24. DELIRIUM AND ACUTE CONFUSION

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CHAPTER 24. DELIRIUM AND ACUTE CONFUSION
Catherine Vena

DEFINITION AND INCIDENCE

Patients in palliative care likely are of an advanced age, experience severe exacerbations of chronic illnesses, and use multiple medications—all of which put them at risk for changes in mental and cognitive function. Frequently, the new onset of behavior labeled as “confusion” is indicative of the acute syndrome of delirium. Delirium is a serious neuropsychiatric complication that, unlike dementia, is potentially reversible. It must be properly diagnosed and promptly treated in the palliative care setting (Friedlander, Brayman, & Breitbart, 2004). The presence of delirium is associated with increased mortality and morbidity including prolonged hospital stays, functional decline, long-term care placement, and, in the case of the imminently dying, a distressing and uncomfortable death (Breitbart & Strout, 2000; Ely, Margolin, Francis et al., 2001c; Inouye, Rushing, Foreman et al., 1998; Marcantonio, Simon, Bergmann et al., 2003; McCusker, Cole, Abrahamowicz et al., 2002; Pitkala, Laurila, Strandberg et al., 2005).
Descriptions of behaviors commonly noted in delirious patients can be found in medical writings from the time of Hippocrates to the present (Clary & Krishnan, 2001). Despite this history, terminology has been inconsistent, overlapping, poorly defined, and often adapted to the discipline or specialty observing the condition. Historically, terms such as organic brain syndrome, acute secondary psychosis, exogenous psychosis, and sundown syndrome have been used synonymously with delirium (Lipowski, 1990). A review of the recent literature reveals a continuing use of a variety of terms to characterize delirium, including acute brain failure, acute confusional state, terminal restlessness or agitation, and ICU psychosis (Barber, 2003; Cacchione, Culp, Laing et al., 2003; Maluso-Bolton, 2000; McGuire, Basten, Ryan et al., 2000; Travis, Conway, Daly et al., 2001). The American Psychiatric Association (APA) first established the term “delirium” and defined diagnostic criteria in 1980 (APA, 1980). Increasingly, practitioners from various disciplines have adopted the term. To prevent miscommunication among health care professions, the clinician must always carefully characterize the mental and cognitive status of patients and use the term “delirium” when appropriate.
The most recent diagnostic criteria for delirium from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) are listed in Box 24-1. Based on these criteria, delirium may be defined as an acute and fluctuating organic brain syndrome characterized by global cerebral dysfunction that includes disturbances in attention, level of consciousness, and basic cognitive functions (thinking, perception, and memory) (APA, 2000). Other features commonly associated with delirium include increased or decreased psychomotor activity, disturbances in the sleep-wake cycle, and emotional lability (Burns, Gallagley, & Byrne, 2005). Delirium is frequently unrecognized by clinicians or misdiagnosed (Laurila, Pitkala, Strandberg et al., 2004). The fact that demented, depressed, and anxious patients may develop delirium makes the diagnosis additionally difficult (Insel & Badger, 2002). The diagnosis of delirium is primarily clinical and requires careful observation and a thorough history. Because the signs and symptoms of delirium are nonspecific, the clinician must look for a constellation of findings, identify the rapidity of onset, and assess for associated medical and environmental risks to determine an appropriate diagnosis.
Box 24-1

Disturbance of consciousness with reduced ability to focus, sustain, or shift attention
Change in cognition or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia
Disturbance develops in a short period of time and fluctuates over the course of the day
Evidence from history, physical examination, or laboratory findings that the disturbance
Is the physiological consequence of a general medical condition
Developed during substance intoxication or medication use
Developed during or shortly after a withdrawal syndrome
Has more than one etiology (e.g., more than one medical condition or a general medical condition plus substance intoxication or medication side effect)
Data from American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (4th ed., text revision). Washington, DC: Author.

Key Features of Delirium

Disturbance of Consciousness

Disturbance of consciousness refers to impairments in attention and the ability to be aware of and sustain attention to the environment (APA, 1999b). Attention is typically fluctuating and may present as a change in the level of consciousness that does not reach the level of stupor or coma. Patients may demonstrate slowed or inadequate reactions to stimuli or manifest distractibility. Individuals may be unable to follow conversations or complete simple tasks, may have slow response time, may be unable to maintain eye contact, or may fall asleep between stimuli. Increasing stimuli (touch, sound) may be needed to elicit a response. Conversely, patients may be hyperalert and overattentive to cues or objects in the environment. The ability to focus can be assessed by the patient’s ability to complete a particular task such as spelling the word “world” backward, subtracting serial 7s, or listing the days of the week in reverse order (Tune, 2000).

