Delirium

❓What❓

• “Delirium may be considered something of a diagnostic chameleon, as its varied presentations can result in misdiagnoses that span almost every major category of mental illness … often mistaken for depression (withdrawn/flat affect), mania (agitation/confusion), anxiety (restless/hypervigilant), dementia (cognitive impairments), & substance abuse (impairment in consciousness)”

• Other diagnostic labels for “delirium” include:

• As a signifier of underlying somatic illness, delirium has an extremely large DDx in addition to its divergent clinical presentations & numerous diagnostic labels

❓Epidemiology❓

• Most common cause of agitation, & most patients referred to inpatient psychiatry with purported depression are ultimately delirious

• Prevalence of ~23% among all medical inpatients
• Prevalence of ~32% among all ICU inpatients
• Prevalence of ~82% among those requiring intubation

❓Presentation❓

• Inattention
• Acute-onset
• Waxing/waning course
• Disturbance of consciousness

• More common = hypoactive
• Less common = hyperactive
• Mixed (fluctuating hypo- vs. hyperactivity)

• Confusion
• Psychosis* (hallucinations, delusions)
• Emotional symptoms (anxiety/restlessness, agitation, withdrawn affect)
• Sundowning (day-night reversal + nocturnal hyperactivity)

⚪ Despite psychosis being a common symptom of delirium, the psychosis is not infrequently so severe that it directs the diagnostician’s focus away from the core features of delirium (namely, inattention)

❓Diagnosis❓

• Attention (backwards spelling, forward digit span recollection)*
• Consciousness (e.g. ↓ Glasgow Coma Scale)
• Orientation (self, location, year)
• Mood (patient’s subjective experience)

⚪ Always start with “attention” testing, as poor attention will influence the validity of remainder of the exam

• Multidirectional nystagmus
• Asterixis vs. Diffuse ⊖ myoclonus (e.g. abrupt, transient loss of truncal tone)

• EEG with generalized/diffuse slowing to the theta-delta range is a consistent finding despite wide-ranging endpoint diagnoses, & resolution of this change has been shown to indicate effective treatment

❓Treatment❓

• Treatment of underlying cause (i.e. run the AMS DDx)

• Unfortunately, environmental & psychosocial changes rarely effective alone

• As “reorientation” is rarely effective alone & treatment of the underlying trigger often requires an extended period of time, the purpose of “bridging” patients with hyperactive delirium using pharmacologic treatments is to keep them physically safe & psychologically comfortable until the brain recovers from the somatic insult

• Neuroleptics are agent of choice, with haloperidol being most common due to its minimal effects on cardiopulmonary physiology, & IV delivery being most preferred due to several disadvantages associated with IM delivery (e.g. ↓ IM absorption if patients has tissue malperfusion, ↑ patient perception of being attacked, ↑ serum CK, ↑ probability of inducing extrapyramidal symptoms)

• A pharmacologic strategy that stops the agitation quickly & completely at the outset is preferred to a strategy that “barely keeps up”

• Using haloperidol as an example, the initial bolus dose varies from 0.5 to 20mg, with the smaller dosing being used for geriatric patients, & higher dosing being used for severe agitation in the young. Since the mean distribution time of haloperidol is ~10 minutes, escalating doses can be staggered by at least 30-minute intervals (goal = calm)

• Since “goal = calm,” additional agents can be coadministered to abort agitated episode, namely benzodiazapines (e.g. lorazepam 1-2 mg)

• Haloperidol should not be used in patients with Parkinson’s disease & Lewy Body disease due to exacerbation of those conditions by dopamine blockade; for this reason, quetiapine, which has a very low affinity for dopamine receptors, can be trialed

📚 References 📚

• MGH Handbook of General Hospital Psychiatry, 8th Edition

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