Delirium is an acute confusional state that commonly occurs in the ICU. It can be hyperactive, hypoactive, or mixed. Delirium increases mortality, length of stay, costs, and long-term cognitive impairment. It results from neurotransmitter imbalances and higher cortical dysfunction exacerbated by predisposing patient factors and precipitating insults like medications and critical illness. Screening tools like ICDSC and CAM-ICU can help diagnose delirium which non-pharmacological prevention bundles, reducing deliriogenic medications, and treatments like haloperidol or dexmedetomidine may help address.

1. Delirium in ICU
Dr.Tinku Joseph
DM Resident
Department of Pulmonary Medicine
AIMS, Kochi.
Email: tinkujoseph2010@gmail.com

2. Overview
 What is delerium ?
 How is it categorised?
 Why does it matter?
 Why does it happen?
 How do we diagnose/monitor it?
 How do we prevent and treat it?

3. What is Delirium?
An acute confusional state
with:
Fluctuating mental status
Disordered attention
Disorganised thinking or altered
consciousness

4.  DSM –IV definition:
 “A disturbance of consciousness with
inattention accompanied by a change in
cognition or perceptual disturbance that
develops over a short period (hours to
days) and fluctuates with time”
What is Delirium?
Synonyms:
ICU psychosis, septic encephalopathy, ICU
syndrome, acute brain failure, acute confusional
state

5.  Delirium develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
Delirium is typically caused by a:
 Medical condition
 Substance intoxication
 Medication side effect.
What is Delirium?

6. How is Delirium Categorized?
HyperactiveHyperactive
HypoactiveHypoactive
MixedMixed
1.6% of cases, “ICU psychosis”,
agitation, restlessness, pulling lines and
tubes emotional lability
1.6% of cases, “ICU psychosis”,
agitation, restlessness, pulling lines and
tubes emotional lability
54.1% % of cases54.1% % of cases
43.5% of cases, “encephalopathy”,
often unrecognized, withdrawal,
apathy, lethargy, decreased
responsiveness, may be misdiagnosed
as depression.
Far more common, likely due to
sedating medications
43.5% of cases, “encephalopathy”,
often unrecognized, withdrawal,
apathy, lethargy, decreased
responsiveness, may be misdiagnosed
as depression.
Far more common, likely due to
sedating medications

7. Why does delirium matter?
 Increased reintubation risk (OR=3)
 Increased ICU & hospital stay* (up to 10 days extra)
 Each day in delirium increases risk of longer stay by 20%
 Increased mortality in ICU & out to 6 months** (OR=3)
 Each day spent in delirium increases risk of death by 10%
 Increased ICU & hospital costs***
 10-24% risk of long-term cognitive impairment
 Increased dementia risk
 Reduced functional status at 3 & 6 months
* Ely et al, Intensive Care Med 2001; 27: 1892-1900 ** Ely et al, JAMA 2004; 291: 1753-62 *** Milbrandt et al, CCM 2004; 32: 955-62

9. Why does delirium happen?
 Higher cortical dysfunction (on functional neuroimaging)
 Pre-frontal cortex, non-dominant posterior parietal regions,
anterior thalamus, basal ganglia, temporal-occipital cortex
 Neurotransmitter dysfunction
 Reduced acetylcholine levels – blockade or deficiency
 Endogenous anticholinergic substances
 Opiates/hypoxia/inflammation
 Serotonin fluctuation
 Dopamine excess
 Glutamate excess (2o
to IFN-γ, LPS, hypoxia, hypoglycaemia)
 Predisposition (baseline vulnerability)
 Precipitants (clinical, iatrogenic, organisational risk factors)

10. Why does delirium happen?
Serotonin
Acetylcholine
Dopamine
Serotonin
Acetylcholine
Dopamine
Opioids & benzo’sOpioids & benzo’s
2o
cerebral infection2o
cerebral infection
Decreased cerebral
metabolism
Decreased cerebral
metabolism
1o
intracranial
disease
1o
intracranial
disease
Systemic diseaseSystemic disease
HypoxiaHypoxia
Metabolic
derangement
Metabolic
derangement
Withdrawal
syndromes
Withdrawal
syndromes
ToxinsToxins

11. Predisposing factors (host factors)
 Present before ICU admission
1. Age
2. Alcoholism
3. Smoking
4. Hypertension
5. Apolipoprotein 4 polymorphism
6. Cognitive impairment
7. Hearing/visual impairment
8. Depression
Risk factors

12. Precipitating factors.
 Occur during course of critical illness
 May involve factors of acute illness or
be iatrogenic;

13. Factors of critical illness
1. Acidosis
2. Anemia
3. Infection/sepsis
4. Hypotension
5. Metabolic disturbances
6. Respiratory disease
7. High severity of illness
Iatrogenic factors
1. Immobilization
2. Medication (opoids,
BDZ)
3. Sleep disturbances

14. Modifiable Risk factors

15. AgeAge
SeveritySeverity
Benzo’sBenzo’sPun & Ely, Chest 2007; 132: 624–636
Pandharipande et al, Anesthesiology 2006; 104: 21-26

