This document provides an overview of delirium, including its definition, history, characteristics, epidemiology, risk factors, causes, pathophysiology, clinical features, diagnosis, differential diagnosis, course and prognosis, and treatment. Some key points covered include: - Delirium is defined as an acute impairment of attention, consciousness, and cognition that fluctuates in severity. - Risk factors include older age, medical illnesses, cognitive impairment, and polypharmacy. - Causes include infections, withdrawal, toxins/drugs, hypoxia, and metabolic disturbances. - The pathophysiology is not fully understood but may involve neurotransmitter imbalances and blood-brain barrier disruption. - Diagnosis involves

1. 1
 PRESENTER-
DR.CHARAN SINGH
JILOWA
 UNDER GUIDANCE OF–
DR.LALIT BATRA

2. What we will cover
2
1. What is delirium ?
2. History.
3. Characteristics
4. Synonyms.
5. Epidemiology.
6. Risk factors
7. Causes .
8. Pathophysiology
9. Clinical features.
10. Diagnosis.
11. D.D.
12. Course and prognosis.
13. Treatment.
14. Preventions .

3. What is Delirium?
 Rapid onset of impairment and fluctuation in
CONCENTRATION.
 Altered CONSCIOUSNESS.
 Impaired COGNITION.
 Delirium is a syndrome,
not a disease.
3

4. HISTORY
 The Word delirium exist in medical litrature since
last 2500 years.
 Almost 50 years ago, George L. Engel and John
Romano postulated that delirium was a reversible
cerebral insufficiency due to decreased brain
metabolic activity, based on
electroencephalogram (EEG) slowing in patients
with delirium.
 In 1980, the third edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-III)
was the first attempt to standardize delirium
nomenclature.
4

5. Clinical characteristics of
delirium
 Acute onset of mental status change with
fluctuating course .
 Attentional deficits .
 Disorganized thinking .
 Altered level of consciousness .
 Perceptual disturbances .
 Disturbed sleep-wake cycle .
 Altered psychomotor activity
 Disorientation and memory impairment .
 Other cognitive deficits behavioral and
emotional abnormalities .
5

6. Delirium - Synonyms
1 Intensive care unit psychosis.
2 Acute confusional state.
3 Acute brain failure
4 Toxic metabolic state.
5 Central nervous system toxicity.
6 Paraneoplastic limbic encephalitis.
7 Sundowning.
8 Cerebral insufficiency.
9 Organic brain syndrome.
6

7. Epidemiology
 According to DSM-IV-TR, the point prevalence of
delirium in the general population is 0.4 percent for
people 18 years of age and older and 1.1 percent
for people 55 and older.
 Approximately 10 to 30 percent of medically ill
patients who are hospitalized exhibit delirium.
 Approximately 30 percent of patients in surgical
intensive care units and cardiac intensive care
units and 40 to 50 percent of patients who are
recovering from surgery for hip fractures have an
episode of delirium.
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8. Epidemiology
 The highest rate of delirium is found in
postcardiotomy patients, more than 90 percent
in some studies.
 An estimated 20 percent of patients with
severe burns and 30 to 40 percent of patients
with AIDS have episodes of delirium while they
are hospitalized.
 Delirium develops in 80 percent of terminally ill
patients.
8

9. Who gets it?-risk factors
 Vision impairment .
 Hypertension .
 Medical illnesses (severity and
quantity).
 COPD.
 Preoperative cognitive
impairment
 Cognitive impairment
 Alcohol abuse.
 Functional limitations .
 Older than 70 years .
 Smoking history .
 History of delirium
 Blood urea nitrogen to
creatinine ratio >18.
 Abnormal sodium level
Abnormal potassium,
sodium, or glucose test.
 Use of physical
restraints.
 Preoperative use of
benzodiazepines
 Malnutrition..
 Abnormal bilirubin level.
 Preoperative use of
narcotic analgesics.
 More than three
medications added.