Change in Cognition

Many aspects of cognitive function are impaired in delirium, including orientation, memory, language, thinking, and perception (APA, 1999b; Tune, 2000). Disorientation usually manifests relevant to time or place, with time disorientation being the first to be affected. Disorientation to other persons occurs commonly, but disorientation to self is very rare. Short-term memory deficits are the most evident memory impairments. Immediate memory (over a period of seconds) is demonstrated by the digit span (a healthy older adult should be able to repeat at least five) while anterograde memory (over a period of minutes) is demonstrated by the ability to remember three objects after 5 to 10 minutes (Burns et al., 2005; Goy & Ganzini, 2003). However, because these tests also reflect attention, severe deficits in this area will affect results. Language disturbances include a lack of fluency and spontaneity (long pauses and use of repetitious phrases), a tendency to ramble and switch from topic to topic, and difficulty finding the correct word to use in conversation or naming objects (anomia). Thinking is usually disorganized as evidenced by incoherent speech, deficits in logic, and responses that are irrelevant to questions asked. Perceptual disturbances may include misinterpretations, illusions, or hallucinations. Visual misperceptions and hallucinations are most common, but auditory, tactile, gustatory, and olfactory misperceptions or hallucinations can also occur. The individual with delirium may have the delusional conviction that the hallucination is real and exhibit emotional and behavioral responses consistent with the hallucination’s content.

Acute Onset and Fluctuating Course

The features of confusion that develops over a short period and fluctuates over the course of the day are important defining criteria for delirium. Symptoms develop over hours or days but are likely to be intermittent in presentation and severity. A typical presentation is worsening of symptoms at night with lucid periods during the day where the patient may function normally (Cole, 2004). Noting the onset of the disturbances in consciousness or cognition assists in differentiating delirium from other syndromes that cause mental status changes, such as dementia.

Etiological Evidence

An important criterion for the diagnosis of delirium is evidence that the changes are a physiological consequence of an underlying medical condition, substance or medication intoxication or withdrawal, or combination of these factors. In palliative and end-of-life care, it may be difficult to identify the exact cause of delirium. An individual may have several potential causes at any one time (see “Etiology and Pathophysiology”). The challenge for the clinician is to identify which of the potential causes is the most likely and then determine the appropriate approach to this problem.

Additional Features of Delirium

Although not required for the diagnosis of delirium, a variety of other features often accompany delirium; these include sleep-wake disturbances, psychomotor activity changes, and emotional lability. The clinician should assess for these symptoms and monitor patients for any changes over time to prevent or at least minimize distress for both patients and their caregivers (Breitbart, Gibson, & Tremblay, 2002).

Sleep-Wake Disturbances

Disturbances in sleep patterns include daytime sleepiness, nocturnal insomnia, disturbed sleep continuity, and excessive dreaming. Some patients may experience a complete reversal of the sleep-wake cycle characterized by diurnal sleep periods and nighttime agitation and insomnia, whereas others may have fragmentation of the circadian sleep-wake cycle characterized by short periods of sleep and waking across the 24-hour day (Burns et al., 2005; Trzepacz, Mittal, Torres et al., 2001).

Psychomotor Activity

Patients with delirium may also exhibit disturbed psychomotor activity. Continuing research has indicated that there are several subtypes of delirium based on motor activity. These include a hyperactive-hyperalert subtype, a hypoactive-hypoalert subtype, and a mixed subtype that features components of the other two (Camus, Burtin, Simeone et al., 2000; Meagher & Trzepacz, 2000; Ross, Peyser, Shapiro et al., 1991). Patients with hyperactive-hyperalert delirium show evidence of sympathetic nervous system overactivity manifested in restlessness or agitation. This subtype is the most commonly recognized probably due to the expected presentation of agitation and/or inappropriate behavior (Inouye, Foreman, Mion et al., 2001). Characteristics of hyperactive-hyperalert delirium include plucking at bedclothes, wandering, verbal or physical aggression, increased alertness to stimuli, psychosis, and mood lability. Hypoactive-hypoalert patients appear lethargic and drowsy, respond slowly to questions, and do not initiate movement. This type of delirium is characterized by withdrawal from people and usual activities and decreased responsiveness to stimuli. Because they are quiet and withdrawn, the delirium in these patients is often overlooked or attributed to dementia, depression, or senescence (Casarett, Inouye, & American College of Physicians, 2001; Inouye et al., 2001). Differentiating delirium from normal aging processes, dementia, or depression requires careful and repeated assessment. A patient with a mixed subtype shows alternating periods of both types of behavior. Periods of lethargy may be seen as clinical improvements, when in fact the delirium may be continuing and increasing in severity (Clary & Krishnan, 2001; Milisen, Foreman, Godderis et al., 1998). A complete assessment of all symptoms of delirium is required before a change in behavior can be labeled as an improvement.

