Diagnostic ultrasound ( PDFDrive )

CHAPTER 45 Neonatal and Infant Brain Imaging 1543
occurs is more important than the classiication. he key causes
of poor neurologic outcome relate to hydrocephalus and parenchymal
extension into the descending white matter tracts
(Table 45.2).
Sonography is the most efective method for detecting this
hemorrhage in the newborn period and for follow-up in the
subsequent weeks. Most hemorrhage (90%) occurs in the irst
7 days of life, but only one-third of these occur in the irst 24
hours. 101 he optimal cost-efective timing to screen premature
infants is at 10-14 days of life, to identify patients with signiicant
hemorrhage as well as those developing hydrocephalus. 102 Small
SEHs (grade I) might be missed when screening late if they
resolve quickly, but these have not proven clinically important.
A late screen for PVL should performed at 1 month to search
for the cystic changes of PVL, 103,104 because the clinical course
or irst brain ultrasound will not predict the later development
of hydrocephalus or PVL. An examination should be performed
earlier if required by the patient’s condition. Term-equivalent
age studies with MRI are now frequently done to determine the
extent of damage. Careful recent studies with ultrasound done
at term-equivalent age by Daneman and colleagues 3 have demonstrated
that many of the noncystic indings can be identiied
with high-resolution transducers focused on the brain parenchyma
in areas that are not periventricular where the noncystic WMIP
occurs.
Optimal Brain Ultrasound Screening in
Premature Infants (Less Than 30 Weeks’
Gestation or Less Than 1500 g)
FIRST SCAN: 10 TO 14 DAYS
Germinal matrix hemorrhage
Posthemorrhagic hydrocephalus
SECOND SCAN: 4 WEEKS OF AGE
Cystic PVL
Cystic PVL lesions coalesce, leaving only thin white matter
after 4 weeks
Ventricular enlargement
THIRD SCAN: TERM-EQUIVALENT AGE
White matter injury of prematurity (beyond only PVL)
Best seen by ultrasound or magnetic resonance imaging
PVL, Periventricular leukomalacia.
Complications of SHE and IVH are IVOH, usually at the
foramina of Monro or the sylvian aqueduct, and EVOH, at the
arachnoid granulations. Complications of IPH are permanent
areas of damaged brain that can become necrotic, leading to
porencephalic cysts.
TABLE 45.2 Grades of Germinal Matrix
Hemorrhage
Grade
I
II
III
IV
Type and Description
Subependymal hemorrhage
Intraventricular extension without hydrocephalus
Intraventricular hemorrhage with hydrocephalus
Intraparenchymal hemorrhage with or without
hydrocephalus
Subependymal Hemorrhage
(Grade I Hemorrhage)
On sonographic examination, acute SEH appears as a homogeneous,
moderately to highly echogenic mass (Fig. 45.36). he
echogenic clot oten causes focal hemorrhage in the caudothalamic
groove. he choroid plexus is normally quite thick at the trigone
of the lateral ventricle and tapers progressively anteriorly, descending
between the head of the caudate and the thalamus just
above the foramen of Monro. SEH may appear as a bulge in the
choroid plexus (Fig. 45.37, Video 45.9 and Video 45.10). As the
hematoma ages, the clot becomes less echogenic, with its center
becoming sonolucent. Over time the clot retracts, and necrosis
A
B
FIG. 45.36 Subependymal Hemorrhage (SEH), Bilateral. (A) Coronal sonogram shows echogenic SEH bilaterally. (B) Parasagittal sonogram
shows the hemorrhage located in the caudothalamic notch. See also Video 45.9 and Video 45.10.