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|Classification and external resources|
|Classification and external resources|
Delirium, or acute confusional state, is a syndrome that presents in two basic forms. In its hyperactive form, it is manifested as severe confusion and disorientation, developing with relatively rapid onset and fluctuating in intensity. In its hypoactive form, it is manifested by an equally sudden withdrawal from interaction with the outside world. Delirium as a syndrome is one which occurs more frequently in people in their later years. However, when it occurs in the course of a critical illness, delirium has been found to occur in young and old patients at relatively even rates.
Delirium represents 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 psychotic features such as hallucinations and delusions. Delirium itself is not a disease, but rather a clinical syndrome (a set of symptoms), which results from an underlying disease, from medications administered during treatment of that disease in a critical phase, from a new problem with mentation or from varying combinations of two or more of these factors.
It is a corollary of the criteria that a diagnosis of delirium 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 demented person who is operating 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 depressants (benzodiazepines and opioids). 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 exception of deliriants.) Delirium must by definition be caused by an organic process, i.e., a physically identifiable structural, functional, or chemical problem in the brain (see organic brain syndrome), and thus, fluctuations of mentation 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 confusion and various impairments in awareness and temporal and spatial orientation), delirium is the common symptomatic manifestation of new organic brain dysfunction (for any reason). Delirium requires both a sudden change in mentation, and an organic cause for this. Thus, without careful assessment and history, delirium can easily be confused 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. 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 treatment of the underlying organic cause(s). In some cases, temporary or palliative or symptomatic treatments are used to comfort patients or to allow better patient management (for example, a patient who, without understanding, is trying to pull out a ventilation tube that is required for survival). Delirium 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 hospitalized 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.
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 required, but may be contribute to the diagnosis.
The core features are:
Delirium is a syndrome encompassing an array of neuropsychiatric symptoms, including a disturbance in consciousness/attention and cognition that develops acutely and tends to fluctuate. The change in cognition (memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance, must be one that is not better accounted for by a pre-existing, established, or evolving dementia. Other symptoms can include disorientation, thought disorder, memory problems, language disorder, sleep disturbance, delusions, mood lability, psychomotor changes (changes in rate of activity/movement), and hallucinations.
Delirium occurs as a stage of consciousness in the continuum between normal awakeness/alertness and coma. During the 20th century, delirium was described as a ‘clouding of consciousness’ but this rather nebulous concept has been replaced by a better understanding of the components of phenomenology that culminate in severely impaired higher order brain functions. Lipowski described delirium as a disorder of attention, wakefulness, cognition, and motor behaviour, while a disturbance in attention is often considered the cardinal symptom. Disrupted sleep-wake cycles can result from a loss of normal circadian rhythm.
Accumulating evidence indicates three core domains of delirium phenomenology: “Cognition”, composed of inattention and other cognitive deficits; “Higher Level Thinking Processes” including impaired executive function, semantic expression and comprehension; and “Circadian Rhythm” including altered motor activity and fragmented sleep-wake cycle. Phenomenology studies suggest that “core” symptoms occur with greater frequency while other less consistent “associated” symptoms may reflect the biochemical influence of particular aetiologies or genetic, neuronal or physiological vulnerabilities.
Inattention is the cardinal and required symptom to diagnose delirium and is noticeable on interview by distractibility and inability to shift and / or sustain attention. More formal testing can include the months of the year backwards, serial sevens or digit span tests. Disorientation (another symptom of confusion, and usually a more severe one) describes the loss of awareness of the surroundings, environment and context in which the person exists. It may also appear with delirium, but it is not required, as noted. Disorientation may occur in time (not knowing what time of day, day of week, month, season or year it is), place (not knowing where one is) or person (not knowing who one is).
Memory impairment occurs and is linked to inattention. Reduction in formation of new long-term memory (which by definition survives withdrawal of attention), is common in delirium, because initial formation of (new) long-term memories generally requires an even higher degree of attention than do short-term memory tasks. Since older memories are retained without need of concentration, previously formed long-term memories (i.e., those formed before the period of delirium) are usually preserved in all but the most severe cases of delirium.
