Diagnostic ultrasound ( PDFDrive )

CHAPTER 45 Neonatal and Infant Brain Imaging 1553
A
B
C
D
FIG. 45.50 Periventricular Leukomalacia (PVL). (A) Coronal sonogram of cystic PVL. (B) and (C) Sagittal sonograms show large and small
affected areas of PVL. (D) Sagittal sonogram shows cystic PVL in the occipital lobe.
simultaneously. 161 Periventricular white matter damage can be
studied with cranial ultrasound if technical factors include careful
attention to focal areas of hyperechogenicity. Leijser and colleagues
162 divided white matter into grade 0, less echogenicity
than choroid plexus; grade 1, same echogenicity as choroid plexus;
and grade 2, brighter than choroid plexus. Only severe grade
(grade 2) predicted a poor neurologic outcome.
MRI has proven to be the best method for WMIP/PVL
diagnosis when done at term-equivalent age in the very-lowbirth-weight
infants most at risk for PVL. 163,164 he increasing
use of MRI has been controversial as a standard of care but
clearly adds to the prognostic value in predicting neurodevelopmental
outcomes of very premature infants. 165,166 he addition
of difusion-weighted imaging 167 and difusion tensor imaging 168
have also been shown to add value in predicting more extensive
white matter injury. Delayed myelination, ventricular enlargement,
and width of extracerebral spaces were not found to be good
predictors of cerebral palsy.
Term Infants With Hypoxic Ischemic Injury
Difuse cerebral edema with or without SAH is a common result
of hypoxic-ischemic events in full-term infants. In some cases,
acute very focal areas of edema may cause increased gray
matter–white matter diferentiation. However, it is common that
when brain edema can be diagnosed on ultrasound, there are
typically slitlike ventricles in a difusely echogenic brain with
poorly deined sulci. his echogenicity may cause efacement
of the sulci so that the sulci seem to disappear (Fig. 45.51). 4 he
brain parenchyma appears echogenic in the distribution of the
injury, and the sulci are diicult to appreciate because of surrounding
echogenic edematous brain. he mechanism of the
increased echogenicity of the brain parenchyma from cerebral
edema is not understood completely. One possibility is that the
increased intracellular luid causes more interfaces.
Color Doppler ultrasound evaluation of severely asphyxiated
infants has demonstrated earlier and at times more focal abnormalities
than gray-scale evaluation alone (see Chapter 46).
Investigators have used Doppler sonography to classify brain
edema and to predict outcome. Outcome of children with signiicantly
abnormal cerebral blood low was noted in 47 patients,
from newborns to 4 years of age. However, loss or reversal of
diastolic low did not necessarily imply a lethal outcome. Survival
was associated with prompt and efective treatment. 169 A few
studies have shown MRI changes early in neonatal life from
asphyxia, but most neonatologists resist moving a very unstable
newborn for magnetic resonance scanning. If the ischemic event
was severe enough to lead to infarction, difuse brain volume
loss occurs within 2 weeks, with ventricular enlargement