They often vary in severity in a short period of time and include attention deficit and behavioral disorganization.
Delirium, also known as an acute confusional state , is an organically caused decline from a previous level of mental function.
It usually involves other cognitive deficits, changes in arousal (hyperactive, hypoactive, or mixed), perceptual deficits, an altered sleep-wake cycle, and psychotic features such as hallucinations and delusions.
Delirium itself is not a disease, but rather a set of symptoms.
It can be the result of an underlying disease, excessive alcohol use, medications administered during the treatment of an illness, drug withdrawal, or any number of health factors.
Delirium can be caused by a disease process outside the brain that affects the brain , such as infection (urinary tract infection, pneumonia) or the effects of drugs, particularly anticholinergics or other central nervous system depressants (benzodiazepines and opioids).
Although hallucinations and delusions are sometimes present in delirium, they are not necessary for diagnosis, and the symptoms of delirium are clinically distinct from those induced by psychosis or hallucinogens (with the exception of delusions).
By definition, delirium must be caused by an organic process, that is, a physically identifiable structural, functional, or chemical problem in the brain.
And therefore fluctuations in mental activity due to changes in purely psychiatric processes or illnesses, such as sudden psychosis due to schizophrenia or bipolar disorder, are (by definition) not called delirium.
Like its components (inability to focus attention, mental confusion, and various deficits in consciousness and temporal and spatial orientation), delirium is the common manifestation of new organic brain dysfunction (for whatever reason).
Delirium requires a sudden change in mentality and an organic cause for this. Delirium can be difficult to diagnose without the proper establishment of a person’s usual mental function.
Without careful evaluation and history, delirium can easily be mistaken for a number of long-term psychiatric disorders or organic brain syndromes, because many of the signs and symptoms of delirium are conditions also present in dementia, depression, and psychosis.
Delirium may appear recently in the context of mental illness, initial intellectual disability, or dementia, without being due to any of these problems.
Treatment of delirium requires treatment of the underlying cause, and multicomponent interventions are considered to be more effective.
In some cases, temporary or palliative or symptomatic treatments are used to comfort the person or to allow other care (for example, a person who, without understanding, tries to remove a ventilation tube that is needed to survive).
Delirium is probably the most common acute disorder affecting adults in general hospitals. It affects 10-20% of all hospitalized adults, and 30-40% of the elderly who are hospitalized and up to 80% of those who are in the intensive care unit (ICU).
Among those who require critical care, delirium is a risk of death within the next year. Antipsychotics are not compatible for the treatment or prevention of delirium among those in the hospital.
When delirium is caused by alcohol or sedative-hypnotic withdrawal, benzodiazepines are generally used.
In common usage, delirium is often used to refer to drowsiness, disorientation, and hallucination.
In medical terminology, however, a number of different symptoms, including temporary disturbances in consciousness, with a reduced ability to focus attention and solve problems, are the main characteristics of delirium.
Occasionally insomnia and severe agitation and irritability are part of the “delirium.” Hallucination, drowsiness, and disorientation are not necessary, but can contribute to the diagnosis.
There are several medical definitions of delirium, including those contained in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and the International Classification of Diseases, Tenth Revision (ICD-10).
However, they all include a few main features:
Disturbance of consciousness (that is, reduced clarity of awareness of the environment, with reduced ability to focus, hold, or shift attention).
Change in cognition (for example, impaired problem solving or memory impairment) or a perceptual disturbance (hallucination). Attacks from hours to days, and tendency to fluctuate.
Behavior can be hyperactive or underactive, and sleep is often disturbed, with loss of the normal circadian rhythm. Thinking is slow and confusing, but content is often complex.
Other clinical features include disorganized thinking, poor memory, delusions, and mood lability.
Signs and symptoms
Delirium is a syndrome that encompasses a variety of neuropsychiatric symptoms, including an impairment in consciousness / attention and cognition that develops acutely and tends to fluctuate.
The change in cognition (memory deficit, disorientation, language impairment), or the development of an impairment, should be one that is not better defined by a pre-existing, established, or evolving dementia.
