It is essential for the evaluation of the premature infant to identify the presence and extent of brain injury. Premature infants are at significant risk for intraventricular hemorrhage (IVH), periventricular leukomalacia (PVL), posthemorrhagic ventricular dilation, and other neurological lesions that may or may not have imaging corollaries.
Through neuroimaging, the neonatologist can initiate interventions and plan supportive care and assess the risk of future neurological deterioration.
In 1968, Abraham Towbin1 described the frequent finding of IVH in necropsies of premature babies, with anomalies almost universally present in those born at less than 28 weeks of gestation.
Ten years later, Papile et al.2 described computed tomography (CT) findings in 46 consecutive very low birth weight (VLBW) infants and demonstrated a much higher incidence of IVH than clinically suspected.
That report described 4 separate grades of hemorrhage: “Grade I: subependymal hemorrhage, grade II: intraventricular hemorrhage without ventricular dilation, grade III: intraventricular hemorrhage with ventricular dilation, and grade IV: intraventricular hemorrhage with parenchymal hemorrhage.”
Since the initial report, Papile’s classification has been modified to grade I, indicating minimal HIV; grade II, with IVH occupying 10% to 50% of the ventricular area; grade III, which represents IVH with > 50% of the ventricular area; and finally, parenchymal hemorrhage, most likely attributable to venous hemorrhagic infarction.3
These findings led to one of the first outcome studies,4 in which the authors described the association of greater developmental and neuromotor disabilities with the finding of more severe IVH (grade III and IV) on computed tomography performed among the 3 and 10 days of life.
Based on these and other studies, the American Academy of Neurology (AAN) published practice parameters in 2002 suggesting universal cranial ultrasound screening for all babies born at less than 30 weeks of gestation.5 The AAN also recommended that ultrasound Initial screening is performed 7 to 14 days after birth and repeated at a corrected age close to term.
In 2001, the Canadian Pediatric Society recommended screening all infants born at less than 32 weeks’ gestation at 2 weeks after birth, with repeat screening 6 weeks later.6
Since the publication of those guidelines, the capabilities of cranial ultrasonography have evolved, and modern ultrasound technology, along with the use of supplemental acoustic windows, can now provide a good structural image of the preterm infant’s brain.7
Computed tomography ( CT) has made it possible to obtain images of the entire brain. This has led to improvements in cranial ultrasound as well as magnetic resonance imaging (MRI), which produces better details and avoids the use of ionizing radiation.8 However, the routine use of MRI for screening premature infants has been identified as of questionable value in the American Academy of Pediatrics (AAP) Choosing Wisely campaign.9
The aim of this clinical report was to provide guidance to clinicians with an evidence-based approach to the use of neuroimaging in the preterm infant.
| Initial screening exams |
The VLBW infant (i.e., birth weight < 1500 g) is at high risk for intraventricular hemorrhage (IVH) and germinal matrix hemorrhage, as well as ischemic white matter injury as identified by cranial ultrasound.
The risk of severe HIV is inversely related to gestational age, with babies born at less than 24 weeks’ gestation being at greatest risk.10
In 2017, the Vermont Oxford Network database demonstrated an overall HIV incidence of 24.6% and a rate of severe HIV of 8.1%, defined as grade III or IV, among more than 50,000 VLBW infants.11
In a survey by the California Quality Perinatal Care Collaborative, 63% of babies born at 22 to 23 6/7 weeks of gestation had HIV, with 36% demonstrating severe HIV.12 This incidence decreased to 14% of those babies with a gestational age at birth of 30 to 31 6/7 weeks with any HIV and 1.4% with a severe degree.
Less severe grades of HIV (grades I and II) may have less prognostic influence on clinical outcomes. In a National Institute of Child Health and Development study of 1,472 infants born at less than 27 weeks’ gestational age,13 there were no significant differences in neurodevelopmental outcomes at 18 to 22 months between infants with and without low-grade hemorrhage. .
PVL is a disorder of the periventricular cerebral white matter that can be cystic or diffuse in nature. Most cystic LPVs occur in infants born between 26 and 30 weeks of gestation, initially appearing as increased periventricular echogenicity with cystic evolution over the course of a few weeks.
