Hypoxic-Ischemic Encephalopathy Follow-up

  • Author: Santina A Zanelli, MD; Chief Editor: Ted Rosenkrantz, MD   more...
 
Updated: Dec 15, 2011
 

Further Inpatient Care

Close physical therapy and developmental evaluations are needed prior to discharge in patients with hypoxic-ischemic encephalopathy (HIE).

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Further Outpatient Care

The goal of follow-up is to detect impairments and promote early intervention for those infants who require it.[92]

Growth parameters including head circumference should be closely monitored in all infants with hypoxic-ischemic encephalopathy.

In infants diagnosed with moderate-to-severe hypoxic-ischemic encephalopathy with either abnormal neurologic examination findings or feeding difficulties, intensive follow-up is recommended. This should include follow-up by developmental pediatrician and pediatric neurologic. Evaluation by a pediatric ophthalmologist is also recommended for these infants because damage to the posterovisual cortex can occur. Hearing testing should occur prior from discharge from the NICU and may need to be repeated in infants at risk for late-onset healing loss (eg, pulmonary hypertension, antibiotic use).

In infants with moderate hypoxic-ischemic encephalopathy but no feeding difficulties and normal neurologic examination findings, routine care is appropriate. If hypothermia therapy was used in the neonatal period, follow-up is recommended for the continued evaluation of the efficacy and safety of this newly introduced therapy. Data should be entered into the available registries, databases, or both whenever possible.

Infants with mild hypoxic-ischemic encephalopathy generally do well and do not require specialized follow-up.

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Inpatient & Outpatient Medications

Continuation of seizure medications should depend on evolving CNS symptoms and EEG findings. Follow-up by a pediatric neurologist is recommended.

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Transfer

Infants who present in a level I or II center may require transfer to a tertiary neonatal ICU for definitive neurodiagnostic studies (EEG and neuroimaging), consultation with a pediatric neurologist, and evaluation for hypothermia therapy.

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Deterrence/Prevention

The use of intrapartum markers such as fetal heart rate monitoring are poor predictors of neonatal outcomes and long-term risk of cerebral palsy.[93]

Most treatments under investigation are discussed above and remain experimental. With the exception of hypothermia therapy, none has consistently shown efficacy in human infants.

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Complications

See Clinical.

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Prognosis

See Mortality/Morbidity for data on outcomes.

Accurate prediction of the severity of long-term complications is difficult, although clinical, laboratory, and imaging criteria have been used.[94] The following criteria have been shown to be the most helpful in outlining likely outcomes:

  • Lack of spontaneous respiratory effort within 20-30 minutes of birth is almost always associated with death.
  • 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.
  • 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.
  • EEG at about 7 days that reveals normal background activity is a good prognostic sign.
  • Persistent feeding difficulties, which generally are due to abnormal tone of the muscles of sucking and swallowing, also suggest significant CNS damage.
  • Poor head growth during the postnatal period and the first year of life is a sensitive finding predicting higher frequency of neurologic deficits.
  • Of note, the use of hypothermia therapy changes the prognostic value of clinical evaluation in infants with hypoxic-ischemic encephalopathy and its impact on predicting outcomes is still under evaluation.[95]
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Contributor Information and Disclosures
Author

Santina A Zanelli, MD  Assistant Professor, Department of Pediatrics, Division of Neonatology, University of Virginia Health System

Santina A Zanelli, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Neuroscience, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Dirk P Stanley, MD  Resident Physician, Department of Pathology, University of Virginia Health System

Disclosure: Nothing to disclose.

David A Kaufman  MD, Associate Professor of Pediatrics, Division of Neonatology, University of Virginia Health System

David A Kaufman is a member of the following medical societies: American Academy of Pediatrics, European Society for Paediatric Infectious Diseases, Medical Society of Virginia, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Ted Rosenkrantz, MD  Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP  Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Director, Neonatal Follow-up Program, Monroe Carell Jr Children's Hospital at Vanderbilt

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, National Hospice and Palliative Care Organization, Society for Pediatric Research, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Carol L Wagner, MD  Professor of Pediatrics, Medical University of South Carolina

Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD  Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Tonse NK Raju, MD, to the development and writing of this article.

