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Delirium せん妄 譫妄、せんもう 섬망 - Wikipedia

Delirium - Wikipedia

Delirium


From Wikipedia, the free encyclopedia
This article is about the mental state and medical condition. For other uses, see Delirium (disambiguation).
Delirium
Delirium
SpecialtyIntensive care medicine, neurology, psychiatry, geriatrics
SymptomsAgitation, confusion, drowsiness, hallucinations, delusions, memory problems
Usual onsetAny age, but more often in people aged 65 and above
DurationDays to weeks, sometimes months (several hours when caused by anticholinergic medications, like dicyclomine, diphenhydramine, doxylamine, promethazine)
TypesHyperactive, hypoactive, mixed level of activity
CausesInconclusive
Risk factorsInfection, chronic health problems, certain medications, neurological problems, sleep deprivation, surgery
Differential diagnosisDementia
TreatmentTreating underlying cause, symptomatic management with medication
MedicationDepending on the underlying cause


Delirium (formerly acute confusional state, an ambiguous term that is now discouraged)[1] is a specific state of acute confusion attributable to the direct physiological consequence of a medical condition, effects of a psychoactive substance, or multiple causes, which usually develops over the course of hours to days.[2][3] As a syndrome, delirium presents with disturbances in attention, awareness, and higher-order cognition. People with delirium may experience other neuropsychiatric disturbances including changes in psychomotor activity (e.g., hyperactive, hypoactive, or mixed level of activity), disrupted sleep-wake cycle, emotional disturbances, disturbances of consciousness, or altered state of consciousness, as well as perceptual disturbances (e.g., hallucinations and delusions), although these features are not required for diagnosis.

Diagnostically, delirium encompasses both the syndrome of acute confusion and its underlying organic process[3] known as an acute encephalopathy.[1] The cause of delirium may be either a disease process inside the brain or a process outside the brain that nonetheless affects the brain. Delirium may be the result of an underlying medical condition (e.g., infection or hypoxia), side effect of a medication such as diphenhydramine, promethazine, and dicyclomine, substance intoxication (e.g., opioids or hallucinogenic deliriants), substance withdrawal (e.g., alcohol or sedatives), or from multiple factors affecting one's overall health (e.g., malnutrition, pain, etc.). In contrast, the emotional and behavioral features due to primary psychiatric disorders (e.g., as in schizophrenia, bipolar disorder) do not meet the diagnostic criteria for 'delirium'.[2]

Delirium may be difficult to diagnose without first establishing a person's usual mental function or 'cognitive baseline'. Delirium may be confused with multiple psychiatric disorders or chronic organic brain syndromes because of many overlapping signs and symptoms in common with dementia, depression, psychosis, etc.[4][5] Delirium may occur in persons with existing mental illness, baseline intellectual disability, or dementia, entirely unrelated to any of these conditions. Delirium is often confused with schizophrenia, psychosis, organic brain syndromes, and more, because of similar signs and symptoms of these disorders.

Treatment of delirium requires identifying and managing the underlying causes, managing delirium symptoms, and reducing the risk of complications.[6] In some cases, temporary or symptomatic treatments are used to comfort the person or to facilitate other care (e.g., preventing people from pulling out a breathing tube). Antipsychotics are not supported for the treatment or prevention of delirium among those who are in hospital; however, they may be used in cases where a person has distressing experiences such as hallucinations or if the person poses a danger to themselves or others.[7][8][9][10][11] When delirium is caused by alcohol or sedative-hypnotic withdrawal, benzodiazepines are typically used as a treatment.[12] There is evidence that the risk of delirium in hospitalized people can be reduced by non-pharmacological care bundles (see Delirium § Prevention).[9] According to the text of DSM-5-TR, although delirium affects only 1–2% of the overall population, 18–35% of adults presenting to the hospital will have delirium, and delirium will occur in 29–65% of people who are hospitalized.[3] Delirium occurs in 11–51% of older adults after surgery, in 81% of those in the ICU, and in 20–22% of individuals in nursing homes or post-acute care settings.[3] Among those requiring critical care, delirium is a risk factor for death within the next year.[3][13]

Because of the confusion caused by similar signs and symptoms of delirium with other neuropsychiatric disorders like schizophrenia and psychosis, treating delirium can be difficult, and might even cause death of the patient due to being treated with the wrong medications.[14][15][16]

Definition

In common usage, delirium can refer to drowsiness, agitation, disorientation, or hallucinations. In medical terminology, however, the core features of delirium include an acute disturbance in attention, awareness, and global cognition.

Although slight differences exist between the definitions of delirium in the DSM-5-TR[3] and ICD-10,[17] the core features are broadly the same. In 2022, the American Psychiatric Association released the fifth edition text revision of the DSM (DSM-5-TR) with the following criteria for diagnosis:[3]

  • A. Disturbance in attention and awareness. This is a required symptom and involves easy distraction, inability to maintain attentional focus, and varying levels of alertness.[18]
  • B. Onset is acute (from hours to days), representing a change from baseline mentation and often with fluctuations throughout the day
  • C. At least one additional cognitive disturbance (in memory, orientation, language, visuospatial ability, or perception)
  • D. The disturbances (criteria A and C) are not better explained by another neurocognitive disorder
  • E. There is evidence that the disturbances above are a "direct physiological consequence" of another medical condition, substance intoxication or withdrawal, toxin, or various combinations of causes

Signs and symptoms

Delirium exists across a range of arousal levels, either as a state between normal wakefulness/alertness and coma (hypoactive) or as a state of heightened psychophysiological arousal (hyperactive). It can also alternate between the two (mixed level of activity). While requiring an acute disturbance in attention, awareness, and cognition, the syndrome of delirium encompasses a broad range of additional neuropsychiatric disturbances.[18]

  • Inattention: A disturbance in attention is required for delirium diagnosis. This may present as an impaired ability to direct, focus, sustain, or shift attention.[3]
  • Memory impairment: The memory impairment that occurs in delirium is often due to an inability to encode new information, largely as a result of having impaired attention. Older memories already in storage are retained without need of concentration, so previously formed long-term memories (i.e., those formed before the onset of delirium) are usually preserved in all but the most severe cases of delirium, though recall of such information may be impaired due to global impairment in cognition.
  • Disorientation: A person may be disoriented to self, place, or time. Additionally, a person may be 'disoriented to situation' and not recognize their environment or appreciate what is going on around them.
  • Disorganized thinking: Disorganized thinking is usually noticed with speech that makes limited sense with apparent irrelevancies, and can involve poverty of speech, loose associations, perseveration, tangentiality, and other signs of a formal thought disorder.
  • Language disturbances: Anomic aphasia, paraphasia, impaired comprehension, agraphia, and word-finding difficulties all involve impairment of linguistic information processing.
  • Sleep/wake disturbances: Sleep disturbances in delirium reflect disruption in both sleep/wake and circadian rhythm regulation, typically characterized by fragmented sleep or even sleep-wake cycle reversal (i.e., active at night, sleeping during the day), including as an early sign preceding the onset of delirium.
  • Psychotic and other erroneous beliefs: Symptoms of psychosis include suspiciousness, overvalued ideation and frank delusions. Delusions are typically poorly formed and less stereotyped than in schizophrenia or Alzheimer's disease. They usually relate to persecutory themes of impending danger or threat in the immediate environment (e.g., being poisoned by nurses).
  • Perceptual disturbances: These can include illusions, which involve the misperception of real stimuli in the environment, or hallucinations, which involve the perception of stimuli that do not exist.
  • Mood lability: Distortions to perceived or communicated emotional states as well as fluctuating emotional states can manifest in delirium (e.g., rapid changes between terror, sadness, joking, fear, anger, and frustration).[19]
  • Motor activity changes: Delirium has been commonly classified into psychomotor subtypes of hypoactive, hyperactive, and mixed level of activity,[20] though studies are inconsistent as to their prevalence.[21] Hypoactive cases are prone to non-detection or misdiagnosis as depression. A range of studies suggests that motor subtypes differ regarding underlying pathophysiology, treatment needs, functional prognosis, and risk of mortality, though inconsistent subtype definitions and poorer detection of hypoactive subtypes may influence the interpretation of these findings.[22] The notion of unifying hypoactive and hyperactive states under the construct of delirium is commonly attributed to Lipowski.[23]
    • Hyperactive symptoms include hyper-vigilance, restlessness, fast or loud speech, irritability, combativeness, impatience, swearing, singing, laughing, uncooperativeness, euphoria, anger, wandering, easy startling, fast motor responses, distractibility, tangentiality, nightmares, and persistent thoughts (hyperactive sub-typing is defined with at least three of the above).[24]
    • Hypoactive symptoms include decreased alertness, sparse or slow speech, lethargy, slowed movements, staring, and apathy.[24]
    • Mixed level of activity describes instances of delirium where activity level is either normal or fluctuating between hyperactive and hypoactive.[3]

