Diagnostic ultrasound ( PDFDrive )

1580 PART V Pediatric Sonography
Duplex sonography may serve as a bedside monitoring modality
for brain injury in a patient on ECMO. Studies have shown
that in neonates without apparent neurologic injury, cerebral
blood low velocity (CBFV) was signiicantly lower than normal
while on ECMO support and that CBFV increased ater decannulation.
Children who developed cerebral hemorrhage had
higher CBFV for days before clinical recognition of a cerebral
hemorrhage. 33
Therapeutic Hypothermia and
Brain Cooling
Brain temperature has been shown to be tightly linked to brain
perfusion. Few data are available on the impact of brain cooling
on the neonatal cerebral hemodynamics. Previous studies have
primarily focused on patients who received cooling for cardiac
surgery or treatment of traumatic brain injury. Hypothermia
was noted to decrease CBFV, whereas increased temperatures
increased CBFV. 34
DIFFUSE NEURONAL INJURY
Hypoxic Ischemic Injury and Asphyxia
he cerebral hemodynamic changes associated with HII or
asphyxia depend on many complex interacting factors including
the severity, time, and duration of the insult; ongoing hypercapnia
and hypoxemia; and maturity of the brain. In the setting of
severe or prolonged asphyxia, brain tissue HII results in the
excessive release of excitatory amino acids, such as glutamate
and aspartate. he subsequent complex cascade of neurometabolic
events results in cerebral vasodilation with subsequent cerebral
edema. 35 In addition to the conventional gray-scale imaging
indings of increased echogenicity of the hemispheric white
matter, increased corticomedullary diferentiation, slitlike ventricles,
and efaced subarachnoid spaces, signiicant changes in
hemodynamic metrics may be observed on duplex sonography.
Increased mean CBFV and decreased RI values (<0.55-0.60)
may be seen on spectral Doppler imaging within 12 hours of
injury, lasting up to several days ater the initial insult (Fig.
46.7). 36,37 Furthermore, RI measurements, in conjunction with
clinical markers, may serve as a safe and cost-eicient method
for prognostication of outcome and success of hypothermic
treatment ater HII (Fig. 46.8). RI values below 0.60 before cooling
may broadly diferentiate neonates who are more likely to have
outcomes of severe neurodevelopmental disability or death by
age 20 to 32 months. 38 Persistent hypoxia or hypercapnia will
also contribute to generalized vasodilation and abnormal Doppler
spectra. Fluctuation of systolic velocities may be caused by
hypoxia-related cardiac ischemia. 39,40
Cerebral Edema
Cerebral edema may be seen in HII, congestive heart failure,
and many infectious processes. In the early phases of brain edema
the RI values typically decrease owing to related vascular vasodilation.
41 As cerebral edema worsens, cerebrovascular resistance
increases, with resultant dampening of the diastolic blood low
velocities. Pulsed wave Doppler imaging typically shows subsequent
progressive elevation of the RI values and may eventually
be accompanied by a reversal of the diastolic low in the intracranial
arteries. 40,42
Brain Death
Depending on local legislation, several strict criteria have to be
fulilled for clinical determination of brain death. Typically, absent
pupillary responses, no cranial nerve relexes, no spontaneous
respiration, and a “lat” electroencephalogram are combined with
neuroimaging techniques conirming absent brain perfusion on
a radionuclide CBF study. Several studies have focused on the
value of duplex sonography for determination of brain death.
Duplex sonography typically shows markedly elevated RI
values (>1.0) with reversal of diastolic low in brain death, likely
secondary to increased ICP. However, it should be recognized
that reversal of the diastolic blood low may also be seen in
children with signiicant hydrocephalus and patent ductus
arteriosus. 43 In brain death, in addition, the pulsations of the
middle and anterior cerebral arteries appear diminished. Eventually,
low during systole becomes diminished and present only
during a brief portion of the cardiac cycle. his represents
nonviable brain blood low 42 (Fig. 46.9).
Although absence of intracranial low demonstrated by Doppler
techniques is a reliable sign of absent cortical function, the
presence of low does not guarantee functional integrity, and
brain death may be present despite preserved intracranial blood
low. 43,44
INTRACRANIAL HEMORRHAGE
AND STROKE
Color low Doppler imaging may be used to show initial displacement,
gradual encasement, and obstruction of the subependymal
and terminal veins by germinal matrix hemorrhage (GMH; Fig.
46.10). In one study, displacement or occlusion of the terminal
vein could be demonstrated in 50% of GMHs and in 92% of
periventricular white matter hemorrhages. 45 his inding may
be useful in the early prediction of infants at risk for worsening
intracranial hemorrhage.
Focal Arterial Ischemic Stroke
Focal disruption of CBF causes arterial ischemic stroke in the
neonatal period. Perinatal complications are the most common
cause of stroke in newborns. Other factors are meningitis, trauma,
polycythemia, dehydration, hypercoagulability, and cerebral
vasculitis. 46,47 hese lesions typically occur in full-term infants,
mostly afect the vascular territory of the MCAs (>50%), and
are usually unilateral.
Not all cerebral infarcts show alterations in regional blood
low. Although magnetic resonance imaging (MRI) and catheter
angiography are the imaging reference standards, during the
subacute phase cranial Doppler sonography can show hypervascularity
characterized by an increased size and number of
visible vessels, and increased mean CBFV in the peripheral,
penumbral region of the ischemic area 47-49 (Fig. 46.11). his