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Delirium and acute confusional states: Prevention, treatment, and prognosis

Author: Joseph Francis, Jr, MD, MPH

Section Editors: Michael J Aminoff, MD, DSc, Kenneth E Schmader, MD
Deputy Editor: Janet L Wilterdink, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2018. | This topic last updated: Aug 13, 2014.

INTRODUCTION — Delirium is an acute confusional state characterized by an alteration of

consciousness with reduced ability to focus, sustain, or shift attention. This results in a cognitive or
perceptual disturbance that is not better accounted for by a preexisting, established, or evolving
dementia. Delirium develops over a short period of time (usually hours to days) and tends to fluctuate
during the course of the day. Delirium is typically caused by a medical condition, substance
intoxication, or medication side effect.

Delirium is considered by some to be a specific type of confusional state that is characterized by

increased vigilance along with psychomotor and autonomic overactivity and manifested as agitation,
tremulousness, and hallucinations. In this discussion, however, the term delirium will be used
synonymously with acute confusional state and will include states characterized by somnolence and
decreased arousal, so-called hypoactive delirium. (See "Diagnosis of delirium and confusional states",
section on 'Definition and terminology'.)

The management of delirium is based primarily upon expert consensus and observational studies, and
only a small number of controlled clinical trials, which are difficult to perform in patients with cognitive
impairment. The preponderance of evidence is most compelling for primary prevention of delirium
using non-pharmacologic, multicomponent approaches targeted broadly at high risk patients [1,2].
Prevention and therapy of delirium are based on the following principles:

● Avoiding factors known to cause or aggravate delirium, such as multiple medications,

dehydration, immobilization, sensory impairment, and sleep disturbance

● Identifying and treating the underlying acute illness

● Providing supportive and restorative care to prevent further physical and cognitive decline

● Where appropriate, controlling dangerous and severely disruptive behaviors using low dose, short
acting pharmacologic agents so the first three steps can be accomplished
The prevention, treatment, and prognosis of delirium will be reviewed here. The definition,
epidemiology, pathogenesis, clinical features, and diagnosis of delirium are discussed separately.
(See "Diagnosis of delirium and confusional states".)

PREVENTION — No intervention or group of interventions reliably prevents delirium; however,

multicomponent, nonpharmacologic interventions that manage many of the modifiable risk factors
appear to reduce the incidence of delirium [3].

Modifying risk factors — A number of factors have been identified as causing or contributing to
delirium in at risk patients. (See "Diagnosis of delirium and confusional states".)

Examples of interventions designed to mitigate risk factors for delirium include:

● Orientation protocols - Provision of clocks, calendars, windows with outside views, and verbally
re-orienting patients may mitigate confusion that results from disorientation in unfamiliar
environments.

● Cognitive stimulation - Patients with cognitive impairment, in particular, may benefit from activity
such as regular visits from family and friends. At the same time, sensory overstimulation should
be avoided, particularly at night.

● Facilitation of physiologic sleep – Nursing and medical procedures, including the

administration of medications, should be avoided during sleeping hours when possible. Night-time
noise should be reduced. One randomized trial found that the use of earplugs at night was
associated with a lower incidence of confusion in ICU patients [4].

● Early mobilization and minimized use of physical restraints for patients with limited
mobility - One study in mechanically ventilated, critically ill patients found that early institution of
physical and occupational therapy along with consequent interruption in use of sedatives, was a
lower rate of hospital days with delirium [5].

● Visual and hearing aids for patients with these impairments

● Avoiding and/or monitoring the use of problematic medications - Medications are often
implicated in precipitating delirium, particularly in those already at risk (table 1). In one systematic
review, the authors concluded that benzodiazepines should be avoided in high risk patients, while
caution should be used in prescribing opioids, dihydropyridines, and antihistamines [6].

In one large cluster-randomized control study based in nursing homes, implementation of a

computerized system to identify the use of problematic medications and trigger a medication
review was associated with a lower incidence of delirium (HR = 0.42) [7].

● Avoiding and treating medical complications – A number of medical conditions are known to
cause or aggravate delirium; these should be managed aggressively and prevented where
possible.

Some studies have focused specifically on early volume repletion for patients with delirium. While
one small study failed to show a benefit for hydration management on the incidence of delirium in
a long-term care setting, the small number of patients (98) and short time period of intervention (4
 weeks) limited the ability of this study to demonstrate efficacy [8].

