Birth Hypoxia in Newborn Baby

by Abhinandan
(Lucknow, India)

Clinical Features Are Perhaps The Best Indicator of The Outcome of Birth Hypoxia

Clinical Features Are Perhaps The Best Indicator of The Outcome of Birth Hypoxia

My son suffered neonatal hypoxia. He didn’t cry at birth, received ventilator support and oxygen supplementation for Hypoxic ischemic encephalopathy.

He has been gradually weaned off oxygen. Now, at the age of 25 days, his breathing is adequate, but he is yet very drowsy and inactive. He is not even able to suck and swallow.

His MRI report is normal.

Doctor, will my baby be normal? When? What will be the future outcome?

The Expert, Ren Chats Answers


Failure to initiate or sustain spontaneous breathing at birth is the commonest cause of subsequent neurologic disabilities like spastic paresis, visual impairment, seizure disorders, and so on. However, newborns who suffer only a mild form of encephalopathy, attributed to poor oxygen saturation during the birth process, usually grow up to be normal infants.

The transition from womb to real world is dramatic, and a complex process. It involves extensive changes in the baby’s breathing and blood circulation dynamics that are most obvious at the time of birth. Therefore mild birth hypoxia occurs almost in all, but the incidence of hypoxic ischemic encephalopathy is only about 6 in 1000 full term newborns, of which only 1 in 10 to 1 in 20 show significant developmental delay.

The injury to the developing brain depends on the degree of hypoxic insult, and the health of the baby. In a compromised baby even a brief episode of hypoxia can set a cascade of events that ultimately lead to neuronal damage. The duration of the insult that is necessary to produce brain injury is inversely proportional to the gestational age of the fetus. Other risk factors for adverse effects of birth hypoxia are as follows:

In the mother:
Low blood pressure, infertility treatment, Thyroid gland dysfunction

During childbirth:
Fever in the mother, difficult forceps delivery, breech extraction, cord prolapse, abruptio placentae (placenta separates from the wall of the uterus before the baby is born).

In the baby:
Placental-fetal blood flow, prematurity, birth weight, energy reserves, congenital heart disease, presence of cerebral anomalies, severe breathing difficulty, sepsis, shock.

The hypoxic ischemic encephalopathy can lead to patchy bilaterally, or diffuse brain injury. The extent of nervous tissue damage is determined by a complex interaction among various vascular, cellular, and metabolic factors, which despite of ongoing treatment often continues for hours to days before manifesting the clinical signs. However, the clues to ongoing system injury usually begin to evolve within 72 hours.

During the first 12 hours of birth the infant may be very irritable with inconsolable shrill cry, or may seem to be sleeping deeply.

The severely affected neonates usually develop excessive jitteriness or seizures within the first 24 hours of life. The medications given to control their abnormal brain activity cause considerable drowsiness. This aggravates the clinical picture of “floppy baby with poor muscular activity” commonly seen in the cases of brain injury, where in startle, grasp, sucking and swallowing neonatal reflexes may also be absent or depressed.

Though clinical seizures are seldom seen in the moderately affected newborns, their EEG (electroencephalogram) recordings often show abnormal paroxysmal discharges. These EEG changes can be helpful in determining the extent of injury caused by birth hypoxa.

The future outcome

Outcome of hypoxic ischemic encephalopathy depends on the severity of birth hypoxia, and consequently the degree of brain damage, both of which are difficult to assess. Apgar Score is commonly recorded to evaluate the neuromuscular and cardiorespiratory status of the newborn at birth, but it has several pitfalls. Nevertheless, it has been noted that babies born with less than 6 Apgar score at 5 minutes have significantly high probability of newborn brain growth restriction, thereby in developing neurological abnormalities.

Clinical features such as seizures, state of consciousness etc are perhaps the best clinical indicator of adverse outcome (see the table given above). Seizures, especially if they present within 12 hours of life, or if they are difficult to control, indicate severe brain injury. Longer the neurological symptoms and signs persist more are the chances of long-term developmental disabilities in the affected infant. On the other hand, normal neurological examination findings at 1 week and at 2 weeks of age correlate with good outcome.

MRI is the most sensitive and specific technique to determine the location and extent of hypoxic ischemic encephalopathy triggered by neonatal hypoxia. It is recommended between days 2 and 8. Even when performed as late as 2 to 3 weeks of life it has been found to be highly predictive of the outcome at 18 months of age. But the flip side is that the MRI evaluation does not show any significant qualitative abnormalities in 20% of cases with developmental disabilities attributed to birth asphyxia.

Moreover, significant recovery from neurological damage caused by birth hypoxia may occur with brain growth and neuronal plasticity. Therefore, neurologic examination findings at the age of 3 months would be a good indicator of long term outcome.

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