Can hypoxic ischemic encephalopathy (HIE) cause brain damage without causing cerebral palsy?

Yes. Hypoxic-ischemic encephalopathy (HIE), commonly known as birth asphyxia, occurs when oxygen deprivation during or near the time of birth results in infant brain damage. This lack of oxygen is caused by reduced oxygen in the baby’s blood (hypoxemia/hypoxia) and a lack of blood flow in the baby’s brain (ischemia).  HIE is estimated to occur in about 2-9 per 1,000 live births.  Roughly 10–60% of affected infants die in the newborn period, and at least 25% of those that survive have significant long-term neurodevelopmental impairments, including mental and physical issues such as cerebral palsyintellectual and developmental disabilities, and seizures. The extent and seriousness of the damage depends on the length of time that the baby was deprived of oxygen and the condition of the baby prior to the oxygen deprivation.  Generally speaking, as the severity of the oxygen deprivation increases, so does the severity of the brain injury. Children diagnosed with HIE can have cerebral palsy, but it is also possible for children with HIE to have normal motor function, depending on the locations of the injured brain cells..


Cerebral Palsy

Cerebral palsy is a term used to describe functional motor deficits in a child.  Cerebral palsy is a motor and postural disorder that originates very early in a child’s life.  It is non-progressive, meaning the damage in the brain does not get worse throughout the child’s life.

Hypoxic-Ischemic Encephalopathy (HIE), Cerebral Palsy and Cognitive Impairments

Recent research that examines neonatal encephalopathy and magnetic resonance imaging (MRI) shows that most brain injury happens at or near the time of birth. The American Congress of Obstetricians and Gynecologists (ACOG) task force on neonatal encephalopathy and cerebral palsy concluded that an acute intrapartum event (such as sudden oxygen deprivation) could only cause spastic cerebral palsy and not isolated cognitve impairments such as intellectual disabilities.  In other words, the task force determined that if oxygen deprivation and HIE damaged the brain enough to cause problems in the child, then these problems would always include motor disabilities (such as problems with movement and posture).  ACOG effectively stated that if a child doesn’t show signs of motor problems (such as cerebral palsy), the child does not have brain damage caused by HIE.

This conclusion by ACOG is incorrect and it ignores well-established research that examines brain injury in children and the resultant developmental problems these children have.  Furthermore, this conclusion by ACOG is irresponsible because it may cause parents and medical professionals to delay treatment in a child whose motor function is normal and not delayed, but who may have learning disabilities and intellectual disabilities resulting from HIE.  Early treatment and intervention is critical for children with cognitive impairments, and for this reason, children with these problems must be identified at the earliest possible age.

Children with Brain Damage from HIE Can Have Normal Motor Function

There are many studies that examine long-term outcomes in children who have brain injury consistent with oxygen deprivation and HIE, but no motor problems.  In these children, the brain damage causes neurodevelopmental, neuropsychological and/or cognitive problems such as seizure disorders, intellectual impairments, memory problems, executive function problems (problems carrying out tasks), speech-language issues, attention deficit and hyperactivity disorder (ADHD), and autism. ACOG essentially takes an all-or-nothing approach to disabilities caused by asphyxia and HIE, which is a reckless dismissal of many subtle yet serious consequences of brain damage.

MRI Imaging Can Show an Evolving Pattern of Asphyxia-Related Injury Over Time

When physicians suspect that a baby experienced oxygen deprivation, the baby should receive an MRI soon after birth (within the first one to two days of life) and be closely watched and monitored for brain injury.  Children with brain injuries should be watched just as closely, even if they do not exhibit motor problems.  It is critical that children with evidence of brain damage but without  functional motor problems be assessed for cognitive/neurodevelopmental and neuropsychological problems as they get older.  These types of impairments may not show up until a child is one year of age, and in many cases, may not be noticed until a child is five or six years old.

When sudden oxygen deprivation near or during the time of delivery is the cause of the brain injury, the MRI will show an evolving pattern of injury.  This means that the damage apparent on the first MRI typically will continue to change over time, though treatments such as brain cooling (hypothermia therapy) may slow down or stop this evolving pattern of injury. If the baby was injured by an event that did not occur close to the time of delivery, the brain damage usually will not show an evolving pattern on MRI as the brain injury will be more established.

How a Brain Injury Manifests Itself Depends on the Location of Damaged Brain Cells

When a sudden and severe oxygen-depriving event (profound asphyxia) causes a baby’s brain injury,  the injury will more likely be in a part of the brain called the deep gray nuclei (the basal ganglia and Basal ganglia and infant brain damage - birth injurythalamus).  When the injury is less severe (partial asphyxia), the damaged part of the brain is usually the white matter of the brain, which transmits signals from one part of the brain to another and controls how the brain learns and functions. Research shows that injury in the deep gray nuclei is associated with severely impaired motor and cognitive function, whereas injury in the white matter results in cognitive impairments that often occur without functional motor deficits (no movement problems).  In other words, brain damage from oxygen deprivation (asphyxia) can cause mental impairments without any physical impairments.

It is thought that cognitive deficits are due to problems outside the deep gray nuclei. Injury in the deep gray nuclei as well as in the white matter are associated with a watershed pattern of injury (injury in the borders of different parts of the brain, including major brain arteries).  In this type of injury, blood flow is decreased and may be blocked in certain areas of the brain.  A watershed pattern – which occurs outside the deep gray nuclei – is associated with cognitive impairment.  In short, the watershed pattern that causes cognitive problems occurs in both deep gray nuclei injury as well as white matter injury.

Hypoxic-Ischemic Encephalopathy (HIE), Cognitive Impairments, and Medical Malpractice

Standards of care must be followed at all times to avoid complications that give rise to hypoxic/ischemic insults.  A mother and baby must be closely monitored during labor and delivery, and proper prenatal testing must be performed in order to avoid conditions that can lead to HIE.  Failure to properly monitor a mother and baby and to follow standards of care is negligence.  If the negligence results in injury to the baby, it is medical malpractice.

Trusted Michigan Hypoxic-Ischemic Encephalopathy (HIE) Attorneys

If your child has been diagnosed with HIE, a review of medical records can determine whether negligence played a role in causing the injury. ABC Law Centers is a national birth injury law firm that has been helping children with birth injuries for over three decades. Contact our award-winning lawyers today for a free consultation. We have numerous multi-million dollar verdicts and settlements that attest to our success, and charge nothing unless the suit is successful.

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Related Resources on Hypoxic Ischemic Encephalopathy (HIE)


Video: Michigan Hypoxic Ischemic Encephalopathy (HIE) Lawyers Discuss HIE

In this video, Michigan  hypoxic ischemic encephalopathy (HIE) lawyers Jesse Reiter and Rebecca Walsh discuss the causes of and treatments for HIE.  Negligence by the medical team is often the cause of HIE and birth asphyxia.


Sources:

van Handel, Mariëlle, Hanna Swaab, Linda S. de Vries, and Marian J. Jongmans. “Long-term cognitive and behavioral consequences of neonatal encephalopathy following perinatal asphyxia: a review.” European journal of pediatrics 166, no. 7 (2007): 645-654.

Gonzalez, F. F., and S. P. Miller. “Does perinatal asphyxia impair cognitive function without cerebral palsy?.” Archives of Disease in Childhood-Fetal and Neonatal Edition 91.6 (2006): F454-F459.

STEVENSON, David K., William E. BENITZ, Philip SUNSHINE, Susan R. HINTZ, and Mauri DRUZIN. “Fetal & neonatal brain injury.” (2009): 576-577.