Delirium …

Neurobehavioral & Cognitive Disorders

Updated 08.11.2025
Released 09.24.2025
Expires For CME 08.11.2028

Delirium in critical illness

Authors: Maria Bruzzone Giraldez MD, Shawniqua Williams Roberson MEng MD

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Editor: Howard S Kirshner MD

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Delirium in critical illness

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Introduction

Overview

Delirium is a frequent but often overlooked complication in critically ill patients. Its detection is crucial because ICU delirium is linked to higher risks of adverse outcomes, including prolonged hospitalization, cognitive decline, and increased mortality. Evidence suggests that timely recognition and management of delirium can lead to better patient outcomes, which emphasizes the need for systematic assessment and intervention in critical care settings.

Key points

	• Delirium is underrecognized in critical care.
	• Delirium is independently associated with worse cognitive impairment after critical illness.
	• Several risk factors for delirium are iatrogenic and reversible.
	• Standard-of-care guidelines recommend routine delirium monitoring in the ICU.
	• Evidence-based interventions for delirium are nonpharmacologic.

Historical note and terminology

The term “delirium” is derived from the Latin word delirare, which means “to go out of the furrow,” ie, to deviate from a straight line or to be deranged (01). This term was first applied to a syndrome of fluctuating mental state attributable to poisoning, fever, or head trauma. The syndrome has been recognized under various other terms since Hippocrates’ publication of his Prognostikon 4 in 500 BC. Delirium is among the most common neurologic syndromes associated with critical illness, particularly among older patients, and its underlying pathophysiology has been the subject of much investigation.

Delirium during critical illness has come to be recognized as an independent risk factor for mortality (24), long-term cognitive impairment (67), new dementia diagnosis (98), and worse other outcomes (97).

These findings have transformed modern thinking about delirium from a benign symptom of extracerebral organ dysfunction to an adverse outcome per se, with the potential to worsen brain injury if not addressed.

This transformation in perspective has driven escalating efforts by intensivists to monitor for and limit the occurrence of delirium during critical illness to understand its neurobiological mechanisms and to develop potential therapeutic interventions (75; 53).

Delirium has been referred to by several names, including encephalopathy, acute confusional state, acute brain dysfunction, acute brain failure, and altered mental status (63). The use of various terms to describe a common clinical presentation has become a significant obstacle to scientific progress in this area, as researchers from different fields employ different terminology (86). An international, interdisciplinary panel of experts in intensive-care medicine, neurology, geriatrics, rehabilitation medicine, pharmacy, anesthesiology, and psychiatry generated an expert consensus for the nomenclature of delirium, acute encephalopathy, and related terms. Delirium is a clinical syndrome, and is characterized by an acute change in attention, awareness, and cognition (101). The panel discourages the use of other terms, such as altered mental status and acute brain dysfunction (86).

The panel refers to acute encephalopathy as a pathobiological brain process that develops quickly, usually in less than 4 weeks, and that manifests clinically as subsyndromal delirium, delirium, or coma. Therefore, the consensus recommendation was that the term “acute encephalopathy” should not be used to describe clinical symptoms observed at the bedside (86).

The DSM-5 defines five specific clinical criteria for delirium diagnosis, which are listed in Table 1. Typically, delirium occurs in the setting of an underlying medical condition, and symptoms are not better explained by a preexisting, evolving, or established neurocognitive disorder (28). Subsyndromal delirium is diagnosed when cognitive changes compatible with delirium are present but do not fulfil all DSM-5 criteria (82). Using clinical characteristics, delirium can further be classified into hyperactive delirium, hypoactive delirium, and mixed based on the presence and intensity of motor manifestations (59).

Table 1. DSM-5 Diagnostic Criteria for Delirium

Criterion	Description
A	Disturbance in attention (reduced ability to direct, focus, sustain, and shift attention) and awareness (impaired orientation to the environment).
B	The disturbance develops over a short period (hours to days), represents a change from baseline, and fluctuates in severity throughout the day.
C	Additional cognitive disturbance (eg, memory deficit, disorientation, language impairment, visuospatial difficulties, or perceptual disturbances).
D	Disturbances in Criteria A and C are not better explained by a preexisting or evolving neurocognitive disorder and do not occur during coma or severely reduced arousal.
E	Evidence from history, physical examination, or laboratory findings indicates the disturbance results from a medical condition, substance intoxication or withdrawal, toxin exposure, or multiple causes.