Delirious patients have diminished comprehension as evidenced by reduced ‘grasp’ of their surroundings and difficulties in connecting with their immediate environment, executive dysfunction affecting abstraction, initiation/perseveration, switching mental sets, working memory, temporal sequencing and organization, insight and judgment. Though none of these cognitive deficits is specific to delirium, the array and pattern is highly suggestive.
Language disturbances in delirium include anomic aphasia, paraphasias, impaired comprehension, agraphia, and word-finding difficulties. Incoherent or illogical / rambling conversation is reported commonly. Disorganised thinking includes tangentiality, circumstantiality and a proneness to loose associations between elements of thought which results in speech that often makes limited sense with multiple apparent irrelevancies. This aspect of delirium is common but often difficult for non-experts to assess reliably.
Disruption of sleep-wake cycle is almost invariably present in delirium and often predates the appearance of a full-blown episode. Minor disturbances with insomnia or excessive daytime somnolence may be hard to distinguish from other medically ill patients without delirium, but delirium typically involves more substantial alterations with sleep fragmentation or even complete sleep-wake cycle reversal that reflect disturbed circadian rhythm regulation. The relationship of circadian disturbances to the characteristic fluctuating severity of delirium symptoms over a 24-hour period or to motor disturbance is unknown.
Motor activity alterations are very common in delirium. They have been used to define clinical subtypes (hypoactive, hyperactive, mixed) though studies are inconsistent as to the prevalence of these subtypes. Cognitive impairments and EEG slowing are comparable in hyperactive and hypoactive patients though other symptoms may vary. Psychotic symptoms occur in both although the prevailing stereotype suggests that they only occur in hyperactive cases. Hypoactive cases are prone to non detection or misdiagnosis as depression. A range of studies suggest that motor subtypes differ regarding underlying pathophysiology, treatment needs, and prognosis for function and mortality though inconsistent subtype definitions and poorer detection of hypoactives impacts interpretation of these findings.
Psychotic symptoms occur in up to 50% of patients with delirium. While the common non-medical view of a delirious patient is one who is hallucinating, most people who are medically delirious do not have either hallucinations or delusions. Thought content abnormalities include suspiciousness, overvalued ideation and frank delusions. Delusions are typically poorly formed and less stereotyped than in schizophrenia or Alzheimer’s disease. They usually relate to persecutory themes of impending danger or threat in the immediate environment (e.g. being poisoned by nurses). Misperceptions include depersonalisation, delusional misidentifications, illusions and hallucinations. Hallucinations and illusions are frequently visual though can be tactile and auditory. Abnormalities of affect which may attend the state of delirium may include many distortions to perceived or communicated emotional states. Emotional states may also fluctuate, so that a delirious person may rapidly change between, for example, terror, sadness and jocularity.
It was thought for many years that all delirium was a transient state of brain dysfunction that fluctuated on an hourly basis. Interestingly, Barrough noted in 1583 that 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 meeting criteria for delirium for an alarmingly long time. For example, in ICU cohorts, it is common to find that 10% of patients still have delirium at the time of hospital discharge.
Dementia is supposed to be an entity that continues to decline, such as Alzheimer’s disease. Another way of looking at dementia, however, is not strictly based on the decline component but on the degree of memory and executive function problems. It is now known, for example, that between 50% and 70% of ICU patients have tremendous problems with ongoing brain dysfunction that looks a lot like the degree of problems experienced by Alzheimer’s or TBI (traumatic brain injury) patients and which leaves too many ICU survivors disabled and unable to go back to work and unable to serve effectively as the matriarchs and patriarchs of their families. This is a distressing personal and public health problem that is getting an increasing amount of scrutiny in ongoing investigations. The implications of such an “acquired dementia-like illness” (note: the term here is being used in a circumstance in which not all patients continue to decline as some have persistent yet stable brain dysfunction and others with newly acquired brain problems can recover fully) are profound at the private level, dismantling the person’s life in very practical ways such as inability to find a car in a parking lot or even complete shopping lists or job-related tasks done previously for years. The societal relevance is also huge when one considers work-force issues related to the inability of a young wage earner being unable to work because of either being a newly disabled ICU survivor him/herself or because he/she now has to care for their family member who is now suffering this “dementia-like” illness following ICU care.
