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Summary Table

Category	Details
Risk Factors	Age >65, pre-existing dementia or cognitive impairment, recent surgery (especially hip fracture repair), ICU admission, polypharmacy (anticholinergics, benzodiazepines, opioids), sensory impairment (poor vision/hearing), dehydration, urinary catheter use, physical restraints, sleep deprivation, alcohol use disorder
Etiology	Multifactorial: infections (UTI, pneumonia), metabolic derangements (hyponatremia, hypercalcemia, hepatic/uremic encephalopathy, hypoglycemia), medications (anticholinergics, benzodiazepines, opioids, corticosteroids), substance intoxication/withdrawal (alcohol, benzodiazepines), postoperative state, pain, urinary retention, fecal impaction, hypoxia
Patient Presentation	Acute onset of confusion, inattention, disorientation, fluctuating mental status over hours to days. Family or nurse often reports "the patient is not acting like themselves." Often worse at night ("sundowning").
Classic Physical Exam	Inattention (cannot spell "WORLD" backwards, cannot recite months in reverse), disorganized thinking, altered level of consciousness (ranges from agitated/combative to lethargic/obtunded), psychomotor agitation or retardation, perceptual disturbances (visual hallucinations), sleep-wake cycle disruption
Key Diagnostic Results	Clinical diagnosis using the Confusion Assessment Method (CAM). Labs to identify the cause: CBC, BMP, urinalysis, blood cultures, chest X-ray, liver function tests, thyroid function, arterial blood gas, drug levels, toxicology screen. Brain imaging and lumbar puncture only if structural lesion or meningitis/encephalitis is suspected.
Management	Identify and treat the underlying cause (this is the single most important step). Non-pharmacologic interventions first (reorientation, sleep hygiene, mobilization, remove catheters/restraints, correct sensory deficits). Low-dose haloperidol or second-generation antipsychotics only for severe agitation posing danger to patient or staff. Avoid benzodiazepines unless the cause is alcohol or benzodiazepine withdrawal.
Keywords	"Acute onset," "waxing and waning," "fluctuating consciousness," "inattention," "sundowning," "elderly postoperative confusion," "visual hallucinations in the elderly," "acutely agitated hospitalized patient"

1. Pathophysiology

Delirium is fundamentally an acute failure of global cerebral function. Unlike focal neurological deficits (stroke, mass lesion), delirium reflects a diffuse breakdown in the brain's ability to maintain attention, integrate sensory input, and sustain organized cognition. The hallmark is inattention, which is the single most important clinical feature and the feature that separates delirium from nearly all psychiatric mimics.

The leading neurochemical model centers on cholinergic deficiency and dopaminergic excess. Acetylcholine is the primary neurotransmitter for sustained attention and memory consolidation. When cholinergic transmission drops, whether from anticholinergic medications, metabolic insults, or systemic inflammation, attention collapses. This is why anticholinergic drugs are among the most common pharmacologic triggers. Conversely, dopamine excess contributes to the psychomotor agitation, hallucinations, and perceptual disturbances seen in the hyperactive subtype. This dopaminergic-cholinergic imbalance is also the rationale for using dopamine-blocking agents (antipsychotics) as symptomatic treatment.

A second critical mechanism is neuroinflammation. Systemic illness (sepsis, pneumonia, UTI) triggers peripheral cytokine release (IL-1, IL-6, TNF-alpha), which crosses the blood-brain barrier and activates microglial cells. This inflammatory cascade impairs synaptic function and neurotransmitter balance. This explains why even a "simple" UTI in an elderly patient with low cognitive reserve can produce a dramatic delirious state. The concept of cognitive reserve is central: a patient with pre-existing dementia has a lower threshold for delirium because the brain has fewer compensatory mechanisms to absorb additional insults.

The fluctuating course ("waxing and waning") directly reflects the dynamic interplay between the precipitating insult and the brain's attempts at compensation. This fluctuation is a defining feature and one of the strongest clinical clues on examination questions.

Visual hallucinations in delirium, as opposed to auditory hallucinations in primary psychotic disorders, arise from disruption of the visual association cortex and thalamic relay pathways. This is a high-yield discriminator: an elderly patient with acute-onset visual hallucinations is far more likely to have delirium than schizophrenia.