Periventricular hemorrhagic infarcts ( PVHI) (i.e., formerly IVH grade 4) occur primarily in infants born at 26 weeks of gestation14 and occur infrequently in infants born after 30 weeks.15
| A periventricular hemorrhagic infarction (PVHI) is a parenchymal lesion generally associated with large IVH and, based on current understanding, is believed to be caused by venous infarction. An IHPV is not, as has been believed, an extension of IVH in the parenchyma. |
The severity of IVH in the most immature infants is consistent with the changes in the development of the subependymal germinal matrix, since it decreases in size from 2.5 mm in the premature neonate at 24 weeks until its involution at approximately 36 weeks. gestational age.3
For these and other reasons that affect vascular integrity, more moderate and late preterm neonates (born between 32 and 36 6/7 weeks of gestation) are at less risk for significant intracranial injury.
In a retrospective study of moderately preterm neonates born between 29 and 33 weeks’ gestation, 60% of a cohort of 7,021 infants underwent imaging, and 15% of these 4,184 infants had abnormalities on ultrasound.16 Rates of IVH and cystic LPV were 1.7% and 2.6%, respectively, in this population.15
The authors noted that low Apgar scores, maternal risk factors, lack of prenatal steroids, and vaginal delivery were associated with ultrasound abnormalities, including intracranial hemorrhage, PVL, and ventriculomegaly.
The presence of risk factors such as abnormal neurological examination, intrauterine growth restriction, abnormal head circumference, low Apgar scores, and need for ventilation or surfactant increased the chance of detecting an anomaly fourfold in a group of more mature preterm neonates born between 33 and 36 weeks of gestational age.17
In a similar study, infants born at > 30 weeks’ gestation who were found to have significant US abnormalities typically had clinically significant events, such as placental abruption, seizures, hypotension, and hydrocephalus, warranting study with cranial US.18
Risk factors also play a role in the most immature premature babies. In a study of 303 infants born at <30 weeks’ gestation, no asymptomatic infants required clinical intervention based solely on screening ultrasound performed at 7 to 14 days.19 All infants who required clinical interventions had precipitating factors. ultrasound, including anemia, metabolic acidosis, pulmonary hemorrhage, and hypotension.
Similar results have been reported for infants born <32 weeks’ gestation with risk factors for severe IVH, including lack of prenatal steroids, birth status, asphyxia, significant acidosis, and/or hypotension.10
Therefore, the risk of severe HIV is associated with a gestational age ≤ 30 weeks, with higher risk in babies born at < 24 weeks of gestation. Infants born >30 weeks gestation have a low risk of severe HIV unless they have additional clinical risk factors.
| Time of occurrence of HIV |
The vast majority of IVHs in premature neonates occur within the first 3 days of life.20-24 Of these, approximately 50% of hemorrhages occur within the first 5 hours, and approximately 70% occur within first 24 hours of life. By 7 days, 95% of HIVs will have occurred, with a small percentage appearing at 7 to 10 days.21,22
In an analysis of infants who required neurosurgical intervention for post-hemorrhagic hydrocephalus, the average age of development of IVH was 2 days, with ventriculomegaly apparent by 3 days of life.24
In this study, timed neurosurgical procedures were performed 3 weeks after the development of IVH. Therefore, frequent monitoring of significant IVH until resolution or stabilization will likely allow determination of ventricular dilation and potential need for treatment.
| Repetition of the brain image |
PVL may initially be observed during the first week of life in the VLBW infant as increased echogenicity of the periventricular white matter, sometimes described as echogenic “flare.” Since the periventricular white matter may normally have slightly increased echogenicity, the echogenic choroid plexus can be used as an internal comparison for this increased echogenicity.25
Normal periventricular white matter should be less echogenic than the choroid plexus. These areas of abnormal white matter may become cystic on ultrasound within 2 to 5 weeks and/or cause ventriculomegaly due to loss of white matter volume, which may be visible on repeat ultrasound at age equivalent to term (TEA).
In light of these findings, the Canadian Pediatric Society recommended screening at 6 weeks of age, while the AAN suggested a study near term.5,6 These suggested variable time frames may lead to different study times in the premature newborn.
Given that screening at 4 to 6 weeks is sensitive in identifying LPV and that term-equivalent ultrasound findings are associated with adverse neurodevelopmental outcomes, screening during both time periods is recommended.
