Hypoxic-Ischemic Encephalopathy (H.I.E.)

There are many signs to look for in an infant with Hypoxic Ischemic Encephalopathy:

• Tense and react more to stimulation than most newborns
• Floppy and hardly react to stimulation
• Visually inactive (no eye contact)
• Move abnormally or even have seizures
• Having problems feeding because their suck is too weak and the muscles in their mouth and throat are not working properly
• Display a very weak cry
• Meconium-stained amniotic fluid
• Low heart rate
• Poor muscle tone
• Weak breathing or no breathing at all
• Bluish or pale skin color
• Excessive acid in the blood

Symptoms can appear mild, such as dizziness and lack of concentration, although long-term symptoms can include more serious complications like damage to the cerebral cortex, the hippocampus, and occipital lobe. This can cause issues with brain development, including learning reading and linguistic skills, as well as other learning disabilities.

Mild hypoxic-ischemic encephalopathy

• Muscle tone may be slightly increased and deep tendon reflexes may be brisk during the first few days
• Transient behavioral abnormalities, such as poor feeding, irritability, or excessive crying or sleepiness (typically in an alternating pattern)
• Typically resolves in 24 hours

Moderately severe hypoxic-ischemic encephalopathy

• The infant is lethargic, with significant hypotonia and diminished deep tendon reflexes
• The grasping, Moro, and sucking reflexes may be sluggish or absent
• The infant may experience occasional periods of apnea
• Seizures typically occur early within the first 24 hours after birth
• Full recovery within 1-2 weeks is possible and is associated with a better long-term outcome

Severe hypoxic-ischemic encephalopathy

• Seizures can be delayed and severe and may be initially resistant to conventional treatments
• The seizures are usually generalized, and their frequency may increase during the 24-48 hours after onset, correlating with the phase of reperfusion injury
• As the injury progresses, seizures subside and the electroencephalogram becomes isoelectric or shows a burst suppression pattern. At that time, wakefulness may deteriorate further, and the fontanelle may bulge, suggesting increasing cerebral edema.
• Stupor or coma is typical; the infant may not respond to any physical stimulus except the most noxious
• Breathing may be irregular, and the infant often requires ventilator support
• Generalized hypotonia and depressed deep tendon reflexes are common
• Neonatal reflexes (sucking, swallowing, grasping, Moro) are absent
• Disturbances of ocular motion, such as a skewed deviation of the eyes, nystagmus, bobbing, and loss of “doll’s eye (ie, conjugate) movements may be revealed by cranial nerve examination
• Pupils may be dilated, fixed, or poorly reactive to light
• Irregularities of heart rate and blood pressure are common during the period of reperfusion injury, as is death from cardiorespiratory failure
• An initial period of well-being or mild hypoxic-ischemic encephalopathy may be followed by sudden deterioration, suggesting ongoing brain cell dysfunction, injury, and death; during this period, seizure intensity may increase

Causes of HIE include the following:

• Preeclampsia
• Placental insufficiencies, placental abrution, placental blood clots
• Maternal diabetes
• Maternal cardiovascular collapse
• Maternal blood clotting disorders
• Maternal low blood pressure
• Fetal maternal hemorrhage
• Meconium aspiration, aspiration causing asphyxia event
• Umbilical cord accidents/issures, cord prolapse, true umbilical knots, cord compression
• Uterine rupture
• Prolonged late stages of labor, failure to progress, trauma during deliver
• Abnormal fetal position, shoulder dystocia
• Infections, viral infections, bacterial or viral infections such as meningitis or sepsis
• Brain skull trauma