Causes

Delirium arises through the interaction of a number of predisposing and precipitating factors.[25][26]

Individuals with multiple and/or significant predisposing factors are at high risk for an episode of delirium with a single and/or mild precipitating factor. Conversely, delirium may only result in low risk individuals if they experience a serious or multiple precipitating factors. These factors can change over time, thus an individual's risk of delirium is modifiable (see Delirium § Prevention).

Predisposing factors

Important predisposing factors include the following:[26][27]

Precipitating factors

Acute confusional state caused by alcohol withdrawal, also known as delirium tremens

Any serious, acute biological factor that affects neurotransmitter, neuroendocrine, or neuroinflammatory pathways can precipitate an episode of delirium in a vulnerable brain.[28] Certain elements of the clinical environment have also been associated with the risk of developing delirium.[29] Some of the most common precipitating factors are listed below:[26][30]

Pathophysiology

The pathophysiology of delirium is still not well understood, despite extensive research.

Animal models

The lack of animal models that are relevant to delirium has left many key questions in delirium pathophysiology unanswered. Earliest rodent models of delirium used atropine (a muscarinic acetylcholine receptor blocker) to induce cognitive and electroencephalography (EEG) changes similar to delirium, and other anticholinergic drugs, such as biperiden and hyoscine, have produced similar effects. Along with clinical studies using various drugs with anticholinergic activity, these models have contributed to a "cholinergic deficiency hypothesis" of delirium.[37]

Profound systemic inflammation occurring during sepsis is also known to cause delirium (often termed sepsis-associated encephalopathy).[38] Animal models used to study the interactions between prior degenerative disease and overlying systemic inflammation have shown that even mild systemic inflammation causes acute and transient deficits in working memory among diseased animals.[39] Prior dementia or age-associated cognitive impairment is the primary predisposing factor for clinical delirium and "prior pathology" as defined by these new animal models may consist of synaptic loss, abnormal network connectivity, and "primed microglia" brain macrophages stimulated by prior neurodegenerative disease and aging to amplify subsequent inflammatory responses in the central nervous system (CNS).[39]

Cerebrospinal fluid

Studies of cerebrospinal fluid (CSF) in delirium are difficult to perform. Apart from the general difficulty of recruiting participants who are often unable to give consent, the inherently invasive nature of CSF sampling makes such research particularly challenging. However, a few studies have managed to sample CSF from persons undergoing spinal anesthesia for elective or emergency surgery.[26][40][41]

A 2018 systematic review showed that, broadly, delirium may be associated with neurotransmitter imbalance (namely serotonin and dopamine signaling), reversible fall in somatostatin, and increased cortisol.[42] The leading "neuroinflammatory hypothesis" (where neurodegenerative disease and aging leads the brain to respond to peripheral inflammation with an exaggerated CNS inflammatory response) has been described,[43] but current evidence is still conflicting and fails to concretely support this hypothesis.[42]

Neuroimaging

Neuroimaging provides an important avenue to explore the mechanisms that are responsible for delirium.[44][45] Despite progress in the development of magnetic resonance imaging (MRI), the large variety in imaging-based findings has limited our understanding of the changes in the brain that may be linked to delirium. Some challenges associated with imaging people diagnosed with delirium include participant recruitment and inadequate consideration of important confounding factors such as history of dementia and/or depression, which are known to be associated with overlapping changes in the brain also observed on MRI.[44]

Evidence for changes in structural and functional markers include: changes in white-matter integrity (white matter lesions), decreases in brain volume (likely as a result of tissue atrophy), abnormal functional connectivity of brain regions responsible for normal processing of executive function, sensory processing, attention, emotional regulation, memory, and orientation, differences in autoregulation of the vascular vessels in the brain, reduction in cerebral blood flow and possible changes in brain metabolism (including cerebral tissue oxygenation and glucose hypometabolism).[44][45] Altogether, these changes in MRI-based measurements invite further investigation of the mechanisms that may underlie delirium, as a potential avenue to improve clinical management of people with this condition.[44]

Neurophysiology

Electroencephalography (EEG) allows for continuous capture of cortical activity in the brain, and is useful in understanding real-time physiologic changes during delirium.[46] Since the 1950s, delirium has been known to be associated with slowing of resting-state EEG rhythms, with abnormally decreased background alpha power and increased theta and delta frequency activity.[46][47]

From such evidence, a 2018 systematic review proposed a conceptual model that delirium results when insults/stressors trigger a breakdown of brain network dynamics in individuals with low brain resilience (i.e. people who already have underlying problems of low neural connectivity and/or low neuroplasticity like those with Alzheimer's disease).[46]

Neuropathology

Only a handful of studies exist where there has been an attempt to correlate delirium with pathological findings at autopsy. One research study has been reported on 7 people who died during ICU admission.[48] Each case was admitted with a range of primary pathologies, but all had acute respiratory distress syndrome and/or septic shock contributing to the delirium, 6 showed evidence of low brain perfusion and diffuse vascular injury, and 5 showed hippocampal involvement. A case-control study showed that 9 delirium cases showed higher expression of HLA-DR and CD68 (markers of microglial activation), IL-6 (cytokines pro-inflammatory and anti-inflammatory activities) and GFAP (marker of astrocyte activity) than age-matched controls; this supports a neuroinflammatory cause to delirium, but the conclusions are limited by methodological issues.[49]

A 2017 retrospective study correlating autopsy data with mini–mental state examination (MMSE) scores from 987 brain donors found that delirium combined with a pathological process of dementia accelerated MMSE score decline more than either individual process.[50]

Diagnosis

The DSM-5-TR criteria are often the standard for diagnosing delirium clinically. However, early recognition of delirium's features using screening instruments, along with taking a careful history, can help in making a diagnosis of delirium. A diagnosis of delirium generally requires knowledge of a person's baseline level of cognitive function. This is especially important for treating people who have neurocognitive or neurodevelopmental disorders, whose baseline mental status may be mistaken as delirium.[51]

General settings

Guidelines recommend that delirium should be diagnosed consistently when present.[6][52] Much evidence reveals that in most centers delirium is greatly under-diagnosed.[53][54][55][56] A systematic review of large scale routine data studies reporting data on delirium detection tools showed important variations in tool completion rates and tool positive score rates. Some tools, even if completed at high rates, showed delirium positive score rates that there much lower than the expected delirium occurrence level, suggesting low sensitivity in practice.[57]

There is evidence that delirium detection and coding rates can show improvements in response to guidelines and education; for example, whole country data in England and Scotland (sample size 7.7M people per year) show that there were large increases (3-4 fold) in delirium coding between 2012 and 2020.[58] Delirium detection in general acute care settings can be assisted by the use of validated delirium screening tools. Many such tools have been published, and they differ in a variety of characteristics (e.g., duration, complexity, and need for training). It is also important to ensure that a given tool has been validated for the setting where it is being used.

