Preoperative cranial ultrasound findings in infants with major congenital heart disease

Abstract

Background: Advances in diagnostic testing and surgical techniques have resulted in reduced mortality in neonates with congenital heart disease (CHD) and a major concern for neurological morbidity in the presence of preoperative neurological injury. Objectives: To determine the incidence and nature of preoperative cerebral ultrasound abnormalities in neonates with major CHD and to examine the relationship between cerebral abnormalities and the type of CHD. Methods: Retrospective study; inclusion criteria: (1) neonates with major CHD admitted to the NICU over a 3‐y period, (2) gestational age > 35 wk, (3) documented preoperative cranial ultrasound available; exclusion criteria: (1) small for gestational age, (2) other congenital anomalies and/or chromosomal abnormalities, (3) a 5‐min Apgar score < 7, (4) congenital infection. Cranial ultrasounds (CUS) were reviewed without knowledge of the cardiac defect. CHDs were categorized. Results: Fifty of 108 neonates with CHD met the inclusion criteria. Twenty‐one patients (42%) had abnormalities on CUS. Thirteen of these (26%) had widened ventricular and/or subarachnoid spaces, three (6%) lenticulostriate vasculopathy, one (2%) calcification in the basal nuclei, and four (8%) had acute ischaemic changes. Cerebral abnormalities occurred more frequendy in patients with coarctation or hypoplastic left heart syndrome (HLHS) than transposition of the great arteries (TGA) (63% vs 14%; n.s.). Conclusion: There is a high incidence of preoperative cerebral ultrasound abnormalities in this group of neonates with major CHD.

Brain abnormalities and neurodevelopmental delay in congenital heart disease: systematic review and meta-analysis

“…Another study by the same authors showed that a significant number of babies with HLHS had associated congenital brain abnormalities such as agenesis of the corpus callosum, holoprosencephaly and abnormal cortical mantle formation. Brain lesions detected by cranial ultrasound include cerebral atrophy, widened ventricular or subarachnoid spaces, intraventricular hemorrhage, linear echodensities of the deep gray matter, especially the basal ganglia and the thalamus, and parenchymal echodensities. Similarly, studies using MRI have reported a range of abnormalities including intracranial hemorrhage, ventriculomegaly with dilation of the subarachnoid spaces representing cerebral atrophy, gray matter injury, cerebral venous thromboses, thromboembolisms, infarctions, periventricular leukomalacia and incomplete closure of the operculum.…”

“…Studies have demonstrated an association between CHD and neurodevelopmental delay, which is attributed in part to the risk of brain injury during cardiac surgery. Neuroimaging studies have also demonstrated a high incidence of preoperative brain abnormalities and neurodevelopmental delay. Early identification of fetuses or neonates at increased risk of brain injury would facilitate appropriate surveillance and targeted intervention.…”

Imaging patterns of sonographic lenticulostriate vasculopathy and correlation with clinical and neurodevelopmental outcome

“…Moreover, all three patients with no flow in lenticulostriate vessels on color Doppler had CHD. Several studies have reported an association between LSV and neonatal cardiac diseases . Miller et al demonstrated that newborns with CHD have brain abnormalities before they undergo cardiac surgery.…”

“…Miller et al demonstrated that newborns with CHD have brain abnormalities before they undergo cardiac surgery. Te Pas et al reported that 3 of 108 neonates (6%) with CHD had evidence of LSV on cranial US. Another study demonstrated that all of the included patients with LSV had cardiac lesions characterized by cyanosis, poor cardiac output, or both .…”

“…The explanation may be that causative spasm, thrombus, or embolus may alter the main MCA trunk or the internal carotid arteries, causing LSV to appear quite differently . Hypoxia and ischemia, which are common in CHD, may be conditions that lead to LSV . Decreased brain perfusion may explain the lack of color Doppler flow in patients with high‐grade LSV.…”