Diagnostic ultrasound ( PDFDrive )

1552 PART V Pediatric Sonography
A
B
C
D
FIG. 45.49 Periventricular Leukomalacia (PVL): Echogenic to Cystic. (A) Coronal sonogram shows acute increased areas of echogenicity.
(B) Development of cystic PVL 1 month later. (C) and (D) Sagittal sonograms. See also Video 45.16.
Pathologically, the periventricular white matter undergoes
coagulation necrosis, followed by phagocytosis of the necrotic
tissue. his necrosis usually occurs in the white matter adjacent
to the external angles of the lateral ventricles. his results in
decreased myelination in these areas and focal dilated lateral
ventricles. In more severe cases of PVL, cystic cavities
develop. 40,152,154 Petechial hemorrhages can complicate PVL. In
fact, hemorrhagic PVL has been shown to be much more
common (64%) than thought when there is MRI-ultrasound
correlation. 157
he initial sonographic examination indings in infants who
ultimately develop cystic PVL may be normal. Within 2 weeks
of the initial insult, however, the periventricular white matter
increases in echogenicity until it is greater than the adjacent
choroid plexus. his increased echogenicity is usually caused by
edema from infarction and may also result from hemorrhage 158
(Fig. 45.49A). Two to 4 weeks ater the insult, cystic changes
may develop in the area of abnormal echogenic parenchyma
(Fig. 45.49B-D; Video 45.16). he cysts can be single or multiple
and are parallel to the ventricular border in the deep white matter
and oten lateral and/or superior to the top of the ventricles.
hese cysts measure from millimeters to 2 cm in diameter. he
cystic changes are usually bilateral and oten symmetrical. Cystic
changes in the corpus callosum can progress to later thinning. 139,159
Pathologic studies suggest that sonography actually underestimates
the incidence of PVL. 158,160 In 51 cases of postmortem-proven
PVL, Adcock and colleagues 160 found that in 44% the neurosonogram
failed to make the diagnosis for two main reasons:
(1) most oten the ultrasound examinations were performed
before 1 month of age and missed the cystic stage of PVL, and
(2) the lesions were microcystic and not large enough to ind
on ultrasound.
On subsequent sonograms, the cystic lesions may enlarge or
resolve. 154 herefore normal-appearing white matter on sonograms
obtained several weeks to months ater the insult does not exclude
the occurrence of PVL. MRI becomes more sensitive than either
CT or ultrasound for long-term follow-up of parenchymal injury,
because when myelination progresses, glial scarring from
damaged white matter can be diagnosed (Fig. 45.50), typically
with thinning of the white matter adjacent to an enlarged ventricle
where the cysts have coalesced and are no longer visible. Because
the initial ultrasound examination indings are oten normal in
infants who have sustained a signiicant hypoxic-ischemic event,
late sonograms should be obtained at about 4 weeks ater birth
to exclude evolving PVL. he characteristic distribution of cystic
lesions that are clearly separate from the ventricle in PVL should
distinguish them from the parenchymal hemorrhage that occurs
in grade IV GMH. However, PVL and GMH can occur