Delirium

Abstract

Delirium is an acute, fluctuating disturbance of attention, awareness, and cognition that develops over hours to days and is a direct consequence of an underlying medical condition, intoxication, or drug withdrawal. Its defining features are an *acute onset*, a *fluctuating course* that waxes and wanes across the day, and a *core disturbance of attention* — the patient cannot hold, focus, or shift the spotlight of awareness. This article distinguishes delirium from dementia and from the newer category of acute encephalopathy, describes its hypoactive, hyperactive, and mixed motor subtypes, and explains its assessment with the Confusion Assessment Method. It covers the epidemiology, the multifactorial vulnerability–precipitant model of risk, the neuroinflammatory and neurotransmitter accounts of its mechanism, its link to long-term cognitive decline, and the multicomponent interventions that prevent it.

Keywords: attention, acute confusion, neuroinflammation

Delirium is at once one of the most common and one of the most under-recognised disorders in hospital medicine. An older adult admitted lucid and oriented can, within a day of surgery or infection, become inattentive, disoriented, and unable to follow a conversation — and then, hours later, seem almost herself again, only to slip back by nightfall. That abrupt arrival and that hallmark fluctuation are the intuition the concept was built to capture: a sudden, reversible failure of the brain's capacity to attend, brought on by something wrong in the body (Lipowski, 1989).

The account below moves from what delirium is, through its motor subtypes and its attentional core, to the epidemiology, the bedside assessment, the vulnerability–precipitant model of who develops it, the mechanisms in the brain, the crucial distinction from dementia, and the prevention and treatment that follow. The recurring theme is that delirium is an acute, multiply-determined disturbance of the attentional system — a form of acute brain failure — rather than a psychiatric illness or an inevitable part of ageing.

What Delirium Is

Delirium is an acute disturbance of attention and awareness, accompanied by a change in cognition, that develops over a short period, fluctuates in severity over the course of a day, and is a direct physiological consequence of a medical condition, a substance, or a withdrawal state. Four elements are diagnostic: the disturbance is *acute* in onset and *fluctuating* in course; its centre is a failure of *attention* — the reduced ability to direct, focus, sustain, and shift the spotlight of awareness; it is accompanied by additional cognitive change such as disorientation, memory disturbance, or perceptual distortion; and it is not better explained by a pre-existing, established, or evolving dementia (Inouye, 2006).

The clinical picture was given its enduring modern description by Zbigniew Lipowski, who characterised delirium as a transient disorder of cognition and attention with a characteristically abrupt onset and a fluctuating course, distinguishing it sharply from the slow, stable decline of dementia (Lipowski, 1989). This framing anchored delirium as a *syndrome* — a final common pathway reached by many different bodily insults — rather than a single disease. Contemporary reviews retain that view while sharpening the criteria: the *attentional* disturbance is now understood as the syndrome's core, with disorientation and amnesia following from it, because a mind that cannot hold information in attention cannot register the date, encode the ward, or track a sentence (Wilson et al., 2020).

Two features make delirium distinctive among cognitive disorders. First, it is *acute and reversible in principle*: unlike a neurodegenerative dementia, it develops in hours to days and, when the underlying cause is treated, it typically resolves — though recovery can be slow and, as later sections show, is not always complete. Second, it is *caused by something outside the brain's own primary pathology* far more often than not: pneumonia, a urinary infection, a hip fracture, a new medication, or surgery, acting on a vulnerable brain, is the usual trigger. Delirium is, in this sense, the brain's stereotyped signal that the body is acutely unwell — which is why it is sometimes called *acute brain failure* (Maldonado, 2017).

Types of Delirium

MeSH files Delirium beneath the broader kinds of confusion and neurocognitive disorders, and records one direct descriptor beneath it, *emergence delirium* — the acute, transient confusion that can occur as a patient wakes from general anaesthesia. It is worth stressing that a *classification* is an indexing device, not a theory of the disorder: the MeSH tree records how the literature is catalogued, and its single child sits alongside the clinically central typology — the *motor subtypes* — by which delirium is actually described at the bedside. The two axes are orthogonal, and the everyday clinical subtypes below cross-cut the indexing hierarchy.

