Delirium is an acute mental status change characterized by abnormal and fluctuating attention and reduced ability to direct, focus, sustain, and shift attention. It impairs cognition. It has an acute onset, fluctuating course, and is often caused by a medical condition. The diagnosis involves assessing attention, awareness, cognition, and determining if it is caused by an underlying medical condition based on criteria in the DSM-V. Predisposing factors include older age, dementia, visual impairment and severity of illness. Precipitating factors include medications, physical restraints and infections. It is diagnosed using mental status exams and scales like the CAM.

1. DELIRIUM
On April 7, 2015
By- Dr Saumya Mittal

2. DELIRIUM- A HISTORY
 Hippocrates referred to it as phrenitis, the origin of our word
frenzy.
 Celsus introduced the term delirium, from the Latin meaning
derailment of the mind
 Galen observed that delirium was often due to physical
diseases that affected the mind “sympathetically.”
 Gowers recognized that these patients could be either
lethargic or hyperactive.
 Bonhoeffer established that delirium is associated with
clouding of consciousness.
 Engel and Romano (1959) described alpha slowing with delta
and theta intrusions on EEGs and correlated these changes
with clinical severity. They noted that treating the medical
cause resulted in reversal of both the clinical and EEG
changes of delirium.

3. DELIRIUM
Most common behavioural disorder in a medical-
surgical setting.
Acute mental status change characterized by
abnormal and fluctuating attention.
There is a disturbance in level of awareness and
reduced ability to direct, focus, sustain, and shift
attention – impair cognition.

4. DEFINITIONS OF TERMS USED
 Attention is the ability to focus on specific stimuli to
the exclusion of others.
 Awareness is the ability to perceive or be conscious
of events or experiences.
 Arousal, a basic prerequisite for attention, indicates
responsiveness or excitability into action.
 Coma, stupor, wakefulness, and alertness are states of
arousal.
 Consciousness, a product of arousal, means clarity
of awareness of the environment.
 Confusion is the inability for clear and coherent
thought and speech.

5. OTHER NAMES
 Many terms are used to describe this disorder:
 acute confusional state,
 acute organic syndrome,
 acute brain failure,
 acute brain syndrome,
 acute cerebral insufficiency,
 exogenous psychosis,
 metabolic encephalopathy,
 organic psychosis,
 ICU psychosis,
 toxic encephalopathy,
 toxic psychosis.

6. DSM-V CRITERIA FOR DELIRIUM
 Disturbance in level of awareness and reduced ability to
direct, focus, sustain, and shift attention
 Change in cognition (deficits in orientation, executive ability,
language, visuoperception, learning, and memory):
 Cannot be assessed in face of severely reduced level of
awareness
 Should not be better accounted for by a preexisting
neurocognitive disorder
 There is evidence from the history, examination, or lab that the
disturbance is caused as a consequences of a general
medical condition.
 The disturbance develops over a short period of time (usually
hours to a few days) and tends to fluctuate in severity during
the course of a day.
 Supportive features commonly present in delirium but not key
diagnostic features: sleep/wake cycle disturbance,
psychomotor disturbance, perceptual disturbances (e.g.,
hallucinations, illusions), emotional disturbances, delusions,
labile affect, dysarthria.

7. 10 CLINICAL CHARACTERSTICS
Acute onset of mental status change with fluctuating
course
Attentional deficits
Confusion or disorganized thinking
Altered level of consciousness
Perceptual disturbances
Disturbed sleep/wake cycle
Altered psychomotor activity
Disorientation and memory impairment
Behavioral and emotional abnormalities
Other cognitive deficits

8. ACUTE ONSET WITH FLUCTUATING COURSE
 Delirium develops rapidly over hours or days, but
rarely over more than a week.
 Fluctuations in the course occur throughout the day.
 Lucid intervals interspersed with the daily fluctuations.
 Gross swings in attention and awareness, arousal,
or both occur unpredictably and irregularly and
become worse at night.
 Lucid intervals may be mislead medical personnel
unless the patients are evaluated over time.

9. ATTENTIONAL DEFICITS
 A disturbance of attention
and consequent altered
awareness is the cardinal
symptom of delirium.
 Patients are distractible,
and stimuli may gain
attention indiscriminately,
trivial ones often getting
more attention than
important ones.
 Components of attention
are disturbed-
o selectivity,
o sustainability,
o processing capacity,
o ease of mobilization,
o monitoring of the
environment, and
o the ability to shift
attention when
necessary.

10. CONFUSION OR DISORGANIZED THINKING
 Delirious patients are unable to maintain the stream
of thought with accustomed clarity, coherence, and
speed.
 There are multiple intrusions of competing thoughts
and sensations.
 Patients are unable to order symbols, carry out
sequenced activity, and organize goal-directed
behaviour.

