Ischemic Encephalopathy


Ke-Ni Niko Tien


Hypoxic ischemic encephalopathy (HIE) is impaired gas exchange caused by a decrease in cerebral blood flow that results in hypoxemia (low blood oxygen levels), hypercarbia (elevated CO2 levels), and severe consequence of global cerebral ischemia (Karlsen, 2013; Zanelli, Kaufman, & Stanley, 2016). HIE can also lead to neurologic injuries, seizures, and death. Intrauterine asphyxia, such as clotting of placental arteries, placental abruption, inflammatory process or perinatal infarction are the most common mechanism of hypoxic injury in term infants (Fatemi, Wilson, & Johnston, 2009). Evidence has shown that providing advanced quality care may reduce the incidence and severity of outcome of neonatal encephalopathy by half (Graham, Ruis, Hartman, Northington, & Fox, 2008).

Currently, the most promising therapy is neuroprotective/therapeutic hypothermia as indicated by intentional head or body cooling (Karlsen, 2013; Price-Douglas & Fernandes, 2015). However, cooling is primarily limited to levels III and IV neonatal intensive care units (NICUs), because of complex care issues that the infant may have. The infant may need to be transported to a tertiary care center (Barks, 2008; Price-Douglas & Fernandes, 2015). It is critical for health care providers at delivery to recognize newborns with HIE who may be candidates for cooling.


The incidence of HIE is one in four cases per 1,000 live births in the United States (Wayock et al., 2014; Zanelli et al., 2016). Worldwide, there are approximately 840,000 neonatal deaths as a result of perinatal asphyxia (Zanelli et al., 2016). Severe hypoxemia may lead to the production of lactic acid during anaerobic glycolysis that results in metabolic acidosis (a low pH and an elevated base deficit), which is the most objective assessment of perinatal HIE (Graham et al., 2008; Karlsen, 2013). In addition, studies have shown an increase in seizures if the umbilical arterial pH is less than 7.0, as well as a significant increase in neurologic morbidities (Fatemi et al., 2009; Graham et al., 2008).

The criteria identified in determining intrapartum asphyxia in an infant are late decelerations on fetal monitoring or meconium/meconium-stained fluid at delivery; delayed respiratory effort after birth; arterial cord blood pH less than 7.1; Apgar score less than 7 at 5 minutes of age and multiorgan injury (Graham et al., 2008). However, studies have shown that numerous factors can contribute to low Apgar scores, such as intrapartum maternal sedation or anesthesia, congenital malformation, the appearance of infection, and the effectiveness of 175resuscitation. Therefore, the Apgar score alone is not the most reliable predictor for perinatal hypoxemia (Graham et al., 2008).

Severe HIE can lead to clinical seizures, epileptic activity seen on electroencephalogram (EEG), hypotonia, lack of gag reflex, poor feeding, and a prolonged depressed consciousness status. Infants who survive a birth asphyxia insult may develop neurologic sequelae such as cerebral palsy, mental retardation, learning difficulties, cognitive and motor deficits, as well as other disabilities (Karlsen, 2013; Zanelli et al., 2016).

Several clinical trials have shown the promising results of intentional hypothermia therapy (Fatemi et al., 2009). Clinical investigations have demonstrated an overall reduction in mortality and disability for infants who received hypothermia therapy (cooling) within the first 24 hours of life. Hypothermia therapy reduces cerebral metabolism and the inflammation process triggered by ischemic events (Fatemi et al., 2009). Currently, hypothermia therapy has become a standard of care in moderate to severe HIE treatment.

Accurately predicting the prognosis and severity of long-term complications of HIE is difficult. The lack of spontaneous respiratory effort for 20 to 30 minutes after birth; presence of frequent and uncontrollable seizure activity; prolonged abnormal clinical neurologic findings, including abnormal muscle tone and posture; abnormal background activity on EEG; persistent feeding difficulties because of abnormal sucking and swallowing and poor head growth are the most helpful indicators in determining possible long-term outcomes of HIE (Zanelli et al., 2016).

Clinical Aspects


There are three levels of HIE: mild, moderately severe, and severe (Zanelli et al., 2016). Mild hypertonia, poor feeding, and irritability present during the first few days of life is categorized as mild HIE. Hypotonia, diminished grasp and gag, Moro reflex and suck, seizure activity, and apneic episodes may be seen when HIE is moderately severe. These symptoms may resolve within 1 to 2 weeks and lead to a better long-term outcome. In infants with severe HIE, seizures can be delayed, severe, and show resistance to conventional anticonvulsant therapy. Other symptoms of severe HIE may also include stupor or coma, respiratory failure requiring mechanical ventilation, generalized hypotonia and depressed reflexes, abnormal ocular motion such as nystagmus, dilated or fixed pupils, and arrhythmia as well as hypotension. These symptoms may worsen during the rewarming period and even cause death.

Therapeutic hypothermia/cooling therapy is the most promising treatment for HIE. The gold standard is to initiate cooling within 6 hours of birth to maximize an optimal outcome (Karlsen, 2013). Once cooling therapy is determined, passive (turning off the radiant warmer) or active cooling (placing an infant on a cooling blanket or head cooling) should be implemented.