Hypoxemia and infections are other common complications in high-risk settings and patients.
These may contribute to delirium and should be actively monitored for and treated when
identified. An interventional program administered via a geriatric consultant team that emphasized
avoiding medical complications achieved a one-third reduction in the incidence of delirium among
126 elderly patients undergoing hip surgery [9].

● Managing pain – Pain may be a significant risk factor for delirium. The use of nonopioid
medications should be used where possible, as these are less likely to aggravate delirium.
Clinicians must balance the benefits of using opioids to treat significant pain with the potential for
an opioid-related delirium.

Studies in patients undergoing surgery suggest that pre-emptive pain treatment may reduce the
incidence of delirium. In one study of 58 older patients, administration of ketamine (given as a
single dose during induction of anesthesia for cardiac surgery) was associated with a lower rate
of postoperative delirium (3 versus 31 percent) [10]. In another study, fascia iliaca compartment
block after hip surgery was associated with a reduced incidence of postoperative delirium in
intermediate-risk, but not in high-risk patients [11]. However, making generalized
recommendations from such studies is difficult, because of the small sample, inconsistent use of
nonpharmacological interventions, and lack of information regarding long-term outcomes [12].

Certain classes of opioids are probably best avoided in older patients and others prone to
delirium. Meperidine in particular, has been shown in multiple prospective studies to increase the
risk for delirium [13-15].

Cancer patients with terminal delirium and pain may benefit from switching from shorter-acting
opioids to long-acting agents such as methadone [16]. Clinicians should also consider the
possibility that opioid-induced hyperalgesia may cause breakthrough pain and consider using
nonopioid analgesia for pain control. (See "Prevention and management of side effects in patients
receiving opioids for chronic pain".)

Use of nursing protocols to better manage pain has been demonstrated to reduce the severity
and duration, but not the incidence, of delirium [17].

In one study, a multicomponent intervention used standardized protocols to screen and control for six
risk factors for delirium in 852 hospitalized patients aged 70 or older: cognitive impairment, sleep
deprivation, immobility, visual impairment, hearing impairment, and dehydration [18]. Interventions
such as those listed above were targeted to the identified risk factors. This program resulted in a
significant reduction in the number of delirium episodes compared with usual care (62 versus 90) and
in the total number of days with delirium (105 versus 161); there was no effect upon delirium severity
or the rate of recurrence. The investigators have since reported that community hospitals were able to
successfully implement this program when there was a commitment of resources by hospital
leadership and appropriate adaptation of protocols to local needs [19]. Subsequent randomized
studies have confirmed that such multicomponent interventions can reduce the incidence of delirium
and/or related complications [20-22].
Medications to prevent delirium — The available evidence does not support the use of medications
to prevent delirium in the acute care or intensive care or postoperative care settings [23-25].
Investigators continue to study the potential benefit of cholinesterase inhibitors, antipsychotic agents,
and others:

● Cholinesterase inhibitors (e.g., rivastigmine; donepezil) has been proposed as a means to

prevent delirium in selected patients and high risk settings (eg, older patients with or without
dementia, postoperative and post-stroke settings) [26,27]. However, clinical trials have not
demonstrated a reduction in the prevalence or incidence of delirium, and side effects have been
greater in patients receiving these medications [27-31].

● Antipsychotic agents, given prophylactically and in low dose have been studied in the
postoperative setting, and have been associated with inconsistent, and at best, modest benefits in
the incidence, severity, and duration of delirium [32-37]. In one of these studies, treatment was
associated with increased severity and longer duration of delirium [37]. A 2013 systematic review
and meta-analysis of six studies concluded that such treatment reduced the incidence of delirium,
but not the severity or duration; nor were the incidence of associated adverse events reduced
[35]. In this analysis, second-generation antipsychotics appeared to be more beneficial compared
to haloperidol.

● Gabapentin, in pilot study, reduced the incidence of postoperative delirium, perhaps by reducing
pain and opioid administration [38].

● Melatonin shows promise in the prevention of delirium. The melatonin agonist, ramelteon, was
studied in a randomized trial of 67 older inpatients with serious medical illness [39]. Compared to
placebo, ramelteon 8 mg was associated with a lower risk of delirium (3 versus 32 percent)
despite its lack of effect on sleep parameters. In another randomized study, administration of low
dose melatonin (0.5 mg) in 145 older inpatients was associated with a lower incidence of delirium;
long-term outcomes were not assessed [40]. Finally, in a randomized trial of 222 patients
undergoing hip surgery, preoperative administration of melatonin was associated with a reduced
incidence of postoperative delirium (9 versus 33 percent) [41].