The motor subtypes matter clinically because they carry different risks of being missed and different prognoses. The hyperactive patient — agitated, pulling at lines, hallucinating — matches the lay picture of delirium and is rarely overlooked. The *hypoactive* patient, quietly drowsy and disengaged, is far more common in older and critically ill people and is routinely mistaken for fatigue, depression, or simply “having a bad day,” yet carries a worse prognosis (Inouye et al., 2014). This under-recognition of the quiet form is one reason systematic screening, rather than reliance on obvious agitation, is now emphasised.

Core Features

The single feature that defines delirium and separates it from every other acute change is a disturbance of *attention*. The delirious patient cannot sustain the focus of awareness: asked to recite the months of the year backwards, or to squeeze a hand each time a particular letter is spoken, they lose the thread, capture on irrelevant stimuli, and cannot filter distraction. Because attention is the gateway through which information enters working memory and awareness, its failure cascades: the patient who cannot attend cannot register the date (apparent disorientation), cannot hold a new instruction (apparent amnesia), and cannot follow a line of reasoning (apparent thought disorder). The attentional deficit is thus primary, and the other cognitive failures are largely secondary to it (Wilson et al., 2020).

The second core feature is the *temporal profile*: acute onset and a fluctuating course. Delirium arrives over hours to days — a caregiver can usually name the day the person changed — and then its severity waxes and wanes unpredictably, characteristically worsening in the late afternoon and night, a pattern clinicians call *sundowning*. This fluctuation is diagnostically decisive, because it separates delirium from the steady level of a dementia and from the fixed deficit of a completed stroke (Lipowski, 1989). A patient who is coherent on the morning ward round and floridly confused that evening has, until proven otherwise, delirium.

Beyond the core, delirium disturbs the whole fabric of consciousness. The level of arousal may be depressed or heightened; the sleep–wake cycle is typically fragmented and reversed; perception is distorted, giving rise to illusions and, in the hyperactive form, frank hallucinations; thinking becomes disorganised and, at times, frankly delusional; and emotion is labile. The clinical review literature stresses that this is a *global* disturbance of cerebral function, which is precisely why so many different bodily insults converge on the same syndrome (Inouye, 2006).

Epidemiology and Comorbidity

Delirium is common wherever acutely ill and older people are found. It affects roughly one in five general medical inpatients and a far higher fraction of specific high-risk groups: up to half of older patients after major surgery, and the great majority — commonly cited as up to 80% — of mechanically ventilated patients in the intensive care unit (Inouye et al., 2014). In the community it is uncommon, but at the end of life it is nearly universal. Its frequency rises steeply with age and with pre-existing cognitive impairment, so that the populations most vulnerable to it are precisely those in whom it is hardest to detect.

The most important epidemiological fact is that delirium is *dangerous*, not benign. A landmark cohort of mechanically ventilated patients showed that delirium independently predicted death at six months, tripling the hazard even after adjustment for severity of illness and other confounders (Ely et al., 2004). Beyond mortality, delirium predicts longer hospital stays, more complications, higher rates of discharge to institutional care, and — the finding that most concerns cognitive science — an elevated long-term risk of dementia (Witlox et al., 2010).

Delirium and dementia are tightly, reciprocally linked. Dementia is the single strongest predisposing factor for delirium, raising its risk several-fold; and an episode of delirium, in turn, accelerates the trajectory of cognitive decline and raises the risk of a later dementia diagnosis (Witlox et al., 2010). The two are so entangled that the syndrome of *delirium superimposed on dementia* is a recognised and especially poor-prognosis presentation. This comorbidity is one of the strongest arguments that delirium is not a trivial, self-limited event but a marker — and possibly a cause — of lasting brain injury.

Assessment

Because delirium fluctuates and is often quiet, it is missed unless it is actively sought, and the central task of assessment is to detect the *attentional* disturbance directly. The most widely used instrument is the *Confusion Assessment Method* (CAM), a diagnostic algorithm that operationalises the syndrome into four features: (1) acute onset and fluctuating course, (2) inattention, (3) disorganised thinking, and (4) altered level of consciousness. A diagnosis requires features 1 and 2 plus either 3 or 4 — a structure that places inattention at the mandatory centre of the definition (Inouye et al., 1990). The CAM transformed delirium research and practice by giving non-psychiatrists a reliable, validated way to make the diagnosis in minutes.

