Diagnostic ultrasound ( PDFDrive )

1550 PART V Pediatric Sonography
A
B
FIG. 45.47 Subarachnoid Hemorrhage Is a Secondary Process Following IVH When Blood Flows From the Fourth Ventricle Into the
Cisterna Magna. (A) Axial sonogram of the posterior fossa shows hemorrhage in the subarachnoid space (H) and cisterna magna. (B) Axial
sonogram shows blood in the subarachnoid space and clot (C) within the fourth ventricle and dilated foramen of Magendie (arrows).
parenchymal hemorrhage or injury as described by Daneman 3
and others. 132
Merrill and colleagues 133 reported 13 cerebellar hemorrhages
in 525 infants under 1500 g. Each of these occurred in the irst
week of life in unstable neonates with acidosis or hypotension
requiring intensive resuscitation, but not always associated with
supratentorial hemorrhage. On follow-up to 2 years, four infants
had cognitive deicits and developmental delay without signs of
motor abnormalities. Cerebellar hemorrhage has been followed
to term with MRI in some studies, and cerebellar volume loss
has been reported that has been more extensive than the initial
hemorrhage. he exact mechanism is not known, but Volpe has
postulated that it may be due to selective neuronal necrosis. 134
hree cases of prenatally diagnosed posterior fossa cysts were
found to result from hemorrhage. hese were initially thought
to be congenital posterior fossa arachnoid cysts but were recognized
because of debris in the cysts and hemosiderin on MRI. 135
In neonates, cerebellar hemorrhage has rarely required surgical
intervention, although older children may require emergency
drainage.
Subarachnoid Hemorrhage
he presence of enlarged interhemispheric and sylvian issures
with thickened sulci and increased echogenicity can suggest the
diagnosis of subarachnoid hemorrhage (SAH). SAH may occur
in neonates who have experienced asphyxia, trauma, or disseminated
intravascular coagulation and may be the only hemorrhage
in full-term infants who are not at risk for GMH. Cisternal
SAH has been found ater IVH but can be a diicult diagnosis
on ultrasound. Posterior fossa views can aid in making the
diagnosis (Fig. 45.47). Spread of blood from the ventricular system
into the spinal subarachnoid space ater GMH is common and
can be seen within 24 hours of the initial, severe IVH in premature
infants. 107
Cerebral Edema and Infarction
White Matter Injury of Prematurity or
Periventricular Leukomalacia
WMIP, previously known as “periventricular leukomalacia,” the
principal ischemic lesion of the premature infant, is infarction
and necrosis of the periventricular white matter. In MRI studies 136
the use of difusion-weighted imaging (which shows hyperintense
areas of restricted difusion) have demonstrated that white matter
damage to premature infants oten extends beyond the periventricular
areas into the cerebral white matter and cortex, the
thalamus, basal ganglia, brainstem, and cerebellum. his premature
pattern has been termed “white matter injury of prematurity.”
31,46,54 In some cases, there is a history of cardiorespiratory
compromise, resulting in hypotension and severe hypoxia and
ischemia. he pathogenesis of PVL has been found to relate to
three major factors: (1) the immature vasculature in the periventricular
watershed; (2) the absence of vascular autoregulation
in premature infants, particularly in the cerebral white matter;
and (3) the maturation-dependent vulnerability of the oligodendroglial
precursor cell. hese cells are extremely vulnerable to
attack by free radicals generated in the ischemia-reperfusion
sequence. 46,97
he prevalence of PVL in the very-low-birth-weight infant
(<1000 g) was previously reported as 25% to 40%. 87 Later, Ment
and colleagues 94 reported that PVL incidence decreased to 7%.
However, with both ultrasound and MRI comparison, cystic and
noncystic white matter damage has been shown in 50% of preterm
infants. 31 Because more infants are surviving with WMIP/PVL
(and thus are at risk for cerebral palsy) than in the past, it becomes
even more important to diagnose these lesion. WMIP consists
of cystic changes of PVL, which are more oten visualized on
ultrasound, and noncystic white matter damage, which is better
seen on MRI 137 (Fig. 45.48).