● Analgesics to control pain may reduce the incidence or severity of delirium, as discussed in the
section above.

MANAGEMENT — The principles underlying the management of delirium are summarized in the
Algorithm (algorithm 1). The algorithm includes two pathways that are followed simultaneously: one to
manage the behavior disturbance; and another to find and treat the underlying medical disorder. An
important caveat is that the symptoms of delirium can have a prolonged duration extending many
weeks into the post-acute period, after the underlying causes and risk factors have been corrected.

Treatment of underlying conditions — Virtually any medical condition can precipitate delirium in a
susceptible patient; multiple underlying conditions are often found [42]. When the underlying acute
illness responsible for delirium is identified, specific therapy is directed toward the medical condition.
(See "Acute toxic-metabolic encephalopathy in adults", section on 'Specific etiologies'.)

The conditions noted most commonly in prospective studies of delirium include:

 ● Metabolic encephalopathy – These include the following which are discussed in detail separately.
(See "Acute toxic-metabolic encephalopathy in adults".)

• Fluid and electrolyte disturbances (dehydration, hyponatremia/hypernatremia,

hypo/hypercalcemia)

• Infections (sepsis, urinary tract, respiratory tract, skin and soft-tissue)

• Organ failure (uremia, liver failure, hypoxemia/hypercarbia)

• Hypoglycemia

● Drug toxicity - Drug toxicity causes or contributes to approximately 30 percent of all cases of
delirium (table 1) [43]. Clinicians must be aware that delirium can occur even with "therapeutic"
levels of such agents as digoxin or lithium, particularly in at risk patients.

Certain acute drug poisoning syndromes can be rapidly treated with the appropriate antidote.
(See "General approach to drug poisoning in adults".)

● Withdrawal from alcohol and sedatives - The treatment of alcohol withdrawal is discussed
separately. (See "Management of moderate and severe alcohol withdrawal syndromes", section
on 'Management'.)

While Wernicke encephalopathy is not common, many older hospitalized patients have biochemical
evidence of thiamine deficiency [44]. In addition, chronic alcoholism is often difficult to detect in this
population, and symptoms of persistent alcoholic delirium may be difficult to distinguish from those of
Wernicke encephalopathy [45]. Thiamine supplementation is inexpensive and virtually risk-free; it
should be provided to all hospitalized patients with evidence of nutritional deficiency. (See "Wernicke
encephalopathy".)

Supportive medical care — The delirious patient is at risk for complications of immobility and
confusion, leading to a high prevalence of irreversible functional decline.

It has long been assumed that the outcome of delirium could be improved by earlier identification of
the disorder and comprehensive intervention to treat underlying causes and prevent subsequent
complications such as immobility, aspiration, and skin breakdown. Unfortunately, there are few
controlled studies. One study found that early identification and comprehensive geriatric consultation
for patients with established delirium had little impact on length of stay, functional outcome, or survival
[46]; another found that multicomponent interventions shortened the duration of delirium but had no
impact on mortality or nursing home use [47]. Stronger evidence supports the use of these
interdisciplinary efforts for prevention of delirium. (See 'Modifying risk factors' above.)

Nonetheless, an interdisciplinary approach to delirium should focus upon maintaining adequate

hydration and nutrition, enhancing mobility and range of motion, treating pain and discomfort,
preventing skin breakdown, ameliorating incontinence (seen in over half of delirious patients), and
minimizing the risk of aspiration pneumonitis.

This team approach should also include family or other caregivers who may feel frightened or
exhausted; delirium can be the "last straw" for those who have been caring for the demented.
Caregiver resources must be realistically assessed.

Because delirium may require weeks or months to fully resolve, management often extends into
subacute settings [48,49]. Transfers of care to new settings are periods of particular vulnerability for
older patients, and it is important to effectively communicate information about mental status to the
accepting treatment team [50].

Managing agitation — Managing disruptive behavior, particularly agitation and combative behavior,
is a challenging aspect of delirium therapy. This hyperactive delirium is less common in older patients,
and when it occurs, alternates with periods of hypoactive delirium, which may be less obvious to the
clinical staff [51]. Periods of disruptive and hyperactive behavior place the patient at risk for falls,
wandering off, or inadvertently removing intravenous lines and feeding tubes.

