Magnesium Levels and Neurologic Outcomes in Patients Undergoing Therapeutic Hypothermia After Cardiac Arrest

Abstract

Therapeutic hypothermia (TH) improves neurological outcomes after cardiac arrest by mitigating cerebral reperfusion injury. Serum magnesium (Mg) inhibits glutamate release, restores blood–brain barrier integrity, and decreases brain edema. The neuroprotective role of Mg in cardiac arrest patients undergoing TH is not well established. We analyzed 438 survivors of cardiac arrest who completed a TH protocol from 2008 through 2016. Multivariate and receiver operating characteristic (ROC) analyses examined the association between Mg supplementation and Mg levels before, during, and after TH with neurologic outcomes. Participants were 65.5 ± 15.9 years old, 47% received bystander cardiopulmonary resuscitation, and time to target temperature was 286 ± 196 minutes. Patients with favorable neurologic outcomes had lower Mg levels at presentation (2.1 mg/dL vs. 2.2 mg/dL, p = 0.010; OR [95% CI] = 0.531 [0.329–0.857]) and more frequently received Mg supplementation (39% vs. 25%, p = 0.009; OR [95% CI] = 1.936 [1.171–3.202]). Mg levels on presentation inversely correlated with favorable neurologic outcomes (r = −0.134, p = 0.036). Stratification of patients based on Mg levels demonstrated trends toward worse neurological outcomes at the extremes of the range, though sample sizes were small and the point estimate was not significant. ROC analysis showed no significant Mg level determining favorable outcomes. Mg levels at presentation inversely correlated with neurologic outcomes in cardiac arrest survivors undergoing TH. Intracellular shift and increased renal excretion of Mg may be responsible for the low Mg levels seen in some patients undergoing TH. Whether Mg supplementation could potentiate the beneficial effects of TH remains unclear and deserves further investigation.