Introduction

Hypoxic or hypoxic–ischemic encephalopathy is the result of prolonged oxygen deprivation of the central nervous system (CNS). The pathophysiology is reasonably well understood, from extensive studies in experimental animals.[1–3] At a critical reduced level of blood flow (or oxygen delivery), the electroencephalograph (EEG) trace slows, potassium increases, and ATP and phosphocreatine (PCr) are depleted. These effects are largely reversible; however, if oxygen deprivation is prolonged, increased intracellular calcium and acidosis induce histological signs of necrosis, which become apparent at a much later (24–48 h) time. Free fatty acids appear as phospholipases are activated; cells swell as part of cytotoxic (hypoxic) edema. Excitatory neurotransmitters glutamate and aspartate released from ischemic cells and lactate produced by glycolysis when oxidative metabolism is inhibited by hypoxia are all believed to contribute to the cytotoxicity.

Clinically, hypoxic encephalopathy is encountered in two quite distinct situations: neonatal or perinatal asphyxia, which is mild, moderate or severe and associated with long-term neurological sequelae including spastic diplegia and mental retardation, and in children and adults as one of the most frequent and disastrous cerebral accidents seen in hospital emergency departments.