Examples of tools in use in clinical practice include:

  • Confusion Assessment Method (CAM),[59] including variants such as the 3-Minute Diagnostic Interview for the CAM (3D-CAM)[60] and brief CAM (bCAM)[61]
  • Delirium Observation Screening Scale (DOS)[62]
  • Nursing Delirium Screening Scale (Nu-DESC)[63]
  • Recognizing Acute Delirium As part of your Routine (RADAR)[64]
  • 4AT (4 A's Test)[65]
  • Delirium Diagnostic Tool-Provisional (DDT-Pro),[66][67] also for subsyndromal delirium[68]

Intensive care unit

People who are in the ICU are at greater risk of delirium, and ICU delirium may lead to prolonged ventilation, longer stays in the hospital, increased stress on family and caregivers, and an increased chance of death.[69] In the ICU, international guidelines recommend that every person admitted gets checked for delirium every day (usually twice or more a day) using a validated clinical tool.[70] Key elements of detecting delirium in the ICU are whether a person can pay attention during a listening task and follow simple commands.[71] The two most widely used are the Confusion Assessment Method for the ICU (CAM-ICU)[72] and the Intensive Care Delirium Screening Checklist (ICDSC).[73] Translations of these tools exist in over 20 languages and are used ICUs globally with instructional videos and implementation tips available.[71] For children in need of intensive care there are validated clinical tools adjusted according to age. The recommended tools are preschool and pediatric Confusion Assessment Methods for the ICU (ps/pCAM-ICU) or the Cornell Assessment for Pediatric Delirium (CAPD) as the most valid and reliable delirium monitoring tools in critically ill children or adolescents.[74]

More emphasis is placed on regular screening over the choice of tool used. This, coupled with proper documentation and informed awareness by the healthcare team, can affect clinical outcomes.[71] Without using one of these tools, 75% of ICU delirium can be missed by the healthcare team, leaving the person without any likely interventions to help reduce the duration of delirium.[71][75]

Differential diagnosis

There are conditions that might have similar clinical presentations to those seen in delirium. These include dementia,[76][77][78][79][80] depression,[80][78] psychosis,[5][80][78] catatonia,[5] and other conditions that affect cognitive function.[79]

  • Dementia: This group of disorders is acquired (non-congenital) with usually irreversible cognitive and psychosocial functional decline. Dementia usually results from an identifiable degenerative brain disease (e.g., Alzheimer disease or Huntington's disease), requires chronic impairment (versus acute onset in delirium), and is typically not associated with changes in level of consciousness.[81] Dementia is different from delirium in that dementia lasts long-term while delirium lasts short-term.
  • Depression: Similar symptoms exist between depression and delirium (especially the hypoactive subtype). Gathering a history from other caregivers can clarify baseline mentation.[82]
  • Psychosis: In general, people with primary psychosis have intact cognitive function; however, primary psychosis can mimic delirium when it presents with disorganized thoughts and mood dysregulation. This is particularly true in the condition known as delirious mania.[5]
  • Other mental illnesses: Some mental illnesses, such as a manic episode of bipolar disorder, depersonalization disorder, or other dissociative conditions, can present with features similar to that of delirium.[5] Such condition, however, would not qualify for a diagnosis of delirium per DSM-5-TR criterion D (i.e., fluctuating cognitive symptoms occurring as part of a primary mental disorder are results of the said mental disorder itself), while physical disorders (e.g., infections, hypoxia, etc.) can precipitate delirium as a mental side-effect/symptom.[3]

Prevention

Treating delirium that is already established is challenging and for this reason, preventing delirium before it begins is ideal. Prevention approaches include screening to identify people who are at risk, and medication-based and non-medication based (non-pharmacological) treatments.[83]

An estimated 30–40% of all cases of delirium could be prevented in cognitively at-risk populations, and high rates of delirium reflect negatively on the quality of care.[30] Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition. This includes individuals over age 65, with a cognitive impairment, undergoing major surgery, or with severe illness.[52] Routine delirium screening is recommended in such populations. It is thought that a personalized approach to prevention that includes different approaches together can decrease rates of delirium by 27% among the elderly.[84][9]

In 1999, Sharon K. Inouye at Yale University, founded the Hospital Elder Life Program (HELP)[85] which has since become recognized as a proven model for preventing delirium.[86] HELP prevents delirium among the elderly through active participation and engagement with these individuals. There are two working parts to this program, medical professionals such as a trained nurse, and volunteers, who are overseen by the nurse. The volunteer program equips each trainee with the adequate basic geriatric knowledge and interpersonal skills to interact with patients. Volunteers perform the range of motion exercises, cognitive stimulation, and general conversation[87] with elderly patients who are staying in the hospital. Alternative effective delirium prevention programs have been developed, some of which do not require volunteers.[88]

Prevention efforts often fall on caregivers. Caregivers often have a lot expected of them and this is where socioeconomic status plays a role in prevention.[89] If prevention requires constant mental stimulation and daily exercise, this takes time out of the caregiver's day. Based on socioeconomic classes, this may be valuable time that would be used working to support the family. This leads to a disproportionate number of individuals who experience delirium being from marginalized identities.[86] Programs such as the Hospital Elder Life Program can attempt to combat these societal issues by providing additional support and education about delirium that may not otherwise be accessible.

Non-pharmacological

Delirium may be prevented and treated by using non-pharmacologic approaches focused on risk factors, such as constipation, dehydration, low oxygen levels, immobility, visual or hearing impairment, sleep disturbance, functional decline, and by removing or minimizing problematic medications.[52][78] Ensuring a therapeutic environment (e.g., individualized care, clear communication, adequate reorientation and lighting during daytime, promoting uninterrupted sleep hygiene with minimal noise and light at night, minimizing room relocation, having familiar objects like family pictures, providing earplugs, and providing adequate nutrition, pain control, and assistance toward early mobilization) may also aid in preventing delirium.[9][30][90][91] Research into pharmacologic prevention and treatment is weak and insufficient to make proper recommendations.[78]

Pharmacological

Melatonin and other pharmacological agents have been studied for delirium prevention, but evidence is conflicting.[9][92] Avoidance or cautious use of benzodiazepines has been recommended for reducing the risk of delirium in critically ill individuals.[93] It is unclear if the medication donepezil, a cholinesterase inhibitor, reduces delirium following surgery.[9] There is also no clear evidence to suggest that citicoline, methylprednisolone, or antipsychotic medications prevent delirium.[9] A review of intravenous versus inhalational maintenance of anaesthesia for postoperative cognitive outcomes in elderly people undergoing non-cardiac surgery showed little or no difference in postoperative delirium according to the type of anaesthetic maintenance agents[94] in five studies (321 participants). The authors of this review were uncertain whether maintenance of anaesthesia with propofol-based total intravenous anaesthesia (TIVA) or with inhalational agents can affect the incidence rate of postoperative delirium.

