Vasoplegic syndrome occurs in 8% to 12% of cases that use cardiopulmonary bypass and carries a high mortality. Although the precise cause of this shock state has yet to determined, it is postulated to be related to abnormal nitric oxide (NO)-mediated dilatation of vascular smooth muscle resulting in arterial and venous vasodilatation. Since its first report in 2014, the off-label use of hydroxocobalmin as a rescue therapy for the treatment of refractory vasodilatory shock has gained attention with a mechanism thought to be primarily mediated by the scavenge, binding to, and prevention of the formation of NO. Importantly, no dose-finding study of hydroxocobalamin for the treatment of vasoplegic shock has been published. Consequently, dosing is extrapolated from the treatment of cyanide toxicity (5 g administered by intravenous infusion over 15 min) and the hemodynamic improvement only appears to persist for a few hours when administered as a bolus. Herein we describe twelve patients with vasoplegic shock following cardiac surgery that received an extended duration infusion of hydroxocobalamin administered over a median of 6 h and illustrate the rapidity and durability of the hemodynamic response encountered.
Keywords: CYANOKIT; Hydroxycobalamine; Shock; Vasoplegic syndrome.
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