11.  The patient’s speech reflects this jumbled thinking.
 Speech shifts from subject to subject and is
rambling, tangential, and circumlocutory, with
hesitations, repetitions, and perseverations.
 Decreased relevance of the speech content and
decreased reading comprehension are
characteristic of delirium.
 Confused speech is further characterized by an
abnormal rate, frequent dysarthria, and nonaphasic
misnaming, particularly of words related to stress or
illness, such as those referable to hospitalization.

12. ALTERED LEVEL OF CONSCIOUSNESS
 Consciousness, or clarity of awareness, may be
disturbed.
 The patients may have hypoactive delirium
(lethargy and decreased arousal) or hyperactive
delirium (hyperalert and easily aroused).
 In hyperalert patients the extreme arousal does not
preclude attentional deficits.
 The two extremes of consciousness may overlap or
alternate in the same patient or may occur from the
same causative factor.
 The elderly in particular may have a “quieter,” more
subtle presentation of delirium that may evade
detection.

13. PERCEPTUAL DISTURBANCES
 Perceptions may be multiple, changing, or abnormal in size
or location.
 The most common perceptual disturbance is
 Decreased perceptions per unit of time.
 Illusions
 Hallucinations- in young and hyperactive delirium
 Illusions and other misinterpretation result from abnormal
sensory discrimination.
 Hallucinations are
 usually in the visual sphere, vivid, 3D, and in full colour.
 Patients may see lilliputian animals or people- move about.
 generally unpleasant (patients attempt to fight/escape them).
 Auditory hallucinations with voices commenting on the
patient’s behaviour are unusual.

14. DISTURBED SLEEP/WAKE CYCLE
 This is one of the least specific symptoms and also
occurs in dementia, depression, and other behavioral
conditions.
 Excessive daytime drowsiness and reversal of the
normal diurnal rhythm.
 “Sundowning”—with restlessness and confusion during
the night—is common.
 Nocturnal peregrinations- delirious patient, partially
clothed in a hospital gown, has to be retrieved from the
hospital lobby or from the street in the middle of the
night.
 Disruption of circadian sleep cycles may result in rapid
eye movement or dream-state overflow into waking.

15. ALTERED PSYCHOMOTOR ACTIVITY
 psychomotor
retardation
 lethargy and
 decreased arousal
 Agitated
 overactivity of the ANS
 likely to have delusions
and perceptual disorders
e.g. hallucinations.
 Only about 15% are
strictly hyperactive
 patients being younger
 drug-related causes
 shorter hospital stay
 better prognosis.
Hypoactive-Hypoalert
subtype
Hyperactive-Hyperalert
subtype
There are two subtypes of delirium

16. DISORIENTATION AND MEMORY IMPAIRMENT
 Disturbances in orientation and memory are related.
 Patients are disoriented first to time of day, followed by
other aspects of time, and then to place. Disorientation
to person—in the sense of loss of personal identity—is
rare.
 Disorientation is one of the most common findings in
delirium but is not specific for delirium. It occurs in
dementia and amnesia as well.
 Among patients with delirium, recent memory is
disrupted in large part by the decreased registration
caused by attentional problems.
 Reduplicative paramnesia, a specific memory-related
disorder, results from decreased integration of recent
observations with past memories. Persons or places are
“replaced” in this condition e.g. Capgras syndrome*.

17. OTHER COGNITIVE DEFICITS
 Disturbances occur in visuospatial abilities and in writing.
 Higher visual-processing deficits
 difficulties in visual object recognition,
 environmental orientation, and
 organization of drawings and other constructions.
 Writing disturbance may be the most sensitive language abnormality in
delirium.
 The most salient characteristics are abnormalities in the mechanics of
writing:
 The formation of letters and words is indistinct,
 words and sentences sprawl in different directions
 reluctance to write,
 motor impairments (e.g., tremors, micrographia)
 spatial disorders (e.g., misalignment, leaving insufficient space for the writing
sample).
 perseverations of loops or aspects of the writing.
 Spelling (consonants) and syntax, small grammatical words (prepositions and
conjunctions) are also disturbed
 Writing is easily disrupted in these disorders, possibly because it
depends on multiple components and is the least used language
function.

18. BEHAVIORAL & EMOTIONAL ABNORMALITIES
 Behavioural changes include
 Elementary behavioural changes
 Especially in elderly
 decreased activities of daily living,
 urinary incontinence,
 frequent falls.
 Delusions,
 Persecutory
 Paranoid ideation
 Personality alterations.
 Delusions, like hallucinations
 fleeting,
 changing,
 readily affected by sensory input.
 Some patients can exhibit
facetious humour and playful
behaviour, lack of concern about
their illness, poor insight,
impaired judgement and
confabulation.
 Emotional lability-
 Agitated and fearful or depressed
or quite apathetic.
 Dysphoric (unpleasant)
emotional states are the more
common.
 Depression symptoms.
 The mood changes of delirium
are probably due to direct effects
of the confusional state on the
limbic system and its regulation
of emotions.

