Central nervous system outcomes in children with complex congenital heart disease

Wernovsky, Gil; Shillingford, Amanda J.; Gaynor, J. William

doi:10.1097/01.hco.0000153451.68212.68

Cited by 146 publications

(121 citation statements)

References 53 publications

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“…Relative changes in OEF, BFI, and CMRO 2i in response to hypercapnia, i.e. %DOEF, %DBFI, and %DCMRO 2i , were computed using formulas analogous to equation (4). Changes in StO 2 (DStO 2 ) were quantified as a difference between its hypercapnic and room air values.…”

Section: Magnetic Resonance Imaging Measurementsmentioning

confidence: 99%

“…3,4 Quantification of the hemodynamic and metabolic state of these neonates via measurements of cerebral blood flow (CBF) and the cerebral metabolic rate of oxygen consumption (CMRO 2 ) should provide valuable information toward understanding the interaction between cardiac pathophysiology and subsequent cerebral health. Potentially, such new knowledge could help predict and prevent adverse outcomes.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Jain

Buckley

Licht

et al. 2013

J Cereb Blood Flow Metab

173

192

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Neonatal congenital heart disease (CHD) is associated with altered cerebral hemodynamics and increased risk of brain injury. Two novel noninvasive techniques, magnetic resonance imaging (MRI) and diffuse optical and correlation spectroscopies (diffuse optical spectroscopy (DOS), diffuse correlation spectroscopy (DCS)), were employed to quantify cerebral blood flow (CBF) and oxygen metabolism (CMRO 2 ) of 32 anesthetized CHD neonates at rest and during hypercapnia. Cerebral venous oxygen saturation (S v O 2 ) and CBF were measured simultaneously with MRI in the superior sagittal sinus, yielding global oxygen extraction fraction (OEF) and global CMRO 2 in physiologic units. In addition, microvascular tissue oxygenation (StO 2 ) and indices of microvascular CBF (BFI) and CMRO 2 (CMRO 2i ) in the frontal cortex were determined by DOS/DCS. Median resting-state MRI-measured OEF, CBF, and CMRO 2 were 0.38, 9.7 mL/minute per 100 g and 0.52 mL O 2 /minute per 100 g, respectively. These CBF and CMRO 2 values are lower than literature reports for healthy term neonates (which are sparse and quantified using different methods) and resemble values reported for premature infants. Keywords: cerebral blood flow; cerebral hemodynamics; diffuse optics; MRI; near-infrared spectroscopy; neonatal ischemia INTRODUCTION Congenital heart disease (CHD) affects B35,000 neonates each year in the United States. These patients suffer both short-and long-term neurologic sequelae. Periventricular leukomalacia is the most common cerebral injury found in this population. This type of injury is characterized by focal necrosis in the periventricular white matter, and it is associated with pyknotic glial nuclei and reactive gliosis. 1,2 During the early stages of brain development, the oligodendrocyte (brain glial cells) precursors are metabolically very active and highly susceptible to injury from reduced blood flow and oxygen delivery. Hence, hypoxiaischemia has been implicated as a major cause of this injury in CHD neonates.Periventricular leukomalacia leads to impaired myelination and has been linked to worse neurodevelopmental outcomes in premature infants and postulated to cause (at least in part) the impaired cognition and cerebral palsy commonly seen in this cohort of infants with CHD. 3,4 Quantification of the hemodynamic and metabolic state of these neonates via measurements of cerebral blood flow (CBF) and the cerebral metabolic rate of oxygen consumption (CMRO 2 ) should provide valuable information toward understanding the interaction between cardiac pathophysiology and subsequent cerebral health. Potentially, such new knowledge could help predict and prevent adverse outcomes.

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Section: Magnetic Resonance Imaging Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Jain

Buckley

Licht

et al. 2013

J Cereb Blood Flow Metab

173

192

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show abstract

“…WMI is not exclusively associated with prematurity and it is increasingly appreciated in term infants [23][24][25]. Infants with complex congenital heart disease are at particular risk for WMI and delayed brain maturation [26][27][28]. Because very low birth weight infants comprise approximately 1.5% of the 4 million live births in the United States alone each year, the worldwide social and economic burden is considerable.…”

mentioning

confidence: 99%

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

et al. 2012

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Despite advances in neonatal intensive care, survivors of premature birth remain highly susceptible to unique patterns of developmental brain injury that manifest as cerebral palsy and cognitive-learning disabilities. The developing brain is particularly susceptible to cerebral white matter injury related to hypoxia-ischemia. Cerebral white matter development in fetal sheep shares many anatomical and physiological similarities with humans. Thus, the fetal sheep has provided unique experimental access to the complex pathophysiological processes that contribute to injury to the human brain during successive periods in development. Recent refinements have resulted in models that replicate major features of acute and chronic human cerebral injury and have provided access to complex clinically relevant studies of cerebral blood flow and neuroimaging that are not feasible in smaller laboratory animals. Here, we focus on emerging insights and methodologies from studies in fetal sheep that have begun to define cellular and vascular factors that contribute to white matter injury. Recent advances include spatially defined measurements of cerebral blood flow in utero, the definition of cellular maturational factors that define the topography of injury and the application of high-field magnetic resonance imaging to define novel neuroimaging signatures for specific types of chronic white matter injury. Despite the higher costs and technical challenges of instrumented preterm fetal sheep models, they provide powerful access to clinically relevant studies that provide a more integrated analysis of the spectrum of insults that appear to contribute to cerebral injury in human preterm infants.

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“…[5] It is well-established that 21 to 69% of neonates and infants undergoing cardiac surgery with CPB suffer from long-term adverse neurodevelopmental complications. [6][7][8] The reasons are multi-factorial, and many authors have claimed that abnormal brain development resulting from a cardiac lesion can be blamed for brain injury. [6,9,10] Coagulation during cyanotic coronary heart diseases may be due to the consumption of factors by intravenous coagulation, or liver dysfunction caused by polycythemia and stasis.…”

Section: Discussionmentioning

confidence: 99%

An evaluation of bilateral cerebral oxygen saturation during cyanotic and non-cyanotic cardiac surgery

Demir¹

2016

Turk Gogus Kalp Dama

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Central nervous system outcomes in children with complex congenital heart disease

Abstract: The causes of these late developmental abnormalities are most likely sequential, cumulative and multifactorial.

Cited by 146 publications

References 53 publications

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

An evaluation of bilateral cerebral oxygen saturation during cyanotic and non-cyanotic cardiac surgery

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