In this article, we refer to ICU delirium as the clinical state characterized by a global disturbance in mental functioning (evidenced by confusion, fluctuating levels of arousal, or inattention), which occurs in conjunction with or as a complication of critical illness or the interventions used to treat critical illness.

Clinical manifestations

Presentation and course

	• Delirium is characterized by acute disturbances in attention, awareness, and cognition.
	• Delirium is associated with fluctuating levels of arousal.
	• Delirium typically resolves hours to days after reversal of precipitating factors.
	• Delirium is associated, in a dose-dependent fashion, with worse mortality, higher risk of rehospitalization, and worse long-term cognitive decline after critical illness.

Delirium is a clinical syndrome characterized by the acute onset of disturbances in attention, awareness, and cognition that develop over a short period of time (04). Patients commonly experience confusion and fluctuating levels of arousal and may have alterations in perception and thought content. The condition typically develops over hours to days and is not explained by another established or evolving neurocognitive disorder (eg, nonconvulsive seizure). According to the Diagnostic and Statistical Manual (Version 5), a diagnosis of delirium requires evidence that delirium is a physiologic consequence of a medical condition, toxic exposure or withdrawal, or multiple etiologies. Delirium cannot be diagnosed in the presence of a severely reduced level of consciousness (ie, coma).

One of the earliest manifestations is a difficulty with maintaining focus or attention. Patients may be easily distractible during conversation or while performing simple tasks. Some may also complain of a loss of mental clarity or be easily and frequently disoriented. A hallmark of this disorientation is impaired decision-making, with apparent disregard for the location, time of day, or situation. For example, a delirious patient in the intensive care unit may suddenly declare an intention to get out of bed in the middle of the night to “change the clocks in the living room,” forgetting that they are critically ill with multiple catheters connected.

As the severity of delirium progresses, sudden and frequent fluctuations in the level of consciousness are common, with individuals transitioning from hypersomnolence to hyperarousal and back again over the course of minutes to hours, without clear precipitating factors. Hypersomnolence may present with deep sleep with difficulty opening eyes, even with noxious stimuli, and is referred to as hypoactive delirium. Hyperarousal, known as hyperactive delirium, is typically demonstrated by a heightened state of vigilance, exaggerated startle response with or without the appearance of anxiety or irritability. Yet importantly, in many cases of delirium, individuals may show only subtle behavioral signs, such as somnolence or withdrawn affect with normal levels of arousal (59). This is referred to as normoactive delirium.

The course of delirium is variable. In most cases, the condition resolves over several hours to days after reversal of the precipitating factors. In up to 20% of cases, the episode may persist for weeks to months, particularly when precipitating factors are not mitigated (13).

Prognosis and complications

In patients who experience ICU delirium, both their short-term and long-term prognoses are adversely impacted.

In the short term, ICU delirium has been linked to longer durations of mechanical ventilation and extended ICU length of stay (22; 80). Evidence indicates that patients with delirium spend, on average, 1 day and 9 hours more in the ICU than those without delirium. Similarly, the duration of mechanical ventilation is approximately 1.79 days longer in patients who develop delirium compared to those who do not (80). Studies looking at the relation between ICU delirium and acute mortality have reported inconsistent findings (21; 40).

Long-term prognosis is also affected by ICU delirium, with a documented increase in 30-day mortality (27). Increased likelihood of discharge to a skilled nursing facility, rehabilitation center, or long-term acute care hospital has also been reported after ICU delirium (70).

Post-discharge cognitive impairment, worsening in performance of activities of daily living, and sleep disorders have all been documented in patients who suffered delirium during critical illness (02).

Delirium during critical illness has been increasingly recognized as a predictor of adverse long-term cognitive outcomes. Population-based studies have shown a strong association between delirium and the subsequent development or worsening of dementia.

