HYPOXIC ISCHEMIC ENCEPHALOPATHY
Category: Child Health
Abstract : Further Inpatient Care (hypoxic ischemic encephalopathy): • Close physical therapy and developmental evaluation are needed before discharge. Further Outpatient Care: • As noted before, most infants do not need specific outpatient care. However, they should be monitored in a regular pediatric clinic. Severely disabled children may need to be monitored in multispecialty cl
Further Inpatient Care (hypoxic ischemic encephalopathy):
• Close physical therapy and developmental evaluation are needed before discharge.
Further Outpatient Care:
• As noted before, most infants do not need specific outpatient care. However, they should be monitored in a regular pediatric clinic. Severely disabled children may need to be monitored in multispecialty clinics and by a developmental neurologist.
In/Out Patient Meds (hypoxic ischemic encephalopathy):
• Continuation of seizure medications should depend on evolving CNS symptoms and EEG findings.
o In most infants who are developing normally and have a normal EEG before hospital discharge, phenobarbital is discontinued within 3-4 weeks of birth.
o In those with significant CNS disability with or without persistent episodes of seizures, phenobarbital is continued for 3-6 months; the decision to wean off the drug depends on later changes in EEG and clinical course.
Transfer (hypoxic ischemic encephalopathy):
• Infants delivered in a level I or II center may require transfer to a tertiary neonatal intensive care unit for definitive neurodiagnostic studies (EEG and neuroimaging) and consultation with a pediatric neurologist.
Deterrence/Prevention (hypoxic ischemic encephalopathy):
• The era of neuroprotection may be near. Most of the treatments discussed here are experimental. With the exception of hypothermia, which is still being examined in clinical trials, none of the therapies cited below has been consistently shown to have efficacy in human infants.
o Allopurinol: Slight improvements in survival and CBF were noted in a small group of infants tested with this free-radical scavenger in one clinical trial.
o High-dose phenobarbital: In another study, 40 mg/kg phenobarbital was given over 1 hour to infants with severe HIE. Treated infants had fewer seizures (9 of 15) than untreated control infants (14 of 16). Treated infants also had fewer neurological deficits at age 3 years (4 of 15) than untreated infants (13 of 16). This is the only study showing a benefit of this magnitude in using high-dose phenobarbital for severe HIE. As of this writing, this treatment is not considered the standard of care.
o EAA antagonists: MK-801, an EAA antagonist, has shown promising results in experimental animals and in a limited number of adult trials. It has not been tested in newborn infants. This drug has serious cardiovascular adverse effects.
o Hypothermia: Currently being intensely tested as a neuroprotective therapy, hypothermia's mechanism of protection is not completely understood. Explanations include (1) reduced metabolic rate and energy depletion; (2) decreased excitatory transmitter release; (3) reduced alterations in ion flux; and (4) reduced vascular permeability, edema, and disruptions of blood-brain barrier functions.
The current state-of-the-art on hypothermia is summarized by the following:
�� Brain cooling to about 3-4°C below the baseline temperature (ie, to 33-34°C) may be neuroprotective. The optimal level of hypothermia for maximal neuroprotection is not known. Extreme hypothermia may cause significant systemic side effects.
�� Up to 48-72 hours of cooling may be needed to prevent secondary neuronal loss. The greater the severity of the initial injury, the longer the duration of hypothermia needed for optimal neuroprotection. �� Cooling must be begun early, within 1 hour of injury, if possible; however, favorable outcome may be possible if cooling is begun up to 6 hours after injury.
�� A special device that selectively cools the head is now being tested in clinical studies; it is not available in the market. Some investigators believe that total body cooling (as done for open-heart surgery) may be superior to selective head cooling. The relative merits and limitations of different methods of brain cooling have not been studied.
�� Hypothermia may cause significant side effects, including coagulation defects, leukocyte malfunctions, pulmonary hypertension, and worsening of metabolic acidosis. Until more is learned, hypothermia remains an experimental modality.
Prognosis (hypoxic ischemic encephalopathy):
• Accurate prediction of the severity of long-term complications is difficult, although the following pointers may be used:
o Lack of spontaneous respiratory effort within 20-30 minutes of birth is associated with almost uniform mortality.
o The presence of seizures is an ominous sign. The risk of poor neurological outcome is distinctly greater in such infants, particularly if seizures occur frequently and are difficult to control.
o Abnormal clinical neurological findings persisting beyond the first 7-10 days of life usually indicate poor prognosis. Among these, abnormalities of muscle tone and posture (hypotonia, rigidity, weakness) should be carefully noted.
o Persistent feeding difficulties, which generally are due to abnormal tone of the muscles of sucking and swallowing, also suggest significant CNS damage.
o Poor head growth during the postnatal period and the first year of life is a sensitive finding predicting higher frequency of neurologic deficits.
Medical/Legal Pitfalls (hypoxic ischemic encephalopathy):
• Birth asphyxia, birth injury, and perinatal asphyxia are terms often used incorrectly to describe HIE. This must be avoided, because their improper usage has medicolegal implications.
o Birth injury is a condition in which fetal or neonatal injury has occurred during the process of birth (ie, during the first and second stages of labor). Examples include brachial plexus injury; fracture of the clavicle; forceps-induced damage to the facial nerve or soft tissues; and cuts or bruises from scissors, clips, or scalp monitors.
o Birth asphyxia is similar to birth injury in that asphyxia occurs during the first and second stages of labor when the fetus was otherwise normal.
o Perinatal asphyxia signifies that asphyxia occurred at any time in the perinatal period, namely, from conception through the first month of life.
• The AAP and ACOG recommend using HIE because this term accurately describes the clinical condition, encephalopathy from asphyxia, without implying the time of brain injury. The AAP and ACOG also advise not using the terms perinatal asphyxia or birth asphyxia because it is difficult to identify the time of brain injury and nearly impossible to ascertain that the brain had been "normal" before such injury. These terms are vague and do not reflect all components of HIE.
• Avoid inappropriate designation of the diagnosis as asphyxia and ascribing asphyxia as a cause of any neurological symptom. The medical records should contain objective information on maternal and neonatal history and on clinical findings on the infant.
• The findings from any brain imaging procedures that have been carried out must be included in the total assessment of the infant's clinical status. The findings of neuroimaging tests and EEG (if performed) must be documented.
• No diagnostic tests conclusively prove that a given magnitude of asphyxia has led to a specific neurological injury. Acute perinatal and intrapartum events have been found in only about 20% of children diagnosed as having cerebral palsy.
• Parents must be given realistic explanations about their infant's clinical status and prognosis. It should be emphasized that, except under controlled experimental conditions, cause-and-effect is nearly impossible to establish.
• Good medical records are always better than poor medical records: all details about the infant's status and parental counseling must be documented carefully.
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