sedation in neurocritical care unit

Sedation in neurocritical care unit

Dr. Tushar KumarDA, DNB

PDCC- Neuroanesthesia

Why sedate my patient:

• To control intracranial pressure (ICP) and cerebral perfusion

pressure and decrease the cerebral rate of oxygen utilization

• Blunt central hyperventilation.

• Refractory status epilepsy .

• Patients with traumatic brain injury (TBI)

• To alleviate pain

• Delirium and agitation

What is sedationConscious sedation:Minimally depressed levels of consciousness that retains the patients

ability to independently and continuously maintain an airway and respond appropriately to physical stimulation or verbal command that is produced by pharmacological or non pharmacological or a combination of both.

Sedation in context with neurocritical patients:Defined as incremental reduction in level of consciousness to maintain

a state of amnesia, hypnosis and analgesia, from which patients can be readily recruited to participate in a comprehensive neurological examination.

Sedation practices in the Neurocritical Care Unit Abhijit Lele1, Michael Souter1; 2016 Journal of Neuroanaesthesiology and Critical Care,2

Causes of agitation

• Pain

• Raised ICP

• Hypoxia

• hypercarbia,

• hypoglycaemia

• symptom of drug or alcohol withdrawal

Drugs causing delirium & agitation:

• Benzodiazepines

• Opiates (especially meperidine)

• Anticholinergics

• Antihistamines

• H2 blockers

• Antibiotics

• Corticosteroids

• Metoclopramide

Consequences of inappropriate sedation:

Over sedation: ‑1. Confounding neuro assessment,

2. Need for frequent neuroimaging studies

3. Delayed emergence

4. Disuse atrophy of muscles,

5. Respiratory depression, hypotension, venous thrombosis,

6. Hampers mobility,

7. Increases time on ventilator & ICU length of stay and Cost.

Consequences of inappropriate sedation:

Under sedation:

1. Lead to agitation and anxiety, pain, distress.

2. Elevated ICP,

3. Tachycardia, hypertension, predispose to arrhythmias and myocardial

ischaemia.

4. Tachypnea hypocapnea causing vasoconstriction and reduced CBF.

5. Promote ventilator dyssynchrony,

6. Increased oxygen consumption

7. Wound disruption,

8. Risk and accidental removal of tubes, catheters, lines and drains.

Goals of sedation:

1. Anxiolytic

2. Analgesic

3. Reduce CMRO2

4. Reduce ICP

5. Anti convulsant‑

Assessment of sedation:

• Neurological wake up tests (NWTs) :‑ Gold standard

Frequent neuro checks to assess

neurological functioning.

• Worse outcomes if infusions are continued.

• Daily awakening trials and a need for sedation

Interruption.

Problems in de escalation of sedatives:1. Individual bias regarding agents employed

2. Fear of extubation

3. Decannulation

4. Worsening cardiac ischemia

5. Psychological distress

How to assess sedation:1. Ramsay scale

2. Observer’s assessment of alertness/sedation scale

3. Riker sedation agitation scale‑4. Motor activity assessment scale

5. Minnesota sedation assessment tool

6. Vancouver interaction and calmness scale

7. AVRIPAS (agitation, alertness, heart rate and respiration)

8. Richmond agitation sedation scale (RASS)

9. ATICE (consciousness domain and tolerance Domain)

10. The nursing instrument for the communication of sedation scale

Richmond agitation sedation scale (RASS)

Richmond agitation sedation scale (RASS)

3-step process:

1st step : Alert, restless, or agitated (0 to +4).

2nd : If the patient is not alert and does not show positive motoric

characteristics, the patient’s name is called and the sedation level is

scored, depending on the duration of eye contact (−1 to −3).

3rd : If there is no eye opening with verbal stimulation, the shoulder is

shaken or the sternum is rubbed, and the response is noted (−4 or

−5).

Ramsay sedation scale:

Depth of sedation : ASA 2014

ICU SEDATION

Pharmacological

Conventional

Nonconventional

Non Pharmacological

Benzodiapine, opioids, barbiturates, ketamine, α₂ agonist. Neuroleptics, inhalational agents.

Noise, light, music

Opioids

1. Opioids:

a. Analgesia,

b. Decreased level of consciousness,

c. Respiratory depression,

d. Miosis,

e. Gastrointestinal hypo motility and‑f. Vasodilatation.

Opioids• Acts on opioid receptors (mu (μ), delta (λ), kappa (κ)). • Have central and peripheral effects as agonists, partial

agonists, and mixed agonist-antagonist.• Dose:

• High doses can induced seizure-like activity & myoclonus.

Benzodiazepines

1. Most commonly used drugs

2. Anxiolysis (20% receptor blockade)

3. Sedation (30 50%)‑4. Anterograde amnesia and hypnosis (60% receptor blockade)

5. Muscle relaxation, respiratory depression and anticonvulsant

activity

6. Acts by potentiation of the inhibitory neurotransmitter – ϒ

aminobutyric acid (GABA)

Benzodiazepines• Additive or synergistic effects with other agents

• They decrease the level of consciousness, suppress respiratory drive, or

decrease blood pressure.

