BACKGROUND: Periventricular leucomalacia (PVL) is the most important neuropathologic lesion underlying major neuro-motor deficits of pre-term very low birth weight (VLBW) infants. Published data regarding PVL is not available from our country. OBJECTIVES: A study was planned with main objectives to estimate incidence and describe natural history of PVL among a very low birth weight cohort. STUDY DESIGN: A cohort study was performed on inborn VLBW babies over one year period at a tertiary neonatal intensive care unit. Serial weekly cranial ultrasounds were performed on 97 enrolled subjects until discharge, to diagnose and describe natural history of PVL. RESULTS: 31 out of 97 enrolled subjects developed PVL. No case of PVL developed beyond 19 days of postnatal life. Serial ultrasounds for each baby were tracked until discharge or death. Majority of lesions at onset were flares. Cysts tended to develop in over one third of cases during course of hospital stay. About 50% of ultrasound had normalized at discharge and sequelae such as cerebral atrophy and ventriculomegaly had appeared in few, the rest of lesions being either flares or cysts of PVL. CONCLUSIONS: PVL is fairly common among very low birth weight neonates. Ultrasonographic lesions of PVL undergo dynamic evolution from time of first detection to either progress, regress or leave sequelae before discharge. Ultrasound remains an important bedside diagnostic tool for PVL.
BACKGROUND:Periventricular leucomalacia (PVL) is the most important neuropathologic lesion underlying major neuro-motor deficits of pre-term very low birth weight (VLBW) infants. Published data regarding PVL is not available from our country. OBJECTIVES: A study was planned with main objectives to estimate incidence and describe natural history of PVL among a very low birth weight cohort. STUDY DESIGN: A cohort study was performed on inborn VLBW babies over one year period at a tertiary neonatal intensive care unit. Serial weekly cranial ultrasounds were performed on 97 enrolled subjects until discharge, to diagnose and describe natural history of PVL. RESULTS: 31 out of 97 enrolled subjects developed PVL. No case of PVL developed beyond 19 days of postnatal life. Serial ultrasounds for each baby were tracked until discharge or death. Majority of lesions at onset were flares. Cysts tended to develop in over one third of cases during course of hospital stay. About 50% of ultrasound had normalized at discharge and sequelae such as cerebral atrophy and ventriculomegaly had appeared in few, the rest of lesions being either flares or cysts of PVL. CONCLUSIONS: PVL is fairly common among very low birth weight neonates. Ultrasonographic lesions of PVL undergo dynamic evolution from time of first detection to either progress, regress or leave sequelae before discharge. Ultrasound remains an important bedside diagnostic tool for PVL.