Delirium is defined as a transient, usually reversible, cause of mental dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities. It can occur at any age, but it occurs more commonly in patients who are elderly and have a previously compromised mental status.
Signs and symptoms
The clinical hallmarks of delirium are decreased attention or awareness and a change in baseline cognition. Delirium often manifests as a waxing and waning type of confusion. Symptoms include the following:
Clouding of consciousness
Difficulty maintaining or shifting attention
Fluctuating levels of consciousness
Asterixis in hepatic encephalopathy and uremia
See Clinical Presentation for more detail.
The diagnosis of delirium is clinical. No laboratory test can diagnose delirium.
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for delirium is as follows  :
Disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and awareness.
Change in cognition (eg, memory deficit, disorientation, language disturbance, perceptual disturbance) that is not better accounted for by a preexisting, established, or evolving dementia.
The disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day.
There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a direct physiologic consequence of a general medical condition, an intoxicating substance, medication use, or more than one cause.
Some of the measures used to identify delirium include the following:
Confusion Assessment Method (CAM)
Delirium Symptom Interview (DSI)
Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)
Intensive Care Delirium Screening Checklist (ICDSC)
Delirium symptom severity can be assessed by the Delirium Detection Scale (DDS) and the Memorial Delirium Assessment Scale (MDAS).
See Workup for more detail.
The goal of treatment is to determine the cause of the delirium and stop or reverse it. Components of delirium management include supportive therapy and pharmacologic management.
Fluid and nutrition should be given carefully because the patient may be unwilling or physically unable to maintain a balanced intake. For the patient suspected of having alcohol toxicity or alcohol withdrawal, management should include multivitamins, especially thiamine.
Reorientation techniques or memory cues such as a calendar, clocks, and family photos may be helpful. The environment should be stable, quiet, and well-lighted.
Delirium that causes injury to the patient or others should be treated with medications. The most common medications used are antipsychotic medications. Benzodiazepines often are used for withdrawal states.
Delirium is a transient global disorder of cognition. The condition is a medical emergency associated with increased morbidity and mortality rates. Early diagnosis and resolution of symptoms are correlated with the most favorable outcomes.
Delirium is not a disease but a syndrome with multiple causes that result in a similar constellation of signs and symptoms. Delirium is defined as a transient, usually reversible, cause of mental dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities. The clinical hallmarks are decreased awareness and attention span and a waxing and waning type of confusion.
Based on the level of psychomotor activity, delirium can be described as hyperactive, hypoactive, or mixed. Hyperactive delirium is observed in patients in a state of alcohol withdrawal or intoxication with phencyclidine (PCP), amphetamine, and lysergic acid diethylamide (LSD). These patients often exhibit agitation, restlessness, hallucinations, or delusions. Hypoactive delirium is observed in patients in states of hepatic encephalopathy and hypercapnia and may be more common in older adults. Hypoactive delirium presents with lethargy, drowsiness, apathy, decreased responsiveness, or slowed motor skills. In mixed delirium, individuals display either relatively normal levels of psychomotor activity or rapidly fluctuating levels of activity. [1, 2]
The mechanism of delirium still is not fully understood. Delirium results from a wide variety of structural or physiological insults. The neuropathogenesis of delirium has been studied in patients with hepatic encephalopathy and alcohol withdrawal. Research in these areas still is limited. The main hypothesis is reversible impairment of cerebral oxidative metabolism and multiple neurotransmitter abnormalities. The following observations support the hypothesis of multiple neurotransmitter abnormalities. 
Data from animal and clinical studies support the hypothesis that acetylcholine is one of the critical neurotransmitters in the pathogenesis of delirium.  A small prospective study among patients who have undergone elective hip replacement surgery showed reduced preoperative plasma cholinesterase activity in as many as one quarter of patients. In addition, reduced preoperative cholinesterase levels were significantly correlated with postoperative delirium. 
Clinically, good reasons support this hypothesis. Anticholinergic medications are a well-known cause of acute confusional states, and patients with impaired cholinergic transmission, such those with Alzheimer disease, are particularly susceptible. In patients with postoperative delirium, serum anticholinergic activity may be increased. 