The pathophysiology of delirium is not well understood and a lack of animal models that are relevant to the syndrome has left many key questions in delirium pathophysiology unanswered. Earliest rodent models of delirium used an antagonist of the muscarinic acetylcholine receptors, 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.
Profound systemic inflammation occurring during bacteraemia/sepsis is also known to cause delirium (often termed septic encephalopathy). Modeling this in mice also causes robust brain dysfunction and probably a delirium-like state, although these animals are typically too sick to assess cognitively and measures such as EEG and magnetic resonance imaging/spectroscopy are necessary to demonstrate dysfunction.
Animal models that interrogate interactions between prior degenerative pathology and superimposed systemic inflammation have been developed more recently and these demonstrate that even mild systemic inflammation, a frequent trigger for clinical delirium, induces acute and transient attentional/working memory deficits, but only in animals with prior pathology. Prior dementia or age-associated cognitive impairment is the primary predisposing factor for clinical delirium and ‘prior pathology’ as defined by these new animal models may consist of synaptic loss, network disconnectivity, and primed microglia (brain macrophages that are ‘primed’ by the primary pathology to produce exaggerated responses to subsequent inflammatory insults).
While it is difficult to state with confidence whether delirium is occurring in a non-verbal animal, comparisons with human DSM-IV criteria remain useful. According to DSM-IV, demonstration of acute onset impairments in attention and some other cognitive domain, that cannot be better explained by existing dementia and that are triggered by physiological disturbances resulting from some general medical condition should be present in order to reach a ‘diagnosis’ of delirium. Recent animal models fulfill these criteria reasonably well. Whether the deficit is one of attention or short-term memory is difficult to dissect, but it is undeniably distinct from long-term memory, consistent with observations in patients with delirium. There is an urgent need to understand more about the mechanisms of dysfunction underpinning delirium and data arising from these and other animal models must form part of the discussion on delirium pathophysiology.
Studies of cerebrospinal fluid (CSF) in delirium are difficult to perform. Apart from the general difficulty of recruiting participants who are often unable to give consent, the inherently invasive nature of CSF sampling makes such research particularly challenging. However, a few studies have exploited the opportunity to sample CSF from persons undergoing spinal anaesthesia for elective or emergency surgery. Indeed, spinal anaesthesia may in fact be the anaesthetic modality of choice for frail older patients, so these studies are often undertaken in highly relevant populations.
A systematic review identified 8 studies involving 235 patients (142 with delirium). Overall, 17 different biomarkers were considered and each article identified in the review focused on a narrow range of biomarkers with no overlap between studies. Studies were generally small, studying heterogeneous populations with different times of CSF sampling in relation to delirium, and no clear conclusions could be drawn. Broadly, delirium may be associated with: increased serotoninergic and dopamine signalling; reversible fall in somatostatin; increased cortisol; and increase in some inflammatory cytokines (IL-8), but not others (TNF-α, IL-1β).
One additional study has since been published. Postoperative delirium was strongly associated with pre-operative cognitive decline. However, CSF Aβ1-42, tau, and phosphorylated-tau levels were not associated with delirium status, nor did they correlate significantly with cognitive function before the onset of delirium. The two main explanations for these findings are either: (1) the study was underpowered to detect mediating pathways between premorbid cognitive impairment, Alzheimer’s pathology biomarkers and subsequent delirium; or (2) postoperative delirium arises through pathophysiological pathways that are distinct from Alzheimer's disease.
The neuroimaging correlates of delirium are very difficult to establish. Many attempts to image people with concurrent delirium will be unsuccessful. In addition, there is a more general bias selecting younger and fitter participants amenable to scanning, especially if using intensive protocols such as MRI.
Most of the literature has been summarised by a systematic review. This found 12 articles for inclusion, most with small sample sizes (total number of cases 127). There was substantial heterogeneity in populations, study design, and imaging modalities such that no firm conclusions were made. Generally, structural imaging suggested that diffuse brain abnormalities such as atrophy and leukoaraiosis might be associated with delirium, though few studies could account for differences in key variables such as age, sex, education or underlying cognitive function and education.