16. DELIRIUM(S) - causes
 DD Drugs, dementia
 E Eyes & ears (poor vision and hearing)
 L Low O2 states (CHF, COPD, ARDS, MI, PE)
 I Infection
 R Retention (urine and stool)
 I Ictal states
 U Underhydration/undernutrition
 M Metabolic upset
 (S) Subdural, sleep deprivation

17. I WATCH DEATH
 I Infection
 W Withdrawal (alcohol, sedatives, barbiturates etc.)
 A Acute metabolic (acidosis, alkalosis, electrolytes)
 T Trauma (closed head injury, haematoma etc.)
 C CNS pathology (seizures, stroke, encephalitis)
 H Hypoxia
 D Deficiencies (thiamine, niacin, B12, folate)
 E Endocrinopathies (thyroid, glucose, adrenal)
 A Acute vascular (hypertensive crisis, arrhythmia)
 T Toxins/drugs
 H Heavy metals

20. Diagnosis & monitoring
 Intensive Care Delirium Screening Checklist (ICDSC)
and the Confusion Assessment Method for the ICU
(CAM-ICU)
 Using ICDSC, each patient is assigned a score from 0 to
8; a cut-off score of 4 has sensitivity 99% and
specificity 64% for identifying delirium

22.  CAM-ICU has a more modest
sensitivity ranging from 64% to
81%, high specificity from 88%
to 98%.
Diagnosis & monitoring

27.  S100B protein indicator of glial activation and/or
death. Shown to be elevated in patients with delirium.
 Higher baseline levels of procalcitonin or C-reactive
protein were associated with more days with delirium.
 Other biomarkers elevated-brain-derived
neurotrophic factor, neuron-specific enolase,
interleukins, cortisol.
Biomarkers

28. What should we do to prevent/treatWhat should we do to prevent/treat
delerium in ICU patientsdelerium in ICU patients

29. Treating/Preventing delirium
 Monitoring
 Non-pharmacological
interventions
 Reduction in deliriogenic
medications
 Pharmacological interventions

30. Environmental factors
 Extremes in sensory impairmentExtremes in sensory impairment
eg: hypothermia.eg: hypothermia.
 Deficits in vision or hearingDeficits in vision or hearing
 Immobility or decreased activityImmobility or decreased activity
 Social isolationSocial isolation
 Novel environmentNovel environment
 stressstress

31. A bundle for delirium prevention ??
 Family support (all levels, kids, children)
 Allow family at bed side when ever possible

32.  Orientation improvements:
Day lights, wall clocks,
exterior view from ICU.
 Privacy for patients.
 Hearing aid
 Glasses
 Television/ Music therapy
 Proper sleep
A bundle for delirium prevention ??

35. Role of doctor & Nursing staff
 Introduce yourself, smile and be
friendly with patients.
A bundle for delirium prevention ??

36. Treating/Preventing delirium
Non-pharmacological (Summary)
 Up to 40% risk reduction achieved
 Repeated reorientation of patients
 Early mobilization
 Visual and hearing aids (and wax removal!)
 Early catheter, line etc. removal
 Minimize restraints and sedatives
 Sedation Interval
 Sleep protocol
 Delirium bundle

37.  First address complication of critical illness that may
lead to delirium (hypoxia, hypercapnia, hypoglycemia,
shock, electrolyte imbalances)
 Any drug intended to improve cognition may have
adverse psychoactive effects thus paradoxically
exacerbating delirium.
Pharmacological treatment

38.  Haloperidol recommended as drug of choice for treatment
of ICU delirium by SCCM
 Blocks D2 dopamine receptors, resulting in amelioration
of hallucinations, delusions, unstructured thought patterns
 SCCM guidelines-hyperactive delirium to be treated with
2 mg intravenously, followed by repeated doses (doubling
previous dose) every 15 to 20 minutes while agitation
persists
Haloperidol

39.  Once agitation subsides scheduled doses (every 4 to 6
hours) may be continued for few days, followed by
tapered doses for several days.
 Common doses for ICU patients range from 4 to 20
mg/day
 Adverse effectsAdverse effects – extrapyramidal, prolonged QTc,– extrapyramidal, prolonged QTc,
torsades (3.8%), neuroleptic malignant syndrometorsades (3.8%), neuroleptic malignant syndrome
Haloperidol

40. Treating delirium – atypical antipsychotics
 Olanzepine, quetiapine, risperidone
 Alter multiple neurotransmitters
including DA, NA, serotonin, ACh,
histamine
 Suggestion of decreased
extrapyramidal side-effects compared
to haloperidol
 As effective as haloperidol

44.  Dexmedetomidine, novel α2- receptor agonist that does
not act on GABA receptors, may to be alternative
sedative agent less likely to cause delirium.
 Pandharipande P. et al (2007) showed ICU patients
sedated with dexmedetomidine spent fewer days in
coma and more days neurologically normal than
lorazepam.
 Benzodiazepines are not recommended for management
of delirium
Dexmedetomidine

49. Conclusion
 Delirium is a frequent disease in the
ICU and associated with poor
outcomes.
 Delirium is often under recognized, can
be monitored and rapidly identified.
 New approaches to manage and prevent
delirium are emerging everyday.
 Dexmedetomidine has a place in this
new strategies.