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

ii.

Endothelin activation

iii.

Liberation of hemoglobin results in the scavenging of nitric oxide.

d.Vasospasm is one of the main factors resulting in death or disability after an acute SAH, aside from

initial ictus.

H.Treatment Considerations (Stroke 2023;54:314-70)
1

Surgical management to prevent rebleeding and β€˜secure’ aneurysm

Craniotomy and aneurysm clipping

Endovascular aneurysm coiling

2Agents for preventing vasospasm or delayed ischemic neurologic deficits

Nimodipine (Br Med J 1989;298:636-42)

Is a β€œcerebrovascular-specific” lipophilic dihydropyridine calcium channel blocker

ii.

60 mg orally or by tube every 4 hours Γ— 21 days (dose reduction 30 mg every 2 hours may be

considered if 60 mg dose intolerable): The clinical impact of dose reducing or discontinuing

nimodipine because of hypotension is not well understood but may be associated with

unfavorable outcomes (Neurocrit Care 2016;25:29-39).

iii.

Only U.S. Food and Drug Administration (FDA) label-approved medication to reduce delayed

ischemic neurologic deficits associated with SAH

iv.

Clinical trials did not show a large effect of nimodipine on the occurrence of vasospasm (though

the incidence of delayed ischemic neurologic deficits were significantly less).

Possibly neuroprotective

vi.

Administration issues in patients who require enteral doses – Black box warning against

inadvertent intravenous administration if nursing staff extract nimodipine from the gel capsule

at the bedside.

vii.

Nursing should be prohibited from extracting the gel inside the nimodipine capsule for bedside

administration (may increase the risk of inadvertent intravenous administration, incomplete

extraction from the capsule) (Neurocrit Care 2015;22:89-92).

viii.

There is a commercially available liquid product that is for use in patients with swallowing

difficulty or feeding tubes. Pharmacy compounding of nimodipine syringes from liquid

capsules has been reported but further studies are warranted to determine the optimal enteral

formulation. (Pharmacotherapy 2023;43:279-90).

Antifibrinolytic agents

Use of antifibrinolytic agents such as aminocaproic acid or tranexamic acid has been evaluated

after SAH.

ii.

Older data analyses before the advent of endovascular interventions suggested that rebleeding

is less common with these agents (primarily aminocaproic acid) but that stroke may be more

common.

iii.

More recent data analyses suggest that a short infusion (less than 72 hours) reduces rebleeding

but probably does not affect long-term outcomes.

(a)The 2023 American Heart Association SAH guidelines moderately support this strategy in

early SAH management (Stroke 2023;54:314-70)

(b)For example, use of 1000 mg of tranexamic acid intravenously every 6 hours until the

aneurysm is secured

Statins

Preservation of nitric oxide balance as heme is liberated during SAH hemolysis.

ii.

Phase II data with pravastatin and simvastatin

iii.

Phase III trial (STASH) showed no benefit of applying statins in aneurysmal SAH (Lancet

Neurol 2014;13:666-75).

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