The critically ill patient poses a special problem: intubated and unable to speak, they cannot answer the questions a verbal assessment requires. The *CAM-ICU* solved this by recasting each feature into a nonverbal task — squeezing the assessor's hand at a target letter to test attention, answering yes/no logic questions with head nods — validated against expert psychiatric assessment in ventilated patients (Ely et al., 2001). Together with the level-of-arousal scales that precede it, the CAM-ICU made routine delirium monitoring possible in intensive care, where the disorder is both most common and most consequential. Modern reviews recommend brief, structured screening of attention — not a global impression — as the standard of care (Oh et al., 2017).

Worked Example

The multifactorial nature of delirium can be made concrete with a simple, deliberately illustrative risk calculation built on the vulnerability–precipitant model. Suppose delirium emerges when a patient's *risk index* — combining a stable *predisposing vulnerability* and an acute *precipitating insult* — crosses a threshold. Let vulnerability V (0–1) summarise baseline factors such as age, dementia, and sensory impairment, and let the precipitant P (0–1) summarise the acute insult such as surgery, infection, or a new sedative. Crucially the two *interact*: a highly vulnerable brain needs only a mild insult, while a robust brain can withstand a strong one (Inouye & Charpentier, 1996). Define the risk index

R = 0.40·V + 0.40·P + 0.60·(V·P)

and turn it into the probability of delirium with a logistic function centred at the threshold R = 0.5:

p = 1 / (1 + e^{−6(R − 0.5)})

Consider Patient A, a frail 84-year-old with mild dementia and poor hearing (high vulnerability, V = 0.8) who undergoes a routine, uncomplicated procedure (modest precipitant, P = 0.4). The index is R = 0.40(0.8) + 0.40(0.4) + 0.60(0.8·0.4) = 0.32 + 0.16 + 0.192 = 0.672, giving p = 1 / (1 + e^−1.032) ≈ 0.74 — a 74% probability of delirium from a minor insult.

Now consider Patient B, a fit 84-year-old with no cognitive impairment and intact senses (low vulnerability, V = 0.2) facing the *same* procedure (P = 0.4). The index is R = 0.40(0.2) + 0.40(0.4) + 0.60(0.2·0.4) = 0.08 + 0.16 + 0.048 = 0.288, giving p = 1 / (1 + e^1.272) ≈ 0.22 — only a 22% probability. The identical insult produces delirium in one patient and not the other, because the vulnerable brain sits far closer to the threshold. This is the central lesson of the vulnerability–precipitant model, and it is why prediction tools such as PRE-DELIRIC combine baseline and acute variables rather than relying on either alone (van den Boogaard et al., 2012).

Causes

Delirium is the final common pathway of an enormous range of insults, and its causes are conventionally split into *predisposing* factors, which set the baseline vulnerability of the brain, and *precipitating* factors, which are the acute triggers. The predisposing factors — advanced age, pre-existing dementia or cognitive impairment, sensory impairment, frailty, and multiple comorbidities — determine how little it takes to tip a patient over. The precipitating factors — infection, surgery, metabolic derangement, dehydration, uncontrolled pain, and above all medications, especially those with sedative or anticholinergic action — supply the insult (Inouye & Charpentier, 1996). The two trade off against one another, so that in a highly vulnerable patient a single dose of a sleeping pill may precipitate delirium, whereas a robust patient tolerates major surgery unscathed.

At the level of mechanism, no single pathway explains every case; instead several converging processes are implicated, integrated in Maldonado's *systems* synthesis of the pathophysiology (Maldonado, 2017). The *neuroinflammatory* hypothesis holds that a peripheral insult — infection, surgery, trauma — releases inflammatory cytokines that cross a compromised blood–brain barrier and disrupt neuronal function. The *neurotransmitter* hypothesis emphasises a relative deficiency of acetylcholine and an excess of dopamine, which is why anticholinergic drugs so reliably precipitate delirium and why the syndrome is a global failure of cortical function. Further contributions come from impaired oxidative metabolism, abnormal stress responses with elevated cortisol, and disruption of the sleep–wake cycle. These are not rival theories so much as facets of a single picture of acute, reversible network dysfunction (Wilson et al., 2020).

