Delirium

Delirium is an acute, fluctuating disturbance of consciousness with impaired attention and cognition, typically caused by an underlying medical condition, substance use, or withdrawal.

Exam domain	One-glance essentials
Definition / diagnosis	Acute fluctuating disturbance of attention and awareness due to an underlying cause ^[1] Hypoactive delirium is common and easily missed ^[1]
Epidemiology / risks	Older age, dementia, frailty and sensory impairment predispose ^[1] Infection, drugs, surgery, pain and metabolic disturbance precipitate ^[1]
Core mechanism	Diffuse cerebral dysfunction disrupts attention and arousal ^[1] Multiple small insults can exceed a vulnerable brain's reserve ^[1]
Clinical picture	Hours-to-days onset, fluctuation, inattention and altered consciousness ^[1] Disorganised thinking, hallucinations or reversed sleep cycle may occur ^[1]
Investigations	Confirm bedside inattention and collateral time course ^[2] Search urgently for causes with examination, medication review and targeted tests ^[2]
Management	Treat causes and provide orientation, hydration, mobility and sensory aids ^[3] Medication is reserved for severe distress or immediate danger ^[3]
Complications	Falls, aspiration, pressure injury and prolonged admission ^[4] Delirium predicts mortality, institutionalisation and later cognitive decline ^[4]
Prevention / follow-up	Avoid deliriogenic drugs and use multicomponent inpatient prevention ^[3] Support sleep, mobility, nutrition, hearing and vision ^[3]
Exam traps	*Do not diagnose dementia during an unresolved delirium* ^[2] A quiet withdrawn patient may have high-risk hypoactive delirium ^[3]

References

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p48)

^[2] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p48)

^[3] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12)

^[4] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p23)

Delirium — from the Latin de- ("off, away from") + lira ("furrow, track"), literally meaning "off the track" or "derailed" — is an acute confusional state characterised by impairment in both consciousness and cognition ^[1]^[2].

Think of it this way: the brain's "operating system" has crashed. Unlike dementia, where specific "programs" (memory, language) fail one by one, delirium is a global system failure — the whole computer is glitching. It represents a common final pathway of disrupted cerebral homeostasis ^[2].

Core Concept

Delirium is NOT a disease in itself — it is a syndrome (a clinical manifestation of an underlying medical insult). Finding delirium means you must find the cause. It is the brain's "fever" — a non-specific alarm signal that something is physiologically wrong.

Key definitional features:

Acute onset (hours to days, not weeks to months)
Fluctuating course (classically worse at night — "sundowning")
Impaired attention (the cardinal, hallmark feature)
Altered level of consciousness (distinguishes it from dementia)
Evidence of an underlying medical cause (always)

Setting	Prevalence / Incidence
General hospitalised patients	14–24% at any point ^[2]
Elderly presenting to A&E	10–30% harbour a life-threatening condition ^[2]
Post-surgical (esp. hip fracture, cardiac surgery)	15–53%
ICU patients	60–80% (mechanically ventilated)
Palliative care / terminal illness	Up to 85%
Nursing home residents	10–40%

Prevalence increases with age — because cerebral reserve (the brain's ability to tolerate physiological insults) diminishes with age ^[2]
35–40% 1-year mortality in older patients presenting to A&E with delirium ^[2]
Massively under-recognised: > 70% of delirium cases are missed by clinical teams, especially the hypoactive subtype (the "quiet" delirious patient who is just drowsy) ^[2]

High Yield: Delirium is an independent predictor of mortality. Mortality data: 14% at 1 month, 22% at 6 months, 6× that of non-delirious patients ^[2]. It also confers a 5× increased incidence of dementia within 2 years ^[2].

Hong Kong Context

Hong Kong has a rapidly ageing population (> 20% aged ≥ 65 by 2026). Delirium is extremely common on geriatric, orthopaedic, and medical wards in the Hospital Authority system.
Polypharmacy in elderly patients (multiple chronic medications) is a major driver.
Common precipitants in HK include urinary tract infections, pneumonia, constipation, dehydration, and medication changes (especially after admission).

3. Risk Factors

The concept here is predisposing factors (baseline vulnerability) × precipitating factors (acute insult) = delirium. A patient with high baseline vulnerability (e.g., demented, elderly, sensory impaired) needs only a minor precipitant (e.g., a urinary catheter insertion, constipation) to tip into delirium. A young, healthy patient would need a massive insult (e.g., major surgery, septic shock) ^[2].

Factor	Why it predisposes
Dementia	Reduced cognitive reserve — the brain is already operating at its limit
Previous episode of delirium	Indicates underlying brain vulnerability
Older age	Reduced cerebral reserve, ↓ cholinergic neurons, ↓ cerebral blood flow
Functional impairment	Marker of frailty and reduced physiological reserve
Sensory impairment (vision/hearing)	Reduced external orientation cues → the brain "fills in gaps" with misperceptions
History of cerebrovascular disease	Pre-existing brain damage reduces reserve
Alcohol misuse	Chronic neurotoxicity, thiamine deficiency, liver disease
Severe comorbid illness	Multiple organ systems are already stressed

The classic mnemonic is DELIRIUM(S) ^[2]:

Letter	Category	Examples
D	Drugs	Anticholinergics, opioids, benzodiazepines, steroids, digoxin, diuretics, polypharmacy
E	Electrolytes	Hypo/hypernatraemia, hypercalcaemia, hypo/hyperglycaemia
L	Low oxygen	Hypoxia (pneumonia, PE, COPD exacerbation, post-operative)
I	Infection	UTI, respiratory infection, septicaemia, meningitis/encephalitis
R	Retention (of urine or faeces)	Urinary retention, constipation → surprisingly potent precipitants
I	Ictogenic (seizures)	Post-ictal states, non-convulsive status epilepticus
U	Underhydration / Undernutrition	Dehydration, malnutrition, thiamine/B12 deficiency
M	Metabolic (especially glucose)	Hepatic encephalopathy, uraemia, hypo/hyperglycaemia, metabolic acidosis, abnormal albumin
(S)	Subdural / Structural	Head injury, space-occupying lesions, stroke

Additional precipitants from lecture slides and notes ^[1]^[2]:

Use of physical restraints (worsens agitation, ↓ orientation)
Bladder catheter (discomfort, infection risk, unfamiliar sensation)
Pain (uncontrolled pain is a major precipitant)
Sleep deprivation (disrupts circadian regulation of neurotransmitters)
Constipation (often overlooked!)
Unfamiliar environment (ICU, post-transfer between wards)

Six causes of confusion in alcoholism ^[1]:

Intoxication
Delirium tremens (DT)
Head injury (alcoholics fall frequently)
Metabolic disturbances (e.g., hypoglycaemia)
Hepatic encephalopathy
Wernicke encephalopathy

Clinical Pearl

Never assume a confused alcoholic patient is "just drunk." You must systematically exclude all six causes listed above. Missing Wernicke encephalopathy or a subdural haematoma from a fall is a catastrophic and avoidable error. Always give thiamine BEFORE glucose in alcoholics — glucose without thiamine can precipitate or worsen Wernicke encephalopathy by exhausting remaining thiamine stores.

4. Anatomy and Functional Basis

Understanding delirium requires understanding what "consciousness" and "attention" actually are neuroanatomically.

Consciousness has two components:

Arousal (wakefulness): Governed by the ascending reticular activating system (ARAS) in the brainstem (pons, midbrain), which projects diffusely to the thalamus and cortex. Damage or dysfunction here → reduced level of arousal (drowsiness → stupor → coma).
Awareness (content of consciousness): Governed by the cerebral cortex, especially the association cortices. Damage here → confusion, disorientation, impaired cognition.

In delirium, both arousal and awareness are disrupted — this is what distinguishes it from dementia (where arousal is preserved until very late stages).

Attention is the ability to select and sustain focus on relevant stimuli while filtering out irrelevant ones.
Key structures: prefrontal cortex (executive control), posterior parietal cortex (spatial attention), thalamus (sensory gating), and the reticular formation (alerting).
Acetylcholine (ACh) is the primary neurotransmitter for attentional processing (basal forebrain cholinergic system — nucleus basalis of Meynert).
This is why anticholinergic drugs are such potent precipitants of delirium — they directly impair the attentional system.

The suprachiasmatic nucleus (SCN) of the hypothalamus is the master circadian clock.
It regulates the sleep-wake cycle via melatonin (from the pineal gland) and cortisol.
In delirium, disruption of these circuits (by inflammation, medications, ICU environment) leads to the characteristic sleep-wake cycle disturbance.

System	Role in delirium
Acetylcholine (ACh) ↓	Central to delirium pathophysiology. Reduced cholinergic transmission → impaired attention, memory, and cortical processing. This is why anticholinergic drugs cause delirium and why demented patients (who already have ACh deficiency) are vulnerable.
Dopamine (DA) ↑	Excess dopamine → psychomotor agitation, hallucinations, delusions. This is why antipsychotics (dopamine blockers) help in hyperactive delirium.
GABA	Altered GABAergic tone — relevant in hepatic encephalopathy (excess GABA-ergic activity) and alcohol/benzodiazepine withdrawal (sudden loss of GABA-ergic activity).
Glutamate	Excitotoxicity via NMDA receptors may contribute to neuronal injury in prolonged delirium.
Serotonin (5-HT)	Serotonin syndrome can cause delirium; serotonin excess contributes to agitation and autonomic instability.
Melatonin ↓	Disruption of circadian regulation → sleep-wake cycle disturbance.

5. Pathophysiology

The pathophysiology of delirium is poorly understood ^[2], but several converging hypotheses exist. Think of them as overlapping mechanisms rather than competing theories:

A systemic insult (infection, surgery, trauma) triggers a systemic inflammatory response (↑ IL-1, IL-6, TNF-α).
These pro-inflammatory cytokines cross the blood-brain barrier (BBB), which becomes more permeable with age, illness, and inflammation.
Within the brain, microglial activation occurs → neuroinflammation → impaired neuronal function.
This disrupts neurotransmitter synthesis and release, particularly reducing acetylcholine and increasing dopamine.
The result: global cortical dysfunction → delirium.

Why does this explain the clinical features?

↓ ACh → impaired attention, memory, orientation
↑ DA → hallucinations, agitation, psychosis
Neuroinflammation → diffuse cortical dysfunction → fluctuating symptoms

Acetylcholine is the most critical neurotransmitter for sustained attention and cortical arousal.
Any insult that ↓ ACh synthesis (hypoxia, hypoglycaemia) or blocks ACh receptors (anticholinergic drugs) can precipitate delirium.
Serum anticholinergic activity correlates with delirium severity in some studies.
This is why the elderly are so vulnerable — they already have age-related cholinergic decline.

Cerebral hypoxia, hypoperfusion, or metabolic derangement → impaired oxidative metabolism → reduced ATP production → neuronal dysfunction.
The brain is exquisitely sensitive to metabolic insults because it consumes ~20% of total body oxygen despite being only ~2% of body weight.

Recent neuroimaging studies (fMRI, EEG) show that delirium involves a breakdown of functional connectivity between brain networks — particularly the default mode network, the dorsal attention network, and thalamocortical circuits.
EEG characteristically shows diffuse slowing of background cortical activity ^[2] — reflecting global cortical hypofunction.

