CAM ICU; AGITATION IN ICU

1. DELIRIUM
Dr. Ram Gopal Maurya
MD, PDCC

2. • defined as follows: (1) A disturbance of consciousness (i.e.,
reduced clarity of awareness of the environment) with
reduced ability to focus, sustain, or shift attention. (2) A
change in cognition (e.g., memory deficit, disorientation,
language disturbance) (3) The disturbance develops over a
short period (usually hours to days) and tends to fluctuate
during the course of the day.
One group found that neurology/neurosurgical patients were
at the highest risk, followed by trauma patients, and then
medical intensive care patients. Surgical ICU patients were at
the lowest risk.

3. • Defined by Diagnostic and Statistical Manual
of Mental Disorders(DSM)-IV.
• Delirium is described in the DSM IV-TR as an
acute confusional state characterized by
fluctuating mental status, inattention, and
either altered level of consciousness or
disorganized thinking.

5. • prevalence of 20% to 80%,
• Each aditional day with delirium increases a
patient’s risk of dying by 10%.
• In one large study, mixed delirium was found
to be the mostcommon subset (54.9%), with
hypoactive somewhat less common (43.5%),
and hyperactive agitated delirium was rare
(1.6%)

6. • Delirium can be classified according to
psychomotor behavior into hypoactive delirium,
hyperactive delirium, or a mixed subtype.
Hypoactive delirium, which is the most prevalent
form of delirium, is characterized by decreased
physical and mental activity and inattention. In
contrast, hyperactive delirium is characterized by
combativeness and agitation.
• Hypoactive delirium might actually be associated
with a worse prognosis.

7. Risk Factors for Delirium

11. PATHOPHYSIOLOGY
• is poorly understood
• Neurotransmitter imbalance. Multiple
neurotransmitters have been implicated, including
dopamine (excess), acetylcholine (relative
depletion), γ-aminobutyric acid (GABA), serotonin,
endorphins, norepinephrine, and glutamate.
• Inflammatory mediators. Inflammatory mediators, such
as tumor necrosis factor alpha (TNF-α), interleukin-1
(IL-1), have been implicated in the pathogenesis of
endothelial damage, thrombin formation, and
microvascular dysfunction in the central nervous
system (CNS), contributing to delirium.

13. CLINICAL PRESENTATIONS OF
DELIRIUM
• Fluctuating levels of arousal over the day’s
course is a central hallmark of delirium and a
major diagnostic criterion.
• psychomotor agitation syndrome usually
occurs during the night hours, it has been
termed the sundown syndrome and is virtually
diagnostic of stress-induced delirium.

15. ASSESSMENT
• many scales available for the assessment of
agitation and sedation
1. the Riker Sedation-Agitation scale [ SAS]
2. the Motor Activity Assessment Scale (MAAS)
3. Richmond Agitation-Sedation Scale (RASS)
4. the Adaptation to Intensive care environment
( ATICE)
5. The Minnesota Sedation Assessment Tool
(MSAT).

18. • A number of tools have been developed to aid in
the detection of delirium in the ICU. These tools
have been validated for use in both intubated and
nonintubated patients and measured against a
“gold standard,” the Diagnostic and Statistical
Manual of Mental Disorders (DSM) criteria. The
tools are the Confusion Assessment Method for
the ICU (CAM-ICU) and the Intensive Care
Delirium Screening Checklist (ICDSC).
• A meta-analysis of studies involving these
methods demonstrates a higher sensitivity and
specificity for the CAM-ICU.

19. CAM-ICU
• To perform the CAM-ICU,
patients are first evaluated
for level of consciousness;
patients who respond to
verbal commands (a RASS
score of −3 or higher level
of arousal) can then be
assessed for delirium. The
CAM-ICU comprises four
features: (1) a change in
mental status from
baseline or a fluctuation in
mental status, (2)
inattention, (3)
disorganized thinking, and
(4) altered level of
consciousness.

20. ICDSC
• A score of 4 or above
indicates delirium,
while 0 indicates no
delirium. Patients with
scores between 1 and
3 are considered to
have subsyndromal
delirium,
• which has worse
prognostic
implications than the
absence of delirium
but a better prognosis
than clearly present
delirium.

22. management

25. • The use of ABCDEs (Awakening and Breathing
Trials, Choice of appropriate sedation,
Delirium monitoring and management, and
Early mobility and Exercise) has been shown
to decrease the incidence of delirium and
improve patient outcome.
• IWATCHDEATH and DELIRIUM mnemonics can
be particularly helpful in guiding this initial
evaluation.

26. Pharmacological Treatment of
Delirium
• Anti-Psychotics : Haloperidol (used by 75–80% of
intensivists) and atypical anti-psychotics (used by
35–40% of intensivists) have emerged as the
standard pharmacological treatments for delirium
in the ICU.
• The main mechanisms of action of
haloperidol are thought to be antagonism at
cortical dopamine (D2) receptors [78–81],
nigrostriatal pathway D2 blockade, and
disinhibition of acetylcholine (i.e.,
acetylcholine increase)

27. • haloperidol binds with a high affinity at D2
receptors, relatively low affinity at D1 receptors,
and it exhibits little adrenergic or muscarinic
activity compared to lower potency neuroleptics.
• Haloperidol is administered intravenously or
intramuscularly in the critical care setting [86].
Both methods have high bioavailability (~100%).
the mean half-life of haloperidol is 21 hours. It is
extensively metabolized by the liver.
• Common doses for ICU patients range from 4 to
20 mg/day

28. • Atypical Anti-Psychotics : typical anti-psychotics may be
as efficacious for delirium and were associated with
less EPS or side effects compared with haloperidol and
other neuroleptic anti-psychotics .
1. Olanzapine
2. Amisulpride
3. quetiapine
4. Risperidone
• Medications should be avoided in with prolonged QT
intervals

29. Alpha-2 Agonists: Clonidine and
Dexmedetomidine
• The alpha-2 agonists, such as
dexmedetomidine, have gained popularity in
their use due to decreased respiratory
suppression and recent trials demonstrating
reduced delirium prevalence as compared
with GABA-ergic drugs (e.g., benzodiazepines).