Diagnostic ultrasound ( PDFDrive )

CHAPTER 45 Neonatal and Infant Brain Imaging 1547
A
B
FIG. 45.42 Intraventricular Hemorrhage: Dependent Clot. (A) Coronal sonogram shows dependent clot in an infant with the right side of
the head down. (B) Sagittal sonogram of the left lateral ventricle shows dependent clot (H) separate from the choroid plexus (C). Note also the
extensive echogenicity lining the ventricles, likely due to ventriculitis and blood clot.
A B C
FIG. 45.43 Intraparenchymal Hemorrhage. (A) and (B) Coronal sonograms show acute intraparenchymal hemorrhage in the right parietal
lobe and follow-up 8 days later. Note the change in echogenicity of the clot over time, with some areas that are still echogenic but other areas
that are now more isoechoic to brain parenchyma. (C) Coronal magnetic resonance image shows the clot. See also Video 45.11 and Video 45.12.
severe posthemorrhagic hydrocephalus. 110 Occasionally, a trapped
fourth ventricle may be caused by obstruction of both the
aqueduct and the outlets of the fourth ventricle. In these cases
a ventriculoperitoneal shunt will decompress only the lateral
and third ventricles. Shunting can have long-term side efects,
especially if there is a multiloculated hydrocephalus ater shunt
infection. 111
Intraparenchymal Hemorrhage (Grade IV
Hemorrhage)
IPH is usually in the cerebral cortex and located in the frontal or
parietal lobes, because it oten extends from the subependymal
layer over the caudothalamic groove (Fig. 45.43). Studies
suggest that IPH is caused by hemorrhagic venous infarction. 84,85
Periventricular hemorrhagic infarction (PVI) is believed to
be venous infarction secondary to a large SEH compressing
subependymal veins. hese focal periventricular white matter
infarcts are typically frontal to parieto-occipital and are asymmetrical,
usually unilateral, and if bilateral, asymmetrical in size.
PVI in the temporal lobe is associated with a greater risk of
cognitive, behavioral, and visual problems. 112 Infants with IPH
associated with GMH typically develop hemiparesis, and if there
is periventricular hyperintensity, they may develop cerebral
palsy. 113-118 It is thought that this hyperintensity may relate to
pressure from hydrocephalus. his is in contrast to infants with
periventricular echogenicity and minimal or no IVH, who are at
much higher risk for PVL. hese infarcts typically cause spastic
hemiparesis. 31,113
Acutely, IPH appears as an echogenic homogeneous mass
extending into the brain parenchyma. As the clot retracts, the
edges form an echogenic rim around the center, which becomes
sonolucent. he clot may move to a dependent position, and by
2 to 3 months ater the injury, an area of porencephaly (if there
is communication with the ventricle) or encephalomalacia
develops (Figs. 45.44 and 45.45).
Unusual types and sites of IPH, acute cystic changes, midline
shit, and downward extension of hemorrhage into the thalamus
may result from hemorrhage into PVL, secondary to infarction
or thromboembolism, from a bleeding diathesis (e.g., vitamin