Diagnostic ultrasound ( PDFDrive )

1204 PART IV Obstetric and Fetal Sonography
FIG. 34.31 Echogenic Mineralized Thalamostriate Vessels
(Arrow). These vessels form an echogenic arborizing (branching) pattern
in the thalamus, which may be seen in normal fetuses but can be
associated with many fetal conditions.
efects depending on the individual pathogens and time of
maternal infection. Immunization, prenatal screening, and case
management protocols have been proposed. 232 he Zika infection
(particularly in the irst trimester) tends to be very severe with
micrencephaly, microcephaly, cortical abnormalities, dysgenesis
of the corpus callosum, and calciications, which are oten at the
gray-white junction. 197
In North America, CMV is most common intrauterine infection,
afecting about 0.2% to 2.0% of live births, and is a common
cause of mental retardation and sensorineural hearing loss. he
next most common infections in North America are toxoplasmosis
and herpes simplex. he severity of injury oten relates
more to the age when infection irst occurs and afects brain
development than to the speciic organism. Cerebral and noncerebral
ultrasound indings as noted below for CMV are shared
by many of the infections, so detection of any of these indings
should include general assessment for infections. Unfortunately,
several indings can appear or evolve in late pregnancy, so surveillance
with ultrasound should continue throughout pregnancy,
with MRI employed as appropriate. 11,233-235
Most mothers acquire primary CMV infection through contact
with infected persons, but reinfection can also occur. CMV afects
1% to 2% of pregnancies, and vertical transmission to the fetus
occurs in 30% to 40%. About 10% to 15% of these have symptoms
at birth, and of these about 20% to 30% die and 90% of survivors
have neurodevelopmental handicap. Of the 85% to 90% of infants
who appear normal at birth, 5% to 15% will develop late complications
including hearing loss or developmental delays.
Diagnosis of fetal infection can be made via amniocentesis.
Ultrasound and MRI are used to help determine prognosis but
are imperfect at predicting outcomes. he odds ratio of poor
outcome with noncerebral abnormality is 7.2 and with cerebral
abnormality is 25.5; although the absence of indings is reassuring,
it does not guarantee a good outcome. Cerebral and posterior
fossa indings include VM, increased periventricular echogenicity,
calciications, ventricular synechiae, microcephaly, periventricular
pseudocysts or other cysts, malformations of cortical development,
and cerebellar abnormality (Fig. 34.32). Noncerebral indings
include echogenic bowel, hepatomegaly, IUGR, oligohydramnios
or polyhydramnios, ascites or pleural efusion, liver
calciications, and placental enlargement. 233-237
Congenital toxoplasmosis is caused by the transplacental
passage of the parasite Toxoplasma gondii from an infected mother
who is typically asymptomatic and acquires infection through
contact with raw or undercooked meat, cat litter, or exposure
to infected water or soil (gardening). In the United States, 15%
of childbearing-age women are infected, and incidence of
congenital toxoplasmosis is about 400 to 4000 per year. Interestingly,
transmission to the fetus increases with gestational age
and is estimated at about only 6% to 15% in the irst trimester
but increases to 60% to 81% in the third trimester. If untreated,
about 20% to 50% develop infection. Fetal disease severity,
however, decreases with age and is highest in the irst trimester.
Prenatal cerebral indings may appear late ater 24 weeks and
suggest a poor prognosis and can include VM, cerebral calciications,
echogenic parenchymal nodules, difuse periventricular
echogenicity, callosal dysgenesis, microcephaly, IUGR, and
hydrops. Most fetuses (70%-90%) are infected in later pregnancy
and are asymptomatic at birth, but some manifest the diagnostic
triad (chorioretinitis, hydrocephalus, intracranial calciications)
and hepatosplenomegaly. Asymptomatic infants remain at high
risk of developing late chorioretinitis and neurologic deicits.
Maternal serum testing and amniocentesis can conirm infection.
Prenatal and postnatal therapy can improve outcomes. 232,238-240
VASCULAR MALFORMATIONS
A variety of vascular malformations are described prenatally,
including the vein of Galen aneurysmal malformation, dural
sinus malformation, and pial arteriovenous malformation. 241
he most common is the vein of Galen aneurysmal malformation,
which is a congenital anomaly of midline choroidal and mural
vessels that drain into and dilate the embryonic precursor of the
vein of Galen, the median prosencephalic vein of Markowski,
which in turn drains through an aberrant falcine sinus that can
be mistaken for the vein of Galen. In general, this anomaly
becomes detectable in the third trimester as a cystlike midline
space behind the thalamus with turbulent follow on Doppler
(Fig. 34.33). In prenatal cases 81% are associated other abnormalities
that predict a poor outcome, including heart failure and
cerebral abnormalities such as VM, malformations of cortical
development, and ischemic and hemorrhagic changes. It is not
associated with chromosomal abnormality. Postnatal treatment
is with embolization, which is delayed to about 6 months unless
there is heart failure. Outcome can be good in the few who have
isolated lesions and no heart failure. 11,241-243
Pial arteriovenous malformations are abnormal, usually
supratentorial, supericial arteriovenous communications eventually
draining into and dilating the vein of Galen. hey may result