29.12.2021 Views

Diagnostic ultrasound ( PDFDrive )

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

CHAPTER 45 Neonatal and Infant Brain Imaging 1555

3

B

O

A

B

FIG. 45.52 Brainstem and Cerebellar Hemorrhage. (A) and (B) Sagittal and axial sonograms show highly echogenic hemorrhage in the

brainstem (B), cerebellar vermis, and hemispheres, and posteriorly in the occipital cortex (O), after acute, near-total intrauterine asphyxia. Clot is

also seen in the third ventricle (3) just below the cavum septi pellucidi.

and focal abnormal echogenicity in cerebral cortex and deeper

structures. Doppler ultrasound to look for low luctuations in

resistive indices and low in the dural sinuses is valuable.

In term infants treated with hypothermia for hypoxic ischemic

encephalopathy, there have been rare reports of IVH. 166,172,173

However, outcomes ater hypothermia for HIE from the NICHD

Neonatal Research Network studies show that there is a decrease

in deaths and that hypothermia does not increase rates of severe

disability among survivors.

Neonatal HIE is best evaluated with ultrasound in the irst

few days of life. MRI is the most sensitive and speciic imaging

technique, and is useful in stable term infants. Some authors

suggest that MRI late in the irst week of life may be useful but

term-equivalent age is best for prognosis. However, the brain

may appear normal or near normal at 5 to 7 days ater the event.

For severe hypotensive episodes, thalami, brainstem, and cerebellum

are most sensitive owing to their high metabolic activity.

In premature infants, HIE injury appears as increased echogenicity

on ultrasound, hypoattenuation on CT (may be missed because

of high neonatal brain water content), and hyperintensity from

restricted difusion on difusion-weighted imaging. In term infants,

the lateral thalami, posterior putamen, hippocampus, brainstem,

corticospinal tracts, and sensorimotor cortex are most

afected. 88,89,174

Focal Infarction

Cerebral infarction in the neonate, aside from PVL or periventricular

hemorrhagic venous infarction, is uncommon. Risk

factors are prematurity, severe birth asphyxia, congenital heart

disease (resulting in a let-to-right shunt), meningitis, emboli

(from the placenta or systemic circulation), polycythemia,

hypernatremia, and trauma. 120,175,176 Symptoms vary, ranging from

asymptomatic to seizures with lethargy and coma. he MCA

distribution is the most frequent site, although the anterior and

posterior circulations have also been afected. 46 Single areas of

infarction are more frequently seen in full-term infants, whereas

premature infants oten demonstrate multiple sites of injury.

Cerebral blood low evaluation with color and or power Doppler

sonography are used in unstable neonates, and difusion-weighted

MRI is used in stable infants to identify the earliest signs of

stroke. 177-182

Cerebellar infarction is much less common than cerebral

infarction. However, six cases were reported in 3 years at Hammersmith

Hospital in London, diagnosed by MRI in patients at

several years of age who were born prematurely. 183 All these

patients also had IVH, and thus cerebellar damage was likely a

result of difuse ischemic injury. Only one of the six patients

was diagnosed on sonography as having cerebellar damage.

Because the vermis is so echogenic, edema or hemorrhage can

be a diicult diagnosis in this region. Cerebellar infarction was

also diagnosed with MRI in 13 patients with severe cerebral

palsy who had cerebellar hemispheric and vermian damage. 184

Now that we are routinely evaluating the posterior fossa in detail,

we are more aware of cerebellar infarction at the time of the

injury in premature infants. 185

On sonography, the infarcted brain parenchyma demonstrates

speciic indings within the irst 2 weeks (see Fig. 45.52; Fig.

45.53). hese include echogenic parenchyma, lack of arterial

pulsation, lack of blood low appreciated by pulsed or color

Doppler sonography, mass efect from edema, arterial territorial

distribution of injury, and decreased sulcal deinition. Ater 2

weeks, the echogenic lesions begin to show cystic changes, and

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!