American Delirium Society
[58] Canadian Coalition for Seniors’ Mental Health (2006).
National Guidelines for Seniors’ Mental Health: The As- • European Delirium Association
sessment and Treatment of Delirium. Canadian Coalition
for Seniors’ Mental Health. • Australasian Delirium Association

[59] Siddiqi, N.; House, AO; Holmes, JD (30 June 2006). • CAM-ICU Training Manual
“Occurrence and outcome of delirium in medical in-
patients: a systematic literature review”. Age and Age- • CAM-ICU online
ing 35 (4): 350–364. doi:10.1093/ageing/afl005. PMID
• RADAR tool
16648149.
• Hospital Elder Life Program
[60] Voyer, Philippe; Richard, Sylvie; Doucet, Lise;
Carmichael, Pierre-Hugues (2009). “Detecting Delirium • Healthcare Improvement Scotland delirium re-
and Subsyndromal Delirium Using Different Diagnostic sources
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13 Further reading

• Macdonald, Alastair; Lindesay, James; Rockwood,

Kenneth (2002). Delirium in old age. Oxford [Ox-
fordshire]: Oxford University Press. ISBN 0-19-
263275-2.

• Grassi, Luigi; Caraceni, Augusto (2003). Delirium

: acute confusional states in palliative medicine. Ox-
ford: Oxford Univ. Press. ISBN 0192631993.

• Newman, James K.; Slater, Christopher T. (editors)

(2012). Delirium : causes, diagnosis and treatment.
Hauppauge, N.Y.: Nova Science Publisher’s, Inc.
ISBN 978-1613242940.
 13

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