Sequential ultrasound appears to have the best performance in identifying lesions associated with cerebral palsy. In infants with cerebral palsy, almost one-third were found to have LPV on ultrasound performed after 4 weeks of age.26
Among 12,739 preterm infants who were evaluated at 4 weeks of age and again near TSE, 14% had cystic LPV that was only visible on early imaging and had resolved by the time of subsequent study.27
Subgroup analysis revealed that in infants born at 26 weeks’ gestation, 18.5% of PVL cases were missed by a single ultrasound examination performed at TSE. However, a follow-up study demonstrated that infants who had cystic LPV at any time on ultrasound imaging showed a significantly higher primary outcome of late death or impaired neurodevelopment than those who never had such a finding.28
Therefore, even if the findings were transient, infants with cystic LPV are warranted to have close follow-up observation to evaluate neurodevelopmental alterations. Communication regarding neuroimaging results and follow-up plans between inpatient and outpatient professionals is recommended.
| Standard Cranial Ultrasound Imaging Technique |
Cranial ultrasound has traditionally made use of the anterior fontanelle as an acoustic window and must be performed by a sonographer board certified by the American Registry of Diagnostic Medical Sonography. Brain images are taken in the coronal plane with anterior to posterior views and in the sagittal plane with appropriate left and right angulation.7,29
Use of the posterior fontanel may allow for more detailed evaluation of the periventricular white matter and occipital lobes. These views allow excellent visualization of the supratentorial structures but limited views of the posterior fossa and cerebellum.
The cerebellum has been shown to be a common site of injury, with significant hemorrhage occurring in up to 9% of preterm neonates diagnosed by appropriately performed ultrasound.30,31 For this reason, additional imaging through ultrasound is recommended. of the mastoid fontanelle .
In cases of limited cerebellar hemorrhage, there was much better image sensitivity when mastoid views were obtained (86%) than when only the anterior fontanelle was evaluated (16%).32 However, mastoid views cannot detect cerebellar microbleeds, which only They can be visualized with MRI. Aside from hemorrhage, cerebellar hypoplasia is also associated with motor and cognitive deficits.31
Although most cases of cerebellar hypoplasia have been associated with cerebral white matter injury, other factors, including genetic and neurodegenerative syndromes, medications, stroke, and nutrition, play a role in cerebellar growth and affect neurological outcomes. Therefore, cerebellar imaging may have important diagnostic and prognostic value as part of the ultrasound screening examination.
The addition of high-resolution linear color Doppler images obtained through the anterior fontanelle can be used to evaluate the patency of the superior sagittal sinus. If there is concern for venous sinus thrombosis, the posterior and mastoid windows can also help evaluate the sagittal and transverse sinuses.
Many centers are also measuring anterior cerebral artery resistive index as a marker for vascular compliance and to document normal waveforms and diastolic flow.
| Magnetic resonance |
MRI has become increasingly popular as a means of identifying brain injury in the premature newborn.
MRI provides the most detailed image of the brain and avoids the radiation risks associated with CT.33
Specific absorption rates (a measure of the strength of radiofrequency fields) in patients undergoing MRI procedures appear to be much lower in neonates than in adults and in a safe and acceptable range.34
MRI studies can be performed successfully in the preterm TSE population without the use of any sedative medication.35,36 Protocols that rely on feeding the baby 20 to 30 minutes before the scan and swaddling to limit overall movement have been successful in avoiding significant sedation in most cases.
With the use of non-sedation MRI and the increasing availability of compatible equipment, these images have become more easily affordable. However, controversy persists regarding which children should receive TSE MRI studies.
Abnormal findings on TSE MRI in a group of infants born at <30 weeks’ gestation have shown that this study is predictive of psychomotor retardation and cerebral palsy at 2 years.37 The predictive value of TSE MRI for neurocognitive outcomes at school age is less clear.
One study reported that abnormal TSE brain MRI was predictive of adverse neurodevelopmental outcomes at 7 years of age.38 This association with adverse neurodevelopmental outcomes at 7 years of age was particularly striking for white matter abnormalities, deep gray matter, and cerebellum.
However, other studies have reported39,40 that adding MRI to early and late cranial ultrasound did not improve the prediction of severe intellectual disability or neurodevelopmental impairment between 6 and 7 years of age.
Obtaining routine MRI has also not been shown to have a significant clinical effect on maternal anxiety or improve quality of life, although it may increase the cost of care.41 As the Choosing Wisely campaign has identified,9 there is insufficient evidence to Routine brain MRI to TSE may improve long-term outcomes, and the effects the results may have on an individual family may not be predictable.42,43
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