Neuroanatomy

Delirium is not the product of a single lesion; it is a disturbance of large-scale brain *networks* that support attention and consciousness. Because attention depends on the coordinated activity of a widely distributed system — prefrontal cortex, posterior parietal cortex, the thalamus, and ascending arousal pathways from the brainstem — a global metabolic or inflammatory insult that degrades communication across this system produces the characteristic attentional collapse without destroying any one structure (Maldonado, 2017). This network view explains why delirium is reversible: the circuitry is disrupted, not destroyed, and function returns when the insult is removed.

Neuroimaging supports the network account. Studies reviewed in the neurology literature link delirium to reduced cerebral blood flow, disrupted functional connectivity — particularly involving the thalamus and the connections between the prefrontal cortex and subcortical structures — and, in those who develop delirium, pre-existing markers of brain vulnerability such as white-matter change and atrophy (Fong et al., 2009). The picture that emerges is of a brain whose reserve is already reduced by age or disease and whose fragile attentional networks are then pushed into failure by an acute insult — a neural counterpart of the vulnerability–precipitant model. In both disorders the signature is one of *dysfunction* in a specific, distributed system rather than focal damage (Wilson et al., 2020).

Differential Diagnosis

The most important and most frequent diagnostic distinction is between delirium and dementia. The two share confusion and cognitive impairment, but they differ on the features that matter: dementia is *chronic* and develops over months to years, whereas delirium is *acute*, developing over hours to days; dementia is *stable* from hour to hour, whereas delirium *fluctuates*; and in dementia attention and level of consciousness are relatively preserved until late, whereas in delirium the disturbance of attention is the very core (Inouye, 2006). The temporal profile — when and how fast the change began, and whether it waxes and wanes — is the single most useful discriminator, which is why a collateral history from someone who knows the patient is indispensable.

The distinction is complicated by two facts. First, the disorders coexist: dementia predisposes to delirium, so *delirium superimposed on dementia* is common and easily missed against the baseline confusion. Second, the field has recently clarified its terminology. A consensus statement of ten societies distinguished *delirium* — the clinical syndrome defined by its attentional and behavioural features — from *acute encephalopathy*, the underlying pathobiological process of rapidly developing brain dysfunction, reserving *coma* for the deepest disturbance of arousal (Slooter et al., 2020). Delirium must also be separated from primary psychiatric conditions such as depression (which the hypoactive form mimics) and psychosis, and from focal neurological events; the presence of an acute medical precipitant and the hallmark inattention point back to delirium.

Prevention and Treatment

The most important fact about delirium management is that a large fraction of cases — commonly around a third in at-risk hospitalised older people — can be *prevented*. The evidence-based approach is *multicomponent nonpharmacological* prevention, epitomised by the Hospital Elder Life Program (HELP), which systematically targets the modifiable precipitating factors: reorientation and cognitive stimulation, early mobilisation, protocols to promote sleep without sedatives, provision of glasses and hearing aids, hydration, and prompt treatment of the underlying illness. A meta-analysis of such programmes confirmed that they significantly reduce both the incidence of delirium and the rate of falls (Hshieh et al., 2015). No drug has matched this record for prevention.

Once delirium is established, the cornerstone of treatment is to *identify and reverse the underlying cause* — treat the infection, correct the metabolic derangement, stop the offending drug, control the pain — while supporting the patient with the same nonpharmacological measures used for prevention (Marcantonio, 2017). Antipsychotic medication, long used to manage agitation, does not treat the delirium itself: the MIND-USA randomised trial found that neither haloperidol nor ziprasidone altered the duration of delirium in critically ill patients (Girard et al., 2018). Current critical-care guidelines therefore reserve pharmacological sedation for the patient whose agitation threatens their own safety, emphasise avoiding the deliriogenic drugs (especially benzodiazepines) in the first place, and build prevention into routine care through bundles that manage pain, sedation, delirium, immobility, and sleep together (Devlin et al., 2018).