Interventions for preventing delirium in long-term care or hospital

The current evidence suggests that software-based interventions to identify medications that could contribute to delirium risk and recommend a pharmacist's medication review probably reduces incidence of delirium in older adults in long-term care.[95] The benefits of hydration reminders and education on risk factors and care homes' solutions for reducing delirium is still uncertain.[95]

For inpatients in a hospital setting, numerous approaches have been suggested to prevent episodes of delirium including targeting risk factors such as sleep deprivation, mobility problems, dehydration, and impairments to a person's sensory system. Often a 'multicomponent' approach by an interdisciplinary team of health care professionals is suggested for people in the hospital at risk of delirium, and there is some evidence that this may decrease to incidence of delirium by up to 43% and may reduce the length of time that the person is hospitalized.[83]

Treatment

Most often, delirium is reversible; however, people with delirium require treatment for the underlying cause(s), often to prevent injury and other poor outcomes directly related to delirium.[69]

Treatment of delirium requires attention to multiple domains including the following:[2][30]

  • Identify and treat the underlying medical disorder or cause(s)
  • Addressing any other possible predisposing and precipitating factors that might be disrupting brain function
  • Optimize physiology and conditions for brain recovery (e.g., oxygenation, hydration, nutrition, electrolytes, metabolites, medication review)
  • Detect and manage distress and behavioral disturbances (e.g., pain control)
  • Maintaining mobility
  • Provide rehabilitation through cognitive engagement and mobilization
  • Communicate effectively with the person experiencing delirium and their carers or caregivers
  • Provide adequate follow-up including consideration of possible dementia and post-traumatic stress.[2]

Multidomain interventions

These interventions are the first steps in managing acute delirium, and there are many overlaps with delirium preventative strategies.[96] In addition to treating immediate life-threatening causes of delirium (e.g., low O2, low blood pressure, low glucose, dehydration), interventions include optimizing the hospital environment by reducing ambient noise, providing proper lighting, offering pain relief, promoting healthy sleep-wake cycles, and minimizing room changes.[96] Although multicomponent care and comprehensive geriatric care are more specialized for a person experiencing delirium, several studies have been unable to find evidence showing they reduce the duration of delirium.[96]

Family, friends, and other caregivers can offer frequent reassurance, tactile and verbal orientation, cognitive stimulation (e.g. regular visits, familiar objects, clocks, calendars, etc.), and means to stay engaged (e.g. making hearing aids and eyeglasses readily available).[30][52][97] Sometimes verbal and non-verbal deescalation techniques may be required to offer reassurances and calm the person experiencing delirium.[52] Restraints should rarely be used as an intervention for delirium.[98] The use of restraints has been recognized as a risk factor for injury and aggravating symptoms, especially in older hospitalized people with delirium.[98] The only cases where restraints should sparingly be used during delirium is in the protection of life-sustaining interventions, such as endotracheal tubes.[98]

Another approached called the "T-A-DA (tolerate, anticipate, don't agitate) method" can be an effective management technique for older people with delirium, where abnormal behaviors (including hallucinations and delusions) are tolerated and unchallenged, as long as caregiver safety and the safety of the person experiencing delirium is not threatened.[78] Implementation of this model may require a designated area in the hospital. All unnecessary attachments are removed to anticipate for greater mobility, and agitation is prevented by avoiding excessive reorientation/questioning.[78]

Medications

The use of medications for delirium is generally restricted to managing its distressing or dangerous neuropsychiatric disturbances. Short-term use (one week or less) of low-dose haloperidol is among the more common pharmacological approaches to delirium.[30][52] Evidence for effectiveness of atypical antipsychotics (e.g. risperidone, olanzapine, ziprasidone, and quetiapine) is emerging, with the benefit for fewer side effects[30][99] Use antipsychotic drugs with caution or not at all for people with conditions such as Parkinson's disease or dementia with Lewy bodies.[52] Evidence for the effectiveness of medications (including antipsychotics and benzodiazepines) in treating delirium is weak.[77][69]

Benzodiazepines can cause or worsen delirium, and there is no reliable evidence of efficacy for treating non-anxiety-related delirium.[100] Similarly, people with dementia with Lewy bodies may have significant side effects with antipsychotics, and should either be treated with a none or small doses of benzodiazepines.[52]

The antidepressant trazodone is occasionally used in the treatment of delirium, but it carries a risk of over-sedation, and its use has not been well studied.[30]

For adults with delirium that are in the ICU, medications are used commonly to improve the symptoms. Dexmedetomidine may shorten the length of the delirium in adults who are critically ill, and rivastigmine is not suggested.[69] There is emerging evidence that guanfacine can be helpful in reducing delirium, which may involve strengthening network connections in the prefrontal cortex.[101]

For adults with delirium who are near the end of their life (on palliative care) high quality evidence to support or refute the use of most medications to treat delirium is not available.[102] Low quality evidence indicates that the antipsychotic medications risperidone or haloperidol may make the delirium slightly worse in people who are terminally ill, when compared to a placebo treatment.[102] There is also moderate to low quality evidence to suggest that haloperidol and risperidone may be associated with a slight increase in side effects, specifically extrapyramidal symptoms, if the person near the end of their life has delirium that is mild to moderate in severity.[102]

Prognosis

There is substantial evidence that delirium results in long-term poor outcomes in older persons admitted to hospital.[103] This systematic review only included studies that looked for an independent effect of delirium (i.e., after accounting for other associations with poor outcomes, for example co-morbidity or illness severity).

In older persons admitted to hospital, individuals experiencing delirium are twice as likely to die than those who do not (meta-analysis of 12 studies).[103] In the only prospective study conducted in the general population, older persons reporting delirium also showed higher mortality (60% increase).[104] A large (N=82,770) two-centre study in unselected older emergency population found that delirium detected as part of normal care using the 4AT tool was strongly linked to 30-day mortality, hospital length of stay, and days at home in the year following the 4AT test date.[105]

Institutionalization was also twice as likely after an admission with delirium (meta-analysis of seven studies).[103] In a community-based population examining individuals after an episode of severe infection (though not specifically delirium), these persons acquired more functional limitations (i.e., required more assistance with their care needs) than those not experiencing infection.[106] After an episode of delirium in the general population, functional dependence increased threefold.[104]

The association between delirium and dementia is complex. The systematic review estimated a 13-fold increase in dementia after delirium (meta-analysis of two studies).[103] However, it is difficult to be certain that this is accurate because the population admitted to hospital includes persons with undiagnosed dementia (i.e., the dementia was present before the delirium, rather than caused by it). In prospective studies, people hospitalised from any cause appear to be at greater risk of dementia[107] and faster trajectories of cognitive decline,[107][108] but these studies did not specifically look at delirium. In the only population-based prospective study of delirium, older persons had an eight-fold increase in dementia and faster cognitive decline.[104] The same association is also evident in persons already diagnosed with Alzheimer's dementia.[109]

Recent long-term studies showed that many people still meet criteria for delirium for a prolonged period after hospital discharge, with up to 21% of people showing persistent delirium at 6 months post-discharge.[110]

