Objectives: Aneurysmal subarachnoid hemorrhage often leads
to death and poor clinical outcome. Injury occurring during the
first 72 hours is termed “early brain injury,” with disruption of the
nitric oxide pathway playing an important pathophysiologic role in
its development. Quantitative electroencephalographic variables,
such as α/δ frequency ratio, are surrogate markers of cerebral
ischemia. This study assessed the quantitative electroencephalographic
response to a cerebral nitric oxide donor (intravenous
sodium nitrite) to explore whether this correlates with the eventual
development of delayed cerebral ischemia.
Design: Unblinded pilot study testing response to drug intervention.
Setting: Neuroscience ICU, John Radcliffe Hospital, Oxford,
United Kingdom.
Patients: Fourteen World Federation of Neurosurgeons grades 3,
4, and 5 patients (mean age, 52.8 yr [range, 41–69 yr]; 11 women).
Interventions: IV sodium nitrite (10 μg/kg/min) for 1 hour.
Measurements and Main Results: Continuous electroencephalographic
recording for 2 hours. The alpha/delta frequency ratio was
measured before and during IV sodium nitrite infusion. Seven of 14
patients developed delayed cerebral ischemia. There was a +30% to
+118% (range) increase in the alpha/delta frequency ratio in patients
who did not develop delayed cerebral ischemia (p < 0.0001) but an
overall decrease in the alpha/delta frequency ratio in those patients
who did develop delayed cerebral ischemia (range, +11% to –31%)
(p = 0.006, multivariate analysis accounting for major confounds).
Conclusions: Administration of sodium nitrite after severe subarachnoid
hemorrhage differentially influences quantitative
electroencephalographic variables depending on the patient’s
susceptibility to development of delayed cerebral ischemia. With
further validation in a larger sample size, this response may be
developed as a tool for risk stratification after aneurysmal subarachnoid
hemorrhage.
CORE (COnnecting REpositories)
CORE (COnnecting REpositories)