176All neonates who qualify for cooling therapy are cooled to a rectal temperature of 33.5°C or 92.3°F for 72 hours (Burton et al., 2015; Wayock et al., 2014; Zanelli et al., 2016). The criteria to determine whether or not to initiate cooling are a gestational age greater than or equal to 36 weeks and a birth weight greater than or equal to 1,800 g; umbilical cord blood gas or arterial blood gas obtained in the first hour of life with a pH less than or equal to 7.0; or base deficit greater than 16 mmol/L. Cooling also requires a neurologic examination denoting seizures, level of consciousness, spontaneous activity when awake or aroused, posture, tone, primitive reflexes, heart rate, respiratory rate, and reaction of pupils to light.

Seventy-two hours after being placed on a cooling blanket or cooling hat, a slow and controlled rewarming process should be cautiously performed and monitored. At present, there is limited evidence to indicate the safest way and speed to rewarm severely hypothermic infants. Based on the recommendation, rewarming speed should not exceed 0.5°C per hour to prevent sudden vasodilation, hypotension, and other clinical deterioration (Holton, 2014; Karlsen, 2013). During the rewarming period, vital signs, level of consciousness, neurologic examination, and blood gases should be closely monitored.


It is critical for the nurse to closely monitor heart rate and rhythm, blood pressure, pulses, perfusion, respiratory rate and effort, oxygen saturation, acid–base status, and blood glucoses during both cooling and rewarming phases. Monitoring the rectal temperature is helpful, because the skin temperature of the infant is higher than the rectal temperature during the rewarming period. If an infant deteriorates rapidly during either the cooling or rewarming period, the nurse must be prepared to perform a full cardiopulmonary resuscitation.

It is important to monitor closely for any seizure activity. Continuous EEG monitoring is normally placed during the duration of cooling. A full montage EEG and an MRI should be obtained after an infant is rewarmed and stable.

It is essential to perform a complete neurologic examination with hands-on care, including pupils, level of consciousness, and any signs or symptoms of increased intracranial pressure. It is important to ensure appropriate sedation during cooling therapy to optimize comfort and efficacy of the cooling. Inadequate sedation increases metabolic rate and decreases the effectiveness of cooling.

It is critical to monitor intake and output closely as fluid is normally restricted to avoid fluid overload and cerebral edema. Infants who undergo cooling therapy are at risk for renal impairment and electrolyte imbalance, which requires frequent monitoring and correction of any imbalance.

Infants who receive cooling often are treated with antibiotics for possible infection. It is vital to monitor any signs and symptoms of infection. It is also important to monitor for any signs of coagulopathy such as petechiae. Infants may require transfusions because of coagulopathy induced by hypothermia and decreased platelet function.

177It is critical to frequently assess the skin for possible subcutaneous fat necrosis. Erythematous nodules and plaques over boney areas such as the back, arms, buttocks, and thighs are the characteristic areas of subcutaneous fat necrosis that may worsen during cooling and can be very painful.

Families are an integral part of care for an infant admitted to the NICU. Continuous updates and support are essential to families while their babies undergo cooling therapy. It is important to encourage bonding by allowing parents to touch their baby and help with care.


Perinatal HIE is a major health issue globally. It can lead to neurologic deficits, neurodevelopmental disabilities, long-term functional impairments, and significant learning difficulties later on in a child’s life. Although there are no effective pharmacologic therapies to treat HIE currently, intentional cooling therapy has been the most promising and has become the standard of care for moderate to severe HIE. All cooling criteria and a sound neurologic examination need to be carefully reviewed to determine if the infant is a candidate for this therapy.

Close monitoring of an infant, including thorough frequent assessments, is critical during the cooling and rewarming phase. It is important to understand and recognize any potential side effects. It is also vital to include parents and family in nursing care. Families must understand the reasons behind cooling therapy, the expected length of treatment, and the potential for long-term morbidities.


Current research supports the efficacy of intentional cooling treatment for infants who are more than or equal to 36 weeks gestation and more than or equal to 1,800 g. However, there has been significant research in HIE for multimodal therapeutic approaches, and many clinical trials are in the process to prove that cooling used on infants who are younger than 36 weeks is applicable and effective as well.

Barks, J. (2008). Technical aspects of starting a neonatal cooling program. Clinics in Perinatology, 35(4), 765–775. doi:10.1016/j.clp.2008.07.009

Fatemi, A., Wilson, M. A., & Johnston, M. V. (2009). Hypoxic-ischemic encephalopathy in the term infant. Clinics in Perinatology, 36(4), 835–858. doi:10.1016/j.clp.2009.07.011

Graham, E. M., Ruis, K. A., Hartman, A. L., Northington, F. J., & Fox, H. E. (2008). A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy. American Journal of Obstetrics & Gynecology, 199(6), 587–595. doi:10.1016/j.ajog.2008.06.094

Holton, T. (2014). Clinical guidelines (nursing): Therapeutic hypothermia in the neonate. The Royal Children’s Hospital Melbourne. Retrieved from


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Jun 30, 2018 | Posted by in NURSING | Comments Off on Ischemic Encephalopathy
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