2. Classification and Clinical Manifestation

Subtype	Psychomotor Activity	Clinical Features	Prognosis	Exam Relevance
Hyperactive	Increased	Agitation, restlessness, combativeness, pulling at lines/tubes, hallucinations, emotional lability	Better (detected earlier due to disruptive behavior)	The "classic" vignette presentation; easily recognized
Hypoactive	Decreased	Lethargy, withdrawal, flat affect, reduced responsiveness, appears "quiet" or "sleepy," minimal spontaneous speech	Worse (frequently missed, higher mortality)	The most commonly tested "trap." Often misdiagnosed as depression or fatigue. Exam questions often present a quiet, withdrawn postoperative elderly patient.
Mixed	Fluctuating between both	Alternates between periods of agitation and periods of lethargy throughout the day	Intermediate	Most common subtype in clinical practice; reinforces the "waxing and waning" pattern

Additional clinical features by domain:

Domain	Manifestation
Attention	Cannot maintain focus, easily distractible, unable to follow multi-step commands, fails digit span or serial subtraction
Orientation	Disoriented to time first (most sensitive), then place, then person (last to be lost)
Perception	Visual hallucinations (most common), illusions (misidentification of objects/people), paranoia
Sleep-Wake Cycle	Fragmented sleep, daytime somnolence, nocturnal worsening ("sundowning")
Cognition	Impaired short-term memory, disorganized speech, difficulty with abstract reasoning
Affect	Labile mood: anxiety, fear, irritability, or apathy depending on subtype

3. Diagnostic Workup

Test	Purpose	When to Order
Confusion Assessment Method (CAM)	Bedside screening tool for delirium (best initial clinical tool)	On every patient with suspected altered mental status
CBC with differential	Evaluate for infection (leukocytosis), anemia	Routine for all delirious patients
Basic Metabolic Panel (BMP)	Sodium, glucose, calcium, BUN/creatinine, CO2	Routine: detects hyponatremia, hypercalcemia, uremia, hypoglycemia
Urinalysis and urine culture	UTI is the most common infectious trigger in elderly	Routine
Chest X-ray	Pneumonia screening	Routine, especially if respiratory symptoms or fever present
Liver function tests	Hepatic encephalopathy	If jaundice, liver disease history, asterixis
Thyroid function (TSH)	Myxedema coma or thyrotoxicosis	If no clear precipitant found
Arterial blood gas (ABG)	Hypoxia, hypercarbia, acid-base disturbance	If respiratory compromise suspected
Blood cultures	Bacteremia/sepsis	If febrile or hemodynamically unstable
Toxicology screen / drug levels	Medication toxicity, substance intoxication	If ingestion suspected or medication list includes high-risk drugs (digoxin, lithium, theophylline)
Ammonia level	Hepatic encephalopathy	If liver disease present
Vitamin B12, folate, thiamine	Nutritional deficiency	If malnutrition or alcohol use disorder suspected
CT/MRI of the brain	Rule out stroke, subdural hematoma, mass	Only if focal neurological deficits, recent head trauma, or no identifiable metabolic/infectious cause
Lumbar puncture	Rule out meningitis or encephalitis	Only if fever + neck stiffness, immunocompromised, or no identifiable cause with persistent altered mental status
EEG	Nonconvulsive status epilepticus	If seizures suspected or patient remains unresponsive without clear cause

The diagnosis of delirium is clinical. There is no single laboratory test or imaging study that "confirms" delirium. The Confusion Assessment Method (CAM) is the best initial screening tool and is considered the standard bedside instrument. It requires four features, of which three must be present:

Acute onset and fluctuating course (required)
Inattention (required)
Disorganized thinking
Altered level of consciousness

Features 1 and 2 are mandatory. The presence of either feature 3 or 4 alongside them satisfies the diagnostic criteria. Pay close attention to this: inattention is the cardinal feature. If the patient can attend normally, the diagnosis is not delirium regardless of how confused they appear.

After establishing the diagnosis, the workup shifts entirely to identifying the precipitating cause. This is the part that exam questions focus on most heavily. A reasonable first-pass panel for any delirious patient includes CBC, BMP, urinalysis, chest X-ray, and a medication review. This combination covers the most common triggers: infection, metabolic derangement, and drug effect.

Brain imaging (CT or MRI) is not routine. It is ordered only when there are focal neurological signs (hemiparesis, cranial nerve palsies, new-onset seizures), a history of recent head trauma, or when no metabolic or infectious cause can be identified. An exam question that presents delirium with a clear UTI source and then asks "what is the next step" is testing whether you will waste time ordering a head CT. The answer in that scenario is to treat the UTI, not image the brain.

