Delirium, also referred to as "acute confusional state" or "acute brain syndrome," is a condition of severe confusion and rapid changes in brain function.

1. DELIRIUM

2. Definition
Delirium, also referred to as "acute confusional state" or
"acute brain syndrome," is a condition of severe confusion
and rapid changes in brain function.
Characterized by global impairment of consciousness
(clouding of consciousness), resulting in reduced level of
alertness, attention, perception of the environment and
thence cognitive performance.
A syndrome, not a disease

4. Classification of Organic Mental Disorders

5. Delirium due to General Medical Condition
A disorder characterized by the acute and sudden
development of changes in attention, memory, language
and/or perception that can be etiologically linked to the direct
physiological consequences of a general medical condition.

6. Substitute Terms
acute confusional states
acute brain syndrome
acute organic reaction
toxic psychosis
metabolic (and other acute) encephalopathies

7. Epidemiology
Much more common in elderly (concept of diminished
cerebral reserve)
1-2% in community samples
18-35% on admission to hospital
29-64% in inpatient department. Nearly 30% of older patients
experience delirium at least once during their hospital stay.
More common in surgical, burn, and intensive care units (frail
patients and cardiac surgery have very high rates of delirium)

8. Predisposing Factors
Pre-existing brain damage or dementia (bidirectional: 5X risk of dementia 2 years after delirium episode)
Extremes of age (very old or very young)
Previous episode of delirium
Functional and sensory impairment
Alcohol or drug dependence
Generalized or focal cerebral lesion/Previous CVA
Chronic medical illness
Surgical procedure and postoperative period
Severe psychological symptoms (such as fear)
Treatment with psychotropic medicines
Present or past history of head injury
Individual susceptibility to delirium

10. DELIRIUM
DEFICIENCIES EXCESSES
Drugs & Toxins
Opiates, psychotropics
Anticholinergics, drug
withdrawal
Poisoning
Organ failure
Uremic/Hepatic, CHF
Hypercarbia, Sepsis
Post-operative states
Electrolytes
Hypernatremia,
Hypercalcemia/Mg
Acidosis
LOCAL (CNS)
Etiologies: Threshold phenomenon

11. DELIRIUM
DEFICIENCIES
Hypoxemia
Global ischemia
Severe anemia
Endocrine
Hypothyroid, Hypopit.
Hypophosphatemia
Thiamine dificiency
Electrolytes
Hyponatremia
Hypocalcemia/Mg
Alkalosis
EXCESSES LOCAL (CNS)

12. DELIRIUM
DEFICIENCIES EXCESSES LOCAL (CNS)
Infection Vascular
Trauma/
Post-ictal

13. Etiology & Pathophysiology
Mostly multifactorial, sometimes idiopathic
Pathological basis is unclear. Oversimplified theories.
Severity correlated with slowing of cerebral rhythms on
EEG
Neurotransmitters dopamine and acetylcholine are
implicated in final pathway
Cortical vs Subcortical mechanisms

14. Diagnosis
Important to recognize underlying condition (correctable) although diagnosis can be made
without it. Bedside attention tests (digit span or vigilance “A” test might be helpful.
Rapid onset
Diurnal variation ICD-10 criteria:
Impaired consciousness and attention
Global disturbance of cognition
Psychomotor disturbances
Sleep-wake cycle disturbances
Emotional disturbances

17. Clinical Features
A relatively acute onset
Cardinal feature is disturbed consciousness (drowsiness,
decreased awareness of one’s surrounding, distractibility
and disorientation)
Disorientation (most commonly in time, then in place and
usually later in person)
Can be unresponsive (stuporose) in most severe form, but
impaired consciousness is usually subtle

