Ischemic hypoxic encephalopathy: what is it?

Encephalopathies are part of a particular group of pathologies, characterized by a structural and functional alteration of the brain .

The various types of encephalopathy differ from each other due to the triggering causes - to which they usually owe their names - for the symptoms, for the complications, for the treatment and for the prognosis.

Congenital or acquired, an encephalopathy can last a lifetime ( permanent encephalopathy ) or may have a more or less important margin of healing ( temporary encephalopathy ).

A form of encephalopathy of a usually permanent nature, which arises following an inadequate supply of oxygen to the brain ( cerebral hypoxia ), is the so-called ischemic hypoxic encephalopathy .

Ischemic hypoxic encephalopathy can affect people of any age: in the fetus and newborn, it is a possible complication of the morbid phenomena called perinatal asphyxia and neonatal asphyxia ; in adults or the elderly, it is a possible complication of pathological conditions - such as silent stroke or transient ischemic attack - which deprive the brain of the necessary oxygen.

CAUSES IN THE FETUS AND THE NEWBORN

There are numerous events that can deprive the brain of a fetus or an infant (or in any case a very young child) of the required oxygen. Below are some of the most common ones:

Before birth (therefore during pregnancy) : preeclampsia, maternal diabetes complicated by vascular problems, congenital fetal infections, alcohol or drug abuse, problems with blood supply through the placenta or severe fetal anemia.
During labor and delivery : occlusion, torsion or prolapse of the umbilical cord, rupture of the placenta or uterus, excessive bleeding from the placenta, abnormal fetal positions (breech birth), prolonged labor or severe maternal hypotension.
After labor : premature birth, severe heart or lung disease, significant fetal infections, brain trauma (or head), congenital malformations or severe fetal hypotension.

CAUSES IN THE ADULT

In addition to transient ischemic attack (or TIA ) and silent stroke, the following traumatic events may contribute to the development of cerebral asphyxia (before) and ischemic hypoxic encephalopathy (then):