Index
Module 10 • Neurology
Neurocritical Care
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Data Tables
Neurocritical Care
Keaton S. Smetana ~3 min read Module 10 of 20
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Neurocritical Care

V.INTRACRANIAL PRESSURE TREATMENT
A.General Concepts
1

Elevated ICP decreases tissue perfusion and tissue oxygenation and worsens neurologic outcome.

2Monro-Kellie doctrine: ICP equals cerebral blood volume (10%) plus CSF (10%) plus brain tissue

(80%). Each therapy targeted at decreasing ICP acts on one or more of these components.

3

Most practitioners use a stepwise approach to treating elevated ICP, including the following interventions:

Head-of-bed elevation (30–45 degrees): Optimizes venous return from the brain, reducing venous

pooling

Early treatment of fever (greater than or equal to 37.8Β°C) to maintain normothermia.

Osmotherapy (mannitol or hypertonic saline)

d.Acute hyperventilation: Reduction in Pco2 to around 32 mm Hg causes a compensatory

vasoconstriction, which reduces cerebral blood volume (chronic hyperventilation should be avoided

because of complications such as stroke).

Drainage of CSF by a ventriculostomy

Sedation with or without neuromuscular blockade (avoid benzodiazepines, when possible)

Maintenance of CPP at 60–70 mm Hg

Surgical decompression or hemicraniectomy (depending on the clinical scenario)

Pharmacologic coma (pentobarbital)

Hypothermia (33Β°C–36Β°C) – Clinicians should consider the risk-benefit of moderate hypothermia

versus targeted temperature management for control of ICP.

B.Treatment Thresholds
1

Recommendations are to treat sustained (for greater than 5 minutes) ICP greater than 22 mm Hg as

measured by external ventricular drain, intraparenchymal catheter, or bolt (Neurosurgery 2017;80:6-

15). If subarachnoid hemorrhage, symptom-based dosing over ICP targets is suggested (Neurocrit Care

2020;32;647-66).

2Specific ICP threshold may have interpatient variability.
3

CPP ideally within 60–70 mm Hg

Targeting CPP greater than 80 mm Hg routinely is also associated with an increased incidence of

acute respiratory distress syndrome and mortality in patients with a TBI; thus, patients must be

selected carefully when targeting higher ranges of CPP (Crit Care Med 1999;27:2086-95).

Osmotherapy

C.Comparison of Osmotherapy Agents
Table 8. Comparison of Osmotherapy Agents

Mannitol

Hypertonic Saline

Mechanism of action

Acute increase in cerebral blood flow

results in cerebral vasoconstriction

(because of autoregulation), leading to

decreased cerebral blood volume

Increase in serum osmolality creates

osmotic gradient to pull extracellular

fluid from brain

Osmotic diuretic

Acute increase in cerebral blood flow

results in cerebral vasoconstriction

(because of autoregulation), leading to

decreased cerebral blood volume

Increase in serum osmolality creates

osmotic gradient to pull extracellular

fluid from brain

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