19. PATHOPHYSIOLOGY
Pathophysiology is not entirely understood.
1. Brain areas may be involved
2. Alterations in neurotransmitters
3. Altered BBB permeability by cytokines
4. Abnormal secretion of melatonin
Delirium is the final common pathway of many
pathophysiological disturbances that reduce or
alter cerebral oxidative metabolism .

20.  Brain areas involved in attention are disturbed
 Anterior cingulate cortex- disturbance of management of
attention.
 Bilateral or right prefrontal cortex- attention
maintenance and executive control
 Temporoparietal junction region- disengaging and
shifting attention
 Thalamus- engaging attention*
 Upper brainstem structures-moves focus of attention.
 Right hemisphere is dominant for attention**.

21.  Alterations in neurotransmitters particularly a cholinergic-
dopaminergic imbalance.
 Cholinergic deficit results in delirium.
 Cholinergic neurons project from the pons and the basal forebrain making
cortical neurons more responsive to other inputs.
 A decrease in acetylcholine results in decreased perfusion in the frontal
cortex.
 Anticholinergic agents can induce the clinical and EEG changes of delirium
 Reversible with the administration of cholinergic medications such as
physostigmine.
 The beneficial effects of acetylcholinesterase-inhibitor medications- donepezil,
rivastigmine, and galantamine- used for Alzheimer disease may be partly due to
an activating or attention-enhancing role.
 Hypoglycemia, hypoxia, and other metabolic changes may differentially affect
acetylcholine mediated functions.
 Other neurotransmitters may be involved in delirium, including
dopamine, serotonin, norepinephrine, γ-aminobutyric acid,
glutamine, opiates, and histamine.
 Dopamine has an inhibitory effect on the release of acetylcholine,
hence the delirium-producing effects of l-dopa and other
antiparkinsonism medications.
 Opiates may induce the effects by increasing dopamine and glutamate
activity.

22.  Inflammatory cytokines such as IL, IFN TNF-α,
alter blood-brain barrier permeability further
affecting neurotransmission.
 The combination of inflammatory mediators and
dysregulation of the limbic-hypothalamic-pituitary
axis may lead to exacerbation or prolongation of
delirium.
 Melatonin, a hormone integral to circadian rhythm
and the sleep/wake cycle, may be abnormal in
delirious patients compared to those without
delirium.

23. DIAGNOSIS

24. PRECIPITATING FACTORS
 Four factors independently
predispose to delirium:
 vision impairments (<20/70 binocular),
 severity of illness,
 cognitive impairment, and
 dehydration (high ratio of blood urea
to creatinine).
 Other important predisposing factors
for delirium are
 advanced age, especially older than
80 years, and
 the presence of chronic medical
illnesses.
 Cerebral atrophy or white matter and
basal ganglia ischemic changes.
 deree of physical impairment,
 hip and other bone fractures,
 serum sodium changes,
 infections and fevers, and
 use of multiple drugs- narcotic,
anticholinergic, or psychoactive
properties.
 Five specific factors that can
independently precipitate delirium are
 use of physical restraints,
 malnutrition or weight loss (albumin
levels less than 30 g/L),
 use of indwelling bladder catheters,
 adding more than three medications
within a 24-hour period,
 iatrogenic medical complication.
 Other precipitating factors for incident
delirium after hospitalization include
 electrolyte disturbances
(hyponatremia, hypercalcemia),
 major organ system disease,
 occult respiratory failure,
 occult infection,
 pain,
 specific medications- sedative-
hypnotics or histamine-2 blockers,
 sleep disturbances,
 alterations in the environment
 Novel situations and unfamiliar
surroundings

25.  The predisposing factors for delirium are additive.
 The greater the number of predisposing factors, the
fewer or milder are the precipitating factors needed to
result in delirium.
 Elderly patients with dementia are five times more likely
to develop delirium than those without dementia.
 Heritability of delirium is a new area of investigation. The
presence of genes such as apolipoprotein E (APOE),
dopamine receptor genes DRD2 and DRD3, and the
dopamine transporter gene, SLC6A3, are possible
pathophysiological vulnerabilities for delirium.