Other symptoms may include disorientation, thought disorder, memory problems, language disorder, sleep disorders, delusions, mood lability, psychomotor changes (changes in the rate of activity / movement), and hallucinations.
Delirium occurs as a stage of consciousness on the continuum between normal wakefulness / alertness and coma.
During the 20th century, delirium was described as a “clouding of consciousness,” but this rather hazy concept has been replaced by a better understanding of the components of phenomenology culminating in severely impaired higher-order brain functions.
Lipowski described delirium as a disorder of attention, wakefulness, cognition, and motor behavior, while a disturbance in attention is often considered the cardinal symptom.
Interrupted sleep-wake cycles can be the result of a loss of the normal circadian rhythm.
The accumulation of evidence indicates three central domains of delusion phenomenology:
Cognition, made up of inattention and other cognitive deficits; higher-level thought processes, including impaired executive function, semantic expression, and understanding; and circadian rhythm, including impaired motor activity and the fragmented sleep-wake cycle.
Phenomenology studies suggest that core symptoms occur more frequently, while other less consistent associated symptoms may reflect the biochemical influence of particular etiologies or genetic, neuronal, or physiological vulnerabilities.
Delirium can present in hyperactive, hypoactive, or mixed forms. In its hyperactive form, it manifests as severe confusion and disorientation, developing with a relatively rapid onset and fluctuating in intensity.
In its underactive form, it manifests itself by an equally sudden withdrawal from interaction with the outside world. Delirium can occur in a mixed type in which someone can fluctuate between hyper and hypoactive periods.
Delirium as a syndrome is one that occurs most often in people in their later years. However, when it occurs in the course of critical illness, delirium has been found to occur in young and elderly patients at relatively uniform rates.
Inattention and associated cognitive deficits
Inattention is the cardinal symptom and required to diagnose delirium and is noted in the interview by distraction and the inability to change and / or maintain attention.
The more formal tests can include the months of the previous year, the seven or seven digits. Disorientation (another symptom of confusion, and usually a more serious one) describes the loss of awareness of the environment, surroundings and the context in which the person exists.
It can also appear with delirium, but it is not necessary, as indicated. Disorientation can occur in time (not knowing what time of day, day of the week, month, season, or year), place (not knowing where you are), or person (not knowing who you are).
Memory impairment occurs and is related to inattention.
Reduction in the formation of new long-term memory (which by definition survives withdrawal from attention) is common in delirium, because the initial formation of (new) long-term memories generally requires an even greater degree of attention than short-term memory tasks.
Since older memories are preserved without the need for concentration, previously formed long-term memories (that is, those formed before the delirium period) are generally preserved in all less severe cases of delirium.
Higher level thinking
Delusional patients have decreased understanding as evidenced by:
A lower understanding of their environment and difficulties in connecting with their immediate surroundings, executive dysfunction affecting abstraction, initiation / perseverance, change of mental sets, working memory, temporal sequencing and organization, perception and judgment.
Although none of these cognitive deficits is specific to delirium, the matrix and pattern are highly suggestive.
Language disorders in delirium include anomic aphasia, paraphasia, comprehension problems, agraphia, and difficulty finding words. Incoherent or illogical / incoherent conversation is commonly reported.
Disorganized thinking includes tangentiality, circumstantiality, and a propensity for loose associations between elements of thought resulting in speech that often has limited meaning with multiple apparent irrelevancies.
This aspect of delirium is common, but it is often difficult for non-experts to reliably assess.
Disruption of the sleep-wake cycle is almost invariably present in delirium and often precedes the onset of a full-blown episode.
Minor disturbances with insomnia or excessive daytime sleepiness can be difficult to distinguish from other medically ill patients without delirium.
But delirium generally involves more substantial disturbances with sleep fragmentation or even complete reversal of the sleep-wake cycle reflecting the alteration of circadian rhythm regulation.
The relationship of circadian disturbances to the fluctuating severity characteristic of delirium symptoms over a 24-hour period or to motor disturbance is unknown.