In a 10-year prospective population-based study of adults more than 85 years old, delirium was associated with a more than eight-fold odds of incident dementia (OR 8.7; 95% CI 2.1–35) and with three-fold odds of worsened dementia severity (OR 3.1; 95%CI 1.5–6.3) (14).

Similar associations have been observed in critically ill patients, where a more prolonged duration of delirium correlates with worse cognition up to 1 year after discharge. The BRAIN-ICU study, which enrolled 821 patients in the medical or surgical ICU, demonstrated that longer duration of delirium was an independent risk factor for worse global cognition scores at 3 and 12 months after discharge, and was also an independent risk factor for worse executive function at 12 months (67). Interventions aimed at reducing the burden of delirium among critically ill patients are associated with improved outcomes (75).

Studies have looked at individual motoric subtypes of delirium and their association with outcomes in critically ill patients, including length of mechanical ventilation, ICU stay, mortality, post-discharge disability, depression, post-traumatic stress disorder, and mental health disorders (77). Hypoactive and mixed delirium have been independently associated with in-hospital mortality, but not with 12-month mortality (05). Hypoactive delirium has also been associated with longer ICU stays and prolonged periods of mechanical ventilation (90). Increased duration of hypoactive delirium has been independently associated with a minimal increase in instrumental activities of daily living dependence at 3 months after discharge (77).

Whether delirium is accompanied by normal, decreased, or increased levels of arousal is of prognostic significance. Among hospitalized patients more than 65 years old, the number of days with delirium with normal arousal predicts worse functional and cognitive outcomes at 6 months, even adjusting for pre-illness level of function, severity of illness, and burden of comorbidities (35).

Biological basis

	• Multiple factors, such as sepsis, hypoxia, and metabolic derangements, converge on shared pathways.
	• Cerebral energy failure from impaired blood flow, oxygenation, or glucose use may underlie delirium.
	• Systemic inflammation triggers neuroinflammatory cascades involving cytokines and chemokines.
	• Neurotransmitter imbalances in acetylcholine, dopamine, and GABA contribute, especially in vulnerable brains.
	• Age and neurodegeneration increase susceptibility through synaptic loss and exaggerated glial responses.

Etiology and pathogenesis

Delirium occurs in a wide range of clinical contexts, and various risk factors have been identified. Sepsis, hypoxic respiratory failure, hypotension, drug intoxication (iatrogenic or otherwise), and metabolic disturbances can act as triggers impairing cerebral function and lead to the clinical manifestations of delirium. Our understanding of the pathogenesis of delirium in critical illness is, thus, informed by common mechanistic pathways observed among these conditions.

Delirium underlying pathophysiological pathways

(A) Systemic inflammation, hypoxia‑induced perfusion deficits, and sedative and other drugs exposure constitute some of the principal triggers that affect the brain of the critically ill. (B) These insults precipitate cerebral ...

In the 1940s and 1950s, based on their studies of electroencephalographic changes in normal and delirious individuals, Engel and Romano proposed a hypothesis of cerebral metabolic insufficiency, which posits that delirium is caused by a failure to meet the substantial energy requirements for normal brain function (25). Deficits in cerebral energy metabolism may arise from impaired blood flow (29), impaired glucose regulation (87), or impaired oxygenation (10), conditions that may occur in isolation or in conjunction with other changes that undermine normal brain function.

Importantly, delirium may occur during critical illness even when key metabolic substrates are within normal limits. This finding suggests the brain’s metabolic requirements may increase during delirium, outpacing the normal supply, or that factors are at play to impair the brain’s ability to effectively use its metabolic output to achieve normal neurophysiologic function. Both possibilities may occur during acute systemic inflammatory conditions. Given that conditions such as sepsis and postoperative state are leading risk factors for delirium in critically ill patients, a prevailing hypothesis for delirium pathogenesis lies in the inflammatory mechanistic pathways. Indeed, both septic patients and postoperative patients exhibit increased release and activation of inflammatory mediators such as toll-like receptor 2, interleukin 1beta, and tumor necrosis factor (37). Increases in circulating cytokines, such as IL-6 and TNF, and acute phase proteins (eg, CRP), are associated with increased delirium risk in critically ill adults (09). Peripheral immune signals interact with the blood-brain barrier through complex communication pathways, leading to functional and structural alterations in brain parenchymal cells, including microglia, astrocytes, and neurons. These neuroinflammatory processes are linked to the acute onset of cognitive, behavioral, and emotional disturbances (11).