Systemic insult → Systemic inflammation → BBB breach →
Neuroinflammation (microglial activation) →
↓ Acetylcholine + ↑ Dopamine + ↓ Melatonin →
Impaired attention + psychosis + sleep-wake disruption →
DELIRIUM

6. Aetiology (with Hong Kong Focus)

Category	Common causes	Notes
Infections	UTI, pneumonia, cellulitis, septicaemia, meningitis/encephalitis	UTI and pneumonia are the #1 precipitants in HK elderly
Metabolic	Hypo/hypernatraemia, hypercalcaemia, hypo/hyperglycaemia, uraemia, hepatic encephalopathy, metabolic acidosis, abnormal albumin	Check electrolytes, glucose, renal/liver function
Drugs	Anticholinergics, opioids, benzodiazepines, steroids, digoxin, diuretics ^[2]	Polypharmacy is a huge problem in HK elderly
Substance-related	Alcohol intoxication, withdrawal, delirium tremens ^[1]^[2]	See delirium tremens section below
Hypoxia	Post-operative, pneumonia, PE, COPD, heart failure	Post-operative delirium is extremely common
Organ failure	Renal, hepatic, cardiac failure	Hepatic encephalopathy is a classic cause
Neurological	Post-ictal, head injury, stroke, space-occupying lesion, encephalitis, non-convulsive status epilepticus	Always consider in acute-onset confusion
Nutritional	Thiamine deficiency (Wernicke), B12, folate	Especially in alcoholics and malnourished elderly
Other	Pain, urinary retention, constipation, sleep deprivation, physical restraints, bladder catheter ^[2]	These "minor" precipitants are commonly missed

Delirium tremens is the severe form of alcohol withdrawal ^[1]:

Feature	Detail
Timing	Occurs 24–96 hours after abstention ^[1]
Clinical features	Confusion, hallucinations, severe agitation, seizures ^[1]
Mortality	5% ^[1]
Status	Medical emergency requiring hospitalisation ^[1]

Management of delirium tremens ^[1]:

Benzodiazepines in decreasing dosage (lorazepam/diazepam/others) — first-line
Anticonvulsants (carbamazepine) — for seizure prophylaxis/treatment
Proactive use of parenteral vitamins (thiamine) — ALWAYS give thiamine before glucose
Neuroleptics for control of agitation
Fluid and electrolyte balance

Why benzodiazepines are first-line in DT but second-line in other delirium: In alcohol withdrawal, the problem is sudden loss of GABA-ergic activity (alcohol chronically potentiates GABA receptors → withdrawal removes this → GABA underactivity → excitotoxicity, seizures). Benzodiazepines directly replace the lost GABA-ergic activity. In contrast, in most other forms of delirium, benzodiazepines can worsen confusion because they are sedating and have paradoxical effects in the elderly.

7. Classification

Subtype	Features	Prevalence	Prognosis
Hyperactive	Agitation, restlessness, hallucinations, pulling at lines/tubes, combativeness	~25%	Better (because it gets noticed and treated)
Hypoactive	Drowsiness, lethargy, reduced responsiveness, psychomotor slowing, withdrawn	~25%	Worse prognosis ^[2] — often missed ("quiet delirium")
Mixed	Fluctuates between hyperactive and hypoactive states unpredictably	~35%	Intermediate
Unclassifiable	Does not fit neatly into above categories	~15%	Variable

Clinical Pearl

Hypoactive delirium is the most commonly missed subtype and carries the worst prognosis because it is often mistaken for depression or normal sleepiness, leading to delayed treatment. The patient who is "just a bit drowsy" may be delirious. Always screen for inattention in any patient with altered behaviour.

Substance intoxication delirium
Substance withdrawal delirium
Medication-induced delirium
Delirium due to another medical condition
Delirium due to multiple aetiologies

Acute: hours to days
Persistent: weeks to months

Not superimposed on dementia (F05.0)
Superimposed on dementia (F05.1) — this is extremely common and is the hardest to diagnose

8. Clinical Features

The clinical features of delirium are a variety of neuropsychiatric disturbances ^[2]. I will separate these systematically into symptoms and signs, with the pathophysiological basis explained inline.

8.1 Symptoms (What the Patient/Carer Reports)

Drowsiness, lethargy, reduced arousal → due to disruption of the ascending reticular activating system (ARAS) and thalamocortical circuits by neuroinflammation and neurotransmitter imbalance
Disorientation — classically time > place > person (time orientation is the most fragile and first to go because it requires continuous updating by working memory, which depends on intact attention and prefrontal function) ^[2]
In severe cases → stupor or coma (profound ARAS dysfunction)

Distractibility during conversations ^[2] — the patient cannot maintain focus; they drift off mid-sentence, are drawn to irrelevant stimuli. This is because the prefrontal cortex and basal forebrain cholinergic system (which sustain attention) are dysfunctional.
Inability to follow commands or track a conversation
Cannot maintain a coherent train of thought
Testing: serial sevens (subtract 7 from 100 repeatedly), days of the week backwards, months of the year backwards, digit span ^[2]

High Yield: Impaired attention is the hallmark ^[2] and the most specific feature that distinguishes delirium from other conditions. If attention is normal, it is unlikely to be delirium.

Generally global — involving memory loss, difficulty with language/speech ^[2]
Thinking is slow and muddled, but often rich in content (dream-like) ^[2] — this "dream-like" quality occurs because the brain is generating internal imagery (similar to dreaming) due to disrupted thalamocortical gating. The thalamus normally filters sensory input; when it fails, internal representations intrude into consciousness.
Disorientation (as above)
Memory impairment: Primarily affects registration (laying down new memories) and short-term memory because these depend on sustained attention. Remote memory may be relatively preserved.
Executive dysfunction: Impaired planning, judgment, and problem-solving (prefrontal cortex dysfunction)

Perceptual disturbances: illusions (misinterpretation of real stimuli, e.g., mistaking an IV pole for a person) and hallucinations (especially visual hallucinations) ^[2]
- Why visual hallucinations? Visual processing requires complex cortical integration (occipital → temporal → parietal). When cortical function is globally disrupted, the visual system is particularly vulnerable to generating false percepts. Also, ↑ dopamine in the mesolimbic pathway promotes hallucinations.
- Auditory hallucinations can occur but are less prominent than in primary psychotic disorders
Delusions/abnormal beliefs: typically referential or persecutory but usually transient and poorly elaborated ^[2] — meaning the patient may believe staff are trying to poison them, but they cannot give you a detailed, fixed delusional system (unlike schizophrenia where delusions are often systematised)
Disorganised thinking: disorganised or incoherent speech, rambling or irrelevant conversations ^[2] — reflecting global cortical dysfunction disrupting the language and thought-organisation networks

Can range from daytime drowsiness + nighttime insomnia to complete sleep cycle reversal ^[2]
Another hallmark of delirium ^[2]
Pathophysiology: Disruption of the suprachiasmatic nucleus (SCN) → melatonin circuit. Inflammation, hospital environment (constant light, noise in ICU), and medications all disrupt circadian rhythmicity. ↓ Melatonin secretion has been documented in delirious patients.

Variable, may be labile ^[2]
May involve depression, euphoria, anxiety, anger, fear, apathy ^[2]
Mood lability (rapid swings between emotional states) reflects prefrontal cortical disinhibition and limbic system dysregulation
Fear and anxiety are especially common in hyperactive delirium — imagine being in a dream state where you are confused, misperceiving your environment, and unable to understand what is happening to you

Can be hypo- or hyperactive and can shift between these states unpredictably ^[2]
Hyperactive: agitation, restlessness, pulling at tubes/lines, trying to get out of bed, combativeness
Hypoactive: lethargy, withdrawal, reduced spontaneous movement, minimal speech
Reflects the balance between dopaminergic excess (hyperactive) and cholinergic deficit (hypoactive)

Acute onset with diurnal fluctuation (usually worse at night) ^[2]
Lasting days to months (< 6 months in ICD-10) ^[2]
Why worse at night ("sundowning")? At night: ↓ environmental orientation cues (reduced lighting, fewer staff interactions), ↓ melatonin disruption becomes more apparent, and sensory deprivation increases the brain's tendency to generate internal percepts (hallucinations)

Sign	Description	Pathophysiological Basis
Reduced level of consciousness	GCS may be reduced; patient may be drowsy or difficult to rouse	ARAS dysfunction
Inattention	Cannot follow commands, loses thread of conversation, fails serial sevens or digit span	Cholinergic deficit in prefrontal-basal forebrain circuits
Disorientation	Especially to time; may not know date, day, month, year	Requires continuous updating by working memory (attention-dependent)
Cognitive impairment	MMSE/MoCA scores are acutely reduced from baseline	Global cortical dysfunction
Abnormal speech	Incoherent, rapid or slow ^[2]; may be rambling, disorganised	Disrupted language networks (Wernicke/Broca circuits) + executive dysfunction
Perceptual abnormalities	Visual hallucinations (patient picking at bedsheets — "carphologia"), illusions	Thalamocortical gating failure + dopaminergic excess
Psychomotor changes	Agitation, restlessness, or lethargy, hypokinesia	Dopaminergic-cholinergic imbalance
Autonomic signs (especially in hyperactive delirium)	Tachycardia, hypertension, sweating, tremor, mydriasis	Sympathetic nervous system activation (especially in withdrawal states)
Asterixis (negative myoclonus)	"Liver flap" — if hepatic encephalopathy is the cause	Metabolic encephalopathy disrupting motor cortex
Multifocal myoclonus	Irregular, asymmetric jerking movements	Diffuse cortical irritability from metabolic derangement
Fluctuating examination	Findings change between visits, even within the same day	Inherent property of delirium — fluctuating cortical dysfunction

This table is extremely high yield for exams ^[2]:

Feature	Delirium	Dementia
Onset	Acute	Gradual
Duration	Hours to weeks	Months to years
Course	Fluctuating	Progressive deterioration
Consciousness	Altered	Normal (until very late stages)
Context	New illness/medication	Health unchanged
Perceptual disturbance	Common	Occurs in late stages
Sleep-wake cycle	Disrupted	Usually normal
Orientation	Usually impaired for time and unfamiliar people/places	Impaired in late stages
Speech	Incoherent, rapid or slow	Word finding difficulties
Attention	Profoundly impaired (hallmark)	Relatively preserved until late

Critical Distinction

Delirium and dementia frequently coexist (delirium superimposed on dementia, ICD-10 F05.1). In fact, dementia is the single strongest predisposing factor for delirium. When a demented patient suddenly worsens, always rule out delirium first — do not attribute the deterioration to "progression of dementia." Cognitive fluctuations can occur in dementia (especially Lewy body dementia and as "sundowning" in Alzheimer's), but any change from the patient's baseline pattern of fluctuation should prompt evaluation for delirium ^[2].

Any acute change in cognition or behaviour from baseline
New-onset confusion in any hospitalised patient
Agitation or combativeness in a previously calm patient
Sudden drowsiness or withdrawal not explained by medications
New visual hallucinations
Acute deterioration in a patient with known dementia
Post-operative confusion (especially in elderly after hip fracture or cardiac surgery)
Alcohol withdrawal 24–96 hours after last drink

High Yield Summary

Definition: Acute confusional state = impaired consciousness + impaired cognition. A syndrome, not a disease — always find the cause.

Epidemiology: 14–24% hospitalised patients; > 70% missed; 6× mortality vs non-delirious. 35–40% 1-year mortality in elderly.

Risk Factors: Predisposing (dementia, old age, sensory impairment, alcohol) × Precipitating (DELIRIUM mnemonic: Drugs, Electrolytes, Low O2, Infection, Retention, Ictogenic, Underhydration, Metabolic).

Pathophysiology: Systemic insult → neuroinflammation → ↓ ACh + ↑ DA + ↓ melatonin → global cortical dysfunction.

Core Clinical Features:

Hallmarks: Impaired attention + sleep-wake cycle disruption
Acute onset, fluctuating course (worse at night), disorientation (time > place > person)
Visual hallucinations, transient poorly-elaborated delusions
Psychomotor disturbance (hyper/hypo/mixed)
Mood lability

Subtypes: Hyperactive (25%), Hypoactive (25% — worst prognosis, most missed), Mixed (35%).

Delirium tremens: Severe alcohol withdrawal at 24–96h; confusion, hallucinations, agitation, seizures; 5% mortality; Rx: benzodiazepines + thiamine + fluids.

Key Distinction from Dementia: Acute (not gradual), altered consciousness (not normal), fluctuating (not progressive), impaired attention (hallmark), triggered by illness/medication.

Active Recall - Delirium (Definition to Clinical Features)

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p48) ^[2] Senior notes: ryanho-psych.md (sections 4.1, pages 74–76)

Differential Diagnosis of Delirium

The core challenge of the differential diagnosis of delirium is this: delirium is a syndrome of acute, fluctuating, global brain dysfunction. Several other conditions can mimic parts of this picture — either because they share overlapping features (confusion, hallucinations, agitation, altered consciousness) or because they genuinely coexist with delirium and cloud the clinical picture. Your job is to systematically distinguish them.

The guiding principle is DSM-5 Criterion D: the disturbance is not better explained by another pre-existing, established or evolving neurocognitive disorder and does not occur in the context of a severely reduced level of arousal (e.g., coma) ^[2]. In other words, you need to exclude conditions that look like delirium but are actually something else — and equally, you need to recognise when delirium is superimposed on a pre-existing condition.

This is the most commonly confused differential ^[2].

Feature	Delirium	Dementia
Onset	Acute (hours to days)	Gradual (months to years)
Course	Fluctuating	Progressive deterioration
Consciousness	Altered (key distinguishing feature)	Normal until very late
Attention	Profoundly impaired (hallmark)	Relatively preserved until late
Perceptual disturbance	Common (especially VH)	Late stages only
Sleep-wake cycle	Disrupted	Usually normal
Context	New illness / medication change	Health unchanged
Reversibility	Usually reversible	Irreversible (mostly)

Why is this tricky?