When delirium is manifest by agitation, symptom control is occasionally necessary to prevent harm or
to allow evaluation and treatment. While nonpharmacologic interventions should be the mainstay of
treatment, a cautious trial of psychotropic medication is warranted in these circumstances.
Unfortunately, there are limited data to guide treatment as the available studies have significant
methodologic limitations [24,25].

Nonpharmacologic interventions — Mild confusion and agitation may respond to interpersonal

and environmental manipulations. The hospital environment, characterized by high ambient noise,
poor lighting, lack of windows, frequent room changes, and restraint use, often contributes to
worsening confusion. Special units that address these concerns have improved the functional
outcomes of hospitalization in such frail patients [52]. Frequent reassurance, touch, and verbal
orientation can lessen disruptive behaviors; family members or other familiar persons are preferred,
but professional sitters can also be used to effect. Delusions and hallucinations should be neither
endorsed nor challenged. Other specific interventions are discussed above. (See 'Modifying risk
factors' above.)

Physical restraints should be used only as a last resort, if at all, as they frequently increase agitation
and create additional problems, such as loss of mobility, pressure ulcers, aspiration, and prolonged
delirium. In one study, restraint-use among patients in a medical inpatient unit was associated with a
three-fold increased odds of persistent delirium at time of hospital discharge [53]. Alternatives to
restraint use, such as constant observation (preferably by someone familiar to the patient such as a
family member), may be more effective.

Neuroleptic medications — When indicated, neuroleptic agents are generally used to treat severe
agitation in the patient with delirium, in part because effective alternatives are not available. However,
there are very limited data that support their use [24,54,55]. In a randomized, placebo-controlled,
study low-dose haloperidol was administered as prophylactic treatment to older hospitalized patients
after hip surgery [32]. As described above, treatment did not reduce the incidence of delirium, but did
reduce the severity and duration of episodes. One trial randomly assigned 30 individuals admitted to
the hospital with advanced AIDS and subsequent development of delirium to haloperidol, lorazepam
or chlorpromazine [56]. Treatment with either haloperidol or chlorpromazine (but not lorazepam)
resulted in significant improvement in delirium compared to baseline. Finally, in a randomized study of
101 patients screened for subsyndromal delirium after cardiac surgery, administration of risperidone
(0.5 mg every 12 hours) was associated with a reduced incidence of clinical delirium (34 versus 14
percent) [57].

Because of the longer clinical experience with haloperidol, it remains the standard therapy in this
setting [58]. The newer atypical antipsychotic agents, quetiapine, risperidone, ziprasidone, and
olanzapine have fewer side effects, and in small studies they appear to have similar efficacy to
haloperidol [59-61]. A meta-analysis of three small studies that compared haloperidol with risperidone
and olanzapine found that the three agents were similarly effective in treating delirium [62]. A small
clinical trial compared escalating doses of quetiapine to placebo as add-on treatment to as-needed
haloperidol in 36 patients in the intensive care unit with delirium [63]. Quetiapine was associated with
a shorter duration of delirium, reduced agitation, and higher rates of discharge to home after
hospitalization. In contrast, a randomized trial comparing haloperidol, ziprasidone, and placebo in ICU
patients found that active treatment did not improve outcomes when measured by number of days
alive without altered mental status or the incidence of adverse events [55].

Extrapyramidal side effects are higher in patients treated with high-dose haloperidol (>4.5mg per day),
but were similar among patients treated with low-dose haloperidol, olanzapine, and risperidone [62]. A
systematic review of four trials reached similar conclusions [64]. Sedation can also occur as a side
effect of these medications [63]. Haloperidol is associated with a low frequency of sedation and
hypotension and should also be avoided in patients with underlying parkinsonism, for whom atypical
antipsychotics are preferred. (See "Prognosis and treatment of dementia with Lewy bodies" and
"Management of nonmotor symptoms in Parkinson disease".)

Based on limited evidence, it is recommended that low-dose haloperidol (0.5 to 1.0 mg) be used to
control agitation or psychotic symptoms, up to a maximum dose of 5 mg per day. Haloperidol can be
administered orally, intramuscularly or intravenously. The onset of action is 30 to 60 minutes after
parenteral administration or longer with the oral route. An immediate response is not expected.
Intravenous haloperidol has been associated with clinically significant QT prolongation requiring
additional precautions with its use. (See "Acquired long QT syndrome: Definitions, causes, and
pathophysiology", section on 'Medications'.)

