Hypoxic-ischemic encephalopathy (HIE) is a reduction in the oxygen and/or blood flow to the brain of a newborn baby resulting in brain damage. This condition usually occurs during labor when stresses to the infant are strongest. Children who suffer from HIE will usually go on to have life-long disabilities and cerebral palsy. In fact, in the United States, HIE occurs in 2 to 3 per 1000 births with 15% to 28% of those children being diagnosed with cerebral palsy.  Babies with HIE usually demonstrate abnormalities in feeding, breathing, reflexes, muscle tone, and seizure activity.
HIE When Infant’s Oxygen is Cut Off Completely
There are multiple acute high-risk events that occur during the perinatal period (after 22 weeks of pregnancy) which are known to cause an immediate reduction of oxygen and blood flow to the baby (called terminal asphyxia) which physicians must address by emergency Cesarean Section. Specifically,
The placenta detaches from the wall of the uterus depriving the baby of potentially all blood flow and oxygen.
Umbilical Cord Prolapse:
The umbilical cord drops or prolapses through the open cervix into the vagina and the cord is compressed resulting in a reduction of potentially all blood flow and oxygen to the infant.
The uterus of the mother tears, usually along the scar of a prior c-section resulting in significant blood loss and jeopardizing the life of both mother and baby.
Tight Nuchal Cord:
The umbilical cord is wrapped around the neck of the infant which may result in a significant or complete reduction of oxygen.
The placenta blocks the opening to the cervix, the birth canal, and may result in severe and acute blood loss to both mother and baby.
HIE When Oxygen is Cut Off Periodically
HIE may also cause brain injury over a prolonged period of time where an infant’s oxygenation waxes and wanes during the labor and delivery period. This is also known as a partial prolonged injury to the baby’s brain. Specifically, as blood and oxygen flow to the baby’s brain, it may be significantly reduced and then re-supplied, causing the cells to die off with the continued pattern occurring over an extended period of time. Most obstetricians today use an electronic fetal monitor (external or internal) during labor to provide a window into a baby’s well-being and oxygenation level and the quality of its mother’s contractions. The various patterns on the electronic fetal monitor alert the physician as to whether the infant is demonstrating reassuring signs or is suffering from hypoxia (lack of oxygen). Based upon the correct interpretation of the fetal monitoring strips, the physician is obligated to determine if the labor may continue or the delivery must be expedited by either vacuum, forceps, or Cesarean section.
What Happens During HIE
Whether HIE is caused by terminal asphyxia (immediate reduction in oxygen) or partial prolonged reduction of oxygen, the limited oxygen and blood flow (hypoxia and ischemia) to the newborn will cause a physiologic process in the brain to be triggered. The brain will begin to compensate as a result of the reduction of oxygen and start to convert to other forms of energy to produce oxygen. This will in turn cause a build-up of lactic acid in the bloodstream if oxygen is not restored. This process will continue, leading to cell death in the brain and other organs of the newborn’s body. Once delivery has taken place and the child is resuscitated, there is a further secondary insult to the brain that develops once the brain attempts to restore function. This insult will usually occur anywhere from 6 to 48 hours after the original hypoxic-ischemic injury. Specifically, the newborn’s body will release the response of inflammatory cells and that reaction which is toxic to the healthy cells will contribute to a further exacerbation of the injury all consistent with HIE and potential catastrophic permanent brain damage. 
There are specific markers or findings at birth that indicate that an infant that has suffered HIE:
1) Apgar Score (measurement of infant’s well-being) of less than 5 at 5 minutes and 10 minutes; 2) Fetal Umbilical Artery Acidemia pH less than 7.0 or base deficit greater than or equal to 12 mmol/L; 3) Neuroimaging Evidence of Acute Brain Injury Seen on Brain MRI or MRS consistent with Hypoxia-Ischemia; and 4) Presence of Multisystem Organ Failure Consistent with Hypoxic-Ischemic Encephalopathy
Additionally, the finding of seizures in a newborn is clinically supportive of brain injury.
Cooling Therapy for HIE
Fortunately, today there are neonatal hypothermia treatments (treatments that cool a newborn’s system) that can be administered to newborns diagnosed with HIE that may reduce the extent of the brain injury if they meet the cooling criteria including:
Gestational age of 36 weeks of more;
Apgar score of 5 or less at 10 minutes following birth;
Continued need for resuscitation (endotracheal or mask ventilation) at 10 minutes following birth;
Severe acidosis (pH<7.00, based deficit>16mmol/L from umbilical cord, or an arterial or venous sample from infant within 1 hour following birth); and
Grade II or III encephalopathy (damage to the brain) based on the Sarnat and Sarnat criteria.
The physiologic process behind the cooling therapy is to slow down the metabolic rate of the impaired brain thereby decreasing the rate of cell death and delaying injury. After the infant has been in a cooling state for 48-72 hours the process of rewarming begins stabilizing the brain and limiting inflammation. Neonatal hypothermia is now one of the leading treatments for children diagnosed with HIE improving the outcomes significantly.
The Jacob Fuchsberg Law Firm has been representing the families of catastrophically injured children for generations. We have handled all aspects of obstetrical malpractice which lead to HIE and take significant pride in the results we achieve, which reduce the tremendous financial strains put upon the families of children requiring extraordinary care.
Sources:  Laura D. Selway, MSN, RN. “State of Science Hypoxic Ischemic Encephalopathy and Hypothermic Intervention for Neonates”. Advances in Neonatal Care. Vol 10, No.2 (2010): pp 62-63