Cerebrovascular pressure autoregulation is the physiologic mechanism that holds cerebral blood flow (CBF) relatively constant across changes in cerebral perfusion pressure (CPP). Cerebral vasoreactivity refers to the vasoconstriction and vasodilation that occur during fluctuations in arterial blood pressure (ABP) to maintain autoregulation. These are vital protective mechanisms of the brain. Impairments in pressure autoregulation increase the risk of brain injury and persistent neurologic disability. Autoregulation may be impaired during various neonatal disease states including prematurity, hypoxic-ischemic encephalopathy (HIE), intraventricular hemorrhage, congenital cardiac disease, and infants requiring extracorporeal membrane oxygenation (ECMO). Because infants are exquisitely sensitive to changes in cerebral blood flow (CBF), both hypoperfusion and hyperperfusion can cause significant neurologic injury. We will review neonatal pressure autoregulation and autoregulation monitoring techniques with a focus on brain protection. Current clinical therapies have failed to fully prevent permanent brain injuries in neonates. Adjuvant treatments that support and optimize autoregulation may improve neurologic outcomes.

Near-infrared spectroscopy (NIRS) has been used to study cerebral haemodynamics and oxygenation in the preterm infant for many years, but its use as a clinical tool has remained elusive. This has partly been due to the challenges of providing a continuous quantitative measurement that is valid and reliable, as well as demonstrating that interventions based on NIRS measurements improve clinical outcome. Recent studies investigating cerebral oxygenation targeted treatment, and defining optimal blood pressure based on an assessment of cerebrovascular reactivity, suggest ways in which this technology may yet be clinically useful.

ResumoObjetivo: Verificar a associação de leucomalácia periventricular (LPV) e sepse neonatal em recém-nascidos de muito baixo peso (RNMBP). Métodos AbstractObjective: To investigate the association between periventricular leukomalacia (PVL) and neonatal sepsis in very low birth weight infants (VLBWI). Methods:We studied VLBWI with a clinical suspicion of infection who had been born at our institution between the 1st of August, 2005 and the 31st of July, 2007. Children were excluded if they died before reaching 14 days, had malformations of the central nervous system or congenital infections. Ultrasound brain scans were carried out on the third day and weekly up until the sixth week of life or discharge. Periventricular leukomalacia was diagnosed by persistent diffuse periventricular hyperechogenecity for more than 7 days, or by periventricular cysts. The VLBWI were separated into two groups on the basis of the presence or absence of PVL. Sepsis was defined as clinical manifestation plus a positive culture. The Mann-Whitney, chi-square and t tests were applied followed by logistic regression.Results: A total of 88 VLBWI were studied. Of these, 62 (70.5%) survived and 51 (57.8%) had PVL. Both groups were similar in terms of birth weight, gestational age, Apgar score, type of delivery, SNAPPE-II score, presence of necrotizing enterocolitis, persistent ductus arteriosus and deaths. Sepsis and mechanical ventilation were more common in the group with PVL (23.5 and 2.7%, p = 0.005; 86 and 59%, p = 0.004, respectively). Both of these were identified as, independent risk factors for PVL by logistic regression (p = 0.027 and 0.015, respectively). Conclusions:Chorioamnionitis has been defined as a risk factor for PVL. We have demonstrated that neonatal sepsis is also an important risk factor. We believe that the systemic inflammatory response is the principal factor involved in the etiopathogenesis of PVL among VLBWI.J Pediatr (Rio J). 2008;84(3):211-216