Alterations in motor activity are very common in delirium. They have been used to define clinical subtypes (hypoactive, hyperactive, mixed) although studies are inconsistent in terms of the prevalence of these subtypes.
Cognitive disturbances and slowing of the electroencephalogram (EEG) are comparable in hyperactive and hypoactive patients, although other symptoms may vary.
Psychotic symptoms occur in both, although the prevailing stereotype suggests that they only occur in cases of hyperactivity. Hypoactive cases are prone to undetection or misdiagnosis as depression.
A range of studies suggests that motor subtypes differ in underlying pathophysiology, treatment needs, and prognosis of function and mortality, although inconsistent subtype definitions and poorer underactive detection influence the interpretation of these findings. .
Psychotic symptoms occur in up to 50% of patients with delirium. While the common non-medical vision of a delusional patient is one that he is hallucinating, most people who are medically delusional do not have hallucinations or delusions.
Thought content abnormalities include mistrust, overvalued ideation, and outright delusions. Delusions are often poorly formed and less stereotyped than in schizophrenia or Alzheimer’s disease.
They usually relate to issues of pursuit of imminent danger or threat in the immediate environment (for example, being poisoned by nurses).
Misperceptions include depersonalization, delusional misidentifications, illusions, and hallucinations. Hallucinations and illusions are often visual, although they can be tactile and auditory.
Affect abnormalities that may assist in delusional states may include many distortions to perceived or communicated emotional states.
Emotional states can also fluctuate, so that a delusional person can quickly switch between, for example, terror, sadness, and jocularity.
All delirium was thought for many years to be a transient state of brain dysfunction that fluctuated hourly.
The English medical writer Philip Barrow noted in 1583 that if the delusion resolves, it may be followed by a “loss of memory and reasoning power.”
Recent long-term studies confirm this, showing that many patients end up meeting the criteria for delirium for an alarmingly long time.
For example, in intensive care unit cohorts, it is common to find that 10% of patients still have delirium at the time of hospital discharge.
Dementia in Intensive Care Unit Survivors
Dementia is assumed to be an entity that continues to decline, such as Alzheimer’s disease.
Another way of looking at dementia, however, is not strictly based on the decline component, but on the degree of memory and executive function problems.
It is now known, for example, that between 50% and 70% of intensive care patients have enormous problems of permanent brain dysfunction.
Which is a lot like the measure of problems experienced by patients with Alzheimer’s or traumatic brain injury (TBI).
And which leaves far too many ICU survivors disabled and unable to return to work and unable to serve effectively as matriarchs and patriarchs of their families.
This is a troubling personal and public health issue that is receiving an increased amount of scrutiny in ongoing investigations.
The implications of such an ‘acquired dementia-like illness’ are profound on a private level, dismantling a person’s life in very practical ways.
Like the inability to find a car in a parking lot or even complete shopping lists or tasks related to work previously done for years.
Note : the term here is used in a circumstance where not all patients continue to decline as some have persistent but stable brain dysfunction and others with newly acquired brain problems can fully recover.
The social relevance is also enormous when considering workforce problems related to a young wage earner’s inability to work.
Because you are a recently disabled ICU survivor or because you now have to care for your relative who is now suffering from this ‘dementia-like’ illness after ICU care.
Delirium arises through the interaction of a series of predisposing and precipitating factors.
A predisposing factor could be any biological, psychological, or social factor that increases an individual’s susceptibility to delirium. A person with multiple predisposing factors is said to have a “high baseline vulnerability.”
A trigger is any biological, psychological, or social factor that can trigger the delirium.
The division of causes into “predisposing” and “precipitating” is useful in assessing an individual’s risk for delirium and in guiding the management of delirium, however, there may be a significant degree of overlap between the two categories.
Delirium generally affects old age and health problems. Health outcomes for physical and socioeconomic assets, and opposing factors come from physical and socioeconomic deficits.
People with significant predisposing factors do not compensate for physical or social stressors (“triggers”).
In such an individual, a simple or mild precipitating factor might be sufficient to trigger an episode of delirium. In contrast, delirium can only result in a healthy individual if he suffers from severe or multiple triggers.
