This paradoxical hyperglycemia likely reflects the complex metabolic milieu of resuscitation, including: (1) exogenous dextrose administration (2 mL/kg of 10% solution glucose bolus); (2) endogenous catecholamine release during asphyxia and resuscitation, which stimulates hepatic glycogenolysis and gluconeogenesis while inducing insulin resistance; (3) delayed cellular glucose uptake due to asphyxia-induced metabolic suppression and impaired insulin signaling; and (4) the pharmacodynamics of intravenous porcine insulin in the setting of critical illness. This evidence concerns the gene INS and Hyperglycemia.