Delirium is defined as a transient, usually reversible, cause of mental dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities. It can occur at any age, but it occurs more commonly in patients who are elderly and have a previously compromised mental status.
The clinical hallmarks of delirium are decreased attention or awareness and a change in baseline cognition. Delirium often manifests as a waxing and waning type of confusion. Symptoms include the following:
See Clinical Presentation for more detail.
The diagnosis of delirium is clinical. No laboratory test can diagnose delirium.
Diagnostic criteria
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for delirium is as follows[1] :
Assessment instruments
Some of the measures used to identify delirium include the following:
Delirium symptom severity can be assessed by the Delirium Detection Scale (DDS) and the Memorial Delirium Assessment Scale (MDAS).
See Workup for more detail.
The goal of treatment is to determine the cause of the delirium and stop or reverse it. Components of delirium management include supportive therapy and pharmacologic management.
Fluid and nutrition should be given carefully because the patient may be unwilling or physically unable to maintain a balanced intake. For the patient suspected of having alcohol toxicity or alcohol withdrawal, management should include multivitamins, especially thiamine.
Reorientation techniques or memory cues such as a calendar, clocks, and family photos may be helpful. The environment should be stable, quiet, and well-lighted.
Delirium that causes injury to the patient or others should be treated with medications. The most common medications used are antipsychotic medications. Benzodiazepines often are used for withdrawal states.
See Treatment and Medication for more detail.
Delirium is a transient global disorder of cognition. The condition is a medical emergency associated with increased morbidity and mortality rates. Early diagnosis and resolution of symptoms are correlated with the most favorable outcomes.
Delirium is not a disease but a syndrome with multiple causes that result in a similar constellation of signs and symptoms. Delirium is defined as a transient, usually reversible, cause of mental dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities. The clinical hallmarks are decreased awareness and attention span and a waxing and waning type of confusion.
Delirium is often unrecognized or misdiagnosed as dementia, depression, mania, psychotic disorders, or a typical response of the aging brain to hospitalization.
Based on the level of psychomotor activity, delirium can be described as hyperactive, hypoactive, or mixed. Hyperactive delirium is observed in patients in a state of alcohol withdrawal or intoxication with phencyclidine (PCP), amphetamine, and lysergic acid diethylamide (LSD). These patients often exhibit agitation, restlessness, hallucinations, or delusions. Hypoactive delirium is observed in patients in states of hepatic encephalopathy and hypercapnia and may be more common in older adults. Hypoactive delirium presents with lethargy, drowsiness, apathy, decreased responsiveness, or slowed motor skills. In mixed delirium, individuals display either relatively normal levels of psychomotor activity or rapidly fluctuating levels of activity.[1, 2]
The mechanism of delirium still is not fully understood. Delirium results from a wide variety of structural or physiological insults. The neuropathogenesis of delirium has been studied in patients with hepatic encephalopathy and alcohol withdrawal. Research in these areas still is limited. The main hypothesis is reversible impairment of cerebral oxidative metabolism and multiple neurotransmitter abnormalities. The following observations support the hypothesis of multiple neurotransmitter abnormalities.[3]
Data from animal and clinical studies support the hypothesis that acetylcholine is one of the critical neurotransmitters in the pathogenesis of delirium.[4] A small prospective study among patients who have undergone elective hip replacement surgery showed reduced preoperative plasma cholinesterase activity in as many as one quarter of patients. In addition, reduced preoperative cholinesterase levels were significantly correlated with postoperative delirium.[5]
Clinically, good reasons support this hypothesis. Anticholinergic medications are a well-known cause of acute confusional states, and patients with impaired cholinergic transmission, such those with Alzheimer disease, are particularly susceptible. In patients with postoperative delirium, serum anticholinergic activity may be increased.[6]
In the brain, a reciprocal relationship exists between cholinergic and dopaminergic activities. In delirium, an excess of dopaminergic activity occurs. Symptomatic relief occurs with antipsychotic medications such as haloperidol and other neuroleptic dopamine blockers.
Serotonin: Human and animal studies have found that serotonin is increased in patients with hepatic encephalopathy and septic delirium. Hallucinogens such as LSD act as agonists at the site of serotonin receptors. Serotonergic agents also can cause delirium.