It is important to note that factors that affect an individual’s can change over time, so an individual’s risk of delirium is in a state of flux.
The most important predisposing factors are listed below:
- Advanced age.
- Cognitive impairment / dementia.
- Physical comorbidity (biventricular failure, cancer, cerebrovascular disease).
- Psychiatric comorbidity (such as Depression).
- Sensory impairment (vision, hearing).
- Functional dependency (for example, requires assistance with personal care and / or mobility).
- Dehydration / malnutrition.
- Drugs and drug addiction.
- Alcohol dependence.
Any acute factor that affects neurotransmitter, neuroendocrine, or neuroinflammatory pathways can precipitate an episode of delirium in a vulnerable brain.
Clinical settings can also precipitate delirium, and optimal medical and nursing care is a key component of delirium prevention. Some of the more common triggers are listed below:
- Dehydration, electrolyte imbalance.
- Endocrine disorders (such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), Addison’s disease, hyperthyroidism, hypercalcemia).
- Especially respiratory and urinary tract infections.
- Anticholinergics, dopaminergics, opioids, steroids, recent polypharmacy.
- Stroke / transient ischemic attack.
- Myocardial infarction, arrhythmias, decompensated heart failure.
Physical / psychological stress :
- Iatrogenic event, postoperative mechanical ventilation in the intensive care unit.
- Chronic / terminal illness, cancer.
- Post-traumatic event (such as fall, fracture).
- Immobilization / restriction.
- Severe constipation / fecal impaction.
- Urinary retention.
- Substance extraction (especially alcohol, benzodiazepines).
- Substance intoxication.
- Traumatic head injury.
The pathophysiology of delirium is not well understood and the lack of relevant animal models for the syndrome has left many key questions in the pathophysiology of delirium unanswered.
Early models of rodent delirium used a muscarinic acetylcholine receptor antagonist, atropine, to induce delirium-like EEG and cognitive changes.
Similar anticholinergic drugs such as biperiden and scopolamine have also produced effects similar to delirium.
These models, together with clinical studies of drugs with ‘anticholinergic activity’, have contributed to a hypocolic theory of delirium.
Deep systemic inflammation that occurs during bacteremia / sepsis is also known to cause delirium (often referred to as septic encephalopathy).
Modeling this in mice also causes strong brain dysfunction and probably a delirium-like state.
Although these animals are often too sick to be evaluated cognitively and measures such as EEG and MRI / spectroscopy are required to demonstrate dysfunction.
Recently, animal models have been developed that interrogate interactions between previous degenerative pathology and superimposed systemic inflammation.
They show that even mild systemic inflammation, a frequent trigger of clinical delirium, induces acute and transient deficits of attention / working memory, but only in animals with a history of disease.
Previous dementia or age-related cognitive decline is the main predisposing factor for clinical delirium, and the ‘prior pathology’ defined by these new animal models may consist of:
Synaptic loss, network disconnection, and primed microglia (brain macrophages that are “primed” by the primary pathology to produce exaggerated responses to subsequent inflammatory insults).
While it is difficult to establish with confidence whether delirium is occurring in a nonverbal animal, comparisons with the criteria in the Diagnostic and Statistical Manual of Human Mental Disorders, Fourth Edition (DSM-IV) remain useful.
According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV):
Demonstration of acute onset deficiencies in attention and some other cognitive domain, which cannot be better explained by existing dementia and which are triggered by physiological disturbances resulting from some general disorders, a medical condition must be present to reach a ‘diagnosis’ of delirium .
Recent animal models meet these criteria reasonably well.
If the deficit is one of attention or short-term memory, it is difficult to dissect, but it is undoubtedly different from long-term memory, consistent with observations in patients with delirium.
There is an urgent need to understand more about the mechanisms of dysfunction underlying delirium and the data emerging from these and other animal models should be part of the discussion on the pathophysiology of delirium.
Cerebrospinal fluid biomarkers
Cerebrospinal fluid (CSF) studies in delirium are difficult to perform.
In addition to the general difficulty of recruiting participants who are often unable to consent, the inherently invasive nature of CSF sampling makes such research particularly challenging.