Short term use of antipsychotic agents is advised as these agents have been associated with a higher
risk of mortality and possibly stroke when used in patients with dementia [65]. (See "Management of
neuropsychiatric symptoms of dementia".)

Benzodiazepines — Benzodiazepines have a limited role in the treatment of delirium; they are
primarily indicated in cases of sedative drug and alcohol withdrawal or when neuroleptic drugs are
contraindicated. Surveys of practicing clinicians suggest that benzodiazepines are overprescribed for
patients with delirium [66].

(See "Sedative-analgesic medications in critically ill adults: Selection, initiation, maintenance, and
withdrawal".)

Benzodiazepines (eg, lorazepam 0.5 to 1.0 mg) have a more rapid onset of action (five minutes after
parenteral administration) than the antipsychotics, but they can worsen confusion and sedation [56]. In
a prospective study of intensive care unit (ICU) patients, lorazepam was an independent risk factor for
incident delirium, increasing the risk by approximately 20 percent [67]. A systematic review of
benzodiazepine use in delirium found two studies comparing benzodiazepine versus neuroleptic
agents; one study found no advantage, the other found decreased effectiveness of benzodiazepines
compared with neuroleptics [68]. In two randomized trials of sedative treatment in mechanically
ventilated ICU patients, the benzodiazepine midazolam was associated with significantly more
delirium compared with dexmedetomidine treatment (77 versus 54 percent) [69], while similar
outcomes were observed lorazepam and dexmedetomidine [70].

Cholinesterase inhibitors — Cholinesterase inhibitors do not have a role in the treatment or

symptom management of delirium.

A randomized clinical trial compared rivastigmine to placebo in 104 hospitalized intensive care
patients with delirium who were also prescribed haloperidol. The trial was stopped early because of
higher mortality in the rivastigmine group (22 versus 8 percent) [71]. Median duration of delirium was
also longer in the rivastigmine group (5 versus 3 days, p = 0.06). Cholinesterase inhibitors are also not
helpful in the prevention of delirium. (See 'Prevention' above.)

Managing pain — In the appropriate setting (postoperative, post-trauma), the role of pain as a
contributor to delirium and agitation should be considered, and analgesia provided. As discussed
above, therapies to reduce pain should be administered with some caution as they also have the
potential to contribute to delirium. (See 'Modifying risk factors' above.)

In one randomized study of 53 patients after cardiac surgery, those who received morphine (5 mg IM)
had more rapid improvement of agitation and were less likely to require additional sedatives than
those who were administered haloperidol (5 mg IM) [72]. Other outcomes were not assessed.

Hypoactive delirium — In general, symptomatic treatment is not used for hypoactive delirium.

One study suggested that patients with hypoactive delirium have a similar response to treatment with
haloperidol as those who were agitated [73]. Other case reports and one uncontrolled case series
have suggested that treatment with the stimulant drug methylphenidate may be associated with
improved alertness and cognition [74-76]. However, in the absence of stronger evidence,
psychostimulants such methylphenidate or modanifil cannot be recommended for treating hypoactive
delirium, because of the potential risk of precipitating agitation or worsening psychotic symptoms [77].

Terminal delirium — Delirium is common in palliative care settings and causes significant distress to
family members [78]. Underlying causes are often multifactorial, but up to 50 percent of episodes are
reversible, particularly when the underlying cause is either dehydration or medication-related [79,80].

Hyperactive as well as hypoactive presentations of terminal delirium are both common; the former
may require management with neuroleptic medication, usually haloperidol, as described above
[81,82]. (See 'Neuroleptic medications' above.)

In one small case series, methadone appeared to be effective in the treatment of both refractory pain
and terminal delirium when neuroleptic medication was not [16]. Midazolam sedation has also been
described as a therapeutic option in this setting [83,84]. (See "Overview of managing common non-
pain symptoms in palliative care", section on 'Palliative sedation'.)

Ethical considerations — The treatment of patients with delirium is complicated by the critical nature
of their illness and their impaired capacity to make decisions. The doctrine of "implied consent" allows
the emergency treatment of patients with delirium in order to stabilize a life-threatening process [85].
However, it is important to document the assessment of cognitive abilities and decision-making
capacity. Current practice leaves considerable room for improvement. As an example, in a prospective
study of 173 medical and surgical procedures performed in patients with delirium at a university
hospital, investigators found no documented assessments of competency or decision capacity, and
cognitive assessments in only 4 percent of cases [86]. No informed consent was documented in 19
percent of procedures, and surrogates were used in only 20 percent.