Another leading hypothesis of the mechanism by which common risk factors may lead to delirium lies in the imbalance of one or more neurotransmitter systems of the brain. Disruptions in acetylcholine, dopamine and GABA synthesis, metabolism, and receptor signaling are common effects of many drugs used in the care of critically ill patients. These disruptions may precipitate delirium, particularly in brains that are more vulnerable due to predisposing factors (101).

Any or all these mechanisms may induce earlier or more severe delirium states in brains that are primed for insult, eg, among older individuals or those with neurodegenerative disease. A variety of mechanisms contribute to this enhanced vulnerability. Worsening degenerative cognitive dysfunction is associated with progressive thalamic synaptic loss and axonal pathology (15). Microglia and astrocytes in individuals with neurodegenerative disease mount exaggerated pro-inflammatory responses to secondary inflammatory stimuli (38). With increasing age and worsening dementia, there is also degeneration of cholinergic and noradrenergic neuronal populations (81; 52), which may yield higher sensitivity to subtle neurotransmitter imbalances.

The pathways by which pathological metabolic, inflammatory, or neurotransmitter function led to the clinical manifestations observed in delirium are incompletely understood. A central hypothesis is rooted in disruptions to network connectivity in the brain (57). Although this may be a global phenomenon, certain neuroanatomic structures and functional connections are likely either more sensitive or more susceptible to inflammatory and metabolic changes. Disruptions in network connectivity have been observed using fMRI and EEG recordings during delirium (95). These likely lead to the clinical manifestations of delirium by disrupting sensory, perceptive, memory, computation, and arousal processes supporting normal cognitive function.

Epidemiology

Approximately 31% of adult medical and surgical ICU admissions are complicated by delirium (50). More than half of delirium cases present with hypoactive signs (eg, somnolence, with paucity of movement), whereas roughly 13% of cases are hyperactive in nature. Patients requiring mechanical ventilation are at higher risk, with prevalence estimates ranging from roughly 50% to 80% in this population (24; 34).

Risk factors for delirium in the critically ill are common. It is estimated that the typical patient in the medical intensive care unit has more than 11 risk factors for delirium onset (23). Risk factors for delirium in the ICU are usually divided into predisposing (baseline), related to the patient’s clinical characteristics and comorbidities, and precipitating (hospital-related), referring to the patient’s acute illness and its treatment (44).

Predisposing and precipitating risk factors for delirium

(Contributed by Dr. Maria Giraldez.)

Examples of predisposing risk factors include advanced age (103) and cognitive impairment before admission (72; 96). Age greater than 65 years is an important predisposing risk factor, with an estimated prevalence of 19% to 82% among critically ill older adults (44). This is important because delirium significantly increases the likelihood of functional decline after admission among hospitalized adults 65 years of age or older (OR 2.51; 95%CI 2.31-2.73) (31).

Precipitating risk factors for delirium include the use of certain medications like benzodiazepines, opiates and anticholinergic agents (71); factors related to the ICU course, like high severity of illness (65) and prolonged mechanical ventilation (96); and factors related to the ICU environment that usually lead to poor sleep, which have also been associated with delirium development (99). In general, baseline risk factors are less modifiable than hospital-related risk factors, and preventive measures for delirium are mostly focused on the latter.

Prevention

Strategies to prevent delirium in critical care environments begin with recognizing individual risk factors for its development and necessitate a comprehensive approach that involves interventions in the intensive care unit and with the individual patient (66).

