Delirium in the hospital: Emphasis on the management of geriatric patients

Although delirium has many descriptive terms (Table 1), a common unifying term is “acute global cognitive dysfunction,” now recognized as delirium; a consensus supported by DSM-5¹ and ICD-10² (Table 2). According to DSM-5, the essential feature is a disturbance of attention or awareness that is accompanied by a change in baseline cognition that cannot be explained by another preexisting, established, or evolving neurocognitive disorder (the newly named DSM-5 entity for dementia syndromes).¹ Because delirium affects the cortex diffusely, psychiatric symp­toms can include cognitive, mood, anxiety, or psychotic symp­toms. Because many systemic illnesses can induce delirium, the differential diagnosis spans all organ systems.

Three subtypes
Delirium can be classified, based on symptoms,^3,4 into 3 sub­types: hyperactive-hyperalert, hypoactive-hypoalert, and mixed delirium. Hyperactive patients present with rest­lessness and agitation. Hypoactive patients are lethargic, confused, slow to respond to questions, and often appear depressed. The differential prognostic significance of these subtypes has been examined in the literature, with conflicting results. Rabinowitz⁵ reported that hypoactive delirium has the worst prognosis, while Marcantonio et al⁶ indicated that the hyperactive subtype is associated with the highest mortality rate. Mixed delirium, with periods of both hyperactivity and hypoactivity, is the most common type of delirium.⁷

A prodromal phase, characterized by anxiety, frequent requests for nursing and medical assistance, decreased attention, rest­lessness, vivid dreams, disorientation imme­diately after awakening, and hallucinations, can occur before an episode of full-spectrum delirium; this prodromal state often is iden­tified retrospectively —after the patient is in an episode of delirium.^8,9

Evidence-based guidelines aim to improve recognition and clinical management.^10-13 Disruptive behavior is the main reason for psychiatric referral in delirium.^14,15 Delayed psychiatric consultation because of non-recognition of delirium is related to variables such as older age; history of a pre-existing, comorbid neurocognitive disorder; and the clinical appearance of hypoactive delirium.¹⁴

The case of Mr. D (Box),¹⁶ illus­trates how the emergence of antipsychotic-associated neuroleptic malignant syndrome (NMS) can complicate antipsychotic treat­ment of delirium in a geriatric medical patient, although delirium also is a common presentation in NMS.¹⁷ Delirium developed after an increase in carbidopa/levodopa, which has central dopaminergic effects that can precipitate delirium, particularly in a geriatric patient with preexisting comorbid neurocognitive disorder. Further complicat­ing Mr. D’s delirium presentation was the development of NMS, which had a multifac­torial causation, such as the use of dopamine antagonists (ie, quetiapine, metoclopramide), and an abrupt decrease of a dopaminergic agent (ie, carbidopa/levodopa), all inducing a central dopamine relative hypoactivity.

Epidemiology
Delirium is more common in older patients,¹⁵ and is seen in 30% to 40% of hospitalized geri­atric patients.¹⁸ Delirium in older patients, compared with other adults, is associated with more severe cognitive impairment.¹⁹ It is com­mon among geriatric surgical patients (15% to 62%)²⁰ with a peak 2 to 5 days postoperatively for hip fracture,²¹ and often is seen in ICU patients (70% to 87%).²⁰ However, Spronk et al²² found that delirium is significantly under-recognized in the ICU. Nearly 90% of terminally ill patients become delirious before death.²³ Terminal delirium often is unrecognized and can interfere with assessment of other clinical problems.²⁴ A preexisting history of comor­bid neurocognitive disorder was evident in as many as two-thirds of delirium cases.²⁵

Pathophysiology and risk factors
The pathophysiology of delirium has been characterized as an imbalance of CNS metab­olism, including decreased blood flow in vari­ous regions of the brain that may normalize once delirium resolves.²⁶ Studies describe the simultaneous decrease of cholinergic transmission and dopaminergic excess.^27,28 Predisposing and precipitating factors for delirium that are of particular importance in geriatric patients include:
• advanced age
• CNS disease
• infection
• cognitive impairment
• male sex
• poor nutrition
• dehydration and other metabolic abnormalities
• cardiovascular events
• substance use
• medication
• sensory deprivation (eg, impaired vision or hearing)
• sleep deprivation
• low level of physical activity.^27,29,30

Table 3 lists the most common delirium-provocative medications.²⁷

Evaluation and psychometric scales
The EEG can be useful in evaluating delir­ium, especially in clinically ambiguous cases. EEG findings may indicate generalized slowing or dropout of the posterior domi­nant rhythm, and generalized slow theta and delta waves, findings that are more common in delirium than in other neurocognitive dis­orders and other psychiatric illnesses. The EEG must be interpreted in the context of the delirium diagnostic workup, because abnor­malities seen in other neurocognitive disor­ders can overlap with those of delirium.³¹

The EEG referral should specify the clini­cal suspicion of delirium to help interpret the results. Delirium cases in which the patient’s previous cognitive status is unknown may benefit from EEG evaluation, such as:
• in possible status epilepticus
• when delirium improvement has reached a plateau at a lower level of cognitive function than before onset of delirium
• when the patient is unable or unwilling to complete a psychiatric interview.²⁷

Assessment instruments are available to diagnose and monitor delirium (Table 4). Typically, delirium assessment includes examining levels of arousal, psychomotor activity, cognition (ie, orienta­tion, attention, and memory), and percep­tual disturbances.