Gamma-aminobutyric acid (GABA): In patients with hepatic encephalopathy, increased inhibitory GABA levels also are observed. An increase in ammonia levels occurs in patients with hepatic encephalopathy, which causes an increase in the amino acids glutamate and glutamine, which are precursors to GABA. Decreases in CNS GABA levels are observed in patients with delirium resulting from benzodiazepine and alcohol withdrawal.
Cortisol and beta-endorphins: Delirium has been associated with the disruption of cortisol and beta-endorphin circadian rhythms. This mechanism has been suggested as a possible explanation for delirium caused by exogenous glucocorticoids.
Disturbed melatonin disturbance has been associated with sleep disturbances in delirium.[7]
Recent studies have suggested a role for cytokines, such as interleukin-1 and interleukin-6, in the pathogenesis of delirium. Following a wide range of infectious, inflammatory, and toxic insults, endogenous pyrogen, such as interleukin-1, is released from the cells. Head trauma and ischemia, which frequently are associated with delirium, are characterized by brain responses that are mediated by interleukin-1 and interleukin-6.[8, 9]
Studies indicate psychosocial stress and sleep deprivation facilitate the onset of delirium.
The specific neuronal pathways that cause delirium are unknown. Imaging studies of metabolic (eg, hepatic encephalopathy) and structural (eg, traumatic brain injury, stroke) factors support the hypothesis that certain anatomical pathways may play a more important role than others. The reticular formation and its connections are the main sites of arousal and attention. The dorsal tegmental pathway projecting from the mesencephalic reticular formation to the tectum and the thalamus is involved in delirium.
Disrupted blood-brain barrier can allow neurotoxic agents and inflammatory cytokines to enter the brain and may cause delirium. Contrast-enhanced MRI can be used to assess the blood-brain barrier.[10, 11]
Visuoperceptual deficits in delirium such as hallucinations and delusions are not due to the underlying cognitive impairment.[12] Visual hallucinations during alcohol-withdrawal delirium are seen in subjects with polymorphisms of genes coding for dopamine transporter and catechol-O-methyltransferase (COMT).[13]
In patients who are admitted with delirium, mortality rates are 10-26%.[14]
Patients who develop delirium during hospitalization have a mortality rate of 22-76% and a high rate of death during the months following discharge.[15] . In a review of 28 studies of critically ill patients the rate of death for patients with delirium was more than doubled.[16]
In patients who are elderly and patients in the postoperative period, delirium may result in a prolonged hospital stay, increased complications, increased cost, and long-term disability.[17]
According to one study, delirium is associated with worse survival and greater resource consumption in those with cardiac critical illness. Among 590 patients included, the prevalence of cardiac (C)ICU delirium was 20.3%. Delirious patients were older, had greater disease severity, required longer ICU stays (5 vs 2 days; P< .001), and had higher mortality (27% vs 3%; P< .001).[18]
Delirium is common in the United States. In a systematic review of 42 cohorts in 40 studies, 10–31% of new hospital admissions met criteria for delirium and the incidence of developing delirium during the admission ranged from 3–29%.[19]
For patients in intensive care units the prevalence of delirium may reach as high as 80%.[2]
Prevalence of postoperative delirium following general surgery is 5–10% and as high as 42% following orthopedic surgery. As many as 80% of patients develop delirium near death. Delirium is extremely common among nursing home residents.
Delirium can occur at any age, but it occurs more commonly in patients who are elderly and have compromised mental status. Delirium can occur on top of an underlying dementia. This diagnosis here requires not only a careful mental status but also a thorough history from the patient's family and the staff as well as a comprehensive chart review.
The diagnosis of delirium is clinical. No laboratory test can diagnose delirium. Obtaining a thorough history is essential.
Because delirious patients often are confused and unable to provide accurate information, getting a detailed history from family, caregivers, and nursing staff is particularly important. Nursing notes can be very helpful for documentation of episodes of disorientation, abnormal behavior, and hallucinations. Learning to record accurate and specific findings in mental status as well as the particular time the finding was observed is imperative for the staff. Staff should not just report "he was confused."
Delirium always should be suspected when (a new onset) or an acute or subacute deterioration in behavior, cognition, or function occurs, especially in patients who are elderly, demented, or depressed.
Patients may have visual hallucinations or persecutory delusions as well as grandiose delusions.
Some patients with delirium also may become suicidal or homicidal. Therefore, they should not be left unattended or alone.