Lumbar puncture follows similar logic: it is reserved for patients with meningeal signs, immunocompromised states, or unexplained persistent encephalopathy.

EEG shows diffuse slowing in delirium (generalized theta and delta waves), which can help confirm the diagnosis in ambiguous cases and is particularly useful for detecting nonconvulsive status epilepticus, a treatable mimic.

4. Management and Treatment

Phase	Intervention	Details
First and most important step	Identify and treat the underlying cause	Antibiotics for infection, correct electrolytes, discontinue offending drugs, treat pain, relieve urinary retention
Non-pharmacologic measures (always first-line)	Environmental and supportive	Reorientation (clock, calendar, familiar objects), sleep hygiene (lights off at night, minimize nocturnal interruptions), early mobilization, correct sensory deficits (glasses, hearing aids), remove unnecessary catheters and restraints, ensure hydration and nutrition, involve family at bedside
Pharmacologic (only if needed)	Low-dose antipsychotics	Haloperidol 0.5 to 1 mg IV/IM/PO, may repeat every 30 to 60 minutes (max approximately 3 to 5 mg/day in elderly). Alternatives: quetiapine 12.5 to 50 mg PO, olanzapine 2.5 to 5 mg IM/PO
Exception: alcohol/benzodiazepine withdrawal	Benzodiazepines	Lorazepam 1 to 2 mg IV, or chlordiazepoxide for alcohol withdrawal protocol. Antipsychotics alone are dangerous in this context (lower seizure threshold).
Prevention (high-yield)	Hospital Elder Life Program (HELP)	Orientation protocols, sleep enhancement, early mobilization, vision/hearing optimization, hydration. Reduces delirium incidence by 30 to 40%.

The foundational principle of delirium management is that delirium is a symptom, not a disease. The treatment is to find and fix the cause. An exam question that offers haloperidol as the "next best step" before a cause has been identified or addressed is almost always wrong.

Step 1: Medication reconciliation. Review every medication the patient is taking. Anticholinergics (diphenhydramine, oxybutynin, promethazine), benzodiazepines (lorazepam, diazepam), opioids, corticosteroids, and fluoroquinolones are among the most common drug triggers. Stopping or substituting the offending agent is often curative. This step is tested repeatedly: a postoperative patient on scheduled diphenhydramine for sleep who becomes acutely confused should have the diphenhydramine discontinued as the next best step.

Step 2: Address physiologic triggers. Treat infections with appropriate antibiotics. Correct electrolyte abnormalities. Ensure adequate oxygenation. Relieve urinary retention (this is a frequently overlooked but very testable cause). Manage undertreated pain, because both uncontrolled pain and excessive opioid use can trigger delirium.

Step 3: Non-pharmacologic interventions. These are always first-line and should be implemented in every case. Reorientation cues (visible clock, calendar, familiar family photos), minimizing room changes, maintaining the sleep-wake cycle (no unnecessary nighttime vitals or lab draws), early ambulation, and ensuring patients have their glasses and hearing aids. Physical restraints should be avoided because they worsen agitation and prolong delirium.

Step 4: Pharmacologic management. Medications are reserved only for patients whose agitation poses a safety risk to themselves or staff (pulling out central lines, endotracheal tubes, or physically combative behavior). Haloperidol remains the most widely referenced agent at a starting dose of 0.5 to 1 mg. It can be given IV, IM, or PO. Monitor the QTc interval, because haloperidol can prolong QT and precipitate torsades de pointes. Second-generation antipsychotics like quetiapine (starting at 12.5 to 25 mg PO at bedtime) are increasingly used, particularly in patients with Parkinson disease or Lewy body dementia where haloperidol is contraindicated due to severe sensitivity to dopamine blockade (can cause irreversible parkinsonism and neuroleptic malignant syndrome).

Critical exception: If the cause of delirium is alcohol withdrawal or benzodiazepine withdrawal, antipsychotics alone are inappropriate and dangerous. These patients require benzodiazepines (lorazepam or chlordiazepoxide) because the underlying mechanism is GABA receptor downregulation. Using only an antipsychotic in alcohol withdrawal can mask symptoms while the patient progresses to withdrawal seizures or delirium tremens. This is one of the most commonly tested "traps" surrounding delirium management.