Discussion

The history of delirium research is a case study in the recovery of a neglected syndrome. For much of the twentieth century delirium was regarded as a transient, unimportant epiphenomenon of physical illness — a nuisance to be sedated and forgotten. Lipowski's synthesis reasserted it as a coherent, describable disorder with a characteristic profile (Lipowski, 1989); Inouye's Confusion Assessment Method made it reliably diagnosable (Inouye et al., 1990); and a wave of cohort studies then showed that it was neither transient nor unimportant, but a predictor of death and lasting cognitive decline (Ely et al., 2004). The field has arrived at a view of delirium as *acute brain failure*: a stereotyped, multiply-determined signal of a brain under acute physiological stress.

That synthesis has practical force. If delirium is multifactorial, then no single test can predict it and no single drug can cure it; prediction must combine baseline and acute variables, and management must be multicomponent (van den Boogaard et al., 2012). If a large fraction of cases is preventable, then prevention — not sedation — is the priority, and the failure to screen for the quiet, hypoactive form is a failure of care. And if delirium marks and perhaps causes lasting brain injury, then it deserves the seriousness accorded to other acute organ failures rather than being dismissed as inevitable confusion in the old and sick (Wilson et al., 2020).

Cognitive Implications

Delirium is, for cognitive psychology, a natural experiment in the role of attention in the architecture of the mind. By acutely and reversibly stripping out the capacity to direct and sustain attention while leaving the underlying knowledge base intact, it demonstrates how much of ordinary cognition — orientation, encoding into memory, coherent thought — depends on an intact attentional gateway. The delirious patient still *knows* the year in the sense of stored knowledge, but cannot bring it to bear, because the system that selects and holds information for processing has failed. Delirium thereby confirms, in a clinical setting, the central place that models of cognition give to attention and its close relationship with working memory (Wilson et al., 2020).

The disorder also carries a sobering lesson about the durability of cognitive injury. The old assumption that delirium fully resolves has been overturned by longitudinal work: patients who develop delirium after critical illness show global cognition and executive function months later that resemble mild traumatic brain injury or early dementia, with longer delirium predicting worse deficits (Pandharipande et al., 2013). Postoperative delirium, likewise, is followed by an accelerated decline in cognitive function over the subsequent year (Saczynski et al., 2012). Whether delirium *causes* this decline or merely unmasks a vulnerable brain remains debated, but the association reframes delirium as an event with consequences for the mind long after the acute confusion has cleared.

Current Directions

Current research is pursuing the mechanism and the long-term consequences of delirium in tandem. On the mechanistic side, work continues to test and integrate the neuroinflammatory and neurotransmitter hypotheses, seeking the biomarkers — inflammatory cytokines, markers of neuronal injury, connectivity signatures — that would identify the vulnerable brain before the insult and clarify whether the different bodily triggers converge on a common final pathway (Maldonado, 2017). The prize is a mechanism specific enough to yield a treatment, an aim that the negative antipsychotic trials have made more, not less, urgent (Girard et al., 2018).

A second front is definitional and preventive. The recent nomenclature statement, separating the clinical syndrome of delirium from the underlying acute encephalopathy, is an attempt to align terminology across the many specialties that encounter the disorder and to make research comparable (Slooter et al., 2020). In parallel, the field is working to embed validated prediction, routine attentional screening, and multicomponent prevention into ordinary hospital and intensive-care practice, so that the substantial preventable fraction is actually prevented (Oh et al., 2017). The synthesis of the last three decades is broad agreement on what delirium is and how to prevent much of it, coexisting with genuine uncertainty about its ultimate mechanism and its treatment once established.

Common Misconceptions

“Delirium is the same as dementia.”

They are distinct. Delirium is acute, fluctuating, and centred on inattention; dementia is chronic, stable, and spares attention until late. Dementia predisposes to delirium, and the two can coexist, but they are not interchangeable (Inouye, 2006).

“Delirium means agitation.”

