Diagnostic ultrasound ( PDFDrive )

1608 PART V Pediatric Sonography
A
B
C
FIG. 47.15 Progression to Moyamoya Angiopathy in
3 1 2-Year-Old Boy With Sickle Cell Disease. (A) Patient had
high normal velocities of the left MCA. MRA performed 2 months
later was normal. (B) At 1-year follow-up screening, abnormally
low low in the left MCA (<40 cm/sec) is noted. (C) MRA at this
time demonstrates moyamoya changes (arrow) with complete
occlusion of the left A1 and M1 segments.
he management of children with conditional velocities is
also being studied. Many remain in the conditional range for
years or eventually normalize, but up to 23% of this cohort convert
over time to abnormal velocities 89,90 (Fig. 47.15). Protocols using
less invasive therapies such as hydroxycarbamide (e.g., hydroxyurea
therapy) in children with conditional velocities show promise
and suggest that following these patients with TCD may be useful
to assess treatment response. 94-96
Vasospasm
Cerebral vasospasm can present as a complication of subarachnoid
hemorrhage secondary to rupture of an intracranial aneurysm, 99
secondary to trauma with or without hemorrhage or secondary
to other pathology. 33,100,101 TCD sonography has become an
important tool in detecting vasospasm before the patient develops
ischemic neurologic deicits or infarct. 37,102 High speciicity has
been described (100%) for vertebral/basilar vasospasm with PSV
greater than 80 and 95 cm/sec, respectively, 102 and with high
speciicity in the diagnosis of MCA vasospasm (98%-100%) when
PSV is greater than 200 cm/sec 103,104 but a sensitivity of only
59%. 105 Digital subtraction angiography continues to be the
reference standard, but because of the cost, high radiation, and
risk of the procedure, it is not as widely used. 37
In adults with aneurysm rupture causing subarachnoid hemorrhage,
vasospasm typically develops 4 to 14 days ater the rupture, 33
gradually increasing and peaking between days 5 and 14. 99 Following
traumatic brain injury, vasospasm can occur (19%-68%
incidence) but usually without clinical deicits (4%-17%). Cerebral
vasospasm in adults with traumatic brain injury presents in the
irst 2 days ater the injury, 99 peaks around day 5 to 7 and has a
shorter overall duration. Posttraumatic vasospasm can also occur
in the absence of subarachnoid hemorrhage and has an even
shorter duration (1.25 days). 99,106 Vasospasm has been seen in
17% of patients with ruptured brain arteriovenous malformation
and presents in 4 to 11 days following rupture. 107 Patients with
persistent severe vasospasm may develop permanent deicits
from cerebral infarction with morbidity and mortality rates of
10% to 30%. 33 In a 2010 study of pediatric patients with moderate