Dementia is the single strongest predisposing factor for delirium. Therefore, delirium superimposed on dementia (ICD-10: F05.1) ^[2] is extremely common and is the hardest diagnostic scenario.
Cognitive fluctuations may occur in dementia, especially in dementia with Lewy bodies and as sundowning phenomenon in Alzheimer's disease ^[2]. In DLB, the fluctuating attention, visual hallucinations, and altered alertness can closely mimic delirium.
The rule: Delirium should be ruled out if there is any change in pattern of fluctuation from baseline ^[2]. If a patient with known DLB suddenly becomes more confused than their usual level, treat it as delirium until proven otherwise.

How to distinguish in practice:

Obtain collateral history from carers about the baseline cognitive state and the tempo of change
Compare current cognitive scores (MMSE/MoCA) to any documented baseline
Look for an identifiable precipitant (new drug, infection, metabolic disturbance)
Impaired attention out of proportion to other cognitive deficits favours delirium

Clinical Pearl

Never say "the patient is just demented" without ruling out superimposed delirium. Any acute worsening in a demented patient is delirium until proven otherwise. Missing this means missing a treatable — and potentially life-threatening — underlying cause.

Non-convulsive status epilepticus often shows no classical ictal features ^[2]. This is one of the most dangerous mimics because it is a treatable neurological emergency that can look identical to delirium.

Supportive clinical features ^[2]:

Abnormal movements: prominent bilateral facial twitching, unexplained nystagmoid eye movements, spontaneous hippus (rhythmic dilation and constriction of the pupils)
Automatisms: lip smacking, chewing, swallowing (these are stereotyped, repetitive movements generated by temporal lobe seizure activity)
Acute aphasia or neglect without a structural lesion (the seizure activity disrupts cortical language/attention networks without causing a stroke)

Why it mimics delirium: Both present with altered consciousness, fluctuating cognition, and inattention. In NCSE, the brain is in a state of continuous abnormal electrical activity — the "confusion" is the clinical manifestation of ongoing subclinical seizures.

Key distinguishing feature: EEG is required for diagnosis ^[2]. The EEG will show continuous or near-continuous epileptiform discharges.

When to suspect NCSE over simple delirium:

Subtle motor phenomena (facial twitching, oral automatisms)
History of epilepsy or recent brain insult (stroke, head injury, neurosurgery)
Rapid fluctuation (seconds to minutes rather than hours)
Poor response to standard delirium management
Unexplained nystagmus or hippus

Delirium is characterised by vivid hallucinations, delusions, language disturbances and agitation, which may resemble psychotic disorders or mood disorders with psychotic features ^[2].

Feature	Delirium	Primary Psychosis (e.g., Schizophrenia)
Consciousness	Altered	Clear (this is the key distinction)
Attention	Profoundly impaired	Relatively preserved (unless very disorganised)
Hallucinations	Predominantly visual	Predominantly auditory (especially 3rd-person running commentary, thought echo)
Delusions	Transient, poorly elaborated, fluctuating	Systematised, fixed, persistent
Onset	Acute, identifiable precipitant	May be insidious (prodromal phase)
Age	Any age; more common in elderly	Typically young adult (peak onset 18–25 M, 25–35 F)
Course	Fluctuating, worse at night	Relatively stable within an episode
Medical cause	Present	Absent (diagnosis of exclusion)
EEG	Diffuse slowing	Normal

Why this distinction matters: Treating delirium with antipsychotics alone (without finding the medical cause) is dangerous. Conversely, diagnosing a young patient with "schizophrenia" when they actually have NMDA-receptor encephalitis or a drug-induced delirium has devastating consequences.

Guidance from the notes on distinguishing primary (psychiatric) vs secondary (medical) psychosis ^[2]:

Secondary psychosis (including delirium) is suggested by: visual hallucinations, older age of onset, acute onset, altered consciousness, disorientation, abnormal vital signs, focal neurological signs, and an identifiable medical precipitant.

This is a specific and high-yield differential to understand:

Alcoholic hallucinosis ^[1]:

Occurs in chronic heavy drinkers
Auditory hallucinations (not visual — this is the key difference from DT)
In clear consciousness (sensorium is not clouded — unlike DT where consciousness is altered)
Distressing in content
Some develop schizophrenia, some remit after stopping alcohol use
Treatment with antipsychotics and advice to abstain from alcohol

The lecture slide explicitly states the distinguishing features: (differentiate from delirium tremens — reduction in alcohol intake, clouded sensorium, visual hallucinations) ^[1].

Feature	Alcoholic Hallucinosis	Delirium Tremens
Consciousness	Clear	Clouded
Hallucinations	Auditory	Visual (predominantly)
Context	Chronic heavy drinking (may still be drinking)	Reduction in / cessation of alcohol intake
Autonomic signs	Absent	Present (tachycardia, sweating, tremor)
Seizures	No	Yes
Treatment	Antipsychotics + abstinence	Benzodiazepines + thiamine + fluids

Fear, anxiety and dissociative symptoms may also occur in some cases of delirium ^[2].

Why this is confusing: A patient who has experienced a traumatic event (e.g., major surgery, ICU stay, assault) may present with:

Disorientation and confusion (dissociative amnesia)
Reduced awareness of surroundings (dissociative detachment)
Emotional numbing or agitation
Altered perception of reality (derealisation/depersonalisation)

How to distinguish:

Feature	Delirium	Acute Stress Disorder
Consciousness	Altered (drowsiness, reduced arousal)	Preserved (may appear "spaced out" but is arousable and oriented once engaged)
Attention	Globally impaired	May be narrowed/focused but not globally impaired
Cognition	Globally disturbed	Intact cognitive testing when engaged
Medical cause	Present	Absent (triggered by psychological trauma)
EEG	Diffuse slowing	Normal
Hallucinations	Visual, vivid	Flashbacks (re-experiencing the trauma — not random hallucinations)
Duration	Days to weeks	3 days to 1 month (by DSM-5 criteria)

The bottom line: If you can engage the patient and their cognitive testing is normal, it is not delirium.

Focal neurological diseases may be associated with focal disturbances in cognition, and delirium may be associated with focal neurological signs if due to brain lesions ^[2].

Notable examples ^[2]:

Condition	What it mimics	Why it's confusing	How to distinguish
Wernicke's aphasia	Confused speech, inability to comprehend language	Looks like "confused" patient who gives incoherent answers	Fluent but paraphasic speech; comprehension disproportionately impaired; repetition impaired; focal lesion in dominant temporal lobe; consciousness and attention otherwise intact
Bitemporal lesions	Memory loss, confusion, behavioural change	Bilateral temporal damage (e.g., HSV encephalitis) causes amnesia and personality change	Usually has identifiable cause (encephalitis, bilateral strokes); may have seizures; neuroimaging shows bilateral temporal pathology
Anton's syndrome	Patient denies blindness, appears confused	Bilateral occipital lobe lesions → cortical blindness with confabulation about visual ability	Patient bumps into objects but insists they can see; test visual fields formally
Bifrontal lesions	Disinhibition, apathy, impaired executive function	Personality and behavioural change looks like delirium	Usually subacute; consciousness preserved; attention may be mildly impaired but arousal is normal; neuroimaging shows frontal pathology

Key principle: Neuroimaging may be required ^[2] to distinguish these from delirium. Focal neurological signs on examination (e.g., hemiparesis, visual field defect, isolated aphasia) should prompt urgent imaging.

This deserves its own section because it is a critical differential, especially in HK where alcohol misuse and nutritional deficiency are not uncommon.

Wernicke's encephalopathy presents with ^[1]:

Confusion
Memory impairment / attention problems / hallucination
Ophthalmoplegia / nystagmus
Ataxia (truncal)
Peripheral neuropathy (50%)
Hypothermia
Apathy
Coma (rare)

Why it mimics delirium: The confusion, inattention, and memory impairment look identical to delirium — and in fact, Wernicke encephalopathy IS a cause of delirium. The distinction matters because the treatment is specific: urgent parenteral thiamine.

How to distinguish Wernicke from "generic" delirium: Look for the classic triad (confusion + ophthalmoplegia + ataxia) — but be aware that the full triad is present in only ~10% of cases. Any confused patient with a history of alcohol misuse or malnutrition should receive empirical thiamine.

Hepatic encephalopathy is staged by the West Haven Criteria ^[1]:

Stage	Features
Stage 1	Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria or depression. Asterixis can be detected.
Stage 2	Lethargy or apathy. Mild disorientation. Inappropriate behaviour. Slurred speech. Obvious asterixis.
Stage 3	Gross disorientation. Bizarre behaviour. Semi-stupor to stupor. Asterixis generally absent.
Stage 4	Coma.

Why it mimics delirium: Stages 1–3 of hepatic encephalopathy present exactly like delirium (inattention, disorientation, sleep-wake cycle disruption, personality change, fluctuating course). Hepatic encephalopathy IS a specific cause of delirium. The distinction is important because the management is specific (lactulose, rifaximin, protein restriction, treat precipitants like GI bleeding or infection).

How to distinguish: Look for stigmata of chronic liver disease (jaundice, spider naevi, palmar erythema, ascites, caput medusae), asterixis ("liver flap"), elevated ammonia (NH3), and abnormal LFTs. The pathophysiology is accumulation of neurotoxins (especially ammonia) due to hepatic failure → these cross the BBB → astrocyte swelling → cerebral oedema → disrupted neurotransmission (especially increased GABAergic tone).

While depression is more commonly confused with dementia (the classic "pseudodementia" scenario ^[2]), severe depression in the elderly can sometimes mimic hypoactive delirium:

Feature	Hypoactive Delirium	Severe Depression
Onset	Acute	Gradual (weeks)
Consciousness	Altered	Clear
Attention	Impaired	May be reduced (poor concentration) but not globally impaired
Cognition	Globally impaired	May perform poorly on testing due to poor effort ("don't know" answers rather than wrong answers)
Diurnal variation	Fluctuating, worse at night	Worse in the morning (morning dysphoria)
Psychomotor slowing	Present	Present (psychomotor retardation)
Medical precipitant	Present	Absent (though medical illness can trigger depression)

Various substances can cause states that mimic delirium or indeed cause delirium:

Substance	Intoxication picture	Withdrawal picture
Alcohol	Confusion, disinhibition, ataxia, slurred speech	DT: confusion, VH, agitation, seizures at 24–96h ^[1]
Benzodiazepines	Drowsiness, slurred speech, ataxia	Similar to alcohol withdrawal (seizures, confusion, agitation)
Opioids	Drowsiness, miosis, respiratory depression	Agitation, sweating, mydriasis, diarrhoea (rarely causes true delirium)
Anticholinergics	Classic delirium: "hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter"	Not typically
Stimulants (amphetamines, cocaine)	Agitation, paranoia, hallucinations, tachycardia	Crash/depression (not typically delirium)
Cannabis	Confusion, paranoia, perceptual disturbances	Mild (rarely delirium)

Differential	Key distinguishing features from delirium
Dementia	Chronic, gradual, consciousness preserved, attention relatively spared until late
NCSE	Subtle motor signs (facial twitching, automatisms); EEG diagnostic
Primary psychosis	Clear consciousness; auditory > visual hallucinations; systematised delusions; younger age
Alcoholic hallucinosis	Clear consciousness; auditory hallucinations; no autonomic signs ^[1]
Acute stress disorder	Preserved consciousness and cognition when engaged; psychological trigger; flashbacks not random VH
Focal neurological disorders	Focal cognitive deficit with preserved consciousness; neuroimaging diagnostic
Wernicke encephalopathy	Ophthalmoplegia, ataxia, peripheral neuropathy; responds to thiamine
Hepatic encephalopathy	Asterixis, stigmata of CLD, elevated NH3; specific treatment (lactulose, rifaximin)
Depression	Gradual onset, clear consciousness, worse in mornings, poor effort on testing

High Yield Summary

Top differentials for delirium (exam favourites):

Dementia — most commonly confused. Key: consciousness preserved in dementia; acute change in a demented patient = delirium until proven otherwise.
Non-convulsive status epilepticus — dangerous mimic; look for facial twitching, automatisms, nystagmus; EEG required.
Primary psychosis — clear consciousness, auditory hallucinations, systematised delusions, younger patient.
Alcoholic hallucinosis vs DT — hallucinosis has clear consciousness + auditory hallucinations; DT has clouded consciousness + visual hallucinations.
Wernicke encephalopathy — confusion + ophthalmoplegia + ataxia; give thiamine empirically.
Hepatic encephalopathy — asterixis, CLD stigmata, elevated NH3; West Haven staging.
Focal neurological disorders — Wernicke's aphasia, Anton's syndrome, bifrontal/bitemporal lesions; neuroimaging needed.
Acute stress disorder — preserved consciousness and cognition when engaged; psychological trigger.

