Delirium is an acute, fluctuating change in mental status, with inattention, disorganized thinking, and altered levels of consciousness.[1] It is a potentially life-threatening disorder characterized by high morbidity and mortality. Guidelines address recognition, risk factors, and treatment for delirium.[2] [3] [4]
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Summary
Introduction
Adverse sequelae
Mortality for those diagnosed with delirium in the hospital is twice that of patients with similar medical conditions without delirium, and may be as high as 14% within 1 month of diagnosis.[5]
Delirium is common in the intensive care unit, especially among mechanically ventilated patients. In critically ill patients, it is associated with an increased length of stay and increased mortality.[6] [7]
Delirium is associated with elevated risks for functional and cognitive decline, poor rehabilitation potential, institutionalization, and rehospitalization.[1] [7][8] [9] [10] [11] While delirium has been considered to be a reversible condition, studies suggest that delirium symptoms can last for weeks to months following onset.[12] Persistent delirium has been found to be frequent in older hospitalized patients, and associated with adverse outcomes.[13] There is growing evidence that delirium may be an independent risk factor for longer term cognitive decline.[14]
Classification
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) notes that in order to be diagnosed with delirium, a patient must show all 4 of the following features.[15]
- A disturbance in attention (i.e., reduced clarity of awareness of the environment) is evident, with reduced ability to focus, sustain, or shift attention. This disturbance in consciousness might be subtle, initially presenting solely as lethargy or distractibility, and might be frequently dismissed by clinicians and/or family members as being related to the primary illness.
- A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance not better accounted for by a pre-existing or evolving dementia.
- The disturbance develops over a short period of time (usually hours to days), represents an acute change from baseline, and tends to fluctuate during the course of the day.
- There is evidence from the history, physical exam, or laboratory findings that the disturbance is caused by the direct physiologic consequences of a general medical condition, substance intoxication, or substance withdrawal. The changes in attention and cognition must not occur in the context of a severely reduced level of arousal, such as coma.
- Hyperactive delirium - a condition where a patient might have heightened arousal, with restlessness, agitation, hallucinations, and inappropriate behavior
- Hypoactive delirium - a condition where a patient might display lethargy, reduced motor activity, incoherent speech, and lack of interest
- Mixed delirium - a combination of hyperactive and hypoactive signs and symptoms.
The term subsyndromal delirium has also been used to define partially resolved or incomplete forms of delirium.
Epidemiology
Delirium occurs in ≥20% of hospitalizations annually, and is the most common hospital-related complication in the US.[19] [20][21] Prevalence of delirium ranges from 10% to 40% in older hospitalized patients.[19]
Delirium affects up to 35% of people on medical floors.[3] [14] Prevalence ranges from: 8% to 18% in the emergency department; 15% to 53% for postoperative patients; and 7% to 50% for intensive care patients.[22] [23] [24] [25] The incidence and prevalence of delirium in medical inpatients appears to have remained broadly stable over the past four decades.[26]
The prevalence of delirium in the community is believed to be 1% to 2%, a figure that increases to 10% for patients ages >85 years.[27]
Delirium is frequently under-recognized. This may be indicative of the fluctuating nature of delirium symptoms, and an overall underappreciation of its clinical significance.
Pathophysiology
The pathophysiology of delirium remains relatively unclear. In general, neuroimaging studies reveal disruptions in higher cortical functioning in multiple disparate areas of the brain, including the prefrontal cortex, subcortical structures, thalamus, basal ganglia, lingual gyri, and frontal, fusiform and temporoparietal cortex.[28] [29] Electroencephalographic (EEG) studies show diffuse slowing of cortical activity.
Theories on the pathogenesis of delirium point to the role of neurotransmitters, inflammation, and chronic stress on the brain. For example, the role of cholinergic deficiency in inducing delirium is strengthened by the clear association of anticholinergic drug use with increased incidence.[30] Studies in surgical patients have demonstrated a dysfunctional interaction between the cholinergic and immune systems in patients who developed postoperative delirium.[31]
Dopaminergic excess is also believed to contribute. Evidence does not appear to support the use of antipsychotic drugs (dopamine antagonists) for the prevention or treatment of delirium, but is not entirely consistent.[32] [33] [34] [35] [36] [37] [38] [39] Other neurotransmitters implicated in the pathophysiology of delirium include norepinephrine, serotonin, gamma-aminobutyric acid, glutamate, and melatonin.
Last updated
Citations
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National Institute for Health and Care Excellence. Delirium: prevention, diagnosis and management in hospital and long-term care. Jan 2023 [internet publication].[Full Text]
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 5th ed., text revision (DSM-5-TR). Washington, DC: American Psychiatric Publishing; 2022
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