However, some studies have exploited the opportunity to collect cerebrospinal fluid samples from people undergoing spinal anesthesia for elective or emergency surgery.
In fact, spinal anesthesia may in fact be the anesthetic modality of choice for frail elderly patients, which is why these studies are often carried out in highly relevant populations.
A systematic review identified 8 studies with 235 patients (142 with delirium):
Overall, 17 different biomarkers were considered and each article identified in the review focused on a narrow range of biomarkers with no overlap between studies.
The studies were generally small, studying heterogeneous populations with different CSF sampling times in relation to delirium, and no clear conclusions could be drawn.
In general terms, delirium may be associated with: increased serotonergic and dopamine signaling; reversible drop in somatostatin; increased cortisol; and increase in some inflammatory cytokines (IL-8, IL-1β), but possibly not others (TNF-α).
An additional study has since been published. Postoperative delirium was strongly associated with preoperative cognitive impairment.
However, Aβ1-42 cerebrospinal fluid, tau, and phosphorylated tau levels were not associated with delirium status, nor were they significantly correlated with cognitive function before delirium onset.
The two main explanations for these findings are:
- The study was underpowered to detect pathways between premorbid cognitive impairment, biomarkers of Alzheimer’s disease, and subsequent delirium.
- Postoperative delirium arises through pathophysiologic pathways that are distinct from Alzheimer’s disease.
Neuroimaging correlates of delirium are very difficult to establish. Many attempts to image people with concurrent delusions will not be successful.
In addition, there is a more general bias that selects the youngest and fittest participants for screening, especially if intensive protocols such as magnetic resonance imaging (MRI) are used.
Most of the literature has been summarized by a systematic review. Twelve articles were found for inclusion, most with small sample sizes (total number of cases 127).
There was substantial heterogeneity in populations, study design, and imaging modalities such that no firm conclusions were made.
Overall, structural imaging suggested that diffuse brain abnormalities such as atrophy and leukoaraiosis could be associated with delirium.
Although few studies could explain differences in key variables such as age, sex, education, or underlying cognitive function and education.
Since the publication of the systematic review, another five studies have been published. The largest-scale report was VISIONS. This prospectively examined neuroimaging correlates of delirium in 47 participants after critical illness.
Duration of delirium was related to measures of white matter tract integrity, and this, in turn, was related to poorer cognitive outcome at 3 and 12 months.
Furthermore, brain volumes were also assessed and related to cognitive outcomes in the same way.
Overall, the study found that longer duration of delirium was associated with smaller brain volume and more white matter disruption, both of which were correlated with worse cognitive scores 12 months later.
Two studies examined the risk of delirium as a postoperative complication after elective heart surgery. Both showed that white matter damage predicted postoperative delirium.
A functional MRI study reported a reversible reduction in activity in areas of the brain that are localized with cognition and attention function.
Electroencephalography (EEG) is an attractive study mode in delirium as it is capable of capturing measures of overall brain function.
There are also opportunities to summarize temporal fluctuations as continuous recordings, compressed into power spectra (quantitative electroencephalogram, quantitative electroencephalography (qEEG)).
Since the work of Engel and Romano in the 1950s, delirium has been known to be associated with a general slowdown in background activity.
A systematic review identified 14 studies for inclusion, representing a range of different populations: 6 in older populations, 3 in intensive care units, sample sizes between 10 and 50).
For most studies, the outcome of interest was relative power measures, in order: alpha, theta, delta frequencies. The relative power of the theta frequency was consistently different between delusional and non-delusional patients.
Similar findings were reported for alpha frequencies. In two studies, the relative power of all these bands was different within patients before and after delirium.
Only a few studies exist where delirium has been correlated with pathological findings at autopsy.
A case series was reported in 7 patients who died during admission to the intensive care unit.
Each case was admitted with a variety of primary conditions, but all had acute respiratory distress syndrome and / or septic shock that contributed to delirium.
6/7 presented evidence of hypoperfusion and diffuse vascular injury, with constant involvement of the hippocampus in 5/7.
