Children with hypoxic-ischemic injury (HII) or hypoxic-ischemic encephalopathy (HIE) can have acute clinical problems, such as seizures, respiratory distress, or rapid deterioriation of consciousness. However, clinical presentation is commonly delayed. Neurological deficits might only become obvious months or years following the event.
Clinical assessment of the extent or severity of the acute event is of limited prognostic value in infants. The immature brain, although more vulnerable to certain adverse stimuli, has an astonishing potential for compensatory functional development.1 Neurological deficits become more obvious when motor, cognitive, and associative demands rise above the level of basic infant functions. Walking, talking, school performance, or refined tests can reveal the limits of the brain's compensatory capacity.2
HIE in infants can be approached by considering the three principal clinical settings: the preterm ventilated infant, the term infant following birth asphyxia, and the infant following intrauterine compromise. Factors that might initiate or predispose to HIE are intrauterine or perinatal infection, metabolic disease, edema, hemorrhage, hypotensive events, and emboli.
When HIE occurs in utero, it may appear as migration or gyration anomaly, cystic brain malformation, hypoplasia, or agenesis. Although a reliable estimate of the hypoxic-ischemic origin of a given lesion may be reached, it is important to be aware that reading the past from imaging presentations can be subject to uncertainty in individual cases.
Imaging modalities have recently become increasingly more sophisticated. Modern ultrasound with high resolution B-mode and color Doppler are effective tools capable of answering many questions about HIE that are posed in the neonatal period and early infancy. In the hands of an experienced and specialized examiner, ultrasound is particularly useful in ill-ventilated premature infants, while having little or no impact on the unstable state of these patients. In term infants, following severe asphyxia, computed tomography (CT) can be helpful when ultrasound is inconclusive. Beyond the immediate postnatal period, magnetic resonance imaging (MRI) is often the most informative and useful imaging modality. It is more versatile than any other method. Acute changes can be accompanied by abnormal brain lactate concentration, intracellular edema, vascular occlusion, or regional perfusion deficits, which can be displayed by more specialized MR techniques, such as MR angiography, MR spectroscopy, diffusion or perfusion imaging. In subacute or chronic HIE, it is helpful to increase the sensitivity for detecting hemorrhage by using a gradient-echo sequence (2D FLASH) for hemosiderin-related susceptibility effects.
Prediction of outcome can be expected to gain considerable impact with increasing sophistication of imaging. In the ill, preterm infant, consistently normal brain imaging constitutes by far the most reliable prognostic factor for normal neurological function beyond infancy.
Medical-legal issues increasingly center on the evidence of HIE supplied by imaging. There is the expectation that modern imaging will solve complex problems. Usually, interest concentrates on timing of hypoxic-ischemic events related to birth. Although many cases of hypoxia-ischemia can be assigned to in utero versus peri-or postnatal events, evaluation based on postnatal imaging should be of sufficient quality and subject to expert reading. In early in utero insults, some major problems encountered are infection versus infarction, malformation versus HIE, and the precise timing of an insult when there is a lack of adequate perinatal imaging.
Minor perinatal events—normally of little risk for inducing HIE—might be superimposed on an already damaged, infective, edematous, metabolically abnormal, or maldeveloped brain, and thus lead to a catastrophic or unfavorable outcome. Imaging appearances should therefore be supplemented by a history of prenatal risk factors and perinatal events. Appearances, such as hydranencephaly or periventricular leukomalacia, are usually linked to one period in the pre-, peri-, or postnatal time frame. Exceptions from this common denotation should be kept in mind and such patterns of brain damage should therefore be regarded as to whether they favor one particular period or clinical setting.
KeywordsWhite Matter Preterm Infant Term Infant Hypoplastic Left Heart Syndrome Subcortical White Matter
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