Targeting strategies focusing on addressing quality, safety and suffering of critically ill patients, including delirium prevention, were addressed by the Society of Critically Care Medicine in its “Pain, Agitation, and Delirium” guideline published in 2013, and updated in the 2018 “Prevention and Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult Patients in the ICU” (PADIS) guideline (69). Following these evidence-based recommendations, several initiatives have been implemented. One of these initiatives is the ABCDEF bundle, where ABCDEF stands for Assess, prevent and manage pain, Both spontaneous awakening trials (SATs) and spontaneous breathing trials (SBTs), Choice of sedation/analgesia, Delirium monitoring and management, Early mobility and exercise, and Family engagement and empowerment (06). This bundle of measures uses a multidisciplinary approach to target several key risk factors for delirium development in the ICU: pain and agitation, sedation, sleep, and mobility (66).

The ABCDEF bundle was successfully implemented in several community hospital ICUs using an interprofessional team model for operationalization of the PADIS guidelines. Several randomized clinical trials have been conducted since, evaluating the bundle intervention for minimization of modifiable risk factors related to ICU delirium (61; 93). However, evidence on the effectiveness of implementing the ABCDEF bundle in the ICU for delirium prevention has been conflicting. Early on, investigators showed that higher bundle compliance was independently associated with more days free of delirium (06) and significantly decreased prevalence of delirium (08). However, a meta-analysis performed to evaluate the impact of bundle interventions on ICU delirium prevalence, duration, and other patient adverse outcomes showed that bundle interventions were not associated with reduced ICU delirium prevalence or shortening of delirium duration. Bundle interventions did show a significant reduction in the proportion of patient-days with coma, hospital length of stay, and 28-day mortality (104). The authors did notice that effectiveness increases when the bundle is entirely implemented. A more recent systematic review and meta-analysis of six studies focused on the implementation of the ABCDEF bundle as a whole and identified decreased delirium incidence and reduced delirium duration when the bundle is implemented (88). The authors mention that although the quality of available studies evaluating the efficacy of bundle measurements for delirium prevention in the ICU is limited, there is an increased body of research that favors the implementation of the ABCDEF bundle for ventilated and nonventilated ICU patients. There is still a need for high-quality randomized controlled trials to better establish the relationship between ABCDEF bundle and delirium outcomes (88).

As described above, effective delirium prevention strategies in the ICU are based on nonpharmacologic strategies. Early studies showed that the use of certain medications, particularly antipsychotics for surgical ICU patients and dexmedetomidine for mechanically ventilated patients, may reduce the prevalence of delirium in the ICU (83). A randomized, multicenter, double-blind, placebo-controlled, investigator-driven study involving 1789 ICU patients did not show any benefit with the use of prophylactic haloperidol compared with placebo in terms of survival improvement (primary outcome) or delirium incidence (secondary outcome) (94). The use of dexmedetomidine as an alternative sedative in the ICU to reduce delirium has been extensively studied. A systematic review showed that the risk of delirium is reduced in mechanically ventilated patients who are sedated with dexmedetomidine (54).

Differential diagnosis

Confusing conditions

Delirium is characterized by a disturbance in attention and cognition that develops over a short period of time, not better explained by a preexisting, evolving, or established neurocognitive disorder. An underlying medical condition causes the disturbance. Processes that cause disturbances in attention and cognition, but are explained by a preexisting or evolving neurocognitive disorder or do not have an underlying medical condition, should be distinguished from delirium (Table 2).

Table 2. Differential Diagnosis of Delirium in Critically Ill Patients

Condition	Key features	Distinguishing characteristics	Diagnostic tools and findings
Nonconvulsive seizures or nonconvulsive status epilepticus	Fluctuating inattention, cognitive changes, possible rhythmic motor movements, and facial myoclonus	No self-directed behavior, slowed responses, perseveration, apraxia, agnosia, dyscalculia, dyslexia; fluctuations similar to delirium	EEG: epileptiform activity; may be normal postictally
Psychiatric conditions (“pseudodelirium”)	Disturbances in attention, awareness, and cognition as seen in catatonia, mania, acute psychosis, and dissociative disorders	Less fluctuation of symptoms; additional features like increased tone in catatonia; may co-exist with delirium	EEG: normal in psychiatric conditions; background slowing favors delirium
Depression	Inattention, poor sleep, or cognitive slowing	More consistent symptoms, absence of acute onset, minimal fluctuation	Clinical assessment; lack of EEG slowing
Dementia	Deficits in attention, memory, and cognition	Gradual onset, step-wise progression, less dramatic fluctuations; high risk of superimposed delirium	History of chronic cognitive decline; baseline cognitive testing

