Neonatal Neurology: Clinical Research
Neonatal Neurology 1: Clinical 1
INDIRA BHAGAT, MD (she/her/hers)
Associate Professor of Pediatrics
Central Michigan University
Central Michigan University
Saginaw, Michigan, United States
The etiology of neonatal arterial ischemic stroke (NAIS) is usually multifactorial and identifying the underlying causes for NAIS may help to mitigate the course of the disease and prevent future stroke. Current guidelines suggest routine echocardiography (ECHO) in the acute period to exclude structural heart lesion, intracardiac thrombus or vegetation in infants with NAIS. Although these conditions precipitate stroke in adults, the need for ECHO in NAIS, especially in an era of routine antenatal fetal sonography, is unclear. We hypothesize that routine postnatal ECHO is unnecessary for NAIS because complex cardiac lesions that might be a source for NAIS, would have already been detected during routine antenatal scanning.
Objective:
To determine the prevalence of significant cardiac risk factors and the need for routine postnatal ECHO evaluation in NAIS in the era of routine fetal anomaly scanning.
Design/Methods: A retrospective cohort study of infants with NAIS confirmed on brain MRI from 2011 to 2022. Infants had ECHO evaluation in the acute period to exclude a cardiac source for NAIS, and the prevalence of complex cardiac anomalies in these infants was compared with that detected through routine antenatal fetal scanning.
Results:
During the study period 54 infants with NAIS were seen at the Michigan Medicine. The majority (89%) were term and 6 were late preterm infants. The median age at presentation was 2 days (IQR 1-2), and clinical seizure was the most common presenting symptom (n=37, 68%).
An ECHO was done in 52 cases (96%) to detect a cardioembolic cause for NAIS. None had intracardiac thrombus or vegetation. Postnatal ECHO detected only 3 infants (5%) with structural heart lesions (AV Canal defect in 1, bicuspid aortic valve in 1, and bicuspid aortic valve with mild hypoplasia of aortic arch in 1) and these 3 cases were prenatally diagnosed to have chromosomal malformation in the form of Trisomy 21, XXX syndrome, and Turner syndrome, respectively. Routine antenatal fetal scanning was abnormal only in the case with AV canal defect (Post versus antenatal scanning: 5% vs. 1.9%, p-value 0.61, 95% CI 0.4-41). Postnatal ECHO was normal in 25 infants (48%), and the remaining 24 infants (47%) had non-complex abnormalities (tiny PFO in 20, small ASD in 3, and tiny VSD in 1) which would seem unlikely to have contributed to the stroke.
Conclusion(s):
The yield of ECHO to exclude a cardiac source for NAIS is so low that routine postnatal ECHO, especially in the era of routine fetal anomaly scanning, is not warranted in infants with NAIS unless accompanied by other syndromic or chromosomal malformations.