9

10. Causes of Delirium
I: Infections........ ............... UTI’s, pneumonia, encephalitis, etc.
W: Withdrawal………..……… alcohol, benzodiazepines, sedative-hypnotics
A: Acute causes…………….. electrolyte disturbance, dehydration, acidosis /
alkalosis, hepatic/renal metabolic failure
T: Toxins, drugs……………. opiates, salycilates,indomethacin, dilantin
C: CNS pathology ………… stroke, TIA, tumors, seizures, hemorrhage, infection
H: Hypoxia…………………….anemia, pulmonary/cardiac failure, hypotension
D: Deficiencies………………..Thiamine (with alcohol abuse), B12
E: Endocrine………………......thyroid, hypo/hyperglycemia, adrenal dysfunction,
hyperparathyroid
A: Acute vascular shock,…… hypertensive encephalopathy
T: Trauma………………………head injury, post-operative, hypo/hyperthermia
H: Heavy Metals……………….lead, m ercury, manganese poisoning
I W A T C H D E A T H
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11. Clinical features
 fluctuation in ability to focus, to shift, and to
sustain attention.
 Easy distractiblity; and impaired memory.
 Associated symptoms include affective lability,
psychomotor abnormalities, and
misinterpretations and hallucinations.
 Affective symptoms often fluctuate and may
include anxiety, fear, apathy, anger, euphoria,
dysphoria, and irritability, all within short time
periods.
 The perceptual disturbances are mostly visual
(described as poorly organized, fragmented
dreams or nightmares.).
11

12. Clinical features
 The hyperactive subtype is psychomotorically
active, hypervigilant, restless, and excitable and
speaks with loud or pressured speech.
 The hypoactive subtype is psychomotorically
slowed, quiet, and withdrawn and has reduced
alertness and decreased speech production.
 The loud patient gains the attention of others and
is more likely to be diagnosed with delirium than
the quiet patient who is not disturbing others.
Because delirium carries an increased risk of
morbidity and mortality, the quietly delirious
patient needs to be identified and appropriately
evaluated and treated.
12

13. Delirium- Pathophysiology
 The proposed theories for delirium
pathophysiology involve -
 Neurochemical abnormalities,
 Alterations in metabolism,
 Involvement of cytokines and acute phase
reactants, and
 Changes in the permeability of the blood–brain
barrier.
13

14. 14 Flacker JM. J Gerontol Biol Sci 1999;54:B239-46

15. Hypotheses about Delirium
Pathophysiology
 Poorly understood
 ACETYLCHOLINE
 The cholinergic system is involved with rapid eye
movement (REM) sleep, attention, arousal, and
memory.
 Anticholinergic agents have been found to cause
delirium in humans and behavioral and EEG
changes in animals.
 The serum anticholinergic levels are increased in
delirious patients and decline as delirium resolves.
 cholinergic agents, such as physostigmine, have
demonstrated benefit in treating anticholinergic
delirium.
15

16. Cont..
 DOPAMINE
 Dopamine is involved in maintaining and shifting
attention via modulation of the frontal cortex.
 Antipsychotic agents that block dopamine receptors
provide symptomatic relief for delirious patients and
may result in a relative decrease in dopamine levels.
 Substances that increase dopamine, such as
psychostimulants, carbidopa and levodopa , bupropion
or amantadine may cause delirium.
 As dopamine levels increase, cholinergic levels
decline, possibly contributing to delirium through the
interaction of the two neurotransmitter systems.
 Reduction in dopaminergic function is associated with
alterations in oxidative metabolism.
16

17. Cont..
 Glutamate
 Glutamate abnormalities are inferred in the
pathophysiology of delirium. Glutamate excitatory
neurotoxicity via the N-methyl-D-aspartate (NMDA)
receptor may cause apoptosis and neuronal death and
has been associated with alcohol intoxication and
withdrawal, conditions that are associated with
delirium.
 GABA and Amonia-
 In patients with hepatic encephalopathy, increased
inhibitory GABA levels are observed.
 An increase in ammonia levels occurs in patients with
hepatic encephalopathy, which causes an increase in
the amino acids glutamate and glutamine, which are
precursors to GABA.
17

18. Cont..
 SEROTONIN
 Excess and attenuated serotonin has been
implicated in delirium.
 Oxidative Metabolism
 Alterations in oxidative metabolism may result in
delirium.
 Blood–Brain Barrier Alterations
 Delirium may be related to capillary endothelial
changes that result in the disruption of the blood–
brain barrier.
18

19. Cont…
 Cytokines
 Rodent models suggest that IL-1
(proinflammatory substance) administration
decreases extracellular Ach in the hippocampus
and increases NE in the hypothalamus.
 Cytokines may change the endothelial
permeability of the blood–brain barrier.
19