In the brain, a reciprocal relationship exists between cholinergic and dopaminergic activities. In delirium, an excess of dopaminergic activity occurs. Symptomatic relief occurs with antipsychotic medications such as haloperidol and other neuroleptic dopamine blockers.
Serotonin: Human and animal studies have found that serotonin is increased in patients with hepatic encephalopathy and septic delirium. Hallucinogens such as LSD act as agonists at the site of serotonin receptors. Serotonergic agents also can cause delirium.
Gamma-aminobutyric acid (GABA): In patients with hepatic encephalopathy, increased inhibitory GABA levels also are observed. An increase in ammonia levels occurs in patients with hepatic encephalopathy, which causes an increase in the amino acids glutamate and glutamine, which are precursors to GABA. Decreases in CNS GABA levels are observed in patients with delirium resulting from benzodiazepine and alcohol withdrawal.
Cortisol and beta-endorphins: Delirium has been associated with the disruption of cortisol and beta-endorphin circadian rhythms. This mechanism has been suggested as a possible explanation for delirium caused by exogenous glucocorticoids.
Disturbed melatonin disturbance has been associated with sleep disturbances in delirium. 
Recent studies have suggested a role for cytokines, such as interleukin-1 and interleukin-6, in the pathogenesis of delirium. Following a wide range of infectious, inflammatory, and toxic insults, endogenous pyrogen, such as interleukin-1, is released from the cells. Head trauma and ischemia, which frequently are associated with delirium, are characterized by brain responses that are mediated by interleukin-1 and interleukin-6. [8, 9]
Stress reaction mechanism
Studies indicate psychosocial stress and sleep deprivation facilitate the onset of delirium.
The specific neuronal pathways that cause delirium are unknown. Imaging studies of metabolic (eg, hepatic encephalopathy) and structural (eg, traumatic brain injury, stroke) factors support the hypothesis that certain anatomical pathways may play a more important role than others. The reticular formation and its connections are the main sites of arousal and attention. The dorsal tegmental pathway projecting from the mesencephalic reticular formation to the tectum and the thalamus is involved in delirium.
Disrupted blood-brain barrier can allow neurotoxic agents and inflammatory cytokines to enter the brain and may cause delirium. Contrast-enhanced MRI can be used to assess the blood-brain barrier. [10, 11]
Visuoperceptual deficits in delirium such as hallucinations and delusions are not due to the underlying cognitive impairment.  Visual hallucinations during alcohol-withdrawal delirium are seen in subjects with polymorphisms of genes coding for dopamine transporter and catechol-O-methyltransferase (COMT). 
In patients who are admitted with delirium, mortality rates are 10-26%. 
Patients who develop delirium during hospitalization have a mortality rate of 22-76% and a high rate of death during the months following discharge.  . In a review of 28 studies of critically ill patients the rate of death for patients with delirium was more than doubled. 
In patients who are elderly and patients in the postoperative period, delirium may result in a prolonged hospital stay, increased complications, increased cost, and long-term disability. 
According to one study, delirium is associated with worse survival and greater resource consumption in those with cardiac critical illness. Among 590 patients included, the prevalence of cardiac (C)ICU delirium was 20.3%. Delirious patients were older, had greater disease severity, required longer ICU stays (5 vs 2 days; P < .001), and had higher mortality (27% vs 3%; P < .001). 
Delirium is common in the United States. In a systematic review of 42 cohorts in 40 studies, 10–31% of new hospital admissions met criteria for delirium and the incidence of developing delirium during the admission ranged from 3–29%. 
For patients in intensive care units the prevalence of delirium may reach as high as 80%. 
Prevalence of postoperative delirium following general surgery is 5–10% and as high as 42% following orthopedic surgery. As many as 80% of patients develop delirium near death. Delirium is extremely common among nursing home residents.
Delirium can occur at any age, but it occurs more commonly in patients who are elderly and have compromised mental status. Delirium can occur on top of an underlying dementia. This diagnosis here requires not only a careful mental status but also a thorough history from the patient's family and the staff as well as a comprehensive chart review.
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