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Ventricular dilation following intraventricular hemorrhage in the premature infant
Insights
Periventricular/intraventricular hemorrhage (PVH/IVH) is common in premature newborns. Hydrocephalus development post-PVH/IVH depends on lesion severity, requiring careful monitoring and tailored treatment based on dilation rate and intracranial pressure.
Area of Science:
- Neonatal Neurology
- Pediatric Neurosurgery
- Perinatal Medicine
Background:
- Periventricular/intraventricular hemorrhage (PVH/IVH) affects 35-45% of premature newborns.
- Hydrocephalus is a common complication of PVH/IVH, with incidence related to hemorrhagic lesion severity.
Purpose of the Study:
- To review the pathophysiology and clinical presentation of hydrocephalus following PVH/IVH in premature infants.
- To discuss diagnostic surveillance and therapeutic strategies for post-hemorrhagic hydrocephalus.
Main Methods:
- Review of current literature on PVH/IVH and subsequent hydrocephalus.
- Analysis of factors influencing hydrocephalus development and progression.
- Evaluation of treatment options based on clinical presentation.
Main Results:
- Ventricular dilation can result from arachnoiditis or intraventricular clot obstruction.
- Hydrocephalus may manifest acutely or progressively 1-3 weeks post-PVH/IVH.
- Classical signs of hydrocephalus may be delayed, underscoring the need for imaging surveillance.
Conclusions:
- Close ultrasound surveillance for ventricular size is crucial after PVH/IVH diagnosis.
- Therapeutic decisions for hydrocephalus depend on the rate of ventricular dilation and intracranial pressure.
- Management options range from CSF production inhibitors and lumbar punctures to ventricular drainage.
Abstract:
Periventricular/intraventricular hemorrhage occurs commonly in the premature newborn. Recent studies indicate an incidence of 35-45%. Following PVH/IVH, the likelihood of developing hydrocephalus is related to the severity of the hemorrhagic lesion. Ventricular dilation may be due to an obliterative arachnoiditis affecting principally the posterior fossa or, less commonly, due to obstruction of flow of cerebrospinal fluid within the ventricular system by clots or other debris. With moderate to severe hemorrhagic lesions, ventricular dilation may occur at the time of PVH/IVH. More commonly, progressive dilation begins one to three weeks following PVH/IVH. The classical signs of hydrocephalus, ie. bulging of anterior fontanelle and inappropriate increase in head circumference, may not appear for days to weeks following onset of ventricular dilation. The precise significance of such normal-pressure hydrocephalus in the genesis of brain injury in the newborn is unknown. Following diagnosis of PVH/IVH, close surveillance of ventricular size with ultrasound scans is indicated. When there is slowly progressive ventricular dilation with normal intracranial pressure, the choice of therapy is made difficult because of frequent spontaneous arrest in such cases. Several modes of therapy have been reported including drugs to decrease the formation of cerebrospinal fluid and the use of serial lumbar punctures. When ventricular dilation is rapid with intracranial hypertension, ventricular drainage is indicated.