20. DSM-IV-TR Diagnostic Criteria for Delirium
Due to General Medical Condition
A. Disturbance of consciousness (i.e., reduced clarity of
awareness of the environment) with reduced ability to
focus, sustain, or shift attention.
B. A change in cognition (such as memory deficit,
disorientation, language disturbance) or the
development of a perceptual disturbance that is not
better accounted for by a preexisting, established, or
evolving dementia.
C. The disturbance develops over a short period of time
(usually hours to days) and tends to fluctuate during
the course of the day.
D. There is evidence from the history, physical
examination, or laboratory findings that the
disturbance is caused by the direct physiological
consequences of a general medical condition.
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21. Diagnostic Tools
Sensitivity Specificity
 CAM* .46-.92 .90.92
 Delirium Rating Scale* .82-.94 .82-.94
 Clock draw .87 .93
 MMSE (23/24 cutoff) .52-.87 .76-.82
 Digit span test .34 .90
 *validated for delirium & capable of distinguishing delirium from dementia
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22. CAM(Confusion Assessment Method)-
22
Uses 4 criterias-
(1) acute onset and fluctuating course.
(2) inattention..
(3) disorganized thinking.
(4) altered level of consciousness.
-- The diagnosis of delirium requires the presence
of criteria:
(1), (2) and (3) or (4)

23. Diagnosis
MMSE & Clock draw-
-Not designed for delirium.
-Useful at separating “normal” from
“abnormal”.
-Not specific for distinguishing
delirium from dementia.
-May be useful as change from
baseline.
23

24. Physical Examination of the Delirious
Patient
s.no. Parameter Finding Clinical implication
1 Pulse bradicardia Hypothyroidism
Increased intracranial pressure
tachycardia Hyperthyroidism
Infection
Heart failure
2 temprature fever Sepsis ,Thyroid storm
Vasculitis
3 Blood pressure hypotension Shock ,Hypothyroidism
Addison's disease
hypertension Encephalopathy
Intracranial mass
4 Respiration Tachypnea Diabetes ,Pneumonia
Cardiac failure, Fever
Acidosis (metabolic)
Shallow Alcohol or other substance
intoxication
5 Carotid vessels Bruits or decreased pulse Transient cerebral ischemia
24

25. Physical Examination of the Delirious Patien
s.no. Parameter Finding Clinical implication
6 Neck Evidence of nuchal rigidity Meningitis
Subarachnoid hemorrhage
7 Eyes Papilledema Tumor
Hypertensive encephalopathy
Pupillary dilatation Anxiety
Autonomic overactivity (e.g.,
delirium tremens)
8 . Mouth Tongue or cheek lacerations Evidence of generalized tonic-
clonic seizures
9 Thyroid enlarged Hyperthyroidism
10 Heart Arrhythmia Inadequate cardiac output,
possibility of emboli
Cardiomegaly Heart failure
Hypertensive disease
Congestion Primary pulmonary failure
Pulmonary edema, Pneumonia
25

26. Laboratory Workup of the Patient
with Delirium
 Standard studies
 Blood chemistries (including electrolytes, renal
and hepatic indexes, and glucose).
 Complete blood count.
 Thyroid function tests.
 Serologic tests for syphilis.
 Human immunodeficiency virus (HIV) antibody
test.
 Urinalysis.
26

27. Cont…
 Electrocardiogram .
 Electroencephalogram(The EEG in delirium frequently
demonstrates generalized slowing).
 Chest radiographBlood and urine drug screen.
• Additional tests when indicated-
 Blood, urine, and cerebrospinal fluid (CSF) cultures
B12, folic acid concentrations.
 Computed tomography or magnetic resonance imaging(
brain scan sub-arachnoid hemorrhage, subdural
hematomas).
 Lumbar puncture and CSF examination.
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28. D.D.
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Relationship of dementia and delirium
Delirium Dementia
A continuum of cognitive disorders.

29. Differentiating Dementia from Delirium
feature dementia delirium
Onset Slow Rapid
Duration Months to years Hours to weeks
Speech Word-finding difficulty Incoherent (slow or rapid)
Attention Preserved Fluctuates
Sleep wake cycle Fragmented sleep Frequent disruption (e.g.,
day night reversal)
Memory Impaired remote memory Impaired recent and
immediate memory
Awareness unchanged reduced
Thoughts Impoverished Reduced
alertness Usually normal Hypervigilent or reduced
29

30. Cont…
 Schizophrenia vs Delirium
 Onset of schizophrenia is rarely after 50.
 Auditory hallucinations are much more common
than visual hallucinations.
 Memory is grossly intact and disorientation is
rare.
 Speech is not dysarthric.
 No wide fluctuations over the course of a day.
30