Emotional Disturbance

Patients with delirium may exhibit emotional disturbances. Anxiety, fear, depression, irritability, anger, euphoria, and apathy are common, with anxiety being the prevailing emotion. The delirious patient may be emotionally labile, rapidly and unpredictably shifting from one emotional state to another (APA, 1999b).

Prodromal and Subsyndromal Signs of Delirium

Some patients have prodromal symptoms such as restlessness, anxiety, irritability, distractibility, or sleep disturbance that progress to overt delirium over 1 to 3 days (APA, 1999b). Recently, Cole and colleagues described a condition known as subsyndromal delirium (SSD) (Cole, McCusker, Dendukuri et al., 2003). The symptoms of SSD are similar to prodromal symptoms, but the patient never progresses to overt delirium. Patients with SSD have the same risk factors and similar outcomes as those with delirium. These findings suggest that delirium is a spectrum disorder in which increasing numbers of symptoms are associated with increasingly adverse consequences. Patients noted to be exhibiting one or more prodromal symptoms or who report feeling “mixed up,” having difficulty judging the passing of time, and having difficulty thinking or concentrating should be assessed for potentially reversible causes of delirium, and appropriate interventions should be initiated.

Prevalence and Outcomes

Researchers have found that the prevalence of delirium ranges from 10% to 80% depending on the population and setting. The palliative care clinician is likely to encounter patients with delirium in a variety of practice settings. In the acute care environment, delirium has been noted in 10% to 30% of general medical and postsurgical patients (Samuels & Neugroschl, 2005; Wise, Hilty, Cerda et al., 2002; Goy & Ganzini, 2003), 40% to 80% of critical care patients (Ely, Inouye, Bernard et al., 2001b; Ely et al., 2001c), and 25% to 50% of cancer inpatients (Fann & Sullivan, 2003). Delirium has also been described in 20% to 45% of patients newly admitted to rehabilitation or skilled nursing facilities (Marcantonio et al., 2003; Pitkala et al., 2005; Samuels & Neugroschl, 2005). From 80% to 90% of terminally ill patients will develop delirium as death approaches (Gagnon, Charbonneau, Allard et al., 2002; Lawlor et al., 2000; Massie, Holland, & Glass, 1983).
The consequences of delirium, including medical and psychosocial morbidity, can be severe for both patients and caregivers. A significant number of patients who recover from delirium remember the episode and report distress from the experience, including anxiety, helplessness, and fear (Breitbart et al., 2002; Laitinen, 1996; Schofield, 1997). Caring for patients with hyperactive delirium has obvious stresses for both families and nurses; however, hypoactive delirium is also stressful, especially for families who regret premature separation from a patient who can no longer communicate (Casarett et al., 2001). Delirium robs patients and families of valuable time. Therefore, because delirium episodes are potentially reversible even in advanced stages of disease, prompt diagnosis and treatment are essential for improving outcomes and quality of life in patients with chronic and advanced illnesses (Lawlor, Fainsinger, & Bruera, 2000).

ETIOLOGY AND PATHOPHYSIOLOGY

Multiple causes have been identified in the development of delirium. Although delirium can occur in a previously healthy person, it is by far more common in people with premorbid conditions. Furthermore, the etiology of delirium is most likely multifactorial. Inouye’s Multifactorial Model for Delirium, consisting of predisposing factors (vulnerability) and precipitating factors (insults), provides a useful framework for predicting individual susceptibility for the development of delirium as well as for identifying potential factors that may have precipitated delirium (Inouye, 1998). Many potential predisposing and precipitating factors associated with delirium are listed in Box 24-2.
Box 24-2

American Psychiatric Press, Inc.

