Delirium

CAM ICU; AGITATION IN ICU

1. DELIRIUM Dr. Ram G opal M aurya 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.

4. 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%)

5. 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.

6. Risk Factors for Delirium

7. 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.

8. 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.

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

10. 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.

11. 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.

12. 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.

13. management

14. 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.

15. 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)

16. 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

17. 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 . Olanzapine Amisulpride quetiapine Risperidone Medications should be avoided in with prolonged QT intervals

18. 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 ).