Dementia in ICU survivors

See also: Post-intensive care syndrome

Between 50% and 70% of people admitted to the ICU have permanent problems with brain dysfunction similar to those experienced by people with Alzheimer's or those with a traumatic brain injury, leaving many ICU survivors permanently disabled.[111] This is a distressing personal and public health problem and continues to receive increasing attention in ongoing investigations.[112][100]

The implications of such an "acquired dementia-like illness" can profoundly debilitate a person's livelihood level, often dismantling his/her life in practical ways like impairing one's ability to find a car in a parking lot, complete shopping lists, or perform job-related tasks done previously for years.[112] The societal implications can be enormous when considering work-force issues related to the inability of wage-earners to work due to their own ICU stay or that of someone else they must care for.[113]

Epidemiology

The highest rates of delirium (often 50–75% of people) occur among those who are critically ill in the intensive care unit (ICU).[114] This was historically referred to as "ICU psychosis" or "ICU syndrome"; however, these terms are now widely disfavored in relation to the operationalized term ICU delirium. Since the advent of validated and easy-to-implement delirium instruments for people admitted to the ICU such as the Confusion Assessment Method for the ICU (CAM-ICU)[72] and the Intensive Care Delirium Screening Checklist (ICDSC),[73] it has been recognized that most ICU delirium is hypoactive, and can easily be missed unless evaluated regularly. The causes of delirium depend on the underlying illnesses, new problems like sepsis and low oxygen levels, and the sedative and pain medicines that are nearly universally given to all people in the ICU p. Outside the ICU, on hospital wards and in nursing homes, the problem of delirium is also a very important medical problem, especially for older patients.[115]

The most recent area of the hospital in which delirium is just beginning to be monitored routinely in many centers is the Emergency Department, where the prevalence of delirium among older adults is about 10%.[116] A systematic review of delirium in general medical inpatients showed that estimates of delirium prevalence on admission ranged 10–31%.[117] About 5–10% of older adults who are admitted to hospital develop a new episode of delirium while in hospital.[116] Rates of delirium vary widely across general hospital wards.[118] Estimates of the prevalence of delirium in nursing homes are between 10%[116] and 45%.[119]

Society and culture

Delirium is one of the oldest forms of mental disorder known in medical history.[120] The Roman author Aulus Cornelius Celsus used the term to describe mental disturbance from head trauma or fever in his work De Medicina.[121] Sims (1995, p. 31) points out a "superb detailed and lengthy description" of delirium in "The Stroller's Tale" from Charles Dickens' The Pickwick Papers.[122][123] Historically, delirium has also been noted for its cognitive sequelae. For instance, the English medical writer Philip Barrow noted in 1583 that if delirium (or "frensy") resolves, it may be followed by a loss of memory and reasoning power.[124]

Costs

In the US, the cost of a hospital admission for people with delirium is estimated at between $16k and $64k, suggesting the national burden of delirium may range from $38 bn to $150 bn per year (2008 estimate).[125] In the UK, the cost is estimated as £13k per admission.[126]

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Further reading

  • Macdonald A, Lindesay J, Rockwood K (2002). Delirium in old age. Oxford [Oxfordshire]: Oxford University Press. ISBN 978-0-19-263275-3.
  • Grassi L, Caraceni A (2003). Delirium: acute confusional states in palliative medicine. Oxford: Oxford University Press. ISBN 978-0-19-263199-2.
  • Newman JK, Slater CT, eds. (2012). Delirium: causes, diagnosis and treatment. Hauppauge, N.Y.: Nova Science Publisher's, Inc. ISBN 978-1-61324-294-0.


==

せん妄

出典: フリー百科事典『ウィキペディア（Wikipedia）』
せん妄
概要
診療科精神医学, 神経学, 心理学
分類および外部参照情報
ICD-10F05
ICD-9-CM293.0
DiseasesDB29284
eMedicinemed/3006
Patient UKせん妄
MeSHD003693

せん妄（譫妄、せんもう、英: delirium）とは意識混濁に加えて奇妙で強迫的な思考や幻覚・錯覚が見られるような状態。健康な人でも睡眠中に強引に覚醒されると同症状が発生する場合がある。特に術後患者や集中治療室(ICU)で管理されている患者によく発生するとされる[1]。医学用語としての具体的な定義はあるものの、あらゆる種類の錯乱状態を総称する言葉として使用されることもしばしばある[2]。

急激な精神運動興奮（カテーテルを引き抜くなど）や、問診上明らかな見当識障害で気がつかれることが多い。大手術後の患者（術後せん妄）、アルツハイマー病、脳卒中、代謝障害、アルコール依存症の患者にもみられる。せん妄とは治療も異なる振戦せん妄は、酒やベンゾジアゼピン系薬物からの離脱によって起こり区別される。

通常は対症療法が行われる。一般に抗精神病薬が使われるが、その効果には議論がある。

症状

覚醒水準の低下の亢進、見当識障害、注意の散漫、判断力・集中力の低下、思考や気分の不安定化、錯覚や幻覚などの意識障害が発生し[3]、攻撃的になったり暴力を起こすこともある[4]。突然生じ経過は短いが、命にかかわることもある緊急事態である[4]。

高齢者にはせん妄がしばしば出現するが、その状態像は認知症と重なる部分が多いため、高齢者の軽い意識障害は仮性認知症と呼ばれる[3]。せん妄の特徴として、発現が急性または亜急性であり、症状の発現に浮動性があり、夜間に増加する傾向があることから[4]、せん妄と認知症の鑑別は時間の経過によって行われる[3]。「入院した途端、急にボケてしまって（認知症のように見える）、自分がどこにいるのか、あるいは今日が何月何日かさえもわからなくなってしまった。」というエピソードが極めて典型的である。

また、高熱とともにせん妄を体験する場合があり、とくに子供に多い[5]。大半の患者はせん妄を覚えており、苦痛な経験だったとの調査報告があり、せん妄は意識障害だから記憶がないというのは誤解である[6]。

こういった症状をおこすせん妄という病態の背景には意識障害、幻視を中心とした幻覚、精神運動興奮があると考えられている。

危険因子

認知症、高齢、重症患者、うつ状態、複数薬物、聴視覚障害（難聴や白内障）、感染症、薬物の中毒症状、アルコールや薬物の離脱症状、疼痛、手術後、身体抑制などがリスクファクターと言われている。

診断基準

『精神障害の診断と統計マニュアル』 (DSM) にも診断基準はあるが、より実践的なConfusion Assessment Methods (CAM) をここでは記す[7]。

  • 急性の発症と症状の動揺
  • 注意力の欠如
  • 思考の錯乱
  • 意識レベルの変化

2つ目までは必須項目であり、あとひとつを満たせば診断してよい。

鑑別診断

認知症では、長期間症状が持続しており意識の混濁はないが、認知症の者にせん妄が生じることもある[4]。急性の脳損傷も似た症状を起こすが早い治療が必要なため、身体疾患の特定も必要となる[4]。

