What Is Hypoxic-Ischemic Encephalopathy (HIE)?
The definition of hypoxic-ischemic encephalopathy (HIE) is a neonatal birth injury caused by oxygen deprivation and limited blood flow to the baby’s brain at or near the time of birth. HIE causes brain injury and can result in cerebral palsy and other cognitive and developmental impairments. Other terms used for HIE include birth asphyxia, perinatal asphyxia, and neonatal encephalopathy.
When blood flow is cut off to parts of the brain, cells begin to break down and release lactic acid and other compounds which can disrupt normal cell function. All cells in the brain are impacted by HIE, but neurons (the cells that transmit and process information in the nervous system) are particularly vulnerable to damage due to hypoxia and ischemia in a kind of brain damage called selective neuronal necrosis. When oxygen or blood is cut off from the brain, brain cells begin to die off in a chain reaction that makes brain damage worse.
Other terms for HIE (and phrases commonly associated with HIE):
Neonatal Encephalopathy – What is it?
Neonatal encephalopathy is used to describe disturbed neurological function in a newborn. HIE falls into this category and is the most common type of neonatal encephalopathy. Some signs and symptoms of neonatal encephalopathy include:
- Respiratory problems
- Feeding Problems
- Depressed reflexes
- Low or high muscle tone
- Seizure Activity.
Other terms for HIE include:
- Oxygen deprivation at birth
- Birth asphyxia
- Fetal oxygen deprivation
- Baby not breathing at birth
- Perinatal asphyxia
How Do You Pronounce Hypoxic-Ischemic Encephalopathy (HIE)?
Overview: Treatment for HIE
HIE is managed using a treatment called hypothermia therapy, where the baby’s brain or body is cooled down below normal temperatures to slow the cascade effect that causes widespread damage. This allows the baby’s brain to recover and reduce the level of disability they may have as they grow. The treatment must be given within 6 hours of birth.
The therapy lasts for around 72 hours, allowing the baby’s metabolic rate to slow. This prevents an injury known as reperfusion injury, which occurs when normal oxygenation and blood flow are restored too quickly to the brain’s cells. While it may seem counter-intuitive that restoring flow quickly could cause further injury, the brain’s cells react differently to rapid oxygenation after being oxygen deprived. After oxygen deprivation injury, rapid oxygenation can cause more inflammation and the release of certain compounds that can harm cells further. Hypothermia treatment works to stabilize the brain’s cells and prevent or limit damaging inflammation.
In addition to hypothermia therapy, medical staff should provide supportive care, which can mean helping the baby breathe, controlling and preventing seizures and low blood sugar, minimizing brain swelling and getting care from specialists.
For more information on hypothermia therapy.
Types and Forms of HIE
HIE is classified into different categories depending on how severe the oxygen deprivation is. If they suspect HIE, medical staff can conduct brain imaging, such as ultrasound and MRI, to see how badly brain tissue in the brain is damaged. Caregivers also do a blood gas test to determine the pH of the baby’s blood, which can also provide some information about the baby’s oxygen levels.
The severity of HIE is determined using Sarnat staging, which takes into account clinical presentation, exam results, seizure presence and illness duration. The results of the Sarnat staging are used together with EEG findings to determine the infant’s prognosis. Mild HIE may have a normal outcome (at least in the short run) but severe HIE has a significant mortality rate, with 80% of survivors showing signs of neurological sequelae. Mild HIE is classified as Sarnat Grade I, and severity increases up to a maximal Stage III.
Prevalence and Incidence of HIE
HIE is estimated to occur in between 2 to 9 per 1,000 live births. Between 10-60% of infants with HIE die in the neonatal period (when they are newborns) and about 25% of those that live with significant brain damage and impairments. Most HIE occurs at the time of labor and delivery.
Life Expectancy for People with HIE and Cerebral Palsy
The life expectancy of people with hypoxic-ischemic encephalopathy depends greatly on the extent to which they are affected and their access to treatments and therapies. For this reason, it’s difficult provide an “average” lifespan for people with HIE. Because many children with HIE are also diagnosed with cerebral palsy, it may be more useful to look at life expectancies for people with cerebral palsy.
People with very mild cerebral palsy are typically expected to live as long as their peers in the general population. Overall, life expectancy for a person with cerebral palsy depends on the extent to which they are affected:
- Lifespan of mild cerebral palsy: For people with fairly mild cerebral palsy (defined as walking unaided), life expectancy in females has been estimated at 70-80 years, and in males at 66-76 years.
- Lifespan of severe cerebral palsy: For those who are more severely affected (defined as an inability to lift the head and being fed through a tube), life expectancies have been estimated to be shorter for both females and males, depending on the qualify of medical care received.
These lifespan numbers were extracted from a 2008 study in Developmental Medicine and Child Neurology. Click here to view the paper, which contains a detailed table on life expectancy for people with cerebral palsy. It takes into account age, sex, movement ability, and feeding mechanism.
More Detailed Information on HIE
For more information on HIE, please visit our Medical Information section, which can provide further information into the causes of HIE, treatment and prevention methods such as hypothermia therapy, associated conditions, and long-term outcomes.
About the HIE Help Center
- Wu, Yvonne, et al. Clinical features, diagnosis, and treatment of neonatal encephalopathy. UptoDate. Accessed 30 Jan. 2017.
- Kurinczuk, Jennifer J. Epidemiology of neonatal encephalopathy and hypoxic–ischaemic encephalopathy, Early Human Development, Volume 86, Issue 6, June 2010, Pages 329-338, ISSN 0378-3782, https://www.ncbi.nlm.nih.gov/pubmed/20554402.