Nonconvulsive seizures and nonconvulsive status epilepticus may present clinically with fluctuating inattention and changes in cognition (26). Some cognitive deficits described during and after nonconvulsive seizures or status epilepticus include no self-directed behavior, slower responsiveness, perseverative behaviors, limited working memory, apraxia, agnosia, dyscalculia, and dyslexia (74; 49). Fluctuation of symptoms has also been described in nonconvulsive seizures or status epilepticus (49). Rhythmic motor movements, as well as the presence of facial myoclonus, if present, should increase the suspicion for nonconvulsive seizures or nonconvulsive status epilepticus (49). The use of electroencephalography can demonstrate underlying epileptogenic activity and explain patient symptoms, but it may not be informative during the postictal state.

Some psychiatric conditions should be considered in the differential diagnosis of delirium. Several psychiatric conditions can present with core features of delirium, and this has been called pseudo-delirium in the past (100). For example, disturbance in attention can be seen in patients with catatonia and mania, disorganized psychosis, or dissociative disorders; these patients can present with disturbance in awareness, and an additional disturbance in cognition can be seen in patients with mania, catatonia, acute psychosis, and dissociative disorders (100). Delirium can be misdiagnosed as depression, which can also present with inattention and poor sleep, but with less fluctuation of symptoms (20). Delirium and psychiatric conditions can also co-exist, making the diagnostic process more complex. In most cases, a detailed evaluation and additional features in psychiatric conditions (eg, increased tone in catatonia) can help guide the diagnosis. EEG can help differentiate delirium from psychiatric conditions; there is usually background slowing in delirium (48), but the EEG is usually normal in psychiatric conditions (64).

Dementia can sometimes be difficult to differentiate from delirium, as both present with deficits in attention and disturbances in cognition; however, the onset of dementia is not acute, and fluctuations are less dramatic and more step-wise (20). It is important to keep in mind that patients with dementia are more susceptible to developing delirium, and the conditions often co-exist. This condition, known as delirium superimposed on dementia (62), presents a diagnostic challenge.

Associated or underlying disorders

The interplay between predisposing risk factors and precipitating risk factors determines an individual’s risk of developing delirium. Predisposing risk factors are inherent to a patient’s characteristics and background. In the critically ill, age has been strongly associated with an increased risk of developing delirium, as have a history of dementia and hypertension (103). The effect of age in delirium is thought to be secondary to the gradual accumulation of damage to somatic brain cells, leading to cellular dysfunction, which increases vulnerability to diseases and death (45). It has been proposed that the increased rate of cerebrovascular disease and head trauma in the elderly could increase their susceptibility to delirium when stressed (44).

Dementia or prior cognitive impairment has been identified as a risk factor for delirium in multiple human (43; 73; 47) and animal studies (15). Moreover, the risk of delirium increases as the severity of dementia worsens (15). Prior studies have found that an MMSE of less than 24 prior to admission was associated with increased risk of developing delirium during hospitalization (43). Some shared pathophysiological mechanisms like cholinergic deficiency, inflammation, and reduced cerebral oxidative metabolism have been postulated as links between dementia and delirium (30).

Hypertension has been consistently described as a risk factor for delirium development in the ICU setting (65; 39; 103). Blood pressure variability has deleterious effects in the brain because it induces microvascular and blood-brain barrier damage secondary to high-frequency pulsatile flow, which has not been adequately buffered during acute critical illness due to impaired cerebral autoregulation. Microvascular and blood-brain barrier damage have been postulated as a significant mechanism in delirium pathophysiology (101).

Several other risk factors have been described in numerous prospective and retrospective studies, including alcohol use, nicotine use, ASA physical status, and cardiac disease; however, the level of evidence for those risk factors has been inconclusive when studied in a meta-analysis (103).