薬の過剰摂取による症状は、薬物相互作用や代謝の低下した高齢者で起こりうる[4]。

振戦せん妄は、アルコールやベンゾジアゼピン系薬あるいはバルビツール酸系薬の離脱症状できたすせん妄状態である。せん妄とは区別され、治療も異なる。

予防

2016年のコクランレビューは、集中治療室以外の入院患者でBispectral indexを用いて麻酔の深さをモニターすることで、せん妄発生率を低下させる中程度の質のエビデンスがあるが、抗精神病薬、コリンエステラーゼ阻害剤、メラトニン、メラトニン受容体作動薬では研究はされているがせん妄の発生率を低下させる明確なエビデンスはないとした[8]。鎮静薬デクスメデトミジンは他の薬剤よりせん妄発生率が低く、特に心臓手術後は有効であった[9]。2018年のレビューでは、16のシステマティックレビューがあり、そこには8つの主要なランダム化比較試験が含まれており、術後の予防的な抗精神病薬の使用はせん妄を発生率を低下させるが、入院期間には影響せず、また死亡率が増加する可能性がある[10]。

予防を目的とした術中のケタミン使用は6つのRCTから、せん妄の発生率に差がなく、術後認知機能障害では保護的なようだが、証拠が限られており結論には限界があった[11]。

2017年のレビューは、5つのランダム化比較試験 (RCT) と1つの非RCTを見出し、メラトニンでは相反する結果であり、1つのラメルテオンでの試験はせん妄発生率を減少させ、L-トリプトファンでは効果がなく、結論としてメラトニン受容体作動薬の定常的な使用は推奨できないとした[12]。2016年のRCTのメタアナリシスは、計669人を含む4つのRCTがあり、メラトニンの服用は内科病棟ではせん妄発生率を減少させ、外科病棟では差がなかった[13]。2015年のレビューには、メラトニンの2つのRCTと、タシメルテオンの1つのRCTが含まれた[14]。

治療

2010年のイギリスのガイドラインでは、ハロペリドール（セレネース）やオランザピン（ジプレキサ）が少量かつ短期間でのみ用いられる[15]。

日本の2015年の『せん妄の治療指針』では、糖尿病がなければ錐体外路症状が最も起こりにくいクエチアピン（やオランザピン）、あればリスペリドン、内服困難ではハロペリドールの注射剤、検査のための深い鎮静には、ハロペリドールや拮抗薬のフルマゼニルを用意したうえでミダゾラム[15]が提示されている。

低活動型せん妄に対しては、専門医が推奨する目立った薬剤はないとする、日本での2016年の調査結果がある[16]。

レビュー

2018年のコクラン共同計画のレビューでは、救急ではない入院患者で治療のための抗精神病薬の使用では、証拠の質が低いがせん妄重症度、死亡率、抗精神病薬（定型か非定型か）による錐体外路症状の発生率に変化はなく、せん妄の時間、入院期間やQOLに影響があったかは判断できない[17]。

2018年の別のレビューは、定型と非定型の抗精神病薬を比較した。ハロペリドールとリスペリドンでは大規模なランダム化比較試験によって偽薬よりも予後不良に結び付いていた。オランザピンとクエチアピンは、大規模な試験ではないが有効性を支持している。大規模RCTが必要とされる[18]。

非薬理学的

非薬理学的な介入では2018年のメタアナリシスで、機器の使用に関する研究が9研究と多く、運動、患者教育、家族参加などは1-2研究存在し、効果量の算出によって有効とされた。研究は不十分である[19]。

参考文献

出典

[脚注の使い方]
  1. ^ “せん妄”. MSDマニュアル プロフェッショナル版. 2018年11月閲覧。 エラー: 閲覧日は年・月・日のすべてを記入してください。（説明）
  2. ^ “せん妄 - 09. 脳、脊髄、末梢神経の病気”. MSDマニュアル家庭版. 2024年1月29日閲覧。
  3. ^ a b c 日本老年行動科学会（編）『高齢者の「こころ」事典』 中央法規 2000年 ISBN 4-8058-1895-6 pp.178-179.
  4. ^ a b c d e f アレン・フランセス 2014, pp. 152–154.
  5. ^ オリヴァー・サックス 2014, pp. 217–237.
  6. ^ “進行性がん患者と介護者における、せん妄のインパクトと苦痛の記憶”. 日本緩和医療学会 (2009年8月). 2016年9月11日時点のオリジナルよりアーカイブ。2016年8月31日閲覧。
  7. ^ “入院中の高齢者のせん妄をボランティアの介入で防ぐ”. 2015年8月18日閲覧。
  8. ^ Siddiqi N, Harrison JK, Clegg A, et al. (March 2016). “Interventions for preventing delirium in hospitalised non-ICU patients”. Cochrane Database Syst Re: CD005563. doi:10.1002/14651858.CD005563.pub3. PMID 26967259.
  9. ^ Pavone KJ, Cacchione PZ, Polomano RC, Winner L, Compton P (November 2018). “Evaluating the use of dexmedetomidine for the reduction of delirium: An integrative review”. Heart Lung (6): 591–601. doi:10.1016/j.hrtlng.2018.08.007. PMID 30266265.
  10. ^ Castro V, Guinguis R, Carrasco M (April 2018). “Are antipsychotics effective for the prevention of postoperative delirium?”. Medwave (2): e7196. doi:10.5867/medwave.2018.02.7195. PMID 29677175.
  11. ^ Hovaguimian F, Tschopp C, Beck-Schimmer B, Puhan M (October 2018). “Intraoperative ketamine administration to prevent delirium or postoperative cognitive dysfunction: A systematic review and meta-analysis”. Acta Anaesthesiol Scand (9): 1182–1193. doi:10.1111/aas.13168. PMID 29947091.
  12. ^ Walker CK, Gales MA (January 2017). “Melatonin Receptor Agonists for Delirium Prevention”. Ann Pharmacother (1): 72–78. doi:10.1177/1060028016665863. PMID 27539735.
  13. ^ Chen S, Shi L, Liang F, et al. (August 2016). “Exogenous Melatonin for Delirium Prevention: a Meta-analysis of Randomized Controlled Trials”. Mol. Neurobiol. (6): 4046–4053. doi:10.1007/s12035-015-9350-8. PMID 26189834.
  14. ^ Chakraborti D, Tampi DJ, Tampi RR (March 2015). “Melatonin and melatonin agonist for delirium in the elderly patients”. Am J Alzheimers Dis Other Demen (2): 119–29. doi:10.1177/1533317514539379. PMID 24946785.
  15. ^ a b 布村明彦、玉置寿男「せん妄：診断・予防・治療」『神経治療学』第34巻第4号、2018年、393-395頁、doi:10.15082/jsnt.34.4_393、NAID 130006386562。
  16. ^ 『せん妄治療の第 1 選択薬に対する専門医の評価に関する研究について』（pdf）（プレスリリース）医療経済研究機構、2016年2月1日。2018年11月25日閲覧。
  17. ^ Burry L, Mehta S, Perreault MM, et al. (June 2018). “Antipsychotics for treatment of delirium in hospitalised non-ICU patients”. Cochrane Database Syst Re: CD005594. doi:10.1002/14651858.CD005594.pub3. PMID 29920656.
  18. ^ Rivière J, van der Mast RC, Vandenberghe J, Van Den Eede F (May 2018). “Efficacy and Tolerability of Atypical Antipsychotics in the Treatment of Delirium: A Systematic Review of the Literature”. Psychosomatics. doi:10.1016/j.psym.2018.05.011. PMID 30181002.
  19. ^ Kang J, Lee M, Ko H, et al. (December 2018). “Effect of nonpharmacological interventions for the prevention of delirium in the intensive care unit: A systematic review and meta-analysis”. J Crit Care: 372–384. doi:10.1016/j.jcrc.2018.09.032. PMID 30300863.