31. Cont…
 Mood disorders vs Delirium
 Mood disorders manifest persistent rather than
labile mood with more gradual onset.
 In mania the patient can be very agitated however
cognitive performance is not usually as impaired.
 Flight of ideas usually have some thread of
coherence unlike simple distractibility.
 Disorientation is unusual in mania.
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32. Why is Delirium missed?
Hard to
see if
you
aren’t
looking
for it.
32

33. Why is Delirium Missed:
Atypical Presentations of Delirium
 Three different symptom patterns:-
 Positive symptoms
 Agitation
 Hallucinations /Delusions
 30%
 Negative symptoms
 Attention deficit
 Hypersomnulence
 25%
 Mixed Symptoms –
 45%
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34. Course and prognosis
 Although the onset of delirium is usually sudden,
prodromal symptoms (e.g., restlessness and
fearfulness) can occur in the days preceding the
onset of florid symptoms.
 The symptoms of delirium usually persist as long
as the causally relevant factors are present,
although delirium generally lasts less than a
week.
 After identification and removal of the causative
factors, the symptoms of delirium usually recede
over a 3- to 7-day period, although some
symptoms may take up to 2 weeks to resolve
completely.
34

35. Course and prognosis
 Recall of what transpired during a delirium,
once it is over, is characteristically spotty; a
patient may refer to the episode as a bad
dream or a nightmare only vaguely
remembered.
 Delirium may progresses to dementia.
 The older the patient and the longer the
patient has been delirious, the longer the
delirium takes to resolve.
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36. TREATMENT
36

37. TREATMENT
 TREATMENT
GOALS PHARMACOLOGIC
AL TREATMENT
NON-
PHARMACOLOGICA
L TREATMENT
37

38. TREATMENT
THREE MAJOR GOALS -
Find and to
reverse the
contributors to
the delirium.
Ensure the patient's
safety while
educating patients,
family, and staff.
Symptomatic
treatment of
behavioral
disturbances
associated
with delirium.
38

39. PHARMACOLOGICAL
TREATMENT
 In general, it is wise not to add additional
medications to the patient's regimen, unless
there is a significant reason to do so. Clinical
situations that might require additional
medications include agitation or psychosis.
 Antipsychotics may be considered if
psychosis, severely disorganized thought
process, or extreme physical or verbal
agitation places the patient or others at risk of
harm.
39

40. Typical Antipsychotics
HALOPERIDOL:-
 try to only use for SEVERE agitation.
 lowest anticholinergic activity of all major neuroleptics
 high potency.
 can be used IM/IV.
 start with 0.5 - 1 mg initial dose, gradually titrating to a
maximum of 4 mg/day.
 Repeat dose q 2-4 h.
 Taper the dose as soon as possible.
 Avoid in individuals with
Parkinson’s Disease.
40

41. Atypical Antipsychotics
Risperidone, Olanzepine, quetiapine
 low dose Risperidone starting at
.25 mg BID
 Olanzapine - 2.5 mg/d as starting
dose
 Quetiapine - 12.5 mg/d starting
dose
41

42. Benzodiazepines
1. It May increase agitation.
2. Best reserved for Delirium 2o to alcohol/
Benzodiazepine withdrawal.
3. Relatively contraindicated in Delirium from
Hepatic Encephalopathy.
42

43. Electroconvulsive Therapy
 ECT is also a treatment for
delirium when other
approaches have failed.
 It has been used as a last
resort for delirious patients
with severe agitation who are
not responsive to
pharmacotherapy.
43

44. Restore Sleep–Wake Cycle
 Delirium is frequently complicated by changes
in the sleep–wake cycle. Attempts to restore
sleep integrity may include moving the
schedule of existing sedating medications
to the hour of sleep or reducing or moving
activating medications and stimulants such as
caffeine to the morning.
 Brief, judicious use of sedating agents, such
as zolpidem or trazodone to reset the sleep–
wake cycle may be appropriate.
44

45. NON PHARMACOLOGICAL
TREATMENT
45

46. Nonpharmacological treatment
 The focus is on safety and orientation with
provision of the appropriate level of stimulation
and education toward the patient and family.
 Nursing care should follow vital sign
measurements and fluid intake and output.
 Care should be given when feeding to reduce or
to prevent aspiration. If possible, feeding should
be done in the lucid intervals, with several small
feedings being desirable in some cases compared
to few large feedings.
46

