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P70 Lenticulostriate vasculopathy in preterm and term infants – a prospective study
  1. Beata Acs1,2,
  2. Lucica Ghiţ&acaron;2,
  3. Vasilica Pl&acaron;iaşu2,
  4. Ionela Voicil&acaron;2,
  5. Iuliana Balint-Boia2,
  6. Simona Andriani2,
  7. Tatiana Ciomârtan1,2
  1. 1University of Medicine and Pharmacy ‘Carol Davila’, Bucharest, Romania
  2. 2National Institute for Mother and Child Health ‘Alessandrescu-Rusescu’, Bucharest, Romania

Abstract

Background and aims Lenticulostriate vasculopathy (LSV) is a sonographic term given to the hyperechogenic vessels in the thalamus and/or basal ganglia detected on routine head ultrasound (HUS) in neonates or infants. LSV is often associated with various perinatal and neonatal abnormalities, but in many cases it seems to be idiopathic. Our aim was to assess the incidence, aetiology and progress of LSV by repeated US scans and to determine the main causes in our study group.

Methods Between 01.07.2015 and 31.12.2016 1948 infants underwent a routine HUS examination performed by the same person using a Toshiba Aplio 500 and Aplio 300 machine. Patients with LSV had repeated follow-up examinations usually at 2 months intervals. In order to determine sonographic LSV progress, at least 2 HUS exams were performed after diagnosis.

Results LSV was detected in 2.87% of the infants who underwent HUS examination. 60.7% of the babies with LSV were born preterm. The median age at the first examination was 35 days of life. Analysing risk factors for LSV we found that 50% had multiple risk factors for LSV (such as neonatal asphyxia and congenital CMV infection, perinatal HIV exposure with congenital heart defect, Down syndrome with congenital heart defect and perinatal hypoxia, extremely preterm birth with perinatal bacterial infection and neonatal asphyxia) In 30.35% of cases LSV was idiopathic and had no associated abnormalities. LSV was bilateral in 58.92% of cases, in 84% located in the thalamus and in 16% in the basal ganglia. In 5 cases appeared at the second HUS examination (babies were followed up for intraventricular haemorrhage) between 3–4 months of life. Sonographic follow up of patients up to 12 months of age showed progression of the hyperechogenic lesions in 7 cases (13%), in 28 cases (50%) complete resolution of lesions between 6–12 months of age, and no change in 13 cases (23%); 8 patients (14%) were lost for follow up after the first HUS exam. In 3 patients cranial magnetic resonance imaging (MRI), performed after LSV was diagnosed, did not detect LSV.

Conclusions LSV is a frequent finding on routine HUS. Although congenital infections were initially considered as the primary cause of LSV, it appears that currently many other conditions can be associated with LSV, whilst in almost a third of the cases it is idiopathic. US may have a higher accuracy for LSV than MRI. It at least half of the cases a complete resolution of LSV lesions was noted.

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