Golden rule: Delirium can coexist with any of these conditions (especially dementia). Always rule out delirium first in any acute confusional state.

Active Recall - Differential Diagnosis of Delirium

References

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p13, p23, p38, p48) ^[2] Senior notes: ryanho-psych.md (sections 4.1–4.2, pages 74–76, 78, 85, 95, 120)

Diagnostic Criteria

Delirium is fundamentally a clinical diagnosis. There is no single blood test, scan, or biomarker that "diagnoses" delirium. You diagnose it at the bedside by recognising the characteristic syndrome, then you investigate to find the underlying cause. Two major classification systems provide formal criteria.

The DSM-5 criteria are the most widely used in clinical practice and research ^[2]:

Criterion	Requirement	Explanation from First Principles
A	A disturbance in attention and awareness	Attention (the ability to direct, focus, sustain, and shift cognitive processing) is the cardinal feature. Awareness refers to reduced orientation to the environment. This reflects cholinergic deficiency in prefrontal-basal forebrain circuits + ARAS dysfunction.
B	The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day	Acute onset distinguishes delirium from dementia (gradual). Fluctuation reflects the inherent instability of a brain in metabolic crisis — neurotransmitter levels, cerebral perfusion, and inflammatory mediators are constantly changing.
C	An additional disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception)	"Additional" means on top of the attention/awareness disturbance. This reflects global cortical dysfunction — not just a single domain (which might suggest a focal lesion).
D	Not better explained by another pre-existing, established, or evolving neurocognitive disorder and does not occur in the context of a severely reduced level of arousal (e.g., coma)	This criterion forces you to distinguish delirium from dementia and from coma. A comatose patient cannot be assessed for attention or cognition, so delirium cannot be diagnosed. A demented patient can develop delirium, but the acute change must be identified.
E	Evidence from history, physical examination, or investigations that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal, or exposure to a toxin, or is due to multiple aetiologies	This is the aetiological criterion — you must demonstrate a medical cause. Delirium is NEVER "idiopathic." If you cannot find a cause, keep looking.

DSM-5 Specifiers ^[2]:

Cause: substance intoxication delirium, substance withdrawal delirium, medication-induced delirium, delirium due to another medical condition, delirium due to multiple aetiologies
Duration: acute (hours to days), persistent (weeks to months)
Activity level: hyperactive, hypoactive, mixed level of activity

The ICD-10 requires ALL of the following ^[2]:

Criterion	Requirement
(a)	Impairment of consciousness and attention
(b)	Global disturbance of cognition (perceptual disturbances, impaired thinking and comprehension, memory impairment, disorientation)
(c)	Psychomotor disturbance (hypo- or hyperactivity with unpredictable shifts)
(d)	Disturbance of sleep-wake cycle
(e)	Emotional disturbances

Additional ICD-10 stipulations ^[2]:

Onset is usually rapid, course diurnally fluctuating with total duration less than 6 months
Diagnosis can be made even if underlying cause is not clearly established

ICD-10 Specifiers ^[2]:

Not superimposed on dementia (F05.0)
Superimposed on dementia (F05.1)
Other delirium (F05.8)
Delirium unspecified (F05.9)

DSM-5 vs ICD-10 — Key Differences

DSM-5 focuses on attention/awareness as the core feature (Criterion A) and mandates identification of a medical cause (Criterion E). ICD-10 is broader, requiring psychomotor disturbance, sleep-wake disruption, and emotional disturbance as mandatory criteria, and notably permits diagnosis even when the underlying cause is not yet established. In practice, use whichever system your institution requires, but understand both for exams.

3. Bedside Screening Tools

Since delirium is often under-recognised ( > 70% missed diagnosis) ^[2], structured screening tools are essential. They do not replace clinical judgement but standardise detection.

The CAM is the most widely validated and used bedside screening tool for delirium worldwide. It operationalises the DSM criteria into four features:

Feature	Assessment	Based on
Feature 1	Acute onset and fluctuating course	Is there an acute change in mental status from baseline? Does the abnormal behaviour fluctuate during the day?
Feature 2	Inattention	Does the patient have difficulty focusing attention (e.g., easily distracted, difficulty keeping track of what is being said)?
Feature 3	Disorganised thinking	Is the patient's thinking disorganised or incoherent (rambling, irrelevant conversation, unclear flow of ideas)?
Feature 4	Altered level of consciousness	Anything other than alert (vigilant, lethargic, stuporous, comatose)?

Diagnostic algorithm: Delirium is present if Feature 1 AND Feature 2 are present, PLUS either Feature 3 OR Feature 4.

Sensitivity: ~94–100%
Specificity: ~90–95%

CAM-ICU: A modified version for patients who cannot speak (e.g., intubated in ICU). Uses visual and motor-based attention tests instead of verbal ones.

High Yield: The CAM is the most commonly asked-about screening tool for delirium in exams. Remember: Features 1 + 2 are mandatory, plus either 3 or 4.

These are used to document change in mental status ^[2]:

Tool	What it tests	Role in delirium
MMSE (Mini-Mental State Examination)	Global cognition (orientation, registration, attention/calculation, recall, language, construction); 30 points	Useful to document cognitive baseline and track change. Not specific for delirium (also abnormal in dementia). Does not specifically assess attention well.
MoCA (Montreal Cognitive Assessment)	More sensitive for executive function and attention; 30 points	Better than MMSE for detecting subtle cognitive impairment. More emphasis on attention and executive function.
Serial sevens	Attention specifically	Subtract 7 from 100 repeatedly (100, 93, 86, 79, 72, 65). Tests sustained attention and working memory — core deficits in delirium.
Digit span	Attention and working memory	Forward: repeat increasing sequences of digits (normal ≥ 5). Backward: repeat in reverse (normal ≥ 3). Impaired in delirium.
Days/months backwards	Attention	Recite days of the week or months of the year in reverse order. Simple, rapid bedside test.

For the specific context of suspected alcohol withdrawal delirium:

Tool	Description
CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol, revised)	Quantifies severity of alcohol withdrawal out of 67 points. Interpretation: < 10 very mild, 10–15 mild, 16–20 modest, > 20 severe ^[2]. Guides benzodiazepine dosing (symptom-triggered therapy for CIWA-Ar ≥ 8).
SADQ (Severity of Alcohol Dependence Questionnaire)	Estimates severity of dependence and predicts risk during detoxification. * > 30 is an indication for in-patient detoxification* ^[2].

The clinical approach to delirium follows a two-step process:

Recognise the syndrome (using clinical assessment ± CAM)
Find the cause (systematic investigations)

The notes emphasise that delirium is often under-recognised ( > 70% missed diagnosis) ^[2], so Step 1 requires a high index of suspicion.

Investigation Modalities

The purpose of investigations in delirium is not to confirm the diagnosis (which is clinical) but to identify the underlying cause. The notes organise investigations into routine and targeted categories ^[2].

These are marked with an asterisk (*) in the original notes ^[2], indicating they should be performed in every case:

Investigation	What you are looking for	Key findings / Interpretation
CBC*	Infection (↑WCC, neutrophilia), anaemia (↓Hb → cerebral hypoxia), thrombocytopaenia (DIC from sepsis, liver disease)	Leucocytosis with left shift suggests bacterial infection. Macrocytic anaemia → consider B12/folate deficiency or alcohol. Pancytopaenia → consider bone marrow failure, severe sepsis.
L/RFT* (Liver/Renal Function Tests)	Organ failure — hepatic encephalopathy (↑bilirubin, ↑ALT/AST, ↓albumin, ↑NH3), uraemia (↑urea, ↑creatinine)	Abnormal albumin ^[2] is itself a risk factor. ↑NH3 with deranged LFT → hepatic encephalopathy. ↑Urea/creatinine → uraemic encephalopathy.
Electrolytes*	Hypo/hypernatraemia, hypo/hyperkalaemia	Hyponatraemia is the most common electrolyte cause of confusion. Rapid correction risks osmotic demyelination syndrome (central pontine myelinolysis).
Blood glucose*	Hypoglycaemia or hyperglycaemia ^[2]	Hypoglycaemia (< 3 mmol/L) is a medical emergency — the brain depends almost entirely on glucose for energy. Hyperglycaemia → hyperosmolar state → dehydration → confusion.
Ca/PO4*	Hypercalcaemia (malignancy, hyperparathyroidism → "stones, bones, groans, moans, and psychiatric overtones")	Hypercalcaemia → ↓neuronal excitability → confusion, drowsiness, coma.
Urinalysis* / MSU*	UTI — the single most common precipitant of delirium in the elderly	Positive nitrites + leucocytes → suggestive of UTI. Send MSU for culture and sensitivity. Remember: asymptomatic bacteriuria is common in the elderly and does not necessarily mean UTI is causing delirium.

2. Targeted Investigations (Based on Clinical Suspicion)

Investigation	When to order	Key findings
CXR	All patients (some consider routine); especially if respiratory symptoms, fever, hypoxia	Consolidation → pneumonia (second most common precipitant after UTI in HK elderly). Pulmonary oedema → heart failure → hypoxia.
Blood culture	Fever, rigors, haemodynamic instability, suspected septicaemia	Positive cultures identify the organism and guide antibiotic therapy. Must be taken BEFORE starting antibiotics.
Sputum culture	Productive cough, CXR consolidation	Organism identification for targeted antibiotic therapy.
Lumbar puncture (LP)	Suspected CNS infection (fever + neck stiffness + confusion), suspected encephalitis	CSF analysis: cell count, protein, glucose, Gram stain, culture, viral PCR (especially HSV). Raised WCC + raised protein + low glucose → bacterial meningitis. Lymphocytosis + raised protein + normal glucose → viral/TB meningitis.

Investigation	When to order	Key findings
CT brain	See specific indications below	Structural lesion: SDH, tumour, stroke, hydrocephalus, cerebral oedema. Normal CT does NOT exclude a neurological cause (encephalitis may have a normal early CT).
EEG	Suspected non-convulsive status epilepticus; when diagnosis is uncertain	Diffuse slowing of background cortical activity ^[2] is the characteristic finding in delirium — reflects global cortical hypofunction. Epileptiform discharges → NCSE.
MRI brain	When CT is non-diagnostic but suspicion for structural/inflammatory pathology remains high	More sensitive than CT for encephalitis (temporal lobe signal change in HSV), small infarcts, white matter disease, posterior reversible encephalopathy syndrome (PRES).
LP	See infection screen above; also for suspected autoimmune encephalitis	NMDA-receptor antibodies, anti-LGI1 antibodies in autoimmune encephalitis.

Indications for neuroimaging in delirium ^[2]:

New focal neurological signs

History or signs of head trauma

Fever (for CNS infection)

No other identifiable cause

Nil or incomplete history

Neurological exam cannot be completed

When to CT the Head

The general principle: neuroimaging has a low yield in delirium ^[2] — most causes are systemic, not structural. But you MUST image if there are focal signs, trauma history, fever suggesting CNS infection, or if you simply cannot find another cause. Think of CT brain as a "rule-out" test for dangerous structural pathology, not a "rule-in" test for delirium.

Investigation	When to order	Key findings
ABG (Arterial Blood Gas)	Suspected hypoxia, respiratory failure, metabolic acidosis	Hypoxia (PaO2 < 8 kPa) → cerebral hypoxia → delirium. Metabolic acidosis → consider DKA, lactic acidosis (sepsis), uraemia, salicylate/methanol poisoning. Respiratory alkalosis → may indicate early sepsis or hepatic encephalopathy (hyperventilation).
ECG	Cardiac cause suspected (arrhythmia, MI), medication monitoring (QTc prolongation from antipsychotics)	Arrhythmias → reduced cardiac output → cerebral hypoperfusion. MI may present atypically in the elderly with confusion rather than chest pain. Check QTc before starting haloperidol.

Investigation	When to order	Key findings
Blood glucose / ketones	All patients (routine); DKA, hypoglycaemia	Already discussed above. Ketones + hyperglycaemia + acidosis → DKA.
Mg (Magnesium)	Alcohol withdrawal, malnutrition, diuretic use	Hypomagnesaemia → neuronal hyperexcitability → seizures, tremor, confusion. Often co-exists with hypokalaemia and hypocalcaemia.
Amylase	Abdominal pain, suspected pancreatitis	Acute pancreatitis can cause delirium via systemic inflammation, pain, and metabolic derangement.
TFT (Thyroid Function Tests)	Suspected thyroid disease (especially in elderly women)	Thyrotoxicosis → agitation, confusion ("thyroid storm"). Myxoedema → drowsiness, hypothermia, confusion ("myxoedema madness").