Delirium is mistaken for dementia or depression, especially when patients are quiet or withdrawn. However, by Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM5) criteria, dementia cannot be diagnosed with certainty when delirium is present. Health professionals can do Mini-Mental Status Exam (MMSE),[20] depression assessment screening using DSM-5 criteria,[1] or the Geriatric Depression Scale (GDS).[21] They can also assess for suicidal and homicidal risk if necessary. Health professionals can directly ask patients about suicidal or homicidal ideation (thoughts), intent, and plan.
Depression symptoms are commonly seen with delirium. In a recent study, patients having symptoms of dysphoric mood and hopelessness are at risk for incident delirium while in the hospital.[22] On the other hand, hypoactive delirium may be mistaken for depression. Up to 42% of patients referred to psychiatry services for suspected depressive illness in the hospital may have delirium.[23] Screening for depression in the presence of delirium is quite challenging.
Delirium is a common cause for psychotic symptoms, bizarre delusions, abnormal behavior, and thought disorders. Agitated patients are at risk for violent and abnormal behavior and in rare circumstances, agitation can lead to attempts of homicide.
The mental status is a bedside or interview assessment that dramatically fluctuates. It includes the patient's appearance, affect (mood), thoughts (especially the presence of hallucinations and delusions), inquiry into self-destructive behavior, homicidal behavior, judgment and, in this diagnosis, orientation, immediate, recent, and long-term memory.
Delirium develops in a short period of time (within hours), and an acute change in consciousness or difficulty focusing on what was being said could occur during the interview. Disturbance of the sleep-wake cycle with insomnia, daytime drowsiness, or disturbing dreams or nightmares can also occur. Patients are often unable to remember why they are in the hospital or the events that occurred during the delirious period (for most patients, it is like a blackout period).
Patients may have false beliefs or thinking (misinterpreting intravenous lines as ropes or snakes) or see or hear things that are not present (picking up things in the air or seeing bugs in the bedclothes). Patients may also misjudge their level of wellness and try to elope from the hospital. Emotional disturbances leading to depression, anxiety, fear, and irritability may be seen in some patients. Delirium in hospitalized seniors may result in the self-removal of catheters or intravenous tubing or attempts to get out of bed, resulting in a fall or injury.
The main symptoms of delirium include the following:
Neurological symptoms may include the following:
Patients with delirium who are hyperactive have an increased state of arousal, psychomotor abnormalities, and hypervigilance. In contrast, patients with delirium who are hypoactive are withdrawn, less active, and sleepy.
Hypoactive delirium sometimes is misdiagnosed as dementia or depression.
In patients who are elderly, delirium often is the presenting symptom of an underlying illness.
Subsyndromal delirium has been defined as the presence of some core diagnostic symptoms that do not meet the criteria for diagnostic threshold. Prevalence rates of 30-50% have been reported in intensive care units.[24, 25]
A prodromal phase lasting for hours to days can occur before full syndromal delirium becomes evident. This includes sleep disturbances, vivid dreams, frequent calls for assistance, and anxiety.[24, 25]
A careful and complete physical examination including a mental status examination is necessary. Testing vital signs such as temperature, pulse, blood pressure, and respiration is mandatory.
Patients have difficulty sustaining attention, problems in orientation and short-term memory, poor insight, and impaired judgment. Key elements here are fluctuating levels of consciousness.
Impaired attention can be assessed with bedside tests that require sustained attention to a task that has not been memorized, such as reciting the days of the week or months of the year backwards, counting backwards from 20, or doing serial subtraction.
DSM-5 diagnostic criteria for delirium[1] is as follows:
Other diagnostic instruments are the Delirium Symptom Interview (DSI) and the Confusion Assessment Method (CAM).[26]
Delirium symptom severity can be assessed by the Delirium Rating Scale (DRS) and the Memorial Delirium Assessment Scale (MDAS).
Table 1. Differentiating Features of Delirium and Dementia
View Table | See Table |
To make an accurate diagnosis, periodic application of diagnostic criteria such as CAM or DSM5 criteria and knowledge of the patient's baseline mental status is imperative.
Gaps in the medical record such as once daily cognitive assessment or no formal assessments on the hallmarks of delirium (attention span and fluctuation) may make diagnosing the condition more difficult. The physicians depend on health records (nursing notes) to identify a fluctuating course. The type of information might also be less than adequate for developing a timely diagnosis. So the recognition of delirium can be delayed by infrequent observation or documentation.[27]
A simple cognitive test like the Mini-Cog can be a predictor of inhospital delirium. At the time of admission to the hospital, if the elderly patient does not have a history of dementia or cognitive impairment, the Mini-Cog can be used to identify patients at high risk for inhospital delirium.
The Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) offers the clinician the opportunity to identify delirium in critical care patients, especially patients on mechanical ventilation. The CAM-ICU makes use of nonverbal assessments to evaluate the important features of delirium.
Another instrument that can be used in ICU settings is the Intensive Care Delirium Screening Checklist (ICDSC). The severity of delirium in the ICU can be estimated by the Delirium Detection Scale (DDS).
A 2012 meta-analysis showed a sensitivity of 75.5% and specificity of 95.8% for CAM-ICU, whereas sensitivity and specificity for the ICDSC were 80.1% and 74.6%, respectively. These results suggest the CAM-ICU is one of the most specific bedside tests that can be used to diagnose delirium in ICU patients.[28]
The CAM-S was developed for measuring the severity of delirium in hospitalized patients (short form) and those in research settings (long form).[29, 30] Developers reported good psychometric properties, high interrater reliability, and strong associations with important clinical outcomes with this tool, which is based on the standardized and validated Confusion Assessment Method (CAM) that screens for the presence—but not the severity—of delirium. The CAM-S was tested in 2 independent cohorts at 3 academic centers comprising 300 patients scheduled for major surgery and 919 medical patients (all patients aged ≥70 y).[29, 30]
Almost any medical illness, intoxication, or medication can cause delirium. Often, delirium is multifactorial in etiology, and the physician treating the delirium should investigate each cause contributing to it. Medications are the most common reversible cause of delirium.
Some of the other common reversible causes include the following:
Other causes of delirium include the following:
Although numerous risk factors have been described, a recent study identified 5 important independent risk factors.
Dementia is one of the strongest most consistent risk factors. Underlying dementia is observed in 25-50% of patients. The presence of dementia increases the risk of delirium 2-3 times. Low educational level, which may be an indicator of low cognitive reserve, is associated with increased vulnerability to delirium.
Dysphoric mood and hopelessness are also risk factors for incident delirium.
Structural changes that may contribute to delirium include the following:
Metabolic causes may include the following:
Hypoperfusion states such as shock congestive heart failure, cardiac arrhythmias, and anemias may contribute to delirium.
Infectious causes may include the following:
Substance intoxication with alcohol, heroin, cannabis, PCP, and LSD may cause symptoms of delirium. Withdrawal from these substances may also contribute.
Medication-induced delirium can be caused by any of the following agents:
Other causes may include postictal state and unfamiliar environment.
Delirium may come about as a result of surgery or operation.
Mild cognitive impairment and vascular risk factors can be independent risk factors for postoperative delirium.[31]
Drugs are a common risk factor for delirium, and drug-induced delirium is commonly seen in medical practice, especially in hospital settings. The risk of anticholinergic toxicity is greater in elderly persons, and the risk of inducing delirium by medications is high in frail, elderly persons and in those with dementia.
Laboratory tests that may be helpful for diagnosis include the following:
See the list below:
Lumbar puncture is indicated when CNS infection is suspected as a cause of delirium or when the source for the systemic infection cannot be determined.
Pulse oximetry is used to diagnose hypoxia as a cause of delirium.
Electrocardiogram is used to diagnose ischemic and arrhythmic causes.
When delirium is diagnosed or suspected, the underlying causes should be sought and treated. Despite every effort, no cause for delirium can be found in a small percentage of patients. Components of delirium management include supportive therapy and pharmacological management.
Fluid and nutrition should be given carefully because the patient may be unwilling or physically unable to maintain a balanced intake. For the patient suspected of having alcohol toxicity or alcohol withdrawal, therapy should include multivitamins, especially thiamine.
Reorientation techniques or memory cues such as a calendar, clocks, and family photos may be helpful. The environment should be stable, quiet, and well-lighted. One study showed a reduction of sound during the night by using earplugs in the ICU setting decreased the risk of delirium by 53%, and improved the self-reported sleep perception of the patient for 48 hours.[34] Sensory deficits should be corrected, if necessary, with eyeglasses and hearing aids. Family members and staff should explain proceedings at every opportunity, reinforce orientation, and reassure the patient. Support from a familiar nurse and family should be encouraged. A meta-analysis of 7 studies that focused on the usefulness of interventions such as physical or occupational therapy, daily reorientation, and the avoidance of sensorial deprivation found a significant reduction in the development of delirium among elderly inpatients.[35]
Physical restraints should be avoided. Delirious patients may pull out intravenous lines, climb out of bed, and may not be compliant. Perceptual problems lead to agitation, fear, combative behavior, and wandering. Severely delirious patients benefit from constant observation (sitters), which may be cost effective for these patients and help avoid the use of physical restraints. These patients should never be left alone or unattended.