Duration: Delirium typically resolves within days once the underlying cause is treated, but in elderly patients, it can persist for weeks. Antipsychotics should be tapered and discontinued as soon as agitation resolves; they are not continued long-term.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Dementia	Both cause confusion, disorientation, and memory impairment in elderly patients	Dementia has an insidious onset over months to years with a stable, progressive course. Attention is preserved until late stages. Delirium has acute onset (hours to days) with a fluctuating course, and inattention is the cardinal feature. A patient who was at their baseline cognition yesterday and is acutely confused today has delirium until proven otherwise, even if they have underlying dementia.
Depression (pseudodementia)	Hypoactive delirium can mimic depression: patient appears withdrawn, apathetic, with psychomotor retardation	Depression develops over weeks, the patient is oriented, attention is intact (though effort may be reduced), and there is a prominent sad or anhedonic mood. The key test: depressed patients can attend if motivated; delirious patients cannot attend regardless of effort.
Schizophrenia / Brief psychotic disorder	Both can present with hallucinations, disorganized thinking, and agitation	Schizophrenia features predominantly auditory hallucinations, a clear sensorium (patient is alert and oriented), intact attention, and onset typically in young adulthood (ages 18 to 25). Delirium features visual hallucinations, altered consciousness, and inattention in an older patient with an identifiable medical trigger.
Nonconvulsive status epilepticus (NCSE)	Can present as altered mental status with minimal or no motor manifestations, mimicking delirium	Suspect NCSE if altered mental status is persistent and unexplained by metabolic workup. EEG is diagnostic. Subtle findings may include nystagmus, eyelid fluttering, or automatisms.
Wernicke encephalopathy	Confusion, altered mental status, often in malnourished or alcohol-dependent patients	Classic triad: encephalopathy + oculomotor dysfunction (nystagmus, ophthalmoplegia) + ataxia. The full triad is present in only about one-third of cases, so have a low threshold if the patient has alcohol use disorder or malnutrition. Treat empirically with IV thiamine before giving glucose.
Hepatic encephalopathy	Confusion, fluctuating mental status, can look identical to delirium	Look for asterixis (flapping tremor), elevated ammonia, history of cirrhosis, and precipitating factors (GI bleed, infection, constipation, excess protein intake). Treatment is lactulose and rifaximin, not antipsychotics.
Sundowning in dementia	Worsening confusion in the evening in a patient with known dementia	Sundowning is a behavioral pattern in dementia, not a new acute process. The patient's baseline cognitive status is already impaired, and there is no new precipitant. However, always rule out superimposed delirium ("delirium superimposed on dementia"), which is extremely common and carries the worst prognosis.

6. Traps and High-Yield Pearls

The single most common way students lose points on delirium questions is by failing to recognize hypoactive delirium. Exam vignettes deliberately present a quiet, lethargic, withdrawn elderly postoperative patient and offer depression, dementia, or "normal postoperative fatigue" as answer choices. The correct answer is delirium, and the giveaway is that the change was acute (over hours to days) and the patient demonstrates inattention on bedside testing. Remember: hypoactive delirium is the most commonly missed subtype in real life and therefore the most commonly tested subtype on examinations.

The second major trap involves management sequencing. When a question asks for the "next best step" in a delirious patient, the answer is almost never "give haloperidol." The answer is to find and treat the cause: check a urinalysis, discontinue the anticholinergic medication, correct the sodium, obtain a chest X-ray. Jumping to pharmacologic management before addressing the underlying trigger is the classic wrong-answer pathway. Antipsychotics are a bridge for safety, not a treatment for delirium itself.

Third, never forget the alcohol and benzodiazepine withdrawal exception. If the vignette describes a patient 48 to 72 hours after hospital admission or after abruptly stopping alcohol/benzodiazepines, with tremors, autonomic instability (tachycardia, hypertension, diaphoresis), agitation, and visual hallucinations, the treatment is benzodiazepines, not antipsychotics. Using haloperidol alone in this setting is a patient safety error and a reliably tested wrong answer.

Finally, understand the concept of delirium superimposed on dementia. A patient with known Alzheimer disease can absolutely develop delirium. Many students see "dementia" in the history and assume the confusion is baseline. The discriminator is the tempo of change: if the family says "she has been like this for years," it is dementia. If the family says "she was fine yesterday and today she does not recognize me," it is delirium on top of dementia, and you must search for a precipitant.

The core competency being tested across all delirium questions is the ability to recognize an acute, fluctuating change in attention as a medical emergency requiring cause-directed evaluation, not simply symptomatic sedation.

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