18. Symptoms vary in individual case. Patient “isn’t acting quite right” may be
noticed by family members. Do not attribute distractibility initially to age,
dementia or fatigue.
Some are hyperactive, restless, irritable and have psychotic symptoms while
other group of patients might be hypoactive with retardation and
perseveration
Repetitive, purposeless movements are common
Thinking is slow and muddled but often, rich in content (dream-like)
Ideas of reference and delusions of persecution can be present but often
transient and poorly elaborated

19. Marked perceptual disturbances such as illusions,
misinterpretations, and hallucinations also occur (mostly visual
but also auditory and tactile). Experiences of depersonalization
and derealization can also occur.
Disturbance of sleep-wake cycle (mostly insomnia at night
with daytime drowsiness)
Diurnal variation is marked, usually with worsening of
symptoms in the evening and night ( D/D: sundowning)

20. Impairment of registration and retention of new memories
(Amnesia for the period of delirium)
Psychomotor disturbance, usually in form of agitation and
occasionally retardation, is present
Generalized autonomic dysfunction, speech and thought
disturbances (such as slurring of speech, incoherence, dysarthria,
and fleeting delusions) are often present
Lability of affect is usually present
Motor and verbal perseveration, dysnomia, agraphia and impaired
comprehension can also be seen

21. The motor symptoms in delirium can include:
1. Asterixis
2. Multifocal myoclonus,
3. Carphologia or floccillation (picking movements
at cover-sheets and clothes),
4. Occupational delirium (elaborate pantomimes as
if continuing their usual occupation in the hospital
bed)
5. Tone and reflex abnormalities

22. Differential Diagnosis
When in doubt, the most useful rule of thumb is to assume delirium
and attempt to rule out common medical etiologies.
Dementia (protracted course except caused by vascular dementia
caused by stroke, beclouded dementia/delirium superimposed on
dementia. DLB is even more confusing, mimics AD)

23. Features Delirium Dementia
Onset Acute Insidious
Duration Days to weeks Protracted (months to years)
Course Fluctuating Chronically progressive
Consciousness Fluctuating Usually normal
Perception Illusions, visual hallucinogens
present
Hallucinogens less common (except
sundowning)
Diurnal variation Marked Usually absent
Sleep-Wake Cycle Impaired Usually normal
Psychomotor activity Retarded, agitated or mixed Normal
Affect Anxious, irritable Labile but usually not anxious
Orientation Disturbed, at least periodically Usually normal, at least initially
Attention &
Concentration
Prominently impaired Less impaired
Memory Recent memory impaired Both recent and remote memory impaired
Reversibility Often reversible Majority not reversible

24. Differential Diagnosis
1. Sundowning (assumed to be related to disruption in circadian rhythm secondary
to decreased melatonin production, nocturnal institutional settings like reduced
staffing, noise, neuropathological changes in suprachiasmatic nucleus,
anticipation of food (increased dopamine so antagonistic effects). Chronic course,
not associated with acute medical problem, not associated with increased
mortality risk in institutionalized individuals.
2. Schizophrenia (psychotic symptoms more constant and better organized)
3. Depression (can be confused with quite, withdrawn behavior or hypoactive
symptoms. EEG findings are helpful). Up to 40 % in a research study.
4. Dissociative disorders (can show spotty amnesia but lack of global cognitive
impairment and abnormal PMA and sleep patterns)
5. Focal syndromes (viz. Wernicke’s aphasia, Anton syndrome, bifrontal lesions) or
NCSE

25. Prevention
More interventions to prevent (particularly nonpharmacological) than to treat
Hospital Elder Life Program (prevent cognitive and functional decline)
Daily Visitor Program
Therapeutic Activities Program
Early Mobilization Program
Feeding & Meal Assistance Program
Relaxation Program
Cognitive Friendly Hospital Programme
Low dose antipsychotics (gabapentin) and melatonin have some level of benefits, same
with cholinesterase inhibitors
Preventive measures though are appealing, often not possible or resources not available
and cost effective

