One has the impression that the brain tolerates hypoxia and reduced blood flow in the immediate postnatal period better than at any other time in life. Indeed, animal experimentation supports this view. Not until the arterial oxygen tension is reduced dramatically to 10 to 15 percent of normal does brain damage occur, and even then the impaired function of other organs contributes to the damage. It is probably correct to think of the encephalopathy in terms of both hypoxia and ischemia, both of which usually occur in utero and are expressed postnatally by recognizable clinical syndromes.
Fenichel (1990), following the original work of Sarnat and Sarnat and of Levene and colleagues, has found it helpful to divide the encephalopathies that follow a complicated birth into three purely descriptive groups according to their severity, each having a prognostic value beyond that of the Apgar score: (1) In newborns with mild hypoxic-ischemic encephalopathy, the symptoms are maximal in the first 24 h and take the form of hyperalertness and tremulousness of the limbs and jaw (the “jittery baby”) and a low threshold of the Moro reaction. The tone of the limbs is normal except for a mild increase in head lag during traction. The reflexes are brisk and there may be ankle clonus. The anterior fontanel is soft. The EEG is normal. Recovery is usually complete and the risk of handicap is low. (2) Newborns with moderate hypoxic-ischemic encephalopathy are lethargic, obtunded, and hypotonic, with normal movements. After 48 to 72 h, the neonate may improve (having passed through a jittery hyperactive phase) or worsen, becoming less responsive in association with convulsions, cerebral edema, hyponatremia, and hyperammonemia from liver damage. The EEG is abnormal. Fenichel associates epileptiform activity and voltage suppression with an unfavorable outcome. Abnormal visual and auditory evoked potentials are other poor prognostic signs. (3) In neonates with severe hypoxic-ischemic encephalopathy, stupor or coma is present from birth; respirations are irregular, requiring mechanical ventilation. There are usually convulsions within the first 12 h. The limbs are hypotonic and motionless even during attempts to elicit the Moro response. Sucking and swallowing are depressed or absent, but pupillary reactions and eye movements may at first be retained, only to be lost as the coma deepens.
It is in the second and third categories, that is, the states of moderate to severe encephalopathy, where correction of the respiratory insufficiency and the metabolic abnormalities permits survival, that a number of motor abnormalities (corticospinal, extrapyramidal, and cerebellar) and developmental delay eventually emerge. Included in the category of severe hypoxic-ischemic encephalopathy are also newborns with a variety of developmental anomalies of the brain and other organs. However, clouding the issue of causality is the absence of perinatal complications in a large number of children with cerebral palsy and the large number of normal babies who are born after complicated deliveries. Notably, only a few cases result from often blamed intrapartum factors such as forceps delivery, breech presentation, cord prolapse, abruptio placentae, and maternal fever.