関連項目

外部リンク


==

선망 [일어한역] 

출처 : 무료 백과 사전 "Wikipedia (Wikipedia)"
선망
개요
진료과정신의학 , 신경학 , 심리학
분류 및 외부 참조 정보
ICD - 10F 05
ICD - 9-CM293.0
DiseasesDB29284
eMedicinemed/3006
Patient UK선망
MeSHD003693

센망 (譫妄, 센토,英: delirium )이란 의식 혼탁에 가세해 기묘하고 강박적인 사고나 환각 · 착각을 볼 수 있는 상태. 건강한 사람이라도 수면 중에 억지로 각성되면 동증상이 발생할 수 있다. 특히 수술 후 환자나 집중치료실 (ICU)에서 관리되는 환자에서 자주 발생한다고 한다 [ 1 ] . 

의학 용어 로서의 구체적인 정의는 있지만, 모든 종류의 착란 상태를 총칭하는 단어로서 사용되는 경우도 자주 있다 [ 2 ] .

급격한 정신운동 흥분( 카테터 를 빼내는 등)이나, 문진상 분명한 견당식 장애 로 느껴지는 경우가 많다. 대수술 후 환자(술후 섬망), 알츠하이머병, 뇌졸중 , 대사장애, 알코올 중독증 환자 에게도 나타난다 . 센망과는 치료도 다른 진전 센망은 술이나 벤조디아제핀 계 약물 로부터의 이탈에 의해 일어나 구별된다.

일반적으로 대증 치료가 수행됩니다. 일반적으로 항정신병약이 사용되지만 그 효과에는 논란이 있다.

증상

각성 수준의 저하 항진, 전망식 장애, 주의 산만, 판단력·집중력 저하, 사고나 기분 불안정화, 착각과 환각 등의 의식장애가 발생하여 [ 3 ] , 공격적으로 되거나 폭력을 일으킬 수도 있다 [ 4 ] . 갑작스럽게 발생하는 경과는 짧지만 생명과 관련되기도 하는 긴급 사태이다 [ 4 ] .

고령자 에게는 섬망이 종종 출현하지만, 그 상태상은 치매 와 겹치는 부분이 많기 때문에, 고령자의 가벼운 의식장애를 가성치매라고 한다 [ 3 ] . 섬망의 특징으로서, 발현이 급성 또는 아급성이며, 증상의 발현에 부동성이 있고, 야간에 증가하는 경향이 있기 때문에 [ 4 ] , 섬망과 치매의 감별은 시간의 경과에 의해 행해진다 [ 3 ] . “입원하자마자 갑자기 흐려져서(인지증처럼 보인다), 자신이 어디에 있는지 , 혹은 오늘이 몇 달 며칠 조차도 모르게 되어 버렸다.”라는 에피소드가 매우 전형적이다.

또한, 고열 과 함께 섬망을 체험하는 경우가 있어, 특히 아이에게 많다 [ 5 ] . 대부분의 환자는 섬망을 기억하고, 고통스러운 경험이었다는 조사보고가 있고, 센망은 의식장애이기 때문에 기억이 없다는 것은 오해이다 [ 6 ] .

이런 증상을 일으키는 선망이라는 병태의 배경에는 의식장애, 환시를 중심으로 한 환각, 정신운동 흥분이 있다고 생각된다.

위험 요인

치매, 노인, 중증 환자, 우울증 상태, 복수 약물, 청시각 장애(난청 이나 백내장), 감염증, 약물 중독 증상, 알코올이나 약물의 이탈 증상, 통증, 수술 후 신체 억제 등 이 리스크 팩터로 알려져 있다.

진단 기준

정신 장애 진단 및 통계 매뉴얼 (DSM)에도 진단 기준이 있지만 , 보다 실용적인 Confusion Assessment Methods (CAM)를 여기에 적는다 [ 7 ] .

  • 급성 발병과 증상 동요
  • 주의력 부족
  • 사고의 혼란
  • 의식 수준의 변화

2번째까지는 필수 항목이며, 하나를 채우면 진단해도 좋다.

감별 진단

치매 에서는 장기간 증상이 지속되어 의식의 혼탁은 없지만, 치매의 사람에게 섬망이 생길 수도 있다 [ 4 ] . 급성 뇌 손상도 비슷한 증상을 일으키지만 빠른 치료가 필요하기 때문에 신체 질환의 식별도 필요하다 [ 4 ] .

약물의 과다 복용 으로 인한 증상은 약물 상호 작용 과 신진 대사가 적은 노인에서 발생할 수 있습니다 [ 4 ] .

진전 섬망은 알코올이나 벤조디아제핀계 약 혹은 바르비툴산계 약의 이탈 증상이 생긴 수선망상태이다. 섬망과는 구별되며 치료도 다르다.

예방

2016년 코 클란 검토는 집중치료실 이외의 입원 환자에서 Bispectral index 를 이용하여 마취 의 깊이를 모니터링 함으로써, 섬망 발생률을 저하시키는 중간 정도의 질의 근거 가 있지만, 항정신병약 , 콜린에스테라아제 억제제 , 멜라토닌 , 멜라토닌 수용체 작용제에서는 연구는 되었지만 섬망의 발생률을 저하 시키는 명확한 근거 는 진정제 덱스 메데 토미딘 은 다른 약제보다 망망 발생률이 낮고, 특히 심장 수술 후 효과적이었다 [ 9 ] . 2018년 검토에서는 16개의 체계적 검토가 있으며, 여기에는 8가지 주요 랜덤화 비교 시험이 포함되어 있으며, 수술 후 예방적인 항정신병제의 사용은 섬망을 발생률을 저하시키지만, 입원 기간에는 영향을 주지 않고 사망률이 증가할 가능성이 있다 [ 10 ] .

예방을 목적으로 한 수술중의 케타민 사용은 6개의 RCT로부터, 섬망의 발생률에 차이가 없고, 수술 후 인지기능장애에서는 보호적인 것 같지만, 증거가 한정되어 있어 결론에는 한계가 있었다 [ 11 ] .

2017년의 리뷰는 5개의 랜덤화 비교시험 (RCT)과 1개의 비RCT를 찾아내고, 멜라토닌에서는 상반되는 결과이며, 1개의 라멜테온에서의 시험은 전망발생률을 감소시키고 L-트립토판에서는 효과가 없고 결론적으로 멜라토닌 수용체 작용약 의 정 . 2016년 RCT의 메타분석은 총 669명을 포함한 4개의 RCT가 있었고, 멜라토닌 복용은 내과 병동에서는 전망 발생률을 감소시키고, 외과 병동에서는 차이가 없었다 [ 13 ] . 2015년의 리뷰에는 멜라토닌의 2개의 RCT와 타시멜테온의 1개의 RCT가 포함되었다 [ 14 ] .

치료

2010년 영국 가이드라인에서는 할로페리돌 (셀레네스)과 올란자핀 (디플렉서)이 소량이고 단기간에만 사용된다 [ 15 ] .

일본의 2015년의 「선망의 치료 지침」에서는, 당뇨병이 없으면 추체 외로 증상이 가장 일어나기 어려운 퀘 티아핀 (이나 오란자핀 ), 있으면 리스페리돈 , 내복 곤란 에서는 할로페리돌 의 주사제 , 검사 를 위한 깊은 진정 에 할로페리 다르나 15 ]가 제시되었습니다.

저활동형 섬망에 대해서는, 전문의가 추천하는 눈에 띄는 약제는 없다고 하는, 일본에서의 2016년의 조사 결과가 있다 [ 16 ] .