PREDISPOSING FACTORS

Demographic

Older age
Male gender

Lifestyle

Drug or alcohol dependence

General Health

Frailty
Impairments in perception (vision, hearing)
Poor nutritional status
Insufficient sleep
Depression

Chronic Illness

Neurological disorder (e.g., dementia, Parkinson’s disease, multiple sclerosis, stroke)
AIDS
Cancer
Endocrine disorder (hypothyroidism or hyperthyroidism, Cushing’s disease)
Organ system failure (renal, hepatic)

PRECIPITATING FACTORS

Environment

Physical restraint or immobility
Unfamiliar surroundings
Sensory overload or deprivation
Admission to intensive care unit

Disease Related

Metabolic abnormalities (hypercalcemia, hyponatremia, uremia)
Anemia
Hypoxemia
Infection or sepsis
Liver failure
Acute neurological disorder (hemorrhage, infection, metastasis, edema)

Physical Discomfort

Constipation
Urinary retention
Dyspnea
Pain
Sleep disturbance

Emotional or Spiritual

Anxiety
Guilt
Spiritual distress or unfinished business

Medications

Polypharmacy
Anticholinergics
Opioids (especially meperidine)
Steroids
Chemotherapeutic and immunotherapeutic agents
Sedatives-hypnotics (benzodiazepines, barbiturates)
H 2 blockers
Phenothiazines

Medication Withdrawal

Alcohol
Benzodiazepines
Nicotine
Opioids
Steroids
Data from Burns, A., Gallagley, A., & Byrne, J. (2005). Delirium. J Neurol Neurosurg Psychiatry, 75, 362-367; Clary, G.L. & Krishnan, K.R. (2001). Delirium: Diagnosis, neuropathogenesis, and treatment. J Psychiatric Pract, 7(5), 310-323; Friedlander, M.M., Brayman, Y., & Breitbart, W.S. (2004). Delirium in palliative care. Oncology (Huntington), 18(12), 1541-1550; discussion 1551-1543; Inouye, S.K. (1998). Delirium in hospitalized older patients: Recognition and risk factors. J Geriatr Psychiatry Neurol, 11, 118-125; Johnson, M.H. (2001). Assessing confused patients. J Neurol Neurosurg Psychiatry, 71(Suppl 1), i7-i12; Samuels, S.C. & Neugroschl, J.A. (2005). Delirium. In B.J. Sadock & V.A. Sadock (Eds.). Kaplan & Sadock’s comprehensive textbook of psychiatry (8th ed., pp. 1054-1067). Philadelphia: Lippincott Williams & Wilkins; and Tune, L.E. (2000). Delirium. In C.E. Coffey & J.L. Cummings (Eds.). Textbook of geriatric neuropsychiatry (2nd ed., pp. 441-452). Washington, DC: American Psychiatric Press, Inc.
Very little is known about the underlying pathophysiological mechanisms of delirium, but analysis of symptomatology and known precipitating factors has lead to at least two explanatory models (Breitbart & Cohen, 2000). In the first model, delirium is seen as a global and nonspecific disorder of the brain characterized by generalized dysfunction in cerebral metabolism. The second model proposes that derangements in specific neurotransmitter systems precipitate brain pathology. There is evidence to support both models. Delirium probably represents a variety of disorders in which either specific or multiple interacting neurotransmitter systems (Table 24-1) are impaired as a result of aberrant metabolic activity, hypoxia, or exogenous agents (Samuels & Neugroschl, 2005).
TABLE 24-1 Possible Neurochemical Changes in Delirium
Data from Balan, S., Leibovitz, A., Zila, S.O., et al. (2003). The relation between the clinical subtypes of delirium and the urinary level of 6-SMT. J Neuropsychiatry Clin Neurosci, 15(3), 363-366; Clary, G.L. & Krishnan, K.R. (2001). Delirium: Diagnosis, neuropathogenesis, and treatment. J Psychiatric Pract, 7(5), 310-323; Flacker, J.M. & Lipsitz, L.A. (1999). Neural mechanisms of delirium: Current hypotheses and evolving concepts. J Gerontol. Series A, Biological Sciences and Medical Sciences, 54A(6), B239-B246; Lewis, M.C. & Barnett, S. R. (2004). Postoperative delirium: The tryptophan dysregulation model. Medical Hypotheses, 63(3), 402-406; Michaud, L., Burnand, B., & Stiefel, F. (2004). Taking care of the terminally ill cancer patient: Delirium as a symptom of terminal disease. Ann Oncol, 15(Suppl 4), iv199-iv203; Samuels, S.C. & Neugroschl, J.A. (2005). Delirium. In B.J. Sadock & V.A. Sadock (Eds.). Kaplan & Sadock’s comprehensive textbook of psychiatry (8th ed., pp.1054-1067). Philadelphia: Lippincott Williams & Wilkins; Trzepacz, P. T. (2000). Is there a final common neural pathway in delirium? Focus on acetylcholine and dopamine. Semin Clin Neuropsychiatry, 5(2), 132-148; and van der Mast, R.C., & Fekkes, D. (2000). Serotonin and amino acids: Partners in delirium pathophysiology? Semin Clin Neuropsychiatry, 5(2), 125-131. © 2005
System and Function Alteration Precipitating Factors Sequelae
Cholinergic System ↓ Acetylcholine (ACh) Hypoxia, hypoglycemia, thiamine deficiency, anticholinergic medication, increased cytokines Decreased ability to focus, maintain, or shift attention
Attention, arousal, memory, rapid eye movement sleep Impaired cognition
Dopamine System ↑ Dopamine Opioids, hypoxia, hypoglycemia Increased motor activity, perceptual impairments, stereo-typical behaviors, mood alteration
Movement, memory, motivation, emotional response, perception Dopamine has a reverse-parallel relationship with cholinergic system (decreases in ACh are associated with increases in dopamine)
γ- Aminobutyric Acid (GABA) System ↑ GABA activity Hepatic failure, elevated serum ammonia levels, benzodiazepine intoxication Hypoactive-hypoalert features
Major inhibitory neurotransmitter ↓ GABA activity Benzodiazepine, alcohol withdrawal Hyperactive-hyperalert features
Serotonin System ↓ Serotonin (5-hydroxytryptamine [5-HT]) Reduced tryptophan (5-HT precursor) availability secondary to illness or surgery (catabolic states, stress) Impaired memory, somnolence, hypoactive-hypoalert features
Modulation of pain, mood, sleep, emotion, cognition, memory, and attention; precursor of melatonin
↑ Serotonin Liver failure, multiple serotonin agonist use Cognitive dysfunction, tremor, restlessness, sleep disturbance hyperactive-hyperalert features