Relying upon implied consent or substituted judgment in cases of delirium introduces other difficulties
since clinicians and proxies do not always make the same decisions as patients. Every effort should
be made to determine what the patient’s own treatment preferences are, and not assume that
decision-making capacity is “all or none”. In some cases, for example, psychopharmacological
treatment of delirium may restore sufficient mental capacity to allow a discussion of treatment
preferences [87]. In addition, since delirium typically fluctuates in severity, there may also be periods
of lucidity in which a discussion of treatment preferences may take place.

OUTCOMES — Delirium has an enormous impact upon the health of older persons. Patients with
delirium experience prolonged hospitalizations, functional and cognitive decline, higher mortality and
higher risk for institutionalization, even after adjusting for baseline differences in age, comorbid illness,
or dementia [88-95].

Mortality — Mortality associated with delirium is high. A report of pooled results from several studies
estimated the one and six month mortality to be 14 and 22 percent, respectively, approximately twice
that of patients without delirium [96]. These findings were likely due in part to the presence of
concomitant dementia and severe physical illness (eg, sepsis). However, prospective observational
studies that adjusted for dementia and other potential confounding factors still found that delirium was
an independent marker for mortality at 6 or 12 months after hospitalization [88,97-100].

Studies have also found a relationship between the duration of delirium and mortality [101,102]. In one
study, protracted delirium (ie, persistent symptoms of confusion at six months) was associated with
increased one-year mortality compared with those whose symptoms had resolved more quickly,
regardless of whether or not patients also had underlying dementia [100].

Persistant cognitive dysfunction — Signs of delirium may persist for 12 months or longer,
particularly in those with underlying dementia [103].

One long-term follow-up study found that after two years, only one-third of patients who had
experienced delirium still lived independently in the community [104]. Another prospective study of
225 patients after heart surgery, found that those who experienced delirium were more likely to have
persistent drop in MMSE scores over baseline at six months compared to those who did not suffer
delirium (40 versus 24 percent); at 12 months the differences were not quite statistically significant (31
versus 20 percent, p=0.055) [105]. In a study of 821 patients admitted to medical or surgical intensive
care, the duration of delirium was associated with worse cognitive function at 3 and 12 months. While
only 6 percent had cognitive impairment at baseline, at 12 months, 34 percent had deficits that were
similar to patients with moderate traumatic brain injury [106]. Other studies have found that patients
with delirium are more likely to have long-term cognitive problems than hospitalized patients who did
not suffer from delirium [107]. Thus, although delirium is considered potentially reversible, impairments
may be prolonged and perhaps permanent, particularly in frail, older patients.
Episodes of delirium during hospitalization adversely affect the course of the disease in patients with
Alzheimer disease (AD). Of 263 participants in the Massachusetts Alzheimer Disease Research
Center patient registry who experienced hospitalization, 56 percent developed delirium during
hospitalization. Although the AD patients with and without delirium had similar rates of cognitive
decline prior to hospitalization, after hospitalization, deterioration proceeded at twice the rate in the
year after hospitalization compared with patients who did not develop delirium. The higher rate of
cognitive decline was evident for up to five years after the hospital stay [108,109]. Patients with AD
who experienced delirium also had an increased risk of death and institutionalization [94].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The
Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at
the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and who
prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and
are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)

● Basics topic (see "Patient education: Delirium (confusion) (The Basics)")

● Beyond the Basics topic (see "Patient education: Delirium (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS — Delirium is an acute confusional state characterized by

an alteration of consciousness with reduced ability to focus, sustain, or shift attention.

● Effective measures to prevent delirium include avoiding where possible, those factors known to
cause or aggravate delirium, orientation protocols, environmental modification and
nonpharmacologic sleep aids, early mobilization and minimizing use of physical restraints, and
visual and hearing aids. (See 'Prevention' above.)

● Prophylactic medications (cholinesterase inhibitors, antipsychotic agents) have not been

conclusively demonstrated to prevent delirium. (See 'Prevention' above.)

● Thiamine supplementation should be considered in all patients with delirium. (See 'Treatment of
underlying conditions' above.)

