[Hypoxic-ischemic encephalopathy in the full-term newborn infant. Recent advances, markers of hypoxia and therapeutic options].

BACKGROUND

Hypoxic-ischemic encephalopathy is the neurological consequence of a nonprogressive encephalopathic clinical picture of the hypoxic-ischemic syndrome, caused by a mixture of reduced oxygenation of the blood with increased carbon dioxide (asphyxia) and a lack of tissue perfusion (ischemia). It is the chief cause of death during the perinatal period, and of nonprogressive neurological deficits in childhood.

CONCLUSIONS

Regarding neurophysiological factors, we emphasise the importance of re-perfusion and reoxygenation in hypoxia-ischemia, with increased oxidative stress, accumulation of oxygen and of hydroxyl radicles which lead to reduced local blood flow and changes in the DNA, enzyme systems and cell membranes. Most of the brain damage in the hypoxic-ischemic syndrome is due to activation of the inflammatory response itself occurring in the central nervous system. In this article we discuss the most important neuropathological lesions, their relation to the clinical findings, and neurological course in hypoxic-ischemic encephalopathy. Finally, we analyze current prognostic markers which have a clearly shown scientific basis to confirm their usefulness, and the most important aspects of treatment which may be used in full-term newborn babies with hypoxic-ischemic encephalopathy.