Investigation	When to order	Key findings
History review	ALWAYS — this is the most important "investigation"	Review the drug chart meticulously. Look for new medications, dose changes, anticholinergic drugs, opioids, benzodiazepines, steroids, digoxin, diuretics. Calculate the anticholinergic burden.
Urine toxicology screen	Suspected substance abuse, unknown ingestion, young patients with unexplained delirium	Detects amphetamines, benzodiazepines, opioids, cannabis, cocaine, barbiturates.
Serum alcohol level	Suspected intoxication or withdrawal	Elevated → intoxication. Low/absent in a known drinker → consider withdrawal.
Anion gap	Suspected toxic ingestion (methanol, ethylene glycol)	Elevated anion gap metabolic acidosis with osmolar gap → toxic alcohol ingestion.

Investigation	When to order	Key findings
Thiamine (Vitamin B1)	Alcoholism, malnutrition, prolonged vomiting (hyperemesis), refeeding	Low thiamine → Wernicke encephalopathy. Do NOT wait for the result — treat empirically with parenteral thiamine if clinically suspected. Pathophysiology: thiamine is a cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase → deficiency → impaired oxidative metabolism → neuronal death in mammillary bodies and periventricular grey matter.
B12, folate	Macrocytic anaemia, chronic alcohol use, malnutrition, elderly	B12 deficiency → subacute combined degeneration of the cord + cognitive impairment. Folate deficiency → megaloblastic anaemia + neuropsychiatric symptoms.

The EEG deserves additional discussion because it is both diagnostically relevant and commonly asked about ^[2].

Aspect	Detail
Characteristic finding in delirium	Diffuse slowing of background cortical activity ^[2] — the normal alpha rhythm (8–13 Hz) is replaced by slower theta (4–7 Hz) and delta (< 4 Hz) activity. This reflects global cortical hypofunction.
Diagnostic yield	Not reliable: false negative 17%, false positive 22% ^[2]
Primary role	Limited role; useful when suspecting non-convulsive seizures, especially if suspicious of brain insult ^[2]
Exception — alcohol/sedative withdrawal	In withdrawal states, the EEG may show fast (beta) activity rather than slowing, because the brain is in a hyperexcitable state (loss of GABAergic inhibition).
Exception — hepatic encephalopathy	Triphasic waves — characteristic but not pathognomonic. These are high-amplitude, sharp waves with a triphasic morphology, most prominent frontally.

Why "diffuse slowing"? The normal alpha rhythm depends on intact thalamocortical oscillatory circuits. When the thalamus is disrupted by metabolic derangement, inflammation, or neurotransmitter imbalance, these circuits slow down — just like a computer processor slowing down when overheated.

High Yield Summary

Diagnostic Criteria:

DSM-5: 5 criteria (A–E). Core = disturbance in attention/awareness (A) + acute onset with fluctuation (B) + additional cognitive disturbance (C) + not explained by pre-existing neurocognitive disorder or coma (D) + evidence of medical cause (E). Specify: cause, duration (acute/persistent), subtype (hyperactive/hypoactive/mixed).
ICD-10: ALL of (a)–(e) required: consciousness/attention + global cognition + psychomotor + sleep-wake + emotional. Duration < 6 months. Specify: superimposed on dementia or not.

Screening: CAM is the gold standard bedside tool. Delirium = Features 1+2 (mandatory) PLUS either 3 or 4.

Investigations — Two Tiers:

Routine (ALL patients): CBC, L/RFT, electrolytes, glucose, Ca/PO4, urinalysis/MSU.
Targeted: CXR, blood cultures, ABG, ECG, CT brain (6 indications), EEG (for NCSE), urine tox, serum alcohol, thiamine/B12/folate, LP.

EEG: Diffuse slowing of background activity; limited yield (FN 17%, FP 22%); main role is to exclude NCSE.

Neuroimaging: Low yield; 6 indications — new focal signs, head trauma, fever, no other cause, incomplete history, cannot complete neuro exam.

CIWA-Ar: For alcohol withdrawal severity (out of 67); ≥ 8 triggers benzodiazepine therapy.

Active Recall - Diagnostic Criteria and Investigations for Delirium

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p48) ^[2] Senior notes: ryanho-psych.md (sections 4.1, pages 74–76, 105)

Management of Delirium

The overarching philosophy of delirium management is simple but critical: *delirium is a medical emergency ^[2]. The confusion itself is not the disease — it is a symptom of an underlying medical insult that is threatening the brain. Therefore, the management hierarchy is:

Treat the underlying cause (this is the definitive treatment)
Provide supportive care (keep the patient safe and oriented)
Manage behavioural disturbance (non-pharmacological first, then pharmacological only when necessary)
Prevent delirium in at-risk patients (proactive multicomponent strategies)

This is the most important step. Most cases recover rapidly when the underlying cause is treated ^[2]. Without treating the cause, no amount of antipsychotic or reorientation will fix delirium.

Underlying Cause	Specific Treatment	Rationale
Infection (UTI, pneumonia, sepsis)	Appropriate antibiotics based on cultures / empirical guidelines	Infection → systemic inflammation → neuroinflammation → delirium. Killing the source stops the inflammatory cascade.
Metabolic derangement	Correct specific abnormality: IV normal saline for hyponatraemia (carefully!), calcium for hypercalcaemia, insulin for DKA, dextrose for hypoglycaemia	Neuronal function depends on precise ionic and metabolic milieu. Correction restores normal neurotransmission.
Drug-related	Stop or adjust the offending medication — review anticholinergics, opioids, benzodiazepines, steroids, digoxin, diuretics	The drug is directly disrupting neurotransmitter balance (e.g., anticholinergics block ACh → impaired attention). Removal allows cholinergic recovery.
Hypoxia	Supplemental O2, treat underlying cause (pneumonia, PE, COPD, HF)	The brain consumes ~20% of total O2. Hypoxia → impaired oxidative metabolism → neuronal dysfunction.
Organ failure	Hepatic encephalopathy: lactulose, rifaximin. Renal failure: dialysis if indicated. Cardiac failure: diuretics, afterload reduction.	Organ failure → accumulation of toxins (NH3, uraemic toxins) → direct neurotoxicity.
Alcohol withdrawal / DT	See dedicated section below	Sudden loss of GABAergic inhibition → neuronal hyperexcitability.
Urinary retention / constipation	Catheterisation (if retention confirmed), laxatives/enema	These "minor" causes are surprisingly potent precipitants. Relief of discomfort and visceral afferent stimulation resolves the delirium.
Pain	Appropriate analgesia (but avoid opioids if possible — use paracetamol, regional anaesthesia)	Uncontrolled pain → cortisol and catecholamine surges → neuroinflammation and sleep disruption. Paradoxically, opioids for pain can also cause delirium — hence the preference for non-opioid approaches.
Nutritional deficiency	Thiamine (parenteral) → BEFORE glucose ^[1], B12, folate replacement	Thiamine is a cofactor for oxidative metabolism; B12 for myelin synthesis and methionine metabolism.

Alcohol Withdrawal / Delirium Tremens — Specific Management

Delirium tremens is a medical emergency requiring hospitalisation ^[1].

Component	Detail
Setting	Indications for in-patient detox: severe dependence (SADQ > 30), history of severe withdrawal (seizures, DT), very high consumption ( > 30 units/day), concomitant BZD misuse, significant medical/psychiatric comorbidity ^[2]
Supportive	NPO if necessary, correct volume deficits, stabilise haemodynamics ^[2]
Correct metabolic derangements	HypoGly, hypoK, hypoMg, hypoPO4, ketoacidosis ^[2]
Thiamine	Proactive use of parenteral vitamins (thiamine) ^[1] — give BEFORE glucose. This prevents Wernicke encephalopathy. Thiamine is a cofactor for pyruvate dehydrogenase; glucose loading without thiamine exhausts remaining stores.
Nutritional supplements	Multivitamins with folate ^[2]
Benzodiazepines (first-line)	Benzodiazepines in decreasing dosage (lorazepam/diazepam/others) ^[1]. Symptom-triggered dosing using CIWA-Ar ≥ 8 ^[2] is preferred (requires intensive monitoring, e.g., hourly); fixed-schedule dosing if symptom-triggered is not feasible. Prefer long-acting BZDs, e.g., diazepam (Valium), chlordiazepoxide (Librium) ^[2].
Anticonvulsants	Carbamazepine ^[1] — for seizure prophylaxis/treatment
Neuroleptics	Neuroleptics for control of agitation ^[1] — used adjunctively for severe agitation/psychosis not controlled by BZDs alone
Fluid and electrolyte balance	Fluid and electrolyte balance ^[1] — DT patients lose large volumes through sweating and have poor oral intake
Refractory DT	Barbiturates or propofol ^[2]; transfer to ICU

Why benzodiazepines are first-line in alcohol withdrawal but second-line in other delirium: Alcohol chronically enhances GABA-A receptor activity. Abrupt cessation → sudden loss of GABAergic inhibition → neuronal hyperexcitability → seizures, autonomic storm, delirium. Benzodiazepines are cross-tolerant with alcohol at the GABA-A receptor, directly replacing the lost inhibition. This is pharmacological substitution therapy — analogous to methadone in opioid withdrawal. In contrast, in non-alcohol delirium, the primary problem is usually cholinergic deficiency and dopaminergic excess, so benzodiazepines (which are GABAergic sedatives) do not address the core pathophysiology and may paradoxically worsen confusion, especially in the elderly.

Supportive care maintains physiological stability while the underlying cause is being treated.

Measure	Rationale
IV fluids / oral hydration	Many delirious patients are dehydrated (fever, poor oral intake, diuretics). Dehydration → reduced cerebral perfusion → worsened delirium.
Nutrition	Ensure adequate caloric intake; consider NG feeding if oral intake is poor. Malnutrition worsens cognitive function and delays recovery.
Early mobilisation	Bed rest → muscle deconditioning, DVT, pressure sores, further cognitive decline. Getting the patient upright and moving (when safe) accelerates recovery.
Thromboprophylaxis	Agitated patients may be restrained or immobilised → ↑ DVT/PE risk. Give LMWH prophylaxis.
Pressure sore prevention	Delirious patients (especially hypoactive) may be immobile for prolonged periods. Regular turning and pressure-relieving mattresses.
Aspiration prevention	Confused patients may aspirate. Sit upright for meals, consider thickened fluids, speech and language therapy assessment for swallowing if needed.
Monitoring	Regular vital signs, fluid balance, cognitive assessment (CAM, MMSE/MoCA), blood glucose, electrolytes. Serial monitoring tracks response to treatment.

Step 3: Management of Behavioural Disturbance

This section primarily applies to hyperactive delirium (agitation, pulling at lines, combativeness) but principles also apply to managing distressing symptoms in hypoactive delirium (hallucinations causing distress, severe anxiety).

Non-pharmacological measures are the mainstay ^[2] of delirium management. They should always be initiated first and continued even when pharmacological treatment is added.

Intervention	Mechanism / Rationale
Frequent reassurance and reorientation ^[2]	The delirious brain has lost its internal compass. Repeatedly telling the patient where they are, what date it is, who you are, and what is happening reduces anxiety and confusion. Place clocks, calendars, and familiar objects at the bedside.
Ensure familiar carer and environment ^[2]	Unfamiliar faces and environments increase disorientation. Having a family member or consistent nurse at the bedside ("specialling") provides a familiar anchor point. Avoid unnecessary ward transfers.
Offer quiet environment and appropriate lighting ^[2]	Excessive noise and stimulation overload the already-compromised brain. However, the environment should not be too dark — appropriate lighting helps maintain the sleep-wake cycle and reduces visual misperceptions (illusions). Nightlights reduce nocturnal hallucinations.
Minimise unnecessary procedures	Every blood draw, catheterisation, or alarm beep is a noxious stimulus that can worsen agitation. Only do what is clinically essential.
Ensure sensory aids	If the patient uses glasses or hearing aids, ensure these are available. Sensory deprivation worsens delirium (the brain fills gaps with hallucinations).
Avoid physical restraints	Restraint as last resort ^[2]. Restraints worsen agitation (the patient fights against them → injury, rhabdomyolysis, DVT, skin breakdown), increase distress, and are associated with worse outcomes. They should only be used when there is immediate danger to the patient or staff and all other measures have failed.
Maintain sleep hygiene	Reduce noise and light at night, cluster nursing interventions to allow uninterrupted sleep, avoid caffeinated drinks in the evening.
Early mobilisation	Getting the patient out of bed (when safe) promotes orientation, maintains muscle strength, and supports circadian rhythm.