• Dose:

• lorazepam has propylene glycol as diluent.

• If infused > 1 mg/kg/day) Propylene glycol toxicity can cause anion gap

metabolic acidosis and acute renal failure, as well as central nervous

system depression or seizures.

• May cause frank delirium.*Sedation in neurological intensive care unit; Birinder S. Paul, Gunchan Paul; Annals of Indian Academy of Neurology, April-June 2013, Vol 16, Issue 2

Intravenous anesthetic agents:

• Propofol :

• sedative and hypnotic

• rapid onset and offset of action

• reduces ICP

• Propofol infusion syndrome” infusion >48 h of high doses

(>80 μg/kg/min)

• high clearance rate

Propofol:

• calorie content (900 cal/Lt) should be considered whenever it

is administered along with parenteral nutrition.

• lacks analgesic effects

• Hypotension and myocardial depression,

• pain on injection

• anaphylactoid reaction.

• Dose:

Propofol:

• Target Controlled Infusion

Propofol is administered via an infusion pump. Patient’s body

weight is entered.

Propofol concentration required in the patient’s blood,

instead of setting the dose rate.

• Optimum depth of sedation in a range of 0.3 4.0 mg/kg/h.‑

Target control infusion pump:

Thiopentone

• Dose dependent sedative, hypnotic, or anesthetic action. ‑• Anticonvulsant and cerebro protective properties.‑• The only indications of continuous infusion of

thiopentone are in the management of refractory status

epilepticus and reduction of refractory intra cranial

hypertension

Thiopentone

Have zero order kinetics.

• Can cause myocardial depression and immunosupression.

• Bronchospasm, Cough, Laryngospasm,

• Angiodema,

• Loss of airway reflexes

• Respiratory depression.• Dose:

α2‑agonists• Presynaptic inhibition of descending noradrenergic activation of

spinal neurons

• Activation of postsynaptic alpha-2 adrenergic receptors coupled

to potassium-channel

• Activating G-proteins : Analgesia, sedation, and anxiolysis.

• Multiple therapies can be avoided

• Arousability is maintained at deeper levels of sedation.

• At higher doses respiratory is maintained.

• But only recommended for 24 hr infusion due to lack of evidence.

α2‑agonists• Dose:

• Cause bradycardia and hypotension specially during the initial

loading period.

• Treatment is supportive and decreased or discontinuation of

the infusion, IV fluids, vesopressors, or vagolytics.

Ketamine

• Phencyclidine derivative

• A non competitive N methyl D aspartate receptor antagonist‑ ‑ ‑ ‑• Causes functional and electrophysiological dissociation

between the thalamo-neocortical and limbic systems.• “sensory isolation”: potent analgesic, sedative, and amnestic• properties.

• Negative effects on CMRO2, CBF and ICP not very popular

• ketamine (dose range of 1.5–3 mg/kg)

Ketamine• Reduce ICP in patients with traumatic brain injury

• CPP, jugular oxygen saturation and middle cerebral artery

blood flow remains almost same.

• Used to facilitate routine bedside procedures.

• Provide good analgosedation after major spine surgeries.

• Opioid sparing effect.‑• Psychomimetic (emergence) phenomenon

• Hypersalivation nausea & vomitting.

Drugs for seadtion:Neuroleptic agents

• Haloperidol / Quetiapine:

• Anti-psychotic

• Central dopaminergic D2 blockade.

• Diminished motor activity, anxiolysis, and indifference to the

external environment.

• Postoperative psychosis and delirium

• Profound sedation with minimal respiratory depression.

Neuroleptic agentsAdverse effects:

a. ECG Changes

b. Hypotension

c. Neurolept malignant syndrome

d. Increased prolactin secretion

e. Larynospasm and bronchospasm.

f. Anticholinergic effects

Sedation and Analgesia in Critically Ill Neurologic Patients John J. Lewin III ; 2013 Neurocritical Care Society Practice Update

Role of Neuromuscular blocking agents

• Do not provide sedation:

Indications include:

1. Invasive ventilation modes

2. Control of ventilation in those with a high respiratory drive

3. Reduction of oxygen consumption in critically hypoxaemic

patients

4. Control of raised intracranial pressure.

Inhalational agents for sedation

• Isoflurane, sevoflurane and desflurane

• Increase CBF and cause cerebral vasodilatation

• Reduce CMRO2

• Burst supression

• logistic challenges

• Inhalational conserving systems AnaConDa® have been used

for sedation in Neurocritical Care Unit.

Isoflurane ; MAC 2

Sevoflurane; MAC4

Inhalational agents for sedation• Ana Con Da : anaesthetic conserving devices.

• Designed to deliver isoflurane and sevoflurane in mechanically

ventilated patient.

• Small device placed between ET tube and Y piece.

• AnaConDa® : Modified heat moisture exchanger (HME).

• Low dead space: 100 mL and can be used with any standard ICU

ventilator.

A review of the practice of sedation with inhalational anaesthetics in the intensive care unit with the AnaConDa® device:Satyajeet Misra, Thomas Koshy; 2012; 56: 6; 518-523.