ASSESSMENT AND MEASUREMENT

Because of differences in presentation and fluctuation of symptoms, delirium is difficult to detect. In fact, research has shown that clinicians caring for patients do not recognize delirium in a majority of cases (Inouye et al., 2001; Laurila et al., 2004). Because diagnosis depends on recognition of a constellation of symptoms in a temporal context, systematic evaluation of vulnerable patients is warranted. Many delirium assessment scales have been developed, some intended for clinical practice and others for research (APA, 1999b). Several review articles are available to provide an overview of the variety of instruments available for detecting, diagnosing, and rating delirium (Hjermstad, Loge, & Kaasa, 2004; Schuurmans, Deschamps, Markham et al., 2003a; Smith, Breitbart, & Platt, 1995). In general, the steps to a comprehensive plan for early detection and monitoring of delirium include regular screening for the presence of cognitive dysfunction, confirmation of diagnosis, and evaluation of severity over time (Cook, 2004, Hjermstad et al., 2004, Milisen, Steeman, & Foreman, 2004; Schuurmans et al., 2003a). The following section discusses those tools most often used in clinical practice.

Screening Instruments

Screening instruments identify the presence of cognitive impairment but are not diagnostic of delirium. They are very helpful for identifying those patients who require additional evaluation. These scales may also be useful for monitoring improvement or deterioration in cognitive status in patients with delirium.

Mini-Mental State Examination

This is one of the most frequently used tools for the clinical evaluation of cognitive changes. It assesses orientation, instantaneous recall, short-term memory, attention, constructional capacities, and use of language (oral and written). A score of less than 24 of a possible 30 indicates cognitive impairment. Because the Mini-Mental State Examination is widely used in practice and research, data are available to support use of scores to rate the severity of impairment as follows: 24 to 30, no impairment; 18 to 23, mild impairment; and 0 to 17, severe impairment (Tombaugh & McIntyre, 1992).