Since publication of the systematic review, five further studies have been published. The largest-scale report was VISIONS. This prospectively examined the neuroimaging correlates of delirium in 47 participants after critical illness. Delirium duration was related to measures of white matter tract integrity and this in turn was related to poorer cognitive outcomes at 3 and 12 months. In addition, brain volumes were also assessed and related to cognitive outcomes in the same manner. Overall, the study found that longer duration of delirium was associated with smaller brain volume and more white matter disruption, and both these correlated with worse cognitive scores 12 months later.
Two studies examined delirium risk as a post-operative complication after elective cardiac surgery. These both showed that white matter damage predicted post-operative delirium. One functional MRI study reported a reversible reduction in activity in brain areas localising with cognition and attention function.
Electroencephalography (EEG) is an attractive mode of study in delirium as it is able to capture measures of global brain function. There are also opportunities to summarise temporal fluctuations as continuous recordings, compressed into power spectra (quantitative EEG, qEEG). Since the work of Engel and Romano in the 1950s, delirium has been known to be associated with a generalised slowing of background activity.
A systematic review identified 14 studies for inclusion, representing a range of different populations: 6 in older populations, 3 in ICU, sample sizes between 10 and 50). For most studies, the outcome of interest was the relative power measures, in order: alpha, theta, delta frequencies. The relative power of the theta frequency was consistently different between delirium and non-delirium patients. Similar findings were reported for alpha frequencies. In two studies, the relative power of all these bands was different within patients before and after delirium.
Only a handful of studies exist where there has been an attempt to correlate delirium with pathological findings at autopsy. A case series has been reported on 7 patients who died during ICU admission. Each case was admitted with a range of primary pathologies, but all had acute respiratory distress syndrome and/or septic shock contributing to the delirium. 6/7 had evidence of hypoperfusion and diffuse vascular injury, with consistent involvement of the hippocampus in 5/7.
A case-control study examined 9 delirium cases with 6 age-matched controls, investigating inflammatory cytokines and their role in delirium. Persons with delirum had higher scores for HLA-DR and CD68 (markers of microglial activation), IL-6 (cytokines pro-inflammatory and anti-inflammatory activities) and GFAP (marker of astrocyte activity). These results might suggest a neuroinflammatory substrate to delirium, but the conclusions are limited by biases from selection of controls.
Delirium arises through the interaction of a number of predisposing and precipitating factors. A predisposing factor might be any biological, psychological or social factor that increases an individual’s susceptibility to delirium. An individual with multiple predisposing factors is said to have ‘high baseline vulnerability’, and this is closely associated with frailty (see below). A precipitating factor is any biological, psychological or social factor that can trigger delirium. The division of causes into ‘predisposing’ and ‘precipitating’ is useful in order to assess an individual’s risk of suffering from delirium, and in guiding the management of delirium – however there may be a significant degree of overlap between the two 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 physical and socioeconomic deficits. Frail individuals (i.e. those with significant predisposing factors) demonstrate an inability to compensate for additional physical or social 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 multiple 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.
The most important predisposing factors are listed below:
Any acute factors that affect neurotransmitter, neuroendocrine 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. Some of the most common precipitating factors are listed below:
Some mental illnesses, such as mania, or some types of acute psychosis, may cause a rapidly fluctuating impairment of cognitive function and ability to focus. However, they are not technically causes of delirium, since any fluctuating 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, physical disorders can be said to produce delirium as a mental side-effect or symptom, although primary mental disorders which produce the symptom cannot be put into this category once identified. However, such symptoms may be impossible to distinguish clinically from delirium resulting from physical disorders, if a diagnosis of an underlying mental disorder is yet to be made.
Differential points from other processes and syndromes that cause cognitive dysfunction:
Delirium represents an organically caused decline from a previously attained level of cognitive functioning. It is a corollary of these differential criteria that a diagnosis of delirium 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 demented person who is operating at their own baseline level of mental ability might appear to be delirious without a baseline functional status against which to compare.