All of the mentioned risk factors increase brain vulnerability, resulting in a failure to show resilience to acute stressors.

Diagnostic workup

The two fundamental steps in diagnosing delirium include a bedside clinical assessment and an evaluation of fluctuations from the patient’s baseline level of functioning. The DSM-5 criteria for delirium diagnosis encompasses the following criteria:

	(A) A disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment).
	(B) The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day.
	(C) An additional disturbance in cognition (eg, memory deficit, disorientation, language, visuospatial ability, or perception).
	(D) The disturbances in Criteria A and C are not explained by another preexisting, established, or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal, such as coma.
	(E) There is evidence from the history, physical examination, or laboratory findings that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal (ie, due to a drug of abuse or to a medication), or exposure to a toxin, or is due to multiple etiologies (04).

In the context of critical illness, this diagnostic approach must be accomplished rapidly, and screening must occur frequently. These pragmatic considerations led to the development of several screening assessments that can be used with good sensitivity and specificity. The CAM-ICU is an instrument derived from the Confusion Assessment Method (CAM). The CAM was developed to improve delirium assessment by nonpsychiatrists, is based on the delirium criteria published by the American Psychiatric Association (42), and has been extensively validated. The CAM was later modified by Ely and colleagues and adapted for use in the critically ill, nonverbal patient; the modified assessment was named CAM-ICU (23). The CAM-ICU can be performed in 2 to 3 minutes, does not require extensive training, and is easy to use; it has demonstrated excellent reliability and validity to detect delirium in ICU patients (23; 33).

Another instrument to detect delirium in the ICU that was developed around the same time as the CAM-ICU is the Intensive Care Delirium Screening Checklist (ICDSC). This checklist contains eight items that were developed based on the psychiatric definition of delirium published in the DSM-4 (07). The ICDSC also demonstrates high sensitivity and reliability to detect delirium in the intensive care setting, and is easy to administer.

Other delirium assessment tools for use in the ICU setting include the Nursing Delirium Screening Scale (36) and Delirium Detection Score (41); these and others can be found on the Network for Investigation for Delirium (NIDUS) webpage.

Management

The cornerstone for delirium management involves nonpharmacological strategies, and those should be tried prior to pharmacologic interventions. Nonpharmacological strategies are based on multicomponent interventions recommended by the Society of Critical Care Medicine’s practice guidelines and aim to reduce modifiable risk factors for delirium, improve cognition, optimize sleep through modification of ICU beds or light systems, and assist with hearing, vision, and mobility in the critically ill (19; 55; 89). Integrated approaches for the management of mechanically ventilated patients incorporate these recommendations and have demonstrated usefulness (78). The most widely used integrated approach is the ABCDEF bundle (58).

This bundle focuses on the importance of pain assessment, prevention, and management (A), awakening and spontaneous breathing trials (B), choice and minimization of analgesia and sedation (C), assessment and management of delirium (D), early mobility (E), and family engagement (F) as ways to prevent and treat delirium. The improvement in compliance with the bundle is associated with a reduction in delirium-free ICU days (75).

Pharmacological interventions for delirium have been extensively studied in the last decades, but evidence supporting effective medications for delirium treatment in the ICU is lacking.

Antipsychotics are often administered in hyperactive delirium and may serve to reduce the occurrence of unsafe behaviors (18). However, a multicenter randomized controlled trial comparing haloperidol, ziprasidone, and placebo among 1183 ICU patients found no difference in delirium duration when using haloperidol or ziprasidone compared to placebo (32).

Benzodiazepine use in the critically ill patient has been associated with increased risk of delirium the next day after administration (102), a worrisome finding considering that benzodiazepines are one of the most common sedatives used in the ICU.

Dexmedetomidine has been studied as an alternative to other sedative and analgesic agents, with several randomized trials showing a reduced rate of delirium in comparison with lorazepam (68), midazolam (79), and propofol (46). However, its use intraoperatively has not been shown to prevent postoperative delirium (17). The use of dexmedetomidine in patients with agitated delirium in the ICU has been demonstrated to increase ventilator-free hours (primary outcome) and accelerate delirium resolution (secondary outcome) (76). More data are still needed to support its use, as dexmedetomidine has a higher cost compared with other sedatives used in the ICU (78).