NEECHAM Confusion Scale

This scale was designed for rapid and unobtrusive assessment and monitoring of acute confusion by the bedside nurse (Neelon, Champagne, Carlson et al., 1996). It can detect changes in mental status as well as physiological and behavioral manifestations of delirium, including those indicative of hypoactive-hypoalert delirium. A score of less than 25 of a possible 30 indicates the presence of cognitive impairment. Repeated measures can be used to monitor changes in mental status (Csokasy, 1999; Milisen et al., 1998; Rapp, 2001).

Delirium Observation Screening Scale

Like the NEECHAM, the Delirium Observation Screening Scale (DOS) was developed to assist nurses in early recognition of delirium based on observations during regular care (Schuurmans, Shortridge-Baggett, & Duursma, 2003b). The 25-item scale, based on DSM-IV criteria for delirium, assesses disturbances in consciousness; attention and concentration; thinking, memory, and orientation; psychomotor activity, sleep-wake pattern; mood; and perception. A reduced, 13-item version of the DOS shows promising results (Schuurmans, Donders, Shortridge-Baggett et al., 2002). The DOS is most applicable to inpatient versus outpatient settings since the scale needs to be administered over three consecutive shifts.

Nursing Delirium Screening Scale

The Nursing Delirium Screening Scale was developed for clinical use as a continuous delirium assessment instrument in busy inpatient units (Gaudreau, Gagnon, Harel et al., 2005). The scale contains five items (disorientation, inappropriate behavior, inappropriate communication, illusions or hallucinations, and psychomotor retardation). Each item is rated on a 0-to-2 scale on each of three shifts. Scores above 2 on any shift indicate the possibility of delirium.

Diagnostic Instruments

Diagnostic instruments are used along with the clinical and cognitive evaluation to make a formal diagnosis of delirium. The following are two examples of diagnostic tools.

Confusion Assessment Method

This valid and reliable tool was designed for efficient and effective detection of delirium (Inouye, van Dyck, Alessi et al., 1990). The four core DSM-IV criteria for delirium can be assessed by nonpsychiatric clinicians in less than 5 minutes. A version of the Confusion Assessment Method (CAM) for critical care patients (CAM-ICU) is also available (Ely et al., 2001b, 2001c). The CAM is useful to confirm delirium in patients who score less than 25 on the NEECHAM Confusion Scale or less than 24 on the Mini-Mental State Examination (Rapp, 2001).

Delirium Rating Scale–Revised-98

This scale, a delirium-specific tool, is a revision of the Delirium Rating Scale (DRS) (Trzepacz, 1999; Trzepacz et al., 2001). The DRS-R-98 contains 16 items: 3 are diagnostic in accordance with DSM-IV criteria, and 13 are severity-based on common symptoms found in delirious patients. The scale yields a total score (maximum of 46) that is diagnostic of delirium and a severity score (maximum of 39) that can be used to rate severity of symptoms over time. Higher severity scores indicate increased delirium.

Delirium Symptom Severity Rating Scales

Delirium symptom severity rating scales are designed to rate the severity of this syndrome. After delirium is diagnosed, these tools are useful for monitoring the effectiveness of interventions.

Memorial Delirium Assessment Scale

This scale was designed to quantify the severity of delirium symptoms for use in clinical intervention studies (Breitbart, Rosenfeid, Roth et al., 1997); it is also useful when assessing delirium in clinical populations (Lawlor et al., 2000). The Memorial Delirium Assessment Scale assesses arousal and level of consciousness, cognitive functioning (memory, attention, orientation, disturbances in thinking), and psychomotor activity. Completion requires about 10 minutes. Scores range from 0 to 30, with higher scores indicating more severe delirium.

Delirium Rating Scale–Revised-98

See earlier description.

Delirium Index

The Delirium Index was developed to specifically measure changes in the severity of symptoms in patients already diagnosed with delirium (McCusker, Cole, Bellavance et al., 1998; McCusker, Cole, Dendukuri et al., 2004). The measure is based on direct observation of the patient and does not rely on information from family members, other care providers, or documentation in the medical record. The Delirium Index contains seven items (each scored between 0 and 3) that yield scores between 0 and 21. Symptom domains include attention, thought, consciousness, orientation, memory, perception, and psychomotor activity. Higher scores indicate increased severity.
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