A case-control study examined 9 cases of delirium with 6 controls of the same age, investigating inflammatory cytokines and their role in delirium.
People with delirum had higher scores for HLA-DR and CD68 (markers of microglial activation), IL-6 (pro-inflammatory and anti-inflammatory cytokine activities), and GFAP (marker of astrocyte activity).
These results may suggest a neuroinflammatory substrate for delirium, but the conclusions are limited by biases in the selection of controls.
Differential points of other processes and syndromes that cause cognitive dysfunction:
Delirium can be distinguished from psychosis, in which consciousness and cognition cannot be affected (however, there may be overlap, as some acute psychoses, especially with mania, are capable of producing delusional states).
Delirium is distinguished from dementia (chronic organic brain syndrome) by describing “acquired” (non-congenital) and generally irreversible cognitive and psychosocial function.
Dementia is usually the result of an identifiable degenerative brain disease (for example, Alzheimer’s disease or Huntington’s disease).
Dementia is generally not associated with a change in the level of consciousness, and a diagnosis of dementia requires chronic deterioration. Delirium is distinguished from depression.
Delirium is distinguished by the passage of time from confusion and inattention that result from long-term learning disorders and varieties of congenital brain dysfunction.
Delirium is also known as “acute confusional state” or “acute brain syndrome.”
The key word in both descriptions is ‘acute’ (ie, recent onset), as delirium may share many of the clinical (ie symptomatic) features of dementia or developmental disabilities, including deficit disorder. attention and hyperactivity, with the important exception of duration of symptoms
Delirium represents an organically caused decline from a previously achieved level of cognitive functioning.
It is a corollary of these differential criteria that a diagnosis of delirium cannot be made without a prior assessment, or knowledge, of the baseline level of cognitive function of the affected person.
In other words, a mentally handicapped or insane person who is operating at his or her own baseline level of mental capacity may appear delusional without a baseline functional state to compare with.
Some mental illnesses, such as a manic episode of bipolar disorder, depersonalization disorder, or some types of acute psychosis can cause a rapidly fluctuating decline in cognitive function and ability to concentrate.
Outwardly, this appears similar to a confused state caused by improper brain metabolism, but in reality it stems from problems in function.
However, they are not technically causes of delirium, as any fluctuating cognitive symptoms that occur as a result of these mental disorders are considered by definition as a mental disorder and as part of it.
Therefore, it can be said that physical disorders produce delirium as a mental side effect or symptom, although the primary mental disorders that produce the symptom cannot be included in this category once identified.
However, such symptoms may be clinically impossible to distinguish from delirium resulting from physical disorders, if a diagnosis of an underlying mental disorder has not yet been made.
Diagnostics in general settings
Multiple guidelines recommend that delirium be diagnosed when presented for health care services.
However, much evidence suggests that delirium is underdiagnosed. Higher delirium detection rates in general settings can be assisted by the use of validated delirium detection tools.
Many of those tools have been published. They differ in duration, complexity, need for training, etc. Examples of tools in use in clinical practice are:
Delirium Observation Screening Scale, Nursing Delirium Screening Scale (Nu-DESC), Confusion Assessment Method, Recognizing Agudo Delirium Como parte de su herramienta Routine (RADAR) y el 4 «A» s Prueba o 4AT.
Diagnosis in intensive care unit
In the intensive care unit, international guidelines recommend that each patient be examined for delirium every day (usually two or more times a day) using a validated clinical tool.
The two most widely used are the Intensive Care Unit Confusion Assessment Method (CAM-ICU) and the Intensive Care Delusions Screening Checklist (ICDSC).
Translations of these tools are available in more than 20 languages and are used worldwide in thousands of intensive care units, and instructional videos and thousands of implementation tips are available.
It is not so important which tool is used for the patient to be monitored.
Without the use of one of these tools, 75% of intensive care unit delirium is missed by the practice team, leaving the patient without likely active interventions to help reduce the duration of their delirium.
The most salient component of the definition of delirium that nurses and other health professionals use at the bedside is whether or not the patient can pay attention and follow simple commands.