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Fetal response to asphyxia illustrating the initial redistribution of blood flow to vital organs. With prolonged asphyxial insult and failure of compensatory mechanisms, cerebral blood flow falls, leading to ischemic brain injury.
Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the initial phase of energy failure, glutamate mediated excitotoxicity and Na+/K+ ATPase failure lead to necrotic cell death. After transient recovery of cerebral energy metabolism, a secondary phase of apoptotic neuronal death occurs. ROS = Reactive oxygen species.
Risk factors for neonatal encephalopathy.
Severe acute hypoxic-ischemic neuronal change in the basal ganglia is noted. Histologic examination reveals severe hypoxic-ischemic neuronal change, characterized by the presence of pyknotic and hyperchromatic nuclei, the loss of cytoplasmic Nissl substance, and neuronal shrinkage and angulation (arrow). These alterations begin to appear approximately 6 hours following hypoxic-ischemic insult. Reactive astrocytosis is evident approximately 24-48 hours after the primary hypoxic-ischemic event.
Significant astrocytosis in the basal ganglia following hypoxic-ischemic insult is observed. An immunohistochemical stain for glial fibrillary acidic protein (GFAP) was performed on the same tissue shown in the previous image to demonstrate the prominent gliosis secondary to the hypoxic-ischemic event. GFAP is a useful marker to study astrocytic response to injury. This gliosis of the basal ganglia, along with subsequent hypermyelination, is responsible for the evolution of status marmoratus over months to years.
Bilateral acute infarctions of the frontal lobe are shown. The infarctions depicted in the figure (arrows) are consistent with watershed infarctions secondary to global hypoperfusion. The lesions depicted in the image are consistent with an acute ischemic event, occurring within 24 hours of death. The regions most susceptible to hypoperfusion include the end-artery zones between the anterior, middle, and posterior cerebral arteries.
A prior hypoxic-ischemic event involving the occipital lobe has resulted in a chronic lesion marked by dyslamination, neuronal loss, and disorganized arrangements of myelinated white matter fibers. Grossly, the lesion was marked by preserved gyral crests and involved sulci, resulting in prominent, mushroom-shaped gyri.
A Luxol-Fast Blue stain was performed on the same tissue shown in the previous image to demonstrate the haphazard arrangement of myelinated white matter fibers projecting into the gray matter of the occipital cortex.
Randomized controlled trials of therapeutic hypothermia for moderate-to-severe hypoxic-ischemic encephalopathy (HIE).
Periventricular leukomalacia is depicted. This cystic lesion, present in the cingulate cortex, is consistent with periventricular leukomalacia. Note the extensive hemorrhage within the cystic space as well as the hemosiderin-laden macrophages around the lesional rim.
Periventricular leukomalacia is depicted. This figure depicts the lesion seen in the previous image at higher magnification. Extensive hemosiderin and reactive astrocytosis is present surrounding the lesion (center of field). Note the proximity of the lesion to the ependymal lining of the lateral ventricle (far right).
Summary of potential neuroprotective strategies.
Table. Sarnat Clinical Stages of Perinatal Hypoxic Ischemic Brain Injury[28]
State 1Stage 2Stage 3
Level of ConsciousnessHyperalertLethargic or obtundedStuporous
Neuromuscular Control
Muscle toneNormalMild hypotoniaFlaccid
PostureMild distal flexionStrong distal flexionIntermittent decerebration
Stretch reflexesOveractiveOveractiveDecreased or absent
Segmental myoclonusPresentPresentAbsent
Complex Reflexes
SuckWeakWeak or absentAbsent
MoroStrong; low thresholdWeak; incomplete; high thresholdAbsent
OculovestibularNormalOveractiveWeak or absent
Tonic neckSlightStrongAbsent
Autonomic FunctionGeneralized sympatheticGeneralized parasympatheticBoth systems depressed
PupilsMydriasisMiosisVariable; often unequal; poor light reflex
Heart RateTachycardiaBradycardiaVariable
Bronchial and Salivary SecretionsSparseProfuseVariable
GI MotilityNormal or decreasedIncreased; diarrheaVariable
SeizuresNoneCommon; focal or multifocalUncommon (excluding decerebration)
EEG FindingsNormal (awake)Early: low-voltage continuous delta and theta



Later: periodic pattern (awake)



Seizures: focal 1-to 1-Hz spike-and-wave



Early: periodic pattern with Isopotential phases



Later: totally isopotential



Duration1-3 days2-14Hours to weeks
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