The hypoactive form — quiet, drowsy, withdrawn — is the most common and the most missed. Waiting for agitation guarantees that most delirium goes undetected (Inouye et al., 2014).

“It is a harmless, temporary confusion.”

Delirium independently predicts higher mortality, longer stays, institutionalisation, and accelerated long-term cognitive decline. It is a marker of serious illness, not a benign nuisance (Witlox et al., 2010).

“Antipsychotics treat delirium.”

They do not shorten it. A large randomised trial found neither haloperidol nor ziprasidone changed the duration of ICU delirium; the treatment is to reverse the cause and support the patient (Girard et al., 2018).

Glossary

Acute brain failure.

A framing of delirium as the brain's stereotyped response to acute physiological stress, analogous to acute failure of the heart or kidneys.

Acute encephalopathy.

The underlying pathobiological process of rapidly developing brain dysfunction, distinguished in recent nomenclature from delirium, its clinical expression.

Attention.

The capacity to direct, focus, sustain, and shift the spotlight of awareness; its disturbance is the diagnostic core of delirium.

CAM-ICU.

A nonverbal adaptation of the CAM for intubated, mechanically ventilated patients who cannot speak.

CAM.

The Confusion Assessment Method, a validated diagnostic algorithm requiring acute onset with fluctuation and inattention, plus either disorganised thinking or altered consciousness.

Dementia.

A chronic, progressive, and stable decline in cognition; the principal predisposing factor for delirium and its main differential diagnosis.

Emergence delirium.

Acute, transient confusion and agitation as a patient wakes from general anaesthesia; the single subtype MeSH files directly under Delirium.

Fluctuating course.

The characteristic waxing and waning of delirium severity over a day, often worse at night; a decisive clue distinguishing it from dementia.

Hyperactive delirium.

The motor subtype marked by agitation, restlessness, and hallucinations; the popular stereotype but the least common pure form.

Hypoactive delirium.

The motor subtype marked by drowsiness, withdrawal, and slowed responses; the most common form and the most frequently missed.

Multicomponent intervention.

A prevention strategy, such as the Hospital Elder Life Program, that targets several modifiable precipitating factors at once.

Precipitating factor.

An acute insult — infection, surgery, a new drug — that triggers delirium in a vulnerable brain.

Predisposing factor.

A stable baseline characteristic — age, dementia, sensory impairment — that raises vulnerability to delirium.

Sundowning.

The worsening of confusion and agitation in the late afternoon and evening, a common expression of delirium's fluctuating course.

Working memory.

The system for briefly holding and manipulating information; it depends on intact attention and fails when attention collapses in delirium.

Key Researchers

E. Wesley Ely

(living). A critical-care physician at Vanderbilt University Medical Center who developed the CAM-ICU, enabling delirium to be diagnosed in ventilated patients, and showed that ICU delirium independently predicts mortality and long-term cognitive impairment. ORCID

Tamara G. Fong

(living). A neurologist at Beth Israel Deaconess Medical Center and the Aging Brain Center at Hebrew SeniorLife whose work connects delirium to neuroimaging markers of brain vulnerability and to long-term cognitive trajectories. ORCID

Timothy D. Girard

(living). A critical-care physician at the University of Pittsburgh who led the MIND-USA trial of antipsychotics for ICU delirium and the BRAIN-ICU study of long-term cognition after critical illness. ORCID

Sharon K. Inouye

(living). A geriatrician at Harvard Medical School and Hebrew SeniorLife who created the Confusion Assessment Method and the Hospital Elder Life Program, and established the predisposing–precipitating model of delirium risk. ORCID

Zbigniew J. Lipowski

(1924–1997). The founder of modern consultation-liaison psychiatry, whose synthesis gave delirium its enduring clinical description as an acute, fluctuating disorder of attention and cognition. Wikipedia

Edward R. Marcantonio

(living). A geriatrician at Beth Israel Deaconess Medical Center whose work established the natural history of postoperative delirium and its association with accelerated long-term cognitive decline. ORCID

Pratik P. Pandharipande

(living). An anaesthesiologist and intensivist at Vanderbilt University Medical Center whose BRAIN-ICU study linked longer delirium duration to worse long-term cognitive impairment after critical illness. ORCID

Frequently Asked Questions

What is delirium?

