), and means to stay engaged (e.g. making hearing aids and eyeglasses readily available). Sometimes verbal and non-verbal deescalation techniques may be required to offer reassurances and calm the person experiencing delirium. Restraints should rarely be used as an intervention for delirium. The use of restraints has been recognized as a risk factor for injury and aggravating symptoms, especially in older hospitalized people with delirium. The only cases where restraints should sparingly be used during delirium is in the protection of life-sustaining interventions, such as endotracheal tubes.Another approached called the "T-A-DA (tolerate, anticipate, dont agitate) method" can be an effective management technique for older people with delirium, where abnormal patient behaviors (including hallucinations and delusions) are tolerated and unchallenged, as long as caregiver and patient safety is not threatened. 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. Medications
Low-dose haloperidol when used short term (one week or less) is the most studied and standard drug for delirium. Evidence for efficacy of atypical antipsychotics (i.e. risperidone, olanzapine, ziprasidone, and quetiapine) is emerging, with the benefit for fewer side effects Use antipsychotic drugs with caution or not at all for people with conditions such as Parkinsons disease or dementia with Lewy bodies. Evidence for the effectiveness of medications (including antipsychotics and benzodiazepines) in treating delirium is weak.Benzodiazepines themselves can trigger or worsen delirium, and there is no reliable evidence for use in non-alcohol-related delirium.
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.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 Alzheimers disease). 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 patients who died during ICU admission. 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.A 2017 retrospective study correlating autopsy data with 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.