The advent of daily monitoring of delirium, facilitated by the confusion assessment method for the intensive care unit and other assessment tools, as well as adequate documentation.
It has led to major changes in the culture of intensive care units and rounds in which the whole team can now analyze the brain and how it is in terms of being “on” (not delusional) or “inactive” (delusional) and then focus. in the various most probable causes of delirium in a specific patient.
Therefore, it is not the monitoring itself that changes the clinical course of the patient, but it is this combination of monitoring and transmitting information in rounds in the intensive care unit.
This is what makes a big difference in understanding this form of organ dysfunction and then makes a difference in clinical outcomes.
Delirium episodes can be prevented by identifying hospitalized people at risk for the condition:
People over 65, people with known cognitive impairment, people with hip fracture, those with serious illness. Close observation is recommended for the first signs in such people.
Systematically address common contributing factors (such as constipation, dehydration, and polypharmacy).
As well as providing a therapeutic environment (such as adequate lighting, minimizing noise, clear communication, minimizing relocation, signage, ways to tell time, and helping the person walk and be mobile) can prevent delirium.
Rates with several interventions together decrease rates to 0.72 from baseline in the elderly.
It is believed that 30-40% of all cases of delirium are preventable and that high rates of delirium negatively reflect the quality of care.
Melatonin and other pharmacological agents have been studied for the prevention of postoperative delirium, but the evidence is not clear.
In critically ill people, it has been recommended to avoid or use benzodiazepines with caution to reduce the risk of delirium.
It is not clear whether the drug donepezil, a cholinesterase inhibitor, reduces delirium after surgery. There is also no clear evidence to suggest that citicoline, methylprednisolone, or antipsychotics prevent delirium.
The treatment of delirium involves two main strategies: first, the treatment of the alleged underlying acute cause or causes; second, by optimizing conditions for the brain.
This involves ensuring that the person with delirium has adequate oxygenation, hydration, nutrition, and normal metabolite levels, that the effects of medications are minimized, constipation is treated, pain is treated, and so on.
Detecting and managing mental stress is also important.
Therefore, the traditional concept that the treatment of delirium is “treating the cause” is not adequate; people with delirium require a very detailed and expert analysis of all the factors that may be altering brain function.
Non-drug treatments are the first step in delirium, unless there is severe agitation that puts the person at risk of harming self or others.
Avoiding unnecessary movements, involving family members, having recognizable faces at the bedside, having means of orientation available (such as a clock and a calendar) may be enough to stabilize the situation.
If this is insufficient, verbal and non-verbal voice reduction techniques may be required to provide assurance and calm the person experiencing delirium. Only if this fails, or if de-escalation techniques are inappropriate, is drug treatment indicated.
“The TA-NA method (tolerate, anticipate, do not shake)” may be an effective management technique for older people with delirium. All unnecessary attachments (IVs, catheters, NG tubes) are removed allowing for greater mobility.
Patient behavior is tolerated even if it is not considered normal, as long as it does not put the patient or others in danger.
This technique requires patients to be isolated in a specific area designated for elderly patients suffering from delirium symptoms. Patient behavior is anticipated so that caregivers can plan the required care.
Patients are treated to reduce agitation. Reducing agitation may mean that patients do not reorient if the reorientation causes agitation.
Low-quality evidence suggests that hydration interventions do not reduce delirium in institutionalized older people.
A computerized drug search program and a pharmaceutical review can prevent delirium in this population, but more research is needed.
Physical restraints are occasionally used as a last resort with patients in severe delirium. The use of restraints should be avoided as it can increase agitation and the risk of injury. To avoid the use of restraints, some patients may require constant supervision.
Treatment of delirium with medications depends on its cause. Antipsychotics, particularly haloperidol, are the most widely used drugs for delirium and the most studied.
The evidence is weaker for atypical antipsychotics, such as risperidone, olanzapine, and quetiapine.
The British Professional Guidelines from the National Institute of Health and Clinical Excellence advise haloperidol or olanzapine. Antipsychotics, however, are not compatible for the treatment or prevention of delirium among those in the hospital.
