Hemodynamic Instability in Hypoxic Ischemic Encephalopathy: More Than Just Brain Injury-Understanding Physiology, Assessment, and Management.

Hypoxic-ischemic encephalopathy (HIE) can have both transient and long-lasting effects on the neonate, including neurologic, renal, cardiac, hepatic, and hematologic. Both the disease process and the treatment option of therapeutic hypothermia can result in hemodynamic instability. Understanding the effects of HIE on the neonatal myocardium, pulmonary vascular bed, and the cardiac dysfunction that can occur is key to managing infants with HIE. This article focuses on causes of hemodynamic instability in neonates following perinatal asphyxia and how to recognize hemodynamic compromise. It reviews the underlying pathophysiology and associated management strategies to improve hemodynamics and potentially improve outcomes.

Glucose Homeostasis and the Neonatal Brain: A Sweet Relationship.

Glucose is the primary substrate for energy metabolism in the brain and although the brain is dependent on a constant glucose supply for normal function, both local energy stores and the supply of alternate substrates are limited. In utero, the placenta provides a continuous supply of glucose to the fetus while transition to extrauterine life marks an abrupt change in substrate delivery and a major change in glucose metabolism where insufficiencies and disruptions can occur. Hypoglycemia is one of the most common biochemical disturbances in the neonatal period, affecting a wide range of neonates. Prolonged or persistent low plasma glucose concentrations can lead to neonatal brain injury and abnormal neurological outcomes. This article discusses fetal and neonatal metabolic adaptation, the physiology of glucose homeostasis, hypoglycemic brain injury (HBI), and neurodevelopmental long-term outcomes.