Clinical Pearl

Think of non-pharmacological management as restoring the brain's external scaffolding. The delirious brain has lost its internal ability to orient itself, maintain attention, and filter stimuli. By providing a calm, well-lit, familiar, and structured environment with consistent caregivers and frequent reorientation, you are acting as an external "cognitive prosthesis" until the brain recovers.

3B. Pharmacological Management

Pharmacological treatment is indicated only when the patient threatens their own or others' safety, or when behavioural disturbance interferes with essential treatment ^[2] (e.g., pulling out IV lines with antibiotics for sepsis, removing an endotracheal tube, preventing essential investigations).

Haloperidol ("Haldol") is the first-line agent ^[2].

Drug name breakdown: Haloperidol is a butyrophenone — a first-generation (typical) antipsychotic.
Mechanism: Blocks D2 dopamine receptors in the mesolimbic pathway → reduces hallucinations, delusions, agitation, and psychomotor hyperactivity. This directly addresses the dopaminergic excess component of delirium pathophysiology.
Why haloperidol is preferred: Preferred due to its longer clinical experience ^[2]. It has minimal anticholinergic effects (important because you don't want to worsen cholinergic deficiency), minimal hypotension (no alpha-1 blockade compared to chlorpromazine), can be given IM, and has a predictable onset of action.
Dosing: Starts at a very low dose and titrated upwards to achieve desirable calming effect. Typically administered in IM form Q6h at 1–5 mg/day ^[2]. In the elderly, start even lower (0.25–0.5 mg).

Aspect	Detail
Route	Oral, IM (preferred in agitated patients who refuse oral), IV (ICU setting — monitor QTc)
Onset	IM: 15–30 minutes; Oral: 30–60 minutes
Duration	12–36 hours (long half-life)
Target	Calm the patient without over-sedating. The goal is a patient who is settled and can cooperate with care, NOT a sleeping patient.

Contraindications / Cautions for Haloperidol:

Contraindication / Caution	Reason
Parkinson's disease / Lewy body dementia	D2 blockade worsens Parkinsonism catastrophically. DLB patients have antipsychotic sensitivity (30–50%): acute irreversible Parkinsonism, loss of consciousness ± neuroleptic malignant syndrome (NMS) ^[2]. Use quetiapine instead (lowest D2 affinity among antipsychotics).
Prolonged QTc	Haloperidol prolongs the QTc interval → risk of Torsades de Pointes → cardiac arrest. Always check ECG/QTc before starting and monitor during treatment.
Alcohol/sedative withdrawal	Haloperidol lowers the seizure threshold → can precipitate withdrawal seizures. Use benzodiazepines as first-line in this context.
Anticholinergic delirium	While haloperidol has low anticholinergic activity itself, antipsychotics do not address the underlying ACh deficiency. Specific treatment (physostigmine) may be needed.

Alternative antipsychotics ^[2]:

Drug	Class	Advantages	Disadvantages
Risperidone	SGA (atypical)	Oral; effective for agitation	Risk of EPSE at higher doses; stroke risk in elderly with dementia
Olanzapine	SGA (atypical)	IM available; sedating (useful at night)	Metabolic effects; anticholinergic properties; may be associated with ↑ mortality in older patients with dementia ^[2]
Quetiapine	SGA (atypical)	Safest in Parkinson's / DLB (lowest D2 blockade); sedating	More hypotension (alpha-1 blockade); less evidence base

High Yield: Atypical antipsychotics are tested only in small uncontrolled studies and may be associated with ↑ mortality in older patients with dementia ^[2]. This is the reason for the "black box warning" — use the lowest effective dose for the shortest possible duration. Keep lowest dose and shortest period if possible; don't prescribe medications unless significant BPSD ^[3].

Exam Favourite

Which antipsychotic should you AVOID in a patient with Parkinson's disease or Lewy body dementia who develops delirium? Haloperidol (and most typical antipsychotics). Use quetiapine instead. DLB patients have severe antipsychotic sensitivity — even a single dose of haloperidol can cause irreversible Parkinsonism, loss of consciousness, or neuroleptic malignant syndrome.

Benzodiazepines have a limited role in the treatment of delirium ^[2]. They are second-line and reserved for specific indications.

Drug of choice: Lorazepam ^[2]

Drug name breakdown: Lorazepam is a short-to-intermediate-acting benzodiazepine.
Mechanism: Enhances GABA-A receptor activity → increased chloride influx → neuronal hyperpolarisation → sedation, anxiolysis, anticonvulsant effect, muscle relaxation.
Why lorazepam specifically? It has no active metabolites (metabolised by glucuronidation, not oxidation) → safer in hepatic impairment (common in elderly and alcoholic patients). It has a predictable IM absorption (unlike diazepam which is erratically absorbed IM).

Lorazepam is mainly reserved for ^[2]:

Sedative/alcohol withdrawal — benzodiazepines are first-line here (GABA replacement therapy)
Parkinson's disease — when antipsychotics are contraindicated (benzodiazepines do not worsen Parkinsonism)
Neuroleptic malignant syndrome (NMS) — when delirium is caused by antipsychotic-induced NMS, you must stop all antipsychotics and use lorazepam for sedation + dantrolene + bromocriptine ^[2]

Why NOT benzodiazepines routinely? In non-withdrawal delirium:

They cause over-sedation → worsens hypoactive delirium
Paradoxical disinhibition in the elderly (patient becomes MORE agitated)
Respiratory depression (especially when combined with opioids)
They worsen cognitive impairment
They do not address the underlying ACh deficit / DA excess

Benzodiazepine	When to Use in Delirium	When to AVOID
Lorazepam	Alcohol/BZD withdrawal, PD, NMS, seizures	Non-withdrawal delirium in elderly (paradoxical worsening)
Diazepam / Chlordiazepoxide	Preferred for alcohol withdrawal protocol (long-acting → smoother taper) ^[1]^[2]	Hepatic impairment (active metabolites accumulate); non-withdrawal delirium

Agent	Role	Mechanism
Trazodone ^[2]	Useful for insomnia and mild agitation in delirium	Serotonin antagonist and reuptake inhibitor (SARI); potent 5-HT2A/H1 blockade → sedation without the EPSE or anticholinergic effects of antipsychotics. Gentler option for mild nocturnal agitation.
Dexmedetomidine	ICU setting for intubated patients	Alpha-2 agonist → sedation without respiratory depression. Emerging evidence for delirium management in ICU. Not routine in general wards.

Step 4: Prevention of Delirium

Prevention is arguably the most important aspect of delirium management because prevention is far more effective than treatment — delirium, once established, carries significant morbidity and mortality even after resolution.

This is the evidence-based gold standard for delirium prevention, based on the landmark Hospital Elder Life Program (HELP) and subsequent studies.

Modifying risk factors ^[2]:

Intervention	Target	Mechanism
Orientation and therapeutic activities for cognitive impairment ^[2]	Cognitive stimulation	Keeps cortical circuits active; compensates for reduced cerebral reserve
Early mobilisation ^[2]	Physical deconditioning	Immobility → functional decline → ↑ delirium risk. Getting patients moving maintains circadian rhythm and orientation.
Prefer nonpharmacological approaches (minimise psychoactive drug use) ^[2]	Drug-induced delirium	Every sedative, opioid, and anticholinergic added increases the risk. Prescribe only what is essential.
Interventions to prevent sleep deprivation ^[2]	Sleep-wake cycle	Cluster nursing activities, reduce nocturnal noise/light, warm drinks at bedtime, avoid sedative hypnotics.
Communication methods and adaptive equipment for vision and hearing impairment ^[2]	Sensory deprivation	Provide glasses, hearing aids, magnifying glasses, written communication boards. Sensory deprivation removes orientation cues → brain fills gaps with hallucinations.
Early intervention for volume depletion ^[2]	Dehydration	Encourage oral fluids, early IV hydration if needed. Dehydration → reduced cerebral perfusion.

Medications: low-dose antipsychotics, gabapentin, melatonin may be useful ^[2].

Agent	Evidence / Mechanism	Notes
Low-dose antipsychotics (e.g., haloperidol 0.5 mg nocte)	Some evidence for reduced incidence/duration of delirium in high-risk surgical patients	Evidence is mixed; not universally recommended. May reduce severity rather than incidence.
Melatonin (0.5–3 mg nocte)	Restores circadian rhythm; anti-inflammatory properties; neuroprotective	Emerging evidence for prevention (not treatment) of delirium. Safe, well-tolerated, minimal side effects. Addresses the melatonin deficiency seen in delirious patients.
Gabapentin	GABAergic modulation; may reduce post-operative delirium	Limited evidence; used in some post-surgical protocols.
Ramelteon (melatonin receptor agonist)	MT1/MT2 receptor agonist → promotes sleep	Some evidence for prevention in elderly medical/surgical patients.

Prevention vs Treatment

The strongest evidence in delirium management is for non-pharmacological multicomponent prevention (HELP-type interventions), which reduces delirium incidence by ~30–40% in high-risk populations. In contrast, pharmacological treatment of established delirium has a weaker evidence base — we use it to manage dangerous symptoms, not to "cure" the delirium. The cure is treating the underlying cause.

Drug	Class	Indication in Delirium	Dose Range	Key Side Effects / Contraindications
Haloperidol	Typical antipsychotic	1st-line for hyperactive delirium ^[2]	0.25–5 mg/day IM/PO Q6h	QTc prolongation, EPSE, avoid in PD/DLB, lowers seizure threshold
Risperidone	Atypical antipsychotic	Alternative to haloperidol	0.25–2 mg/day PO	EPSE at higher doses, stroke risk in elderly with dementia
Olanzapine	Atypical antipsychotic	Alternative; IM available	2.5–10 mg/day PO/IM	Anticholinergic effects, metabolic syndrome, ↑ mortality in elderly dementia
Quetiapine	Atypical antipsychotic	Preferred in PD / DLB	12.5–200 mg/day PO	Hypotension, sedation; safest re: EPSE
Lorazepam	Benzodiazepine	2nd-line; reserved for alcohol/BZD withdrawal, PD, NMS ^[2]	0.5–2 mg IM/PO Q4-6h	Respiratory depression, paradoxical agitation in elderly, over-sedation
Diazepam	Benzodiazepine	Alcohol withdrawal protocol ^[1]^[2]	Symptom-triggered per CIWA-Ar	Active metabolites (caution in liver disease), long-acting
Chlordiazepoxide	Benzodiazepine	Alcohol withdrawal prophylaxis/treatment ^[2]	Per protocol	Active metabolites, less sedating than diazepam
Trazodone	SARI antidepressant	Insomnia / mild agitation ^[2]	25–100 mg nocte	Priapism (rare), orthostatic hypotension
Carbamazepine	Anticonvulsant	Seizure prophylaxis/treatment in DT ^[1]	Per protocol	Hepatotoxicity, hyponatraemia, Steven-Johnson syndrome
Melatonin	Hormone	Prevention of delirium ^[2]	0.5–3 mg nocte	Minimal side effects; no role in acute treatment

Understanding prognosis reinforces why aggressive management is essential ^[2]:

Outcome Measure	Data
Mortality	Independent predictor of mortality; 14% at 1 month, 22% at 6 months, 6× that of non-delirious patients ^[2]
Recovery	Most cases recover rapidly when underlying cause is treated ^[2]
Poor prognostic factors	Elderly, pre-existing dementia/physical illness, hypoactive profile ^[2]
Relationship with dementia	5× increased incidence of dementia within 2 years following delirium; may accelerate pace of cognitive decline ^[2]
Protracted delirium	Especially poor prognosis — particularly for those with protracted delirium ^[2]

High Yield Summary

Management Hierarchy (in order of priority):

Treat the underlying cause — this is the definitive treatment (antibiotics for infection, correct electrolytes, stop offending drugs, thiamine for Wernicke, etc.)
Supportive care — hydration, nutrition, mobilisation, DVT prophylaxis, monitoring
Non-pharmacological measures (MAINSTAY) — reassurance, reorientation, familiar carers, quiet environment, appropriate lighting, sensory aids, restraint as LAST RESORT
Pharmacological (ONLY if patient threatens safety or interferes with essential treatment):
- 1st-line: Haloperidol (low dose, titrate up; IM Q6h at 1–5 mg/day)
- Alternatives: Risperidone, olanzapine, quetiapine (quetiapine for PD/DLB)
- 2nd-line: Lorazepam (reserved for alcohol/BZD withdrawal, PD, NMS)
- Other: Trazodone for insomnia/mild agitation
Prevention — multicomponent non-pharmacological interventions (orientation, mobilisation, minimise drugs, sleep hygiene, sensory aids, hydration); melatonin and low-dose antipsychotics may be useful

Special Scenarios:

Alcohol withdrawal/DT: BZDs first-line (diazepam/chlordiazepoxide) + thiamine + anticonvulsants + fluids
PD/DLB: AVOID haloperidol → use quetiapine; lorazepam if antipsychotics contraindicated
NMS: Stop all antipsychotics → lorazepam + dantrolene + bromocriptine

Prognosis: 14% 1-month mortality; 22% 6-month mortality; 5× ↑ dementia risk in 2 years. Most recover if cause treated. Hypoactive subtype has worst prognosis.