In the ICU, international guidelines recommend that every patient gets checked for delirium every day (usually twice or more a day) using a validated clinical tool. The two most widely used are the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC). 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. 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 practicing team, which leaves the patient without any likely active interventions to help reduce the duration of his/her delirium.
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). The advent of daily monitoring for delirium 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 combination 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.
There is substantial evidence that delirium results in long-term poor outcomes in older persons admitted to hospital. This systematic review only included studies that looked for an independent effect of delirium (i.e., after accounting for other associations with poor outcomes, for example co-morbidity or illness severity).
In older persons admitted to hospital, individuals experiencing delirium are twice as likely to die than those who do not (meta-analysis of 12 studies). In the only prospective study conducted in the general population, older persons reporting delirium also showed higher mortality (60% increase).
Institutionalisation was also twice as likely after an admission with delirium (meta-analysis of 7 studies). In a community-based population examining individuals after an episode of severe infection (though not specifically delirium), these persons acquired more functional limitations (i.e. required more assistance with their care needs) than those not experiencing infection. After an episode of delirium in the general population, functional dependence increased threefold.
The association between delirium and dementia is complex. The systematic review estimated a 13-fold increase in dementia after delirium (meta-analysis of 2 studies). 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 and faster trajectories of cognitive decline, 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. The same association is also evident in persons already diagnosed with Alzheimer’s dementia.
Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition: those over 65, those with a known cognitive impairment, those with hip fracture, those with severe illness. Close observation for the early signs is recommended in those people. Systematically addressing the common contributing factors (such as constipation, dehydration and polypharmacy), as well as providing a therapeutic environment (such as adequate lighting, minimizing noise, clear communication, minimizing relocation, signage, ways to tell the time, and helping the person to walk and be mobile) may prevent delirium.
It is thought that 30–40% of all cases of delirium could be prevented, and that high rates of delirium reflect negatively on the quality of care.
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 important. 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 expert 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 unnecessary movement, involving family members, having recognizable faces at the bedside, having means of orientation available (such as a clock and a calendar) may be sufficient in stabilizing the situation. If this is insufficient, verbal and non-verbal de-escalation techniques may be required to offer reassurances and calm the person experiencing delirium. Only if this fails, or if de-escalation techniques are inappropriate, is pharmacological treatment indicated.
“The T-A-DA method (tolerate, anticipate, don't agitate)” is an effective management technique for people with delirium. All unnecessary attachments are removed (IVs, catheters, NG tubes) which allows for greater mobility. Patient behavior is tolerated even if it is not considered normal as long as it does not put the patient or other people in danger. This technique requires that patients have close supervision to ensure that they remain safe. Patient behavior is anticipated so care givers can plan required care. Patients are treated to reduce agitation. Reducing agitation may mean that patients are not reoriented if reorientation causes agitation.
Physical restraints are often 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. 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. Evidence is weaker for the atypical antipsychotics, such as risperidone, olanzapine and quetiapine. British professional guidelines by the National Institute for Health and Clinical Excellence advise haloperidol or olanzapine.
Benzodiazepines themselves can cause delirium or worsen it, and lack a reliable evidence base. 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. Similarly, people with dementia with Lewy bodies may have significant side-effects to antipsychotics, and should either be treated with a small dose or not at all.
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. Since the advent of validated and easy-to-implement delirium instruments for ICU patients such as the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checkllist (IC-DSC)., of the hundreds of thousands of ICU patients who develop delirium in ICUs every year, it has been recognized that most of them belong to the hypoactive variety, 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 underlying illnesses, new problems like sepsis and low oxygen 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 problem 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 centers is the Emergency Department, where the prevalence of delirium among older adults is about 10%. A systematic review of delirium in general medical inpatients showed that estimates of delirium prevalence on admission ranged from 10 to 31%. About 5% to 10% of older adults who are admitted to hospital develop a new episode of delirium while in hospital. Estimates of the prevalence of delirium in nursing homes are between 10%  to 45%.
Delirium is one of the oldest forms of mental disorder known in medical history.
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 $150 bn per year (2008 estimate). In the UK, the cost is estimated as £13k per admission.