Psychiatric consultation may be indicated for management of behavioral problems such as agitation or aggressive behavior.
Guidelines for risk reduction and management of delirium were published by the Scottish Intercollegiate Guidelines Network (SIGN) in March 2019.[74]
Detecting delirium
Use the 4 As Test (Arousal, Attention, Abbreviated Mental Test 4 [AMT4], Acute change) for identifying patients with probable delirium in emergency and acute hospital settings. This tool may also be used in community or other settings.
In the ICU setting, use the Confusion Assessment Method for the ICU (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC) to identify patients with probable delirium.
Use CT brain scan in those patients presenting with delirium in the presence of the following:
Consider an electroencephalogram when there is suspicion of epileptic activity or non-convulsive status epilepticus.
Reducing risk of delirium
Consider all of the following as part of a package of care for patients at risk for delirium:
Monitor depth of anesthesia in patients 60 years of age and over undergoing surgery that is expected to last more than 1 hr.
Treating delirium
Consider acute, life-threatening causes of delirium. These may include low oxygen level, low blood pressure, low glucose level, and drug intoxication or withdrawal.
Identify and treat potential causes such as medications and acute illness. Multiple causes are common.
Optimize physiology, environment, and medications to promote brain recovery.
Detect and treat agitation or distress with non-pharmacologic means, if possible.
Communicate diagnosis to patients and caregivers and provide ongoing support.
Attempt to prevent delirium complications such as immobility, falls, pressure sores, dehydration, malnourishment, and isolation.
Monitor patient recovery and refer to a specialist if necessary.
Delirium that causes injury to the patient or others should be treated with medications. The most common medications used are antipsychotic medications. While this is a common and seemingly useful strategy, the literature is still mixed. A 2015 meta-analysis of 15 studies found that second-generation antipsychotics (SGAs) may treat delirium better than placebo, usual care, or haloperidol.[36] A 2016 meta-analysis of 19 studies found that antipsychotic use was not associated with change in delirium duration, severity, or hospital or ICU length of stay.[37]
Benzodiazepines often are used for alcohol and benzodiazepine withdrawal states.
Since decreased anticholinergic activity may be associated with delirium, anticholinesterase inhibitors have been tried. Even though case reports showed evidence that cholinesterase inhibitors may play a role in the management of delirium, larger trials and systematic review did not support this use.[38] A randomized, double-blinded, placebo-controlled, multicenter trial in intensive care unit patients showed rivastigmine did not decrease duration of delirium and increased mortality in these patients. In this trial, the study group had more sicker patients with emergency admissions to the ICU, and this trial had used IV haloperidol, lorazepam, or propofol, in addition to rivastigmine, which might also have contributed to the delirium and increased mortality.[39] A review of 7 trials of anticholinesterase inhibitors found that in 5 of the studies there was no benefit from the medications in either the prevention or management of delirium.[40]
Recent clinical trials showed that the melatonin supplement and its receptor agonist ramelteon may be useful in the prevention and management of delirium. Melatonin levels were found to be altered in delirium subjects.[41] Melatonin is available over the counter in North America. Ramelteon has been approved by the FDA for the treatment of insomnia.[42]
Clinical Context: A butyrophenone high-potency antipsychotic. One of most effective antipsychotics for delirium. High-potency antipsychotic medications also cause less sedation than phenothiazines and reduce risks of exacerbating delirium.
Clinical Context: A newer antipsychotic with fewer extrapyramidal adverse effects than Haldol. Binds to dopamine D2-receptor with 20 times lower affinity than for 5-HT2-receptor. Improves negative symptoms of psychoses and reduces incidence of adverse extrapyramidal effects.