47. Nonpharmacological treatment
 Explanations and reassurance that the medical
team is working together to find the cause of the
delirium may also be helpful. Providing sufficient
and consistent staffing for the delirious patient
also assists in orienting, educating, and protecting
the patient.
 Education about delirium management empowers
staff with an approach to take with patients who
have delirium and their families.
 The psychosocial interventions deepen rapport
with the patient and family and move the
treatment goals forward by improving adherence
and satisfaction.
47

48. Environment
 Attention should be paid to providing the appropriate
level of stimulation and orienting cues.
 Orienting cues include a large clock, calendar, well-
lit room, and provision of eyeglasses and hearing
aides if they are required.
 Darkening the room at night to help with the sleep–
wake cycle is also important. Objects from a
patient's residence may also assist with orienting
and soothing the patient.
 If friends and family are available to assist with
orienting the patient, every effort should be made to
involve them in the treatment.
48

49. Family or Companions
 A cooperative family member may stay with
the patient to provide orientation cues,
reassurance to the patient, and observational
data to the nurses and physicians.
• Restraints
Physical restraints are overused
to manage delirious, agitated
patients.
Several studies point toward
restraint use as an aggravating
factor in the escalation of
agitation.
49

50. Patient and Family Education
 During the delirious episode, families can be
educated as to appropriate ways to be supportive
to the patient, as well as to what information is
important to convey to the medical team.
 As the delirium symptoms resolve, the patient and
family should be educated about the long-term
prognosis.
 The knowledge about delirium's risk of increased
mortality and functional and cognitive decline may
be shared with the patient and family as clinically
appropriate.
50

51. Treatment of Specific Etiologies of
Delirium
 Anticholinergic Intoxication
 Anticholinergic poisoning almost always results in
delirium and is often accompanied by physical
agitation and visual hallucinations.
 Use of cholinesterase inhibitor, such as
physostigmine, has been shown to reduce the
severity of the delirium but requires repeated dosing
because of a short half-life.
 In a comparison study of physostigmine and
benzodiazepines for anticholinergic poisoning, the
physostigmine was effective.
51

52. Cont…..
 Substance Intoxication
 Substance intoxication with alcohol, benzodiazepines,
opiates, or mixed compounds requires attention to the
acute management of the airway and vital organ
functioning.
 The primary concern in managing a patient with
substance intoxication is supportive.
 For benzodiazepine ingestions, the benzodiazepine
receptor antagonist flumazenil may be helpful; however,
repeated administrations might be required
 Opiate intoxication may cause respiratory suppression in
addition to delirium. Reversal with naloxone ,naltrexone
may be considered with adequate support and
monitoring of the cardiovascular and respiratory status.
52

53. Cont…..
 Substance Withdrawal
 Alcohol and benzodiazepine withdrawal are treated by
replacing the offending agent with a benzodiazepine
and gradually reducing the dosage of the medication.
 Benzodiazepine detoxification is often performed at a
slower rate than alcohol detoxification owing to the
longer half-life of most benzodiazepines compared to
alcohol.
 In addition to delirium, opioid withdrawal has a
significant risk of physical discomfort to patients.
Symptomatic treatment with medications such as
clonidine is aimed at targeting GI distress, autonomic
changes, and craving.
53

54. How do we prevent it?
 Identify high risk patients
 Do cognitive assessment as routine
 reduce bad drugs
 maintain adequate analgesia
 maintain Oxygenation, etc
 try not to move patients
 use the same nurse if possible
 familiar things - pictures from home, clothes,
books
54

55. Is it really that bad?
 Increased nursing care.
 Increased length of stay.
 Increased risk of cognitive decline .
 Increased risk of functional decline
 Increased mortality Delay in postoperative
mobilization Prevention of early rehabilitation.
 Increased need for home care services .
 Increased distress to caregivers Barrier to
psychosocial closure in terminally ill patient.
55

56. What we need to remember about
delirium
 Confusion with altered Concentration +
Consciousness.
 Lots of Risk factors – dementia and blindness.
 Look for and treat underlying causes.
 Get history from family/friends..
 Avoid iv lines, catheters, changing rooms.
 Try familiar items, companions.
 Undetectable in 30 to 60 percent cases.
 Remember sedatives can make it worse!
56

57. Add life to years, not years to life.
THANK YOU.
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