리뷰

2018년 코클란 공동계획 검토에서는 응급이 아닌 입원환자에서 치료를 위한 항정신병약의 사용에서는 증거의 질이 낮지만 전망중증도, 사망률, 항정신병약(정형 또는 비정형인지)에 의한 추체외로 증상의 발생률에 변화는 없고, 섬망 의 시간 은 .

2018년의 또 다른 리뷰는 정형과 비정형 항정신병제를 비교했다. 할로페리돌과 리스페리돈에서는 대규모 랜덤화 비교 시험에 의해 위약보다 예후 불량에 연결되어 있었다. 올란자핀과 퀘티아핀은 대규모 시험이 아니지만 효능을 뒷받침한다. 대규모 RCT가 필요하다 [ 18 ] .

비 약리학

비약리학적 개입에서는 2018년 메타분석에서 기기 사용에 관한 연구가 9개 연구로 많았고, 운동, 환자교육, 가족참가 등은 1-2개 연구 존재하여 효과량의 산출에 의해 유효하게 되었다. 연구는 불충분하다 [ 19 ] .

참고문헌

출처

[ 각주 사용법 ]
  1. ↑ “ 선망 ”. MSD 메뉴얼 프로페셔널판. 2018년 11월 열람. 오류 : 열람 일은 연, 월, 일 모두를 기입하십시오. ( 설명 )
  2. ↑ “ 선망 - 09. 뇌, 척수, 말초 신경의 질병 ”. MSD 매뉴얼 가정판 . 2024년 1월 29일에 확인함.
  3. ↑ a b c 일본 노년 행동 과학회 (편) 「고령자의 「마음」사전」 중앙 법규 2000 년 ISBN 4-8058-1895-6 pp.178-179.
  4. ^ a b c d e f 알렌 프랑세스 2014 , pp. 152-154.
  5. ↑ Oliver Sax 2014 , pp. 217–237.
  6. ↑ “ 진행성 암 환자와 개호자에 있어서의, 섬망의 임팩트와 고통의 기억 ” . 일본 완화 의료 학회 (2009년 8월). 2016년 9월 11일 시점의 오리지널 보다 아카이브. 2016년 8월 31일에 확인함.
  7. ↑ “ 입원중의 노인의 선망을 자원봉사의 개입으로 막는 ”. 2015년 8월 18일 열람.
  8. ↑ Siddiqi N, Harrison JK, Clegg A, et al . (March 2016). “Interventions for preventing delirium in hospitalised non-ICU patients”. Cochrane Database Syst Re : CD005563. doi : 10.1002/1465ub . 26967259 . 
  9. ↑ Pavone KJ, Cacchione PZ, Polomano RC, Winner L, Compton P (November 2018). “Evaluating the use of dexmedetomidine for the reduction of delirium: An integrative review”. Heart Lung (6): 591–601. doi : 10.1016/j.hrtlng.2018.08.007 . PMID 30266265 . 
  10. ↑ Castro V, Guinguis R , Carrasco M (April 2018). “Are antipsychotics effective for the prevention of postoperative delirium?”. Medwave (2): e7196. doi : 10.5867/ medwave.2018.02.7195 
  11. ↑ Hovaguimian F, Tschopp C, Beck-Schimmer B, Puhan M (October 2018). “Intraoperative ketamine administration to prevent delirium or postoperative cognitive dysfunction: A systematic review and meta-analysis”. Acta Anaesthesiol Scand (2) . 10.1111/aas.13168 . PMID 29947091 . 
  12. ↑ Walker CK , Gales MA (January 2017). “Melatonin Receptor Agonists for Delirium Prevention”. Ann Pharmacother ( 1 ): 72–78. doi : 10.1177/1060028016665863 . 
  13. ↑ Chen S, Shi L, Liang F, et al. (August 2016). “Exogenous Melatonin for Delirium Prevention: a Meta-analysis of Randomized Controlled Trials”. Mol . Neurobiol . (6): 4046–4053. PMID 26189834 .​ 
  14. ↑ Chakraborti D, Tampi DJ, Tampi RR (March 2015). “Melatonin and melatonin agonist for delirium in the elderly patients”. Am J Alzheimers Dis Other Demen ( 2): 119–29. doi : 10.1177/15333175 24946785 . 
  15. ^ a b 후무라 아키히코, 타마키 스즈오 「선망：진단・예방・치료」『신경치료학』 제34권 제4호, 2018년, 393-395페이지, doi : 10.15082/jsnt.34.4_393 , NAID 13000638 . 
  16. ^ 「선망치료의 제1 선택약에 대한 전문의의 평가에 관한 연구에 대해서」(pdf)(보도자료) 의료경제연구기구, 2016년 2월 1일 . 2018년 11월 25일에 확인함 .
  17. ↑ Burry L , Mehta S, Perreault MM, et al. ( June 2018). “ Antipsychotics for treatment of delirium in hospitalised non- ICU patients” . PMID 29920656 .​ 
  18. ↑ Rivière J, van der Mast RC, Vandenberghe J, Van Den Eede F (May 2018). “Efficacy and Tolerability of Atypical Antipsychotics in the Treatment of Delirium: A Systematic Review of the Literature”. Psychosomatics . doi : 10.10.10.10.10. PMID 30181002 .​ 
  19. ↑ Kang J, Lee M, Ko H, et al. (December 2018). “Effect of nonpharmacological interventions for the prevention of delirium in the intensive care unit: A systematic review and meta-analysis”. J Crit Care : 372–384. doi : 10.1016/j.jcrc.2018.09.032 . PMID 30300863 . 

관련 항목

외부 링크

정신과 행동 장애 ( ICD -F - 290-319 )
==

===

섬망

위키백과, 우리 모두의 백과사전.
섬망
Delirium
진료과정신건강의학과, 노인과, 중환자의학과, 신경과
증상초조함, 혼란, 졸림, 환각, 망상, 기억상실
통상적 발병 시기모든 연령에서 가능하나 65세 이상에서 더 흔함
기간수 일에서 수 주, 간혹 수 개월
유형과활동형, 저활동형, 혼재형
병인잘 알려지지 않음
위험 인자감염, 만성 질환, 특정 약물, 신경질환, 수면부족, 수술
유사 질병치매
치료약물 치료, 기저 원인 치료
투약할로페리돌, 리스페리돈, 올란자핀, 퀘티아핀

섬망(譫妄, 영어: delirium)은 의학적 이유로 인해 일반적으로 수 시간에서 수 일에 걸쳐 나타나는 급성 혼란 상태(acute confusional state)이다. 신체 또는 정신적 질병, 극심한 불안, 약물 또는 다양한 원인으로 발생할 수 있다. 특히 노인, 중환자실에 입원한 환자, 수술 전 또는 끝나고 회복 중인 환자에게서 많이 나타난다. 중환자의 섬망은 높은 사망 위험을 시사한다.

증상은 다양하며 주의력 문제, 기억장애, 방향감각 상실, 무질서한 사고, 언어 장애, 수면 패턴 이상, 정신증이나 망상, 환각 등 지각장애, 정서불안, 활동성의 저하 또는 과잉 등이 나타날 수 있다. 각성 정도는 다양하여 혼수 상태인 경우, 정상적인 각성 상태인 경우, 고조된 과잉 행동 상태인 경우가 모두 있을 수 있으며 여러 상태가 번갈아가며 나타나는 환자도 있다.

외부 링크


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