Active Recall - Management of Delirium

References

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12) ^[2] Senior notes: ryanho-psych.md (sections 4.1, pages 74–76, 105–106) ^[3] Lecture slides: GC 169. My grandmother keeps forgetting things Geriatric psychiatry, Dementia.pdf (p41)

Complications of Delirium

Delirium is far more than just "temporary confusion." It is a systemic brain injury event that carries significant short-term morbidity, long-term cognitive consequences, and independent mortality risk. Think of delirium as analogous to a myocardial infarction of the brain — even after the acute event resolves, there is lasting damage.

The complications can be organised into:

Acute complications (during the episode)
Complications of the underlying cause (if untreated/delayed)
Iatrogenic complications (from treatment or restraint)
Long-term sequelae (after resolution)

1. Acute Complications (During the Delirium Episode)

These arise directly from the delirious state itself — the patient's altered consciousness, agitation, immobility, and inability to cooperate with care.

This is the most critical complication. Delirium is an independent predictor of mortality, especially for those with protracted delirium ^[2].

Timeframe	Mortality
1 month	14% ^[2]
6 months	22% ^[2]
Compared to non-delirious patients	6× higher ^[2]
Delirium tremens (if treated)	< 5% ^[1]^[2]
Delirium tremens (if untreated)	Up to 15–20%

Why does delirium itself increase mortality (independent of the underlying cause)? Several mechanisms:

The underlying cause is often a serious medical condition (sepsis, MI, PE) that carries its own mortality — delirium is the clinical "alarm" that this condition is present
Delirium impairs the patient's ability to cooperate with treatment (pulling out IV lines, refusing medications, refusing investigations)
Delirium triggers a cascade of secondary complications (falls, aspiration, immobility → DVT/PE, pressure injuries)
Neuroinflammation during delirium may cause direct neuronal injury, contributing to long-term brain damage

High Yield: The mortality data (14% at 1 month, 22% at 6 months, 6× non-delirious) ^[2] is a commonly examined statistic. Delirium is NOT benign.

Complication	Mechanism
Falls	Hyperactive delirious patients attempt to get out of bed, climb over bedrails, or wander while disoriented. Impaired attention, disorientation, and motor incoordination all contribute. Falls are the leading cause of acute injury in delirious patients.
Fractures (especially hip fracture)	Falls in elderly, osteoporotic patients → hip fracture → further immobilisation → worsened delirium (a vicious cycle).
Head injury	Falls → subdural haematoma (especially in elderly patients on anticoagulants or with cerebral atrophy). This creates a dangerous feedback loop: delirium → fall → head injury → worse delirium.
Self-extubation / line removal	Agitated patients pull out endotracheal tubes, IV lines, urinary catheters, surgical drains → airway compromise, haemorrhage, treatment interruption.

Delirious patients have impaired consciousness, reduced cough reflex, and often poor swallowing coordination.
Hypoactive patients who are drowsy and lying supine are particularly at risk.
Aspiration of oral secretions or gastric contents → aspiration pneumonitis/pneumonia → further hypoxia → worsened delirium.
This is why supportive care includes sitting the patient upright, assessing swallowing safety, and considering thickened fluids or NG feeding if needed.

Delirious patients — especially the hypoactive subtype — may be profoundly immobile for days.

Complication	Mechanism	Prevention
Venous thromboembolism (DVT/PE)	Immobility → venous stasis (Virchow's triad) → thrombus formation. Dehydration further increases blood viscosity.	Thromboprophylaxis (LMWH), TED stockings, early mobilisation
Pressure ulcers (decubitus ulcers)	Sustained pressure on bony prominences (sacrum, heels, occiput) → tissue ischaemia → necrosis. Confused patients do not shift position spontaneously.	Regular repositioning (2-hourly), pressure-relieving mattresses, skin care
Muscle deconditioning / sarcopaenia	Even a few days of bed rest causes significant muscle protein loss, especially in elderly patients. Loss of 1–3% muscle mass per day of bed rest in the elderly.	Early mobilisation, physiotherapy, adequate protein intake
Contractures	Prolonged immobility → joint stiffness → fixed flexion deformities	Range-of-motion exercises, early mobilisation
Functional decline	Combination of deconditioning, contractures, and cognitive impairment → loss of ability to perform ADLs. Many elderly patients never return to their pre-delirium functional baseline.	Comprehensive geriatric assessment, multidisciplinary rehabilitation

Confused patients forget to drink and eat, or refuse food/fluids.
Hyperactive patients have increased metabolic demands (agitation, fever, sweating) that outstrip intake.
Dehydration → reduced cerebral perfusion → worsened delirium (vicious cycle).
Malnutrition → impaired wound healing, impaired immune function, further cognitive decline.

Loss of cortical inhibition over micturition and defecation → urinary and faecal incontinence.
Incontinence → skin breakdown → pressure ulcers, infection.
Urinary catheterisation (often placed in response to incontinence) is itself a precipitating factor for delirium ^[2] and increases UTI risk → another vicious cycle.

Complication	Detail
Aggression / violence	Hyperactive delirious patients may strike staff or other patients. This is driven by fear, misperception (e.g., believing staff are attackers), and cortical disinhibition.
Absconding	Confused patients may wander off the ward, creating safety risks (falls, exposure, inability to find their way back).
Interference with treatment	Pulling out lines, refusing medications, refusing investigations — delays treatment of the underlying cause.

Delirium is the brain's alarm signal that something serious is happening. If the underlying cause is not identified and treated promptly, the consequences can be devastating:

Underlying Cause	Complication if Untreated
Sepsis	Septic shock → multi-organ failure → death
Myocardial infarction	Heart failure, arrhythmia, cardiogenic shock (MI can present as delirium in the elderly without typical chest pain)
Pulmonary embolism	Cardiovascular collapse, death
Meningitis/encephalitis	Permanent neurological damage, death
Hypoglycaemia	Permanent brain damage (neuroglycopenia → selective neuronal necrosis in hippocampus, cortex, basal ganglia)
Wernicke encephalopathy	Korsakoff syndrome (irreversible) — 84% of Wernicke cases progress to Korsakoff syndrome if untreated ^[2]. Characterised by severe anterograde amnesia with confabulation.
Delirium tremens	Mortality 5% if treated ^[1]; death from arrhythmia, underlying diseases, or hypo/hyperthermia ^[2]
Hepatic encephalopathy	Progressive coma (Stage 4 of West Haven Criteria) ^[1] if precipitant not addressed
Status epilepticus	Permanent neuronal injury, death

Clinical Pearl

The single most dangerous complication of delirium is failure to identify and treat the underlying cause. Delirium that is merely "managed" with antipsychotics while the precipitant remains untreated will result in progressive deterioration and death. Every delirious patient deserves a thorough aetiological workup — not just sedation.

3. Iatrogenic Complications (From Treatment)

The management of delirium can itself cause harm if not carefully executed.

Restraint should be used as a last resort ^[2]. The complications include:

Complication	Mechanism
Worsened agitation	The patient fights against restraints → increased distress, catecholamine surge, autonomic instability
Rhabdomyolysis	Prolonged struggling against restraints → skeletal muscle breakdown → myoglobinuria → acute kidney injury
Skin injury and pressure ulcers	Restraints compress soft tissue over bony prominences
DVT / PE	Complete immobilisation → venous stasis
Strangulation / asphyxia	Improperly applied restraints can compress the airway, particularly if the patient slides down
Psychological trauma	Being physically restrained is terrifying for a confused patient, worsening fear, agitation, and subsequent PTSD
Nerve compression	Tight limb restraints can compress peripheral nerves → neuropraxia

Drug	Iatrogenic Complication	Mechanism
Haloperidol	QTc prolongation → Torsades de Pointes → sudden cardiac death	Blocks cardiac potassium channels (hERG) → delayed repolarisation
Haloperidol	Extrapyramidal side effects (acute dystonia, akathisia, Parkinsonism)	D2 blockade in the nigrostriatal pathway → dopaminergic-cholinergic imbalance in basal ganglia
Haloperidol / antipsychotics in DLB	Antipsychotic sensitivity: acute irreversible Parkinsonism, loss of consciousness ± neuroleptic malignant syndrome ^[2]	DLB patients have severe nigrostriatal dopaminergic depletion; even small doses of D2 blockers cause catastrophic Parkinsonism
Antipsychotics in elderly with dementia	↑ mortality ^[2] (cerebrovascular events, pneumonia, cardiac events)	Black box warning — mechanism not fully understood; possibly related to sedation → aspiration, and pro-thrombotic effects
Neuroleptic malignant syndrome (NMS)	Characterised by rapid onset of neuromuscular rigidity, confusion, autonomic dysfunction, hyperthermia. CK > 1000 IU/L. Mortality can reach 20% if untreated ^[2]	Sudden, profound central dopamine blockade → muscle rigidity → rhabdomyolysis + thermoregulatory failure
Benzodiazepines	Over-sedation, respiratory depression, paradoxical agitation	GABAergic sedation in an already-compromised brain; paradoxical effects due to cortical disinhibition in the elderly
Benzodiazepines	Falls	Sedation + impaired coordination in an already disoriented patient

Delirium prolongs hospital stays (on average, delirium adds 7–10 days to a hospital admission), which itself creates complications:

Complication	Mechanism
Hospital-acquired infections	Prolonged exposure to nosocomial pathogens (MRSA, C. difficile, hospital-acquired pneumonia)
Further functional decline	Longer immobilisation → more deconditioning → more dependence
Increased healthcare costs	Direct costs of prolonged admission + costs of managing complications

4. Long-Term Sequelae (After Resolution of Delirium)

These are among the most important and underappreciated complications. Delirium is not just an acute event — it leaves lasting marks on the brain.

5× increased incidence of dementia within 2 years following delirium; may accelerate the pace of cognitive decline ^[2].

Why does a transient episode of delirium cause permanent cognitive damage? Several hypotheses:

Neuroinflammatory injury: The cytokine storm and microglial activation during delirium cause direct neuronal death, particularly in vulnerable regions (hippocampus, prefrontal cortex). These neurons do not regenerate.
Synaptic damage: Excitotoxicity (from glutamate excess) and oxidative stress damage synapses, reducing the brain's "cognitive reserve" — the buffer that keeps a person above the dementia threshold.
Acceleration of pre-existing neurodegeneration: In patients with subclinical Alzheimer's pathology (amyloid plaques, tau tangles already accumulating), delirium may "unmask" or accelerate the clinical expression of dementia.
Chronic neuroinflammation: A single episode of delirium may trigger sustained microglial activation that persists long after the acute episode resolves, creating a chronic neuroinflammatory state that promotes neurodegeneration.

Critical Long-Term Consequence

Delirium is not "just confusion that goes away." Each episode of delirium causes measurable, often permanent, cognitive decline. In patients with pre-existing dementia, delirium accelerates the trajectory of decline. This is why prevention of delirium is so important — every episode prevented is potential dementia prevented.

Not all delirium resolves completely. Some patients — especially the elderly, those with pre-existing dementia or physical illness, and those with the hypoactive profile ^[2] — have protracted delirium that persists for weeks to months.
Protracted delirium carries especially poor prognosis ^[2].
Some patients never return to their cognitive baseline, transitioning directly from delirium into a new diagnosis of dementia.

Delirium, particularly the hyperactive subtype with vivid hallucinations and persecutory delusions, is a profoundly frightening experience.
Patients who recover often recall fragments of the delirium — terrifying hallucinations, the sensation of being restrained, feeling attacked by staff.
Studies show that 15–25% of patients who recover from delirium develop symptoms of PTSD (intrusive memories, nightmares, avoidance, hypervigilance).
This is an under-recognised complication. Post-delirium psychological follow-up is important.

