Hypoxic Ischemic Encephalopathy

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Hypoxic- Ischemic Encephalopathy

What parents must know if their child suffered oxygen deprivation

Babies are very sensitive to changes in the amount of oxygen they receive before birth. One of the most serious complications that can occur pre-term or during the initial stage of labor is the lack of oxygen to the baby’s brain. Not only can it lead to long-term, permanent injuries and poor cognitive development, it could also be fatal.

Perinatal asphyxia refers to a specific type of injury that occurs when a baby is deprived of oxygen around the time of birth. As many as 4 million babies worldwide are affected each year. Of those 4 million, one million will not survive.

In many cases, the baby fully recovers, but some of these babies that survive will develop Hypoxic Ischemic Encephalopathy, or HIE, where damage to the brain is severe enough to permanently damage the neurological system. As a result, the baby may suffer from a variety of birth injuries, including seizures, cerebral palsy, learning and cognitive disabilities, have difficulty walking, or be unable to walk at all. He may require a lifetime of care. There may also be damage to the heart, lungs, and kidneys.1

The chain of events leading to HIE

Because your baby doesn’t actually breathe before she is born, her oxygen is supplied in the form of blood flow. The oxygen travels by way of the umbilical cord, which connects the baby to the placenta. The umbilical cord usually contains one vein and two arteries:

  • The umbilical vein carries red blood cells that contain oxygen and other nutrients from the placenta to your baby.
  • The two arteries carry blood from the baby back to the placenta. This blood contains carbon dioxide (the gas that we breathe out), as well as other waste products produced by your baby’s body.

The carbon dioxide is transferred from the placenta into your bloodstream, to your lungs, where it leaves your body when you exhale. The waste products are transferred into your bloodstream, where they are removed along with your body’s waste products. Fetal blood and maternal blood do not mix together due to the placental barrier, which is located within the placental intervillous space.

Approximately 17 to 20 ounces of blood reach the uterus every minute. From the uterus, most of this blood travels through the intervillous space of the placenta, through the umbilical vein, to the baby.2 In order for enough blood to reach the intervillous space, it must first flow through the mother’s spiral arteries. If there is not enough blood flowing through these spiral arteries into the intervillous space, the baby does not receive enough oxygen.

Chemoreceptors located in the baby’s cardiovascular system are very sensitive to a decrease in oxygen supply. When they sense that the oxygen supply has been decreased, the chemoreceptors respond by stimulating the vagal nerve. Stimulation of the vagal nerve results in a decrease in the baby’s heartrate, which decreases the amount of oxygen being used.2 If the circumstances causing the decrease in oxygen supply are not resolved, your baby’s body will continue to adjust by rearranging the blood flow, sending more blood to the heart, brain, and adrenal glands, and less blood to the spleen, kidneys, arms, and legs. Aerobic metabolism is able to be maintained until the amount of oxygen in the intervillous space is half of what it normally is.3

HIE occurs in two phases

Phase One

If the decrease in oxygen supply continues, the baby’s body will switch from aerobic (oxygen is present) to anaerobic (no oxygen is present) metabolism. The pH levels in the baby’s blood begin to drop, leading to a condition known as metabolic acidosis.4 By this point, the baby has used all of his reserves attempting to supply his brain with enough oxygen. The end result is brain ischemia.

In addition to oxygen, the blood also carries glucose to the baby’s brain. Glucose and oxygen are required to make ATP (energy) that is vital to the brain cells. Glucose is not stored in the baby’s brain cells, therefore, when the supply runs out, there is no more available. Also, when all of the ATP has been used, the sodium-potassium pump stops working, causing depolarization within the brain cells, which causes them to swell.

Along with this swelling, large amounts of calcium enter the brain cells, destroying the cell membrane. When the cell membrane is destroyed, free fatty acids are released into the spaces within the cells, which produces a substance known as Thromboxane A. This substance causes the blood vessels within the cells to become even narrower than they already are. The end result is death of the brain cells within the baby’s brain.5

Phase Two

The second phase is called the “reperfusion phase.” This phase begins 6 to 8 hours after the initial insult to the brain. When the blood supply to the baby’s brain is finally restored, more damage is done to the brain cells by oxygen-free radicals, resulting in oxidative stress and swelling within the brain.

How well a baby’s brain recovers depends upon how severe the damage is

The severity of the injury is broken down into three categories:

Grade I (Mild). The symptoms caused by the irritation to the baby’s brain come and go. These symptoms improve within 48 hours from the initial injury and there is no permanent neurological damage.6

Grade II (Moderately Severe). The baby’s central nervous system is depressed. His Moro reflex is weaker than normal, and he is difficult to arouse. He may be unable to suck. Seizure activity may be present within the first 24 hours after birth. He may have periods of apnea (not breathing). The baby may fully recover within two weeks of birth, which would give him a better prognosis for the long-term outcome.