The same benzodiazepines can cause or worsen delirium, and there is no reliable evidence for use in non-alcohol related delirium.
If the delirium is due to alcohol withdrawal or benzodiazepine withdrawal or if antipsychotics are contraindicated (such as in Parkinson’s disease or neuroleptic malignant syndrome), benzodiazepines are recommended.
Similarly, people with Lewy body dementia can have significant side effects from antipsychotics, and they need to be treated with a small dose or not treated at all.
The antidepressant trazodone is occasionally used in the treatment of delirium, but it carries a risk of excessive sedation and its use has not been well studied.
There is substantial evidence that delirium produces poor long-term outcomes in hospitalized older people.
This systematic review only included studies that looked for an independent effect of delirium (that is, after taking into account other associations with poor outcomes, for example comorbidity or severity of disease).
In older people admitted to hospital, people who experience delirium are twice as likely to die as those who do not (meta-analysis of 12 studies).
In the only prospective study conducted in the general population, older people who reported delirium also showed higher mortality (60% increase).
Institutionalization was also twice as likely after admission with delirium (meta-analysis of 7 studies).
In a community-based population that examines individuals after an episode of severe infection (although not specifically delirium), these people acquired more functional limitations (that is, they needed more help with their care needs) than those who did not experience the infection. .
After an episode of delirium in the general population, functional dependence tripled.
The association between delirium and dementia is complex. The systematic review estimated a 13-fold increase in dementia after delirium (meta-analysis of 2 studies).
However, it is difficult to be sure that this is accurate because the population admitted to the hospital includes people with undiagnosed dementia (that is, the dementia was present before the delirium, rather than being caused by it).
In prospective studies, people hospitalized for any cause appear to be at higher risk for dementia and have faster trajectories of cognitive decline, but these studies did not specifically look at delirium.
In the only population-based prospective study of delirium, older people had an eight-fold increase in dementia and faster cognitive decline.
The same association is also evident in people already diagnosed with Alzheimer’s dementia.
The highest rates of delirium (often 50% to 75% of people) are seen among those who are critically ill in the intensive care unit.
As a result, this is known as ‘intensive care unit psychosis’ or ‘intensive care unit syndrome’, terms largely abandoned for the more widely accepted term: intensive care unit delirium.
Since the emergence of validated and easy-to-implement delusional instruments for intensive care unit patients, such as the Confusion Assessment Method for the intensive care unit (CAM-ICU) and the Intensive Care Detection Verifier Delirium (IC-DSC).
Hundreds of thousands of intensive care unit patients who develop delirium in intensive care units each year, most of them have been recognized as belonging to the underactive variety.
That management teams cannot actively detect and inspect unless actively controlled with such instruments.
The causes of delirium in such patients depend on the underlying diseases, new problems such as sepsis and low oxygen levels, and the pain and sedative medications that are almost universally administered to all intensive care unit patients.
Outside of the intensive care unit, in hospital wards and in nursing homes, the problem of delirium is also a very important medical problem, especially for older patients.
The newest area of the hospital where delirium is just beginning to be routinely monitored in many centers is the Emergency Department, where the prevalence of delirium among older adults is around 10%.
A systematic review of delirium in hospitalized patients in general showed that estimates of the prevalence of delirium on admission ranged from 10% to 31%.
About 5% to 10% of older adults admitted to the hospital develop a new episode of delirium while they are in the hospital.
Delirium rates vary widely in general hospital wards. Estimates of the prevalence of delirium in nursing homes are between 10% and 45%.
Society and culture
Delirium is one of the oldest forms of mental disorder known in medical history.
Sims (1995, p.31) notes an “excellent detailed detailed description” of delirium in the stroller’s tale, by Charles Dickens, The Pickwick Papers “The Posthumous Papers of the Pickwick Club.”
In the US, the cost of admitting a patient with delirium is estimated to be between $ 16k and $ 64k, suggesting that the national burden of delirium may range from $ 38 billion to $ 150 billion per year ( 2008 estimate). In the UK the cost is estimated at £ 13k per admission.