This class of drugs are the medication of choice in the treatment of psychotic symptoms of delirium. Older antipsychotics such as haloperidol, a high-potency antipsychotic, are useful but have adverse neurological effects. Newer neuroleptics such as risperidone, olanzapine, and quetiapine relieve symptoms while minimizing adverse effects. Initial doses may need to be higher than maintenance doses. Use lower doses in patients who are elderly. Discontinue these medications as soon as possible. Attempt a trial of tapering the medication once symptoms are in control. Antipsychotics can be associated with adverse neurological effects such as extrapyramidal symptoms, neuroleptic malignant syndrome, and tardive dyskinesia. Longer term use is also associated with metabolic syndrome. Doses should be kept as low as possible to minimize adverse effects. Paradoxical and hypersensitivity reactions may occur.
Clinical Context: Preferable because it is short acting and has no active metabolites. In addition, can be used in both IM and IV forms. When patient needs to be sedated for longer than 24 h, this medication is excellent. Commonly used prophylactically to prevent delirium tremens.
Reserved for delirium resulting from seizures or withdrawal from alcohol or sedative hypnotics. Coadministration with antipsychotics is considered only in patients who tolerate lower doses of either medication or have prominent anxiety or agitation. Benzodiazepines are preferred over neuroleptics for treatment of delirium resulting from alcohol or sedative hypnotic withdrawal. They also may be used when unknown substances may have been ingested and may be helpful in delirium from hallucinogen, cocaine, stimulant, or PCP toxicity. Use special precaution when using benzodiazepines because they may cause respiratory depression, especially in patients who are elderly, those with pulmonary problems, or debilitated patients.
Clinical Context: For alcohol withdrawal and in cases of Wernicke encephalopathy.
Clinical Context: Vitamin B-12 deficiency can cause confusion or delirium in patients who are elderly. Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B-12 in humans. Vitamin B-12 is synthesized by microbes but not by humans or plants. Vitamin B-12 deficiency may result from intrinsic factor deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum.
Patients with alcoholism and patients with malnutrition are prone to thiamine and vitamin B-12 deficiency, which can cause delirium.
Clinical Context: Melatonin is a naturally occurring hormone secreted by the pineal gland. The concentration of melatonin is highest in the blood during normal times of sleep and lowest during normal times of wakefulness. The general consensus is that melatonin given during normal waking hours has hypnotic properties.
Clinical Context: Ramelteon is a melatonin receptor agonist with high selectivity for human melatonin MT1 and MT2 receptors. MT1 and MT2 are thought to promote sleep and be involved in maintaining circadian rhythm and a normal sleep-wake cycle. Ramelteon does not cause rebound insomnia or withdrawal symptoms at discontinuation. It is approved for prolonged use. It is indicated for insomnia characterized by difficulty with sleep onset.
Agents in this class may be useful in the prevention and management of delirium.
Following recovery, patient's memories of events of the delirium are variable. Be sure to educate the patient, family, and primary caregivers about future risk factors.
It is not unusual for patients who are elderly to require 6-8 weeks or longer for full recovery. In particular, elderly patients with postacute care complications are at risk for prolonged and persistent delirium.[43]
Carefully assess patients to determine their level of care needs. Assessment should include behavior (24 h), daily mental status, potential for injury, and underlying medical and metabolic status.
Prevention should be the goal because delirium is associated with adverse outcomes and high health care costs.
A multicomponent intervention study that targeted cognitive impairment, sleep deprivation, immobility, visual impairment, hearing impairment, and dehydration showed significant reduction in the number and duration of episodes of delirium in older patients who were hospitalized.
Patients who are at high risk for delirium should be monitored closely as outpatients, during hospitalization, and throughout surgical procedures.
Physicians should become familiar with prescribing practices for patients who are elderly, keeping dosages low and avoiding medications that cause delirium.
Monitoring the patient's mental status as a vital sign helps to diagnose delirium early.
Complications of delirium may include the following:
Delirium significantly worsens prognosis and is associated with increased mortality at discharge and at 12 months. A significant proportion of patients with delirium during their hospital admission continued to demonstrate symptoms of delirium at discharge, 6-month, and 12-month follow-up.[19]
Resolution of symptoms may take longer in patients with poor premorbid cognitive function, incorrect or incomplete diagnosis of contributing factors, and structural brain diseases treated with large doses of psychoactive medications prior to the onset of acute medical illness.
For some patients, the cognitive effects of delirium may resolve slowly or not at all.
See the list below:
Features Delirium Dementia Onset Acute Insidious Course Fluctuating Progressive Duration Days to weeks Months to years Consciousness Altered Clear Attention Impaired Normal, except in severe dementia Psychomotor changes Increased or decreased Often normal Reversibility Usually Rarely