Diagnostic ultrasound ( PDFDrive )

CHAPTER 45 Neonatal and Infant Brain Imaging 1541
smaller, apparently from brain destruction. It is essential to
recognize this pattern and test for glutaric aciduria.
HYPOXIC-ISCHEMIC EVENTS
Hypoxic-ischemic events in the neonate can be divided into
maternal causes and causes attributable to the neonate. Maternal
causes include chronic cardiac or pulmonary lung disease,
placental insuiciency, shock, placental abruption, and cardiorespiratory
arrest, all of which can cause severe birth asphyxia.
An uncommon cause is maternal cocaine use. 82 Some therapeutic
maneuvers in these extremely sick, hypoxic neonates have also
been associated with an increased risk for GMH secondary to
increased venous obstruction. 83 Increased venous pressure has
been demonstrated in infants breathing out of sequence with a
mechanical ventilator, during endotracheal tube suctioning, and
with high peak inspiratory pressure. 84 Tension pneumothorax,
exchange transfusions, rapid infusions of colloid, and myocardial
injury caused by asphyxia are other factors that may greatly
afect hemodynamics and venous pressure. 84-86
Arterial Watershed Determines Regional
Pattern of Brain Damage
he sonographic indings are varied depending on the cause and
the age of the neonate when the hypoxic-ischemic event occurs,
because the watershed areas of the brain change in location during
the last trimester 46,87 (Table 45.1). In premature infants the
TABLE 45.1 Patterns of Hypoxic-
Ischemic Injury in Newborns
Hypotension Premature Infant Term Infant
Mild to
moderate
GMH or
periventricular
hemorrhagic
infarction
White matter
injury of
prematurity
(WMIP a.k.a.
PVL)
Parasagittal cortical
or subcortical
injury
Severe Deep gray matter Lateral thalamus
Brainstem and
cerebellar infarct
Posterior putamen
hippocampus
Corticospinal and
sensorimotor
tracts
WMIP formerly periventricular leukomalacia (PVL) has more extensive
injury into cerebral white matter and cortex, thalamus, basal ganglia,
brainstem, and cerebellum.
GMH, Germinal matrix hemorrhage.
Modiied from Volpe JJ. Brain injury in premature infants: a complex
amalgam of destructive and developmental disturbances. Lancet
Neurol. 2009;8(1):110-124. 46
watershed is in the immediate periventricular region, and thus
GMH and PVL are common pathologic indings. With the
advantage of MRI examinations, noncystic forms of white matter
injury have been increasingly diagnosed in premature infants
that extend beyond the periventricular space to afect the difuse
cerebral white matter, thalamus, basal ganglia, brainstem, and
cerebellum. 46 In full-term infants, damage tends to occur more
in the cortical or subcortical regions, because the watershed
moves to these areas more toward the brain surface, resulting
in parasagittal infarction regions in term infants. 88 How to study
hypoxic-ischemic encephalopathy (HIE) depends on the brain
maturity and stability of the newborn infant. Findings at MRI
complement ultrasound and may more oten predict noncystic
white matter lesions. 89-93
Lack of autoregulation of cerebral blood pressure, which
typically occurs in premature infants and less oten in asphyxiated
full-term infants, will cause cerebral perfusion to be directly
afected by hypertensive or hypotensive episodes. his pressurepassive
system can result in sudden focal hemorrhage or, with
hypotension, difuse or focal infarction.
he neurologic manifestations of brain injury in the premature
infant range from the less severe motility and cognitive deicits
to major spastic motor deicits, including spastic diplegia and
spastic quadriplegia with more profound intellectual deicits. In
the full-term infant the hypoxic-ischemic events may manifest
as seizures, movement disorders including arching and isting,
altered tone, absent suck, and, depending on the severity, intellectual
deicits.
Germinal Matrix Hemorrhage
GMH may lead to IVH, hydrocephalus, and porencephaly.
GMH is a common event that occurs primarily in premature
infants less than 32 weeks’ gestational age. Although the incidence
once was as high as 55%, most nurseries have experienced a
signiicant drop in GMH, such that the range is now 10% to
25% in very-low-birth-weight infants (<1000 g) in most neonatal
intensive care units. 94,95 Infants at greatest risk are those at
gestational ages of less than 30 weeks, with birth weight less
than 1500 g, or both. 96 Severe grades of hemorrhage with
hydrocephalus (grade III) and IPH (grade IV) have stabilized
at about 11%, according to a large outcome study of very-lowbirth-weight
infants (<1500 g) by the National Institute of Child
Health and Human Development (NICHD). 97
Multiple factors are associated with GMH, including prematurity
with complications caused by altered cerebral blood low
such as hypoxia, hypertension, hypercarbia, hypernatremia, rapid
volume increase, and pneumothorax. 84-86 Other causes include
increases in cerebral venous pressure at delivery, congestive heart
failure, increased ventilator pressures, and coagulopathies. 53
Factors associated with decreased incidence of GMH include
increased use of antenatal steroids 98,99 and improved neonatal
respiratory care, such as the efective use of high-frequency
ventilators, oscillators, and surfactant, which decrease pressure
to the lung.
GMH originates below the subependymal layer and may be
contained by the ependyma or may rupture into the ventricular
system or less oten into the adjacent parenchyma and thus can