26. MENTAL STATUS EXAMINATION
 Initial general behavioral observations-
 may range from falling asleep during the interview to agitation and combativenes
 Most important are observations of attentiveness and arousability.
 Bedside tests of attention can be divided into
 serial recitation tasks- digit span test, serial reversal test, spelling of a word
 continuous performance tasks- A vigilance test
 alternate response tasks- repetition of a three-step motor sequence.
 Slow and loosely connected thinking and speech may be present, with
irrelevancies, perseverations, repetitions, and intrusions. Patients may propagate
their errors in thinking and perception by elaboration or confabulation.
 Disturbed recent memory is demonstrated by asking the patient to retain the
examiner’s name or three words for 5 minutes.
 A language examination should distinguish between the language of confusion and
that of a primary aphasia.
 Attempts at simple constructions such as copying a cube may be unsuccessful.
 Hallucinations can sometimes be brought out by holding a white piece of paper or
an imaginary string between the fingers and asking the patient to describe what he
or she sees.

27. DIAGNOSTIC SCALES AND CRITERIA
 Confusion Assessment Method (CAM)- widely used
 Delirium Rating Scale-Revised-98 (DRSR-98).
 Memorial Delirium Assessment Scale (MDAS)- a
10-item scale designed to quantify the severity of
delirium in medically ill patients.
 The Delirium Symptom Interview-may not
distinguish delirium from dementia.
 The Neelon and Champagne (NEECHAM)
Confusion Scale is widely used in the nursing
community. Measures acute confusion rather than
delirium.

29. PHYSICAL EXAMINATION
 Look for signs of-
 focal neurological abnormalities,
 meningismus,
 increased intracranial pressure (ICP),
 cerebrovascular disease, or
 head trauma.
 Less specific findings include-
 an action or postural tremor of high frequency (8-10 Hz),
 asterixis or brief lapses in tonic posture (especially at the wrist),
 multifocal myoclonus or shock-like jerks from diverse sites,
 choreiform movements,
 dysarthria, and
 gait instability.
 Patients may manifest-
 agitation or psychomotor retardation,
 apathy,
 waxy flexibility,
 catatonia, or
 Carphologia (“lint-picking” behavior).
 The presence of hyperactivity of the autonomic nervous system may be
life threatening because of possible dehydration, electrolyte
disturbances, or tachyarrhythmias.

30. LABORATORY TESTS
 EEG changes virtually always accompany delirium-
 disorganization of the usual cerebral rhythms and generalized
slowing are the most common changes.
 mean EEG frequency or degree of slowing correlates with the
degree of delirium.
 Additional EEG patterns from intracranial causes of delirium
include-
 focal slowing,
 asymmetric delta activity, and
 paroxysmal discharges (spikes, sharp waves, and spike-wave
complexes).
 Periodic complexes such as triphasic waves and periodic
lateralizing epileptiform discharges may help in the differential
diagnosis.
 Lumbar puncture and neuroimaging are needed in only
a minority of delirious patients. The lumbar puncture
should be preceded by CT or MRI scan of the brain.

31.  Other essential laboratory tests include-
 complete blood cell count;
 glucose, electrolytes, BUN, creatinine, transaminase
 Ammonia, thyroid function tests, ABG
 chest radiographs; electrocardiogram;
 Urinalysis and urine drug screening.
 antibody tests against Hu or NMDA receptors.

33. PREVENTION AND TREATMENT

34.  There are several steps in the management of delirium.
 1. find the cause and eliminate it.
 2. symptomatic measures involving attention to fluid and
electrolyte balance, nutritional status, and early treatment of
infections.
 3. environmental interventions.
 Reduce unfamiliarity by providing a calendar, a clock, family
pictures, and personal objects.
 Maintain a moderate sensory balance in the patient by
avoiding sensory overstimulation or deprivation.
 Minimize staff changes, limit ambient noise and the number of
visits from strangers, and provide a radio or a television set, a
nightlight, and where necessary, eyeglasses and hearing aids.
 Other environmental measures include providing soft music
and warm baths and allowing the patient to take walks when
possible. Physical restraints should be avoided if possible and
a sitter used instead.
 4. proper communication and support are critical with these
patients

35.  Best to avoid the use of drugs in confused patients.
 All the patient’s medications should be reviewed, and
any unnecessary drugs should be discontinued.
 These patients should receive the lowest possible dose
and should not get drugs such as phenobarbital or long-
acting benzodiazepines.
 Often used is haloperidol starting at 0.25 mg daily.
Haloperidol may be repeated every 30 minutes, PO or
IM, up to a maximum of 5 mg/day.
 The atypical antipsychotics—risperidone, olanzapine,
quetiapine, and aripiprazole—may be used at low
doses. Other medications such as valproate,
ondansetron, or melatonin may be effective and safe in
selected cases.
 Finally, there is no evidence for the preventive use of
haloperidol or related medications prior to the
development of delirium, though it may reduce severity
and duration postoperatively, as well as duration of
hospital stay.

36. THANK YOU