Index
Module 10 • Neurology
Neurocritical Care
36%
Data Tables
Neurocritical Care
Keaton S. Smetana ~3 min read Module 10 of 20
19
/ 53

Neurocritical Care

In contrast to midazolam, propofol is advantageous because of its short half-life and relative lack

of residual sedative effects.

2Benzodiazepines

Not preferred because of long duration of action

Also associated with delirium and cognitive impairment

Potential for withdrawal effect, seizures

3

Dexmedetomidine

No specific considerations in existing guidelines for neurocritical care patients

Hypotension risk may be harmful in specific patient types (e.g., aneurysmal SAH/vasospasm, TBI,

SCI).

May be particularly helpful in patients with paroxysmal sympathetic hyperactivity (PSH)

(β€œstorming”) and facilitating extubation, managing alcohol withdrawal, and sedation requiring

frequent neurologic assessments (DEXPRONE study; J Crit Care 2020;60:79-83)
E.Neuromuscular Blockade
1

Mechanism of action: Decreased systemic oxygen delivery needs; reduced coughing

Neuromuscular blockers have no intrinsic value for reducing ICP, but they may be helpful in select

patients with specific issues that exacerbate ICP elevations.

Prevention of cough, ventilator dyssynchrony (both increase ICP)

ii.

Control Pco2 (increased Pco2 may also increase ICP)

Prevention of shivering during therapeutic hypothermia or targeted temperature management

Reduces intrathoracic pressure

d.May be essential in patients requiring high positive end-expiratory pressure (increased intrathoracic

pressure may increase ICP)

2Various agents may be useful – Depends on patient organ function, prescriber preference

Vecuronium/Rocuronium (particularly if normal organ function)

Cisatracurium (particularly if end-organ dysfunction)

Avoid atracurium, if possible, because of hypotension risk. Laudanosine, a hepatically metabolized

product of Hofmann elimination, is a CNS stimulant that can accumulate with prolonged use.

3

Monitor by train-of-four (goal 1-2/4 twitches with no clinical evidence of neuromuscular function [e.g.,

overbreathing the ventilator rate]).

F.

Metabolic Suppression (pentobarbital)

1

Mechanism of action: Suppression of electrical activity in brain (i.e., β€œburst suppression”) causes

reduced cerebral metabolic rate of oxygen (CMRO2).

2Reduced CMRO2 leads to decreased cerebral blood volume.
3

Pentobarbital sodium is usually used in the United States (thiopental in Europe). When pentobarbital

is initiated, all other sedatives and paralytics should be weaned off after burst suppression is achieved.

4

Risks may outweigh benefit, at least for certain conditions such as large hemispheric infarction.

5

Pentobarbital is no more effective and is potentially more harmful for first-line therapy for ICP control

than mannitol – Early studies led clinicians to begin using pentobarbital only in patients with refractory

ICP elevations (Can J Neurosurg 1984;11:434-40).

6

Typical pentobarbital dosage

25–30 mg/kg intravenous loading dose. Usually given as 10 mg/kg Γ— 1 dose, followed by 5 mg/kg

every hour Γ— 3 or 4 doses to avoid hypotension with large bolus dose

1- to 5-mg/kg/hour infusion after loading dose

7

Titration

Titrated to goal ICP (usually less than 20 mm Hg)

HD Video Explanation β€” Synchronized with PDF
Starts at: minute 18 Open on YouTube