Outcome	Detail
Loss of ADL independence	Many elderly patients who survive delirium never return to their pre-morbid functional level. They require more assistance with basic and instrumental ADLs.
Increased institutionalisation	Delirium is independently associated with new nursing home placement. The combination of cognitive decline + functional decline + caregiver burden often makes return home impossible.
Caregiver burden	Family members who witness a relative's delirium experience significant distress. Ongoing care needs after discharge increase caregiver strain and depression.

Patients who have had one episode of delirium are at markedly increased risk of future episodes (a previous episode of delirium is itself a predisposing factor ^[2]).
Each subsequent episode may cause further cumulative cognitive damage.
Hospital re-admission rates are higher in patients with a history of delirium, both because of recurrent delirium and because the underlying vulnerabilities (frailty, dementia, multimorbidity) persist.

These patients are most likely to develop complications ^[2]:

Factor	Why it worsens prognosis
Elderly	Reduced cerebral reserve, multiple comorbidities, more vulnerable to secondary complications (falls, aspiration, pressure ulcers)
Pre-existing dementia	Already reduced cognitive reserve; delirium accelerates neurodegenerative trajectory; harder to diagnose delirium (superimposed on baseline impairment)
Pre-existing physical illness	Less physiological reserve to withstand the metabolic insult causing delirium
Hypoactive profile	Most commonly missed subtype → delayed recognition → delayed treatment → worse outcomes
Protracted delirium	Longer duration of neuroinflammation → more neuronal damage → higher mortality and cognitive decline

High Yield Summary

Complications of Delirium — Key Points for Exams:

Acute: Mortality (14% 1mo, 22% 6mo, 6× non-delirious); falls/fractures/head injury; aspiration pneumonia; DVT/PE; pressure ulcers; dehydration; incontinence; treatment interference.

Iatrogenic: Restraint injuries (rhabdomyolysis, strangulation, skin breakdown); antipsychotic side effects (QTc prolongation, EPSE, NMS, increased mortality in elderly with dementia); benzodiazepine over-sedation/respiratory depression/paradoxical agitation; hospital-acquired infections from prolonged stay.

Long-term: 5× increased dementia risk within 2 years (most important); accelerated cognitive decline even in patients without prior dementia; PTSD (15–25%); functional decline and institutionalisation; increased recurrence/re-admission.

Alcohol-specific: Untreated DT → death from arrhythmia/hyperthermia; untreated Wernicke → Korsakoff syndrome (84%, irreversible).

Poor prognostic factors: Elderly, pre-existing dementia, pre-existing physical illness, hypoactive subtype, protracted delirium.

The bottom line: Delirium is NOT benign. Prevention is better than cure. Every episode causes measurable, often permanent brain damage.

Active Recall - Complications of Delirium

References

^[1] Lecture slides: GC 161. Alcohol and the Brain From Psychiatric to Neuropsychiatric Perspectives.pdf (p12, p23) ^[2] Senior notes: ryanho-psych.md (sections 4.1, pages 74–76, 105–107)

High Yield Summary

Definition: Acute confusional state = impaired consciousness + impaired cognition. A syndrome, not a disease — always find the cause.

Epidemiology: 14–24% hospitalised patients; > 70% missed; 6× mortality vs non-delirious. 35–40% 1-year mortality in elderly.

Pathophysiology: Systemic insult → neuroinflammation → ↓ ACh + ↑ DA + ↓ melatonin → global cortical dysfunction.

Core Clinical Features:

Hallmarks: Impaired attention + sleep-wake cycle disruption
Acute onset, fluctuating course (worse at night), disorientation (time > place > person)
Visual hallucinations, transient poorly-elaborated delusions
Psychomotor disturbance (hyper/hypo/mixed)
Mood lability

Subtypes: Hyperactive (25%), Hypoactive (25% — worst prognosis, most missed), Mixed (35%).

Delirium tremens: Severe alcohol withdrawal at 24–96h; confusion, hallucinations, agitation, seizures; 5% mortality; Rx: benzodiazepines + thiamine + fluids.

Key Distinction from Dementia: Acute (not gradual), altered consciousness (not normal), fluctuating (not progressive), impaired attention (hallmark), triggered by illness/medication.

High Yield Summary

Top differentials for delirium (exam favourites):

Dementia — most commonly confused. Key: consciousness preserved in dementia; acute change in a demented patient = delirium until proven otherwise.
Non-convulsive status epilepticus — dangerous mimic; look for facial twitching, automatisms, nystagmus; EEG required.
Primary psychosis — clear consciousness, auditory hallucinations, systematised delusions, younger patient.
Alcoholic hallucinosis vs DT — hallucinosis has clear consciousness + auditory hallucinations; DT has clouded consciousness + visual hallucinations.
Wernicke encephalopathy — confusion + ophthalmoplegia + ataxia; give thiamine empirically.
Hepatic encephalopathy — asterixis, CLD stigmata, elevated NH3; West Haven staging.
Focal neurological disorders — Wernicke's aphasia, Anton's syndrome, bifrontal/bitemporal lesions; neuroimaging needed.
Acute stress disorder — preserved consciousness and cognition when engaged; psychological trigger.

Golden rule: Delirium can coexist with any of these conditions (especially dementia). Always rule out delirium first in any acute confusional state.

High Yield Summary

Diagnostic Criteria:

DSM-5: 5 criteria (A–E). Core = disturbance in attention/awareness (A) + acute onset with fluctuation (B) + additional cognitive disturbance (C) + not explained by pre-existing neurocognitive disorder or coma (D) + evidence of medical cause (E). Specify: cause, duration (acute/persistent), subtype (hyperactive/hypoactive/mixed).
ICD-10: ALL of (a)–(e) required: consciousness/attention + global cognition + psychomotor + sleep-wake + emotional. Duration < 6 months. Specify: superimposed on dementia or not.

Screening: CAM is the gold standard bedside tool. Delirium = Features 1+2 (mandatory) PLUS either 3 or 4.

Investigations — Two Tiers:

Routine (ALL patients): CBC, L/RFT, electrolytes, glucose, Ca/PO4, urinalysis/MSU.
Targeted: CXR, blood cultures, ABG, ECG, CT brain (6 indications), EEG (for NCSE), urine tox, serum alcohol, thiamine/B12/folate, LP.

EEG: Diffuse slowing of background activity; limited yield (FN 17%, FP 22%); main role is to exclude NCSE.

Neuroimaging: Low yield; 6 indications — new focal signs, head trauma, fever, no other cause, incomplete history, cannot complete neuro exam.

CIWA-Ar: For alcohol withdrawal severity (out of 67); ≥ 8 triggers benzodiazepine therapy.

High Yield Summary

Management Hierarchy (in order of priority):

Treat the underlying cause — this is the definitive treatment (antibiotics for infection, correct electrolytes, stop offending drugs, thiamine for Wernicke, etc.)
Supportive care — hydration, nutrition, mobilisation, DVT prophylaxis, monitoring
Non-pharmacological measures (MAINSTAY) — reassurance, reorientation, familiar carers, quiet environment, appropriate lighting, sensory aids, restraint as LAST RESORT
Pharmacological (ONLY if patient threatens safety or interferes with essential treatment):
- 1st-line: Haloperidol (low dose, titrate up; IM Q6h at 1–5 mg/day)
- Alternatives: Risperidone, olanzapine, quetiapine (quetiapine for PD/DLB)
- 2nd-line: Lorazepam (reserved for alcohol/BZD withdrawal, PD, NMS)
- Other: Trazodone for insomnia/mild agitation
Prevention — multicomponent non-pharmacological interventions (orientation, mobilisation, minimise drugs, sleep hygiene, sensory aids, hydration); melatonin and low-dose antipsychotics may be useful

Special Scenarios:

Alcohol withdrawal/DT: BZDs first-line (diazepam/chlordiazepoxide) + thiamine + anticonvulsants + fluids
PD/DLB: AVOID haloperidol → use quetiapine; lorazepam if antipsychotics contraindicated
NMS: Stop all antipsychotics → lorazepam + dantrolene + bromocriptine

Prognosis: 14% 1-month mortality; 22% 6-month mortality; 5× ↑ dementia risk in 2 years. Most recover if cause treated. Hypoactive subtype has worst prognosis.

High Yield Summary

Complications of Delirium — Key Points for Exams:

Acute: Mortality (14% 1mo, 22% 6mo, 6× non-delirious); falls/fractures/head injury; aspiration pneumonia; DVT/PE; pressure ulcers; dehydration; incontinence; treatment interference.

Alcohol-specific: Untreated DT → death from arrhythmia/hyperthermia; untreated Wernicke → Korsakoff syndrome (84%, irreversible).

Poor prognostic factors: Elderly, pre-existing dementia, pre-existing physical illness, hypoactive subtype, protracted delirium.

The bottom line: Delirium is NOT benign. Prevention is better than cure. Every episode causes measurable, often permanent brain damage.

Delirium

1. Definition

2. Epidemiology

3. Risk Factors

3.1 Predisposing Factors (Baseline Vulnerability)

3.2 Precipitating Factors (Acute Insult)

3.3 Six Causes of Confusion in Alcoholism (Lecture Slide — High Yield)

4. Anatomy and Functional Basis

4.1 Consciousness

4.2 Attention

4.3 Circadian Rhythm

4.4 Neurotransmitter Systems Involved

5. Pathophysiology

5.1 Neuroinflammatory Hypothesis (Most Important)

5.2 Cholinergic Deficiency Hypothesis

5.3 Oxidative Stress Hypothesis

5.4 Neural Network Disconnection

5.5 Neurotransmitter Imbalance Summary

6. Aetiology (with Hong Kong Focus)

6.1 Classification by Cause

6.2 Delirium Tremens (DT) — Special Case

7. Classification

7.1 By Psychomotor Activity

7.2 By Aetiology (DSM-5)

7.3 By Duration (DSM-5)

7.4 By Relationship to Dementia (ICD-10)

8. Clinical Features

8.1 Symptoms (What the Patient/Carer Reports)

8.1.1 Impaired Consciousness

8.1.2 Impaired Attention (The Hallmark of Delirium)

8.1.3 Cognitive Disturbance

8.1.4 Psychosis-like Symptoms

8.1.5 Sleep-Wake Cycle Disturbance (Another Hallmark)

8.1.6 Mood Disturbance

8.1.7 Psychomotor Disturbance (Reported by Carers)

8.1.8 Course (How the Symptoms Evolve Over Time)

8.2 Signs (What the Clinician Observes on Examination)

8.3 Delirium vs Dementia — Key Distinguishing Features

8.4 Clinical "Red Flags" That Should Prompt You to Think Delirium

9. Summary of Pathophysiology → Clinical Feature Connections

Active Recall - Delirium (Definition to Clinical Features)

References

Overview of Key Differential Diagnoses

1. Dementia

2. Non-Convulsive Status Epilepticus (NCSE)

3. Psychosis (Primary Psychotic Disorders)

Alcoholic Hallucinosis vs Delirium Tremens

4. Acute Stress Disorder / Dissociative States

5. Other Focal Neurological Disorders

6. Wernicke Encephalopathy

7. Hepatic Encephalopathy

8. Depression (Especially in the Elderly)

9. Substance Intoxication/Withdrawal (Beyond Alcohol)

Summary Table: Key Differentiating Features

Active Recall - Differential Diagnosis of Delirium

Diagnostic Criteria

1. DSM-5 Diagnostic Criteria for Delirium

2. ICD-10 Diagnostic Criteria for Delirium (F05)

3. Bedside Screening Tools

3.1 Confusion Assessment Method (CAM) — Gold Standard Screening Tool

3.2 Cognitive Assessment Tools

3.3 Alcohol Withdrawal Assessment

Diagnostic Algorithm

Investigation Modalities

1. Routine Investigations (Do for ALL Patients with Delirium)

2. Targeted Investigations (Based on Clinical Suspicion)

2.1 Infection Screen

2.2 Neurological Investigations

2.3 Organ Failure Workup

2.4 Metabolic Investigations

2.5 Drug Toxicity / Substance Screen

2.6 Nutritional Investigations

3. EEG — Special Considerations

4. Investigation Algorithm Summary

Active Recall - Diagnostic Criteria and Investigations for Delirium

References

Management Algorithm

Step 1: Treat the Underlying Cause

Step 2: Supportive Care

Step 3: Management of Behavioural Disturbance