Grade III (Severe). Babies that show signs of severe and permanent brain injury are often comatose. Seizure activity is common and may be frequent during the first 48 hours, which corresponds with the second phase of brain injury. Half of the babies diagnosed with Grade III HIE do not survive.6

Causes of asphyxia

Any event or condition that occurs that limits the amount of oxygen that is transported to a baby before birth can cause asphyxia. Some of the more common causes are:

Treatment for asphyxia and HIE

Treatments that may be necessary for babies suffering from a brain injury due to a lack of oxygen are many. Immediately after birth, she may not be breathing and not have a pulse. In this case, she would require immediate resuscitation by delivery room staff specifically trained in neonatal resuscitation. She may need a ventilator to breathe for her, as well as medications to raise her heart rate and blood pressure. She may need medications to stop seizure activity, correct pH levels in her bloodstream, intravenous fluids, and a blood transfusion.

Therapeutic Hypothermia

A promising treatment for babies that have suffered an injury to the brain during the birth process is Therapeutic Hypothermia. Decreasing the baby’s body temperature will reduce, or slow down, functions in the brain and heart, as well as the baby’s metabolism. This may stop additional brain cells from being injured, as well as allow some of the cells in the baby’s brain a chance to recover partial function. It may also prevent further cells from being damaged during the second phase (reperfusion phase) of HIE.

Therapeutic Hypothermia is not appropriate for every baby. There are guidelines in place to identify which babies should receive this treatment, and which ones shouldn’t. In order for it to be effective, it must be started within the first 6 hours after birth. The baby must be born no earlier than the 36th week of pregnancy and show specific signs that indicate a brain injury.7

It is important that the medical team caring for your baby determines if she is eligible for therapeutic hypothermia treatment. Larger hospitals may have a team of physicians and nurses that are readily available make that decision and have the necessary equipment to begin therapy. If your baby is born in a smaller, community hospital, it is very important that the medical staff contact the closest neonatology team to provide the specialized care that is needed.

These are many of the injuries our clients’ children have sustained

Cognitive, Developmental and Intellectual DisabilitiesInfant Spina Bifida
Brachial Plexus Injuries, Klumpke’s Palsy and Erb’s PalsyInfant Spinal Cord Damage
Cerebral PalsyInfant Subconjunctival Hemorrhage
Hypoxic Ischemic EncephalopathyNeonatal Hyperbilirubinemia
Intracranial HemorrhageKernicterus
Shoulder DystociaNeonatal Stroke and Infant Brain Ischemia
Epidural Birth InjuriesPersistent Pulmonary Hypertension of the Newborn (PPHN)
Horner’s SyndromeVacuum Extraction Injury
HydrocephalusWrongful Birth
Infant Bell’s PalsyUmbilical Cord Prolapse
Infant Broken Bones and Skull FracturesVacuum Extraction and Forceps Injuries
Infant Cervical Dystonia / Infant Torticollis / Infant Dystonia DisorderMeconium Stained Amniotic Fluid
Infant Meningitis

There for you and your baby after a serious birth injury has occurred

If you or your loved one was seriously injured by an act of medical negligence, Crandall & Pera Law may be able to help. We are a nationally recognized team of medical malpractice and birth injury attorneys serving clients throughout Ohio and Kentucky. To learn more about who we are, or to schedule a consultation with an experienced birth injury attorney, please call 877-955-0020 or fill out our contact form.

  1. Fattuoni, C., Palmas, F, Noto, A., Fanos, V., & Barberini, L. (2015). Perinatal asphyxia:     A review from a metabolomics perspective. Molecules, 20(4), 7000-7016. doi: 10.3390/molecules20047000
  2. Blecker, O., Kloosterman, G., Mieras, D., Oosting, J., & Salle, H. (1975). Intervillous space during uterine contractions in human subjects: an ultrasonic study. American Journal of Obstetrics & Gynecology, 123(7), 697-699. Retrieved from www.ncbi.nlm.nih.gov
  3. Petra, C., van Geijn, B., & van Geijn, H. (2008). Uterine activity: implications for the condition of the fetus. Journal of Perinatal Medicine, 36(1), 30-37. doi: 10.1515/JPM2008.003
  4. Omo-Aghoja, L. (2014). Maternal and fetal acid-base chemistry: A major determinant of perinatal outcome. Annals of Medical & Health Sciences Research, 4(1), 8-17. doi: 10.4103/2141-9248.126603
  5. King, T., & Parer, J. (2000). The physiology of fetal heart rate patterns and perinatal asphyxia. The Journal of Perinatal & Neonatal Nursing, 14(3), 19-39. doi: 10.1097/00005237-200012000-00003
  6. Robertson, C. (1993). Long-term follow up of term neonates with perinatal asphyxia. Clinics in Perinatology, 20(2), 483-500. Retrieved from www.ncbi.nlm.nih.gov
  7. Rafat, M. (2012). Whole body cooling for infants the hypoxic-ischemic encephalopathy. Journal of Clinical Neonatology, 1(2), 101-106. doi: 10.4103/2249-4847.96777