Outcomes

Interventions aimed at reducing the burden of delirium among critically ill patients are associated with improved outcomes.

Implementation of the ABCDEF bundle in critically ill patients has been linked to substantial improvements in clinical outcomes. Higher adherence to the bundle correlates with reduced mortality, shorter duration of mechanical ventilation, lower incidence of coma and delirium, decreased use of physical restraints, fewer ICU readmissions, and increased likelihood of discharge home rather than to other facilities. Notably, a dose-response relationship indicates that greater bundle compliance leads to progressively better outcomes. However, an increase in reported pain was observed with higher adherence, suggesting the need for balanced pain management within the bundle framework (75).

Special considerations

Pregnancy

Delirium during pregnancy is not frequently reported, which is attributed to improvement in antenatal care and labor analgesia. However, case reports on delirium during pregnancy in COVID-19 positive patients can be found in the literature (56). In these patients, frequent reorientation is needed, with sensitivity to a patient’s specific pregnancy-related fears and mindset, eg, special attention to pregnancy and fetal viability as well as special attention to invasiveness of procedures and how they may be interpreted in a delirious mind.

Anesthesia

Postoperative delirium occurs in up to 52% of older adults and is associated with increased postoperative cognitive decline and mortality (44) and in up to 25% of adults older than 18 years who are admitted to the surgical ICU for more than 24 hours after surgery (12). Risk factors for postoperative delirium in the critically ill patient include age, emergency surgery, acute physiological score, use of benzodiazepines, trauma (84), mechanical ventilation, and diabetes mellitus (12). In nonventilated postoperative patients, the presence of delirium resulted in longer lengths of surgical ICU and hospital stay and higher hospital and surgical ICU mortality (84). Delirium treatment in the postoperative center involves early recognition using validated assessment tools, nonpharmacologic measurements based on a patient-centered approach that focuses on reorientation and restoration of daily routine, and adequate monitoring and management of pain (91).

Pediatrics

Approximately 30% of pediatric ICU admissions are complicated by delirium (85). Risk factors for delirium in the critically ill pediatric population include young age, developmental delay, benzodiazepine exposure, and mechanical ventilation (16). Pediatric ICU delirium has been associated with increased length of stay, duration of mechanical ventilation (03), increased use of resources, and higher medical costs (92) and is also associated with mortality in children (16). Long-term outcomes in pediatric ICU delirium have not been described (60). Despite this data, most pediatric ICU units do not perform consistent delirium assessments (51). In terms of treatment, one study showed that implementing nonpharmacological measures in the form of a developmentally appropriate bundle for the pediatric population reduced the prevalence of delirium in a subgroup of pediatric intensive care patients (60), but the group remarked that further research is needed.

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Maria Bruzzone Giraldez MD

Dr. Bruzzone Giraldez of the University of Florida has no relevant financial relationships to disclose.
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Shawniqua Williams Roberson MEng MD

Dr. Williams Roberson of Vanderbilt University has no financial relationships to disclose.
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Editor

Howard S Kirshner MD

Dr. Kirshner of Vanderbilt University School of Medicine has no relevant financial relationships to disclose.
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Patient Profile

Age range of presentation: Elderly
Sex preponderance: No sex preponderance

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Delirium in critical illness

Differential Diagnosis

Nonconvulsive seizures
Nonconvulsive status epilepticus
Catatonia
Mania
Disorganized psychosis
- Dissociative disorders
- Depression
- Dementia
- Hypertension

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Clinical Categories

Neurobehavioral & Cognitive Disorders

Delirium in critical illness

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Table 1. DSM-5 Diagnostic Criteria for Delirium

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Table 2. Differential Diagnosis of Delirium in Critically Ill Patients

Associated or underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Anesthesia

Pediatrics

Media

References

Contributors

Authors

Editor

Patient Profile

ICD & OMIM codes

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