Delirium is an acute, fluctuating disturbance of attention and awareness, accompanied by other cognitive change, that develops over hours to days as a direct consequence of a medical illness, a drug, or a withdrawal state. Its core is an inability to focus, sustain, and shift attention.

How is delirium different from dementia?

Dementia develops slowly over months to years and is stable from hour to hour, with attention relatively preserved until late. Delirium develops acutely, fluctuates over a single day, and disturbs attention as its very core. The two often coexist, but the time course and the attentional disturbance distinguish them (Inouye, 2006).

What are the types of delirium?

Clinically, delirium is divided by motor activity into hypoactive (quiet, drowsy), hyperactive (agitated), and mixed forms. The hypoactive form is the most common and the most often missed. MeSH also files one specific subtype, emergence delirium, which occurs on waking from anaesthesia.

What causes delirium?

It is multifactorial. A vulnerable brain (predisposed by age, dementia, or sensory impairment) meets an acute precipitant (infection, surgery, a new medication, metabolic upset). Mechanistically, neuroinflammation and a relative deficit of acetylcholine with excess dopamine are leading explanations (Maldonado, 2017).

How is delirium diagnosed?

By structured assessment of attention and the other core features, most often with the Confusion Assessment Method (CAM), or the CAM-ICU for ventilated patients. A diagnosis requires acute onset with fluctuation and inattention, plus disorganised thinking or an altered level of consciousness (Inouye et al., 1990).

Can delirium be prevented?

Often, yes. Multicomponent nonpharmacological programmes such as the Hospital Elder Life Program, which target modifiable precipitants like immobility, sleep deprivation, dehydration, and sensory impairment, prevent roughly a third of cases in at-risk older inpatients (Hshieh et al., 2015).

Do antipsychotic drugs cure delirium?

No. A large randomised trial found that neither haloperidol nor ziprasidone shortened ICU delirium. The treatment is to find and reverse the underlying cause and support the patient; sedatives are reserved for dangerous agitation (Girard et al., 2018).

Does delirium have lasting effects?

It can. Delirium independently predicts higher mortality and is followed by accelerated long-term cognitive decline; after critical illness, longer delirium predicts worse global cognition and executive function months later (Pandharipande et al., 2013).

Support Organizations

• American Delirium Society (ADS) — a professional society advancing delirium research, education, and quality improvement in clinical care.
• European Delirium Association (EDA) — a multidisciplinary body promoting delirium research and evidence-based practice across Europe.
• Hospital Elder Life Program (HELP) — the multicomponent delirium-prevention programme and its resources for hospitals and families.
• National Institute on Aging (NIA) — public information and research funding on cognitive health, delirium, and dementia in older adults.

References

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Witlox, J., Eurelings, L. S. M., de Jonghe, J. F. M., Kalisvaart, K. J., Eikelenboom, P., & van Gool, W. A. (2010). Delirium in elderly patients and the risk of postdischarge mortality, institutionalization, and dementia: A meta-analysis. JAMA, 304(4), 443–451. https://doi.org/10.1001/jama.2010.1013

van den Boogaard, M., Pickkers, P., Slooter, A. J. C., Kuiper, M. A., Spronk, P. E., van der Voort, P. H. J., et al. (2012). Development and validation of PRE-DELIRIC (PREdiction of DELIRium in ICu patients) delirium prediction model for intensive care patients: Observational multicentre study. BMJ, 344, e420. https://doi.org/10.1136/bmj.e420

Saczynski, J. S., Marcantonio, E. R., Quach, L., Fong, T. G., Gross, A., Inouye, S. K., & Jones, R. N. (2012). Cognitive trajectories after postoperative delirium. New England Journal of Medicine, 367(1), 30–39. https://doi.org/10.1056/NEJMoa1112923

Pandharipande, P. P., Girard, T. D., Jackson, J. C., Morandi, A., Thompson, J. L., Pun, B. T., et al. (2013). Long-term cognitive impairment after critical illness. New England Journal of Medicine, 369(14), 1306–1316. https://doi.org/10.1056/NEJMoa1301372

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