26. Prevention
Orientation protocols (Provision of clocks, calendars, windows with
outside views, and verbal reorientation)
Cognitive stimulation (regular daytime visits from family and friends)
Facilitation of physiologic sleep
Early mobilization and minimized use of physical restraints for patients
with limited mobility
Visual and hearing aids for patients with these impairments
Avoiding and/or monitoring the use of problematic medications
(benzodiazepines often implicated)
Pain Management: preferably with non opioids

27. Management
Series of investigations if cause not identifiable by routine
tests (Drugs: side effect or withdrawal always on differential)
Treatment of the underlying cause
Symptomatic measures
Supportive medical and nursing care

28. Non-pharmacological Therapy
Mainstay of therapy is non-pharmacological
Medications less beneficial due to lack of evidence and associated adverse effects
General measures should relieve stress, control agitation and prevent exhaustion
Frequent explanation
Reorientation
Reassurance
Avoid unnecessary changes in caring staffs
Frequent relative visits
Proper lightening at evening sufficient to promote orientation, not prevent sleep
Neither sensory deprivation nor over stimulation (Black-patch delirium in cataract
surgery patients).
Physical restraints should be used only as a last resort, if at all, as they frequently increase agitation
and create additional problems, such as loss of mobility, pressure ulcers, aspiration, and prolonged
delirium

29. Pharmacological Therapy
Major symptoms requiring pharmacological interventions are
psychosis and insomnia
Antipsychotics are the first line medications (off label)
Reserved for severely agitated and patients with psychotic symptoms
Haloperidol as been used conventionally ( low dose 0.5-1 mg PO or IM
usually 1-5 mg per day, elderly may require even less).
Use with caution in:
1) Delirium tremens (risk of precipitating seizures, rather
benzodiazepines lorazepam or chlordiazepoxide is standard)
2) Epilepsy (risk of precipitating seizures)
3) Liver failure (risk of hepatic coma)

30.  In some studies, other drugs like Alpha2 agonist
Dexmedetomidine has been effective in reducing delirium
duration and superior to antipsychotics
Nowadays, atypical antipsychotics like Risperidone, Clozapine,
Olanzapine are preferred though clinical trials are limited
Insomnia best treated with benzodiazepines with short or
intermittent half lives (Lorazepam 1-2 mg HS, half life: 10-20 hrs)
Benzodiazepines with long half lives (viz. Diazepam: 20-100
hrs, Clonazepam: 18-50 hrs and barbiturates) typically avoided
unless used for an underlying disorder like alcohol withdrawal

31. Course & Prognosis
Many cases recover rapidly. After causal factor removed, within 3-7
days, though some symptoms need up to 2 weeks to resolve.
Recall of events during the period is characteristically spotty
Can sometimes followed by depression or PTSD
Worse prognosis if underlying disease or pre-existing dementia
Hypoactive patients have worse prognosis compared to hyperactive
cases
25% mortality in 3 months
2 fold increase in mortality risk in first two years of delirium episode
Delirium and dementia both act synergistically to accelerate the pace
of cognitive decline

32. References
Shorter Oxford Textbook of Psychiatry, 7th edition
Kaplan and Sadock's Comprehensive Textbook of Psychiatry, 10th edition
Joseph Francis et.al, Diagnosis of delirium and confusional states,
https://www.uptodate.com/contents/diagnosis-of-delirium-and-confusional-states
Joseph Francis et.al, Delirium and acute confusional states: Prevention, treatment, and
prognosis, https://www.uptodate.com/contents/delirium-and-acute-confusional-states-
prevention-treatment-and-prognosis
Burry L et.al, Antipsychotics to treat delirium in hospitalized patients, not including
those in intensive care units,
https://www.cochrane.org/CD005594/DEMENTIA_antipsychotics-treat-delirium-
hospitalised-patients-not-including-those-intensive-care-units
Psychiatry, John Geddes et al., 4th edition
A Short Textbook of Psychiatry, Ahuja, 7th edition