● When the underlying acute illness responsible for delirium is identified, specific therapy is directed
toward that condition as the most effective means of reversing the delirium. (See 'Treatment of
underlying conditions' above.)

● Physical restraints should be used only as a last resort, if at all, as they frequently increase
agitation and create additional problems, such as loss of mobility, pressure ulcers, aspiration, and
prolonged delirium. (See 'Nonpharmacologic interventions' above.)

● Frequent reassurance, touch, and verbal orientation from familiar persons can lessen disruptive
behaviors. (See 'Nonpharmacologic interventions' above.)
● A cautious trial of psychotropic medication should be reserved for treatment of severe agitation or
psychosis with the potential for harm. In this setting, we suggest using low-dose haloperidol (0.5
to 1.0 mg po or IM) (Grade 2C). (See 'Neuroleptic medications' above.)

• Haloperidol is associated with a low frequency of sedation and hypotension.

- Haloperidol should be avoided in patients with underlying parkinsonism, for whom

atypical antipsychotics (eg, quetiapine) are preferred.

- Short term use of antipsychotic agents is advised.

● Benzodiazepines should be avoided in patients with or at risk for delirium, except in cases of
sedative drug and alcohol withdrawal or when neuroleptic medications are contraindicated. (See
'Benzodiazepines' above.)

Cholinesterase inhibitors are not effective in preventing or treating the symptoms of delirium, and
often create undesirable side effects. (See 'Cholinesterase inhibitors' above.)

● Delirium may require weeks or months to fully resolve. Episodes of delirium may adversely affect
the course of the disease in patients with Alzheimer disease. Delirium appears to be associated
with increased short and long-term mortality (See 'Outcomes' above.)

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Topic 4823 Version 10.0

GRAPHICS

Drugs believed to cause or prolong delirium or confusional states*

Analgesics Corticosteroids
NSAIDs Dopamine agonists
Opioids (especially meperidine)
Amantadine

Antibiotics and antivirals Bromocriptine

Acyclovir Levodopa

Aminoglycosides Pergolide

Amphotericin B Pramipexole

Antimalarials Ropinirole

Cephalosporins Gastrointestinal agents

Cycloserine
Antiemetics
Fluoroquinolones
Antispasmodics
Isoniazid
Histamine-2 receptor blockers
Interferon
Loperamide
Linezolid
Herbal preparations
Macrolides
Atropa belladonna extract
Metronidazole
Henbane
Nalidixic acid
Mandrake
Penicillins
Jimson weed
Rifampin
St. John's wort
Sulfonamides
Valerian
Anticholinergics
Hypoglycemics
Atropine
Hypnotics and sedatives
Benztropine
Barbiturates
Diphenhydramine
Benzodiazepines
Scopolamine

Trihexyphenidyl Muscle relaxants

Anticonvulsants Baclofen

Cyclobenzaprine
Carbamazepine

Levetiracetam Other CNS-active agents

Phenytoin Disulfiram

Valproate Cholinesterase inhibitors (eg, donepezil)

Vigabatrin Interleukin-2

Antidepressants Lithium

Phenothiazines
Mirtazapine
 Selective serotonin reuptake inhibitors

Tricyclic antidepressants

Cardiovascular and hypertension drugs

Antiarrhythmics

Beta blockers

Clonidine

Digoxin

Diuretics

Methyldopa

NSAIDs: nonsteroidal antiinflammatory drugs; CNS: central nervous system.

* Not exhaustive, all medications should be considered.

Graphic 70449 Version 7.0

 Assessment and management of patient with delirium

CBC: complete blood count; BUN: blood urea nitrogen; EKG: electrocardiogram; CT: computed tomography; EEG:
electroencephalogram; MRI: magnetic resonance imaging.

Graphic 59337 Version 3.0

Contributor Disclosures
Joseph Francis, Jr, MD, MPH Nothing to disclose Michael J Aminoff, MD, DSc Equity
Ownership/Stock Options: Trust (The portfolio may include medical or drug companies). Equity
Ownership/Stock Options (Spouse): Trust (The portfolio may include medical or drug
companies). Kenneth E Schmader, MD Grant/Research/Clinical Trial Support: Merck [Herpes zoster
(Zoster vaccine)]; GlaxoSmithKline [Herpes zoster (Zoster vaccine)]. Janet L Wilterdink, MD Nothing
to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

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