Ana Con Da: About the device

• Miniature porous evaporator rod that converts the volatile

anaesthetic agent from liquid to vapour state.

• The liquid anaesthetic agent is continuously infused into the

evaporator by an infusion pump incorporating a syringe

system.

• Activated carbon fibres in HME adsorb, store and release the

anaesthetic vapours.

Ana Con Da: The device

Ana Con DaAnaesthetic conserving device:


Start of expiration:

Expiration:


Inspiration:

Benefits of volatile anaesthetic agents:

1. Rapid onset, rapid recovery.

2. Hemodynamics are well maintained.

3. Cerebroprotective.

4. Does not require circle absorber so No risk of compound A

formation.

5. Opioid sparing action

6. Active Gas Scavenging is Unnecessary When Using the

AnaConDa Volatile Agent Delivery System*

* Active Gas Scavenging is Unnecessary When Using the AnaConDa Volatile Agent Delivery System;Hosnieh Djafari Marbini; JICS; 2014.

Drawbacks:

a. Change every 24 hrs

b. Mild hypercapnea

c. Slight increase in dead space

d. Autopumping: lead to severe overdose.

e. Technical difficulty: colour coding and marked "Not for

IV use”

Sedation holidays:

Involves stopping the sedative infusions and allowing the

patient to wake.

The infusion is restarted once the patient is fully awake and

obeying commands or until they became uncomfortable or

agitated.

Ideally, this should be performed on a daily basis

To reduce incidence of delirium

Delirium:• Delirium is an acute disturbance of consciousness accompanied

by inattention, disorganized thinking, and perceptual disturbances that fluctuates over a short period of time.

• 20 – 80 % in ICU patient suffers from delirium

• Makes neurological examination impossible

• Types: Hypoactive deliriumHyperactive delirium

Phathophysiology:

• Neurotransmitter imbalance.

• Inflammatory mediators (TNF-α), IL-1, and other cytokines and

chemokines.

• Impaired oxidative metabolism

• Large neutral amino acids.

Risk factors:

Nonpharmacological methods:To promote sleep in ICU:

• Modification of the patient's local environment and reduction of

unnecessary noise.

• Sleep occurs best below 35 Db

• A noise level of 80 dB will cause arousal.

• Lighting of the bed space to mimic the day–night orientation is helpful.

• Targeted music therapy : Decrease heart rate, ventilatory frequency,

myocardial oxygen demand, anxiety scores, and improve sleep.

Prolonged sedation

1. Over sedation‑2. Hemodynamic

instability

3. Prolonged duration of

intubation and ICU

stay.

1. Renal and hepatic

dysfunction

2. Drug-drug interactions,

3. Shock

4. Hypoproteinemia.

5. Active metabolites

Prolonged sedation:

Avoid accumulation and oversedation by:

a. Patient targeted sedation protocol‑

b. Wake up call‑

How to balance sedation:

Analgosedation in ICU has no fixed cook book formula.

Combination of evidence based intervention‑

ABCDE bundle

• A-Spontaneous awakening trial

• B-Spontaneous breathing trial

• C-Choice of sedation

• D-Delirium monitoring

• E-Early mobility and exercise

Sedation regimens for specific situation:

1. Raised ICP:

a. Target : Quiet and motionless

Ramsey level 5 or 6.

b. Preferred sedative : Fentanyl (1 3 μ‑ g/kg/h)

+

Propofol (0.3 3 mg/kg/h)‑

Sedation in neurological intensive care unit; Birinder S. Paul, Gunchan Paul; Annals of Indian Academy of Neurology, April-June 2013, Vol 16, Issue 2


2. Patients receiving ventilator therapy:

a. Target : sedation with relaxation

b. preferred sedative :

– Morphine 2 5 mg IV1 4 h‑ ‑– Fentanyl 0.5 3.0 μ‑ g/kg/h

– Propofol 0.6 6 mg/kg/h‑– Midazolam 0.05 0.1 mg/kg/h‑


Non ventilated patients:‑• Patient controlled analgesia. ‑• Patient controlled narcotic delivery systems ‑• intravenous opioids or epidural infusions of local anesthetics

or opioids.

• Animation: Early mobilization of ICU patients improve

neurocognitive and functional outcomes.


Post operative patients: ‑1. systemic (i.e., opioid and nonopioid)

2. Regional (i.e., neuraxial and peripheral)

3. Multimodal


Myasthenia gravis and other neurological disease:

Common sedative used: Propofol

Benzodiadepines

Opioid

The myasthenia gravis pt should be carefully monitored with

electromyogram or mechanomyogram.

Road map to sedation in ICU:

Summary :

• Physiological derangements

• Require long duration of analgesic and sedative therapy.

• Rapid onset / rapid recovery

• Predictable dose response,

• lack of drug accumulation and toxicity.

• Serial neurological examinations

Recent studies:

A meta analysis done on 1994 patients included 16 randomised

control patients.

Studied on lorazepam, midazolam, propofol and

dexmedetomidine showed that it decreases ICU length of

stay, mechanical ventilation duration and delirium occurrence.

THANK YOU

sedation in neurocritical care unit

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