What Is Delirium and How Should It Be Managed?

Introduction and Scope of the Problem

The word delirium is derived from the Latin term meaning “off track.” Delirium has many descriptors, including acute confusion, altered mental status, sundowning, intensive care unit (ICU) psychosis, organic psychosis, acute brain failure, toxic metabolic state, cerebral insufficiency, and encephalopathy. All of these terms are used to describe an acute cognitive impairment associated with medical illness, which can be labeled as delirium. The American Psychiatry Association Diagnostic and Statistical Manual of Mental Disorders , Fifth Edition (DSM-V), provides the most widely recognized and used definition ( Table 28.1 ). Briefly, delirium is a transient, often reversible cause of cerebral dysfunction that can manifest clinically with a wide range of neuropsychiatric abnormalities. The clinical hallmarks of delirium are decreased attention span and waxing and waning confusion.

Although delirium is a transient global disorder of cognition, affect and behavior are often involved. The increased morbidity and mortality rates associated with delirium make it a medical emergency. Therefore early diagnosis and resolution of symptoms are correlated with the best outcomes. Unfortunately, delirium is often unrecognized or misdiagnosed. It is commonly mistaken for dementia or depression, attributed to hospitalization, or considered a consequence of old age (older patients are expected to become confused in the hospital). For people with dementia in particular, delirium may be the only presentation of a severe medical illness. The tendency of delirium to be mistaken for other psychiatric illnesses makes recognition and timely treatment difficult. This chapter will provide an overview of the prevalence, features, and effects of delirium and describe evidence-based strategies for screening and management.

Relevant Pathophysiology

Delirium results from a wide variety of both physiological and structural insults, and its overall mechanism is still not fully understood. The main hypothesis involves reversible impairment of cerebral oxidative metabolism and multiple neurotransmitter abnormalities, specifically high dopaminergic tone and low cholinergic tone. Dopamine increase in mesolimbic and mesocortical tracts may cause agitation and delusions, whereas acetylcholine decrease in hippocampal and basal forebrain regions may lead to disorientation, hallucinations, and memory impairment. Clinically this hypothesis is supported by the tendency for anticholinergic medications to cause acute confusional states, especially in patients with impaired cholinergic transmission, such as in Alzheimer’s disease, and in patients with postoperative delirium who have increased serum anticholinergic activity. Additional support for this hypothesis is provided by the fact that symptomatic relief can be seen with the administration of neuroleptics, such as haloperidol, which are dopamine blockers. Other neurotransmitters (serotonin, γ-aminobutyric acid, cortisol, melatonin) are also believed to play a role in delirium, but their role is less clearly defined. No specific neuronal pathways causing delirium have been identified; however, imaging studies of metabolic (e.g., hepatic encephalopathy) and structural (e.g., traumatic brain injury, stroke) factors support the hypothesis that certain anatomical pathways may play a more important role than others. Additionally, disruptions in the blood–brain barrier can allow neurotoxic agents and inflammatory cytokines to enter the brain, which may contribute.