Cerebral oxygen saturation before congenital heart surgery

Kurth, C. Dean; Steven, James L; Montenegro, Lisa M.; Watzman, H. Marc; Gaynor, J. William; Spray, Thomas L.; Nicolson, Susan C.

doi:10.1016/s0003-4975(01)02632-7

Cited by 162 publications

(98 citation statements)

References 22 publications

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“…However, some discordance between the two measurements might also be expected, because the optical probe measures focal hemodynamics over the frontal areas of the brain, which tend to be hypometabolic in neonates. 39 Finally, the measured values of StO 2 agree very well with those previously reported by Kurth et al 40 in nonanesthetized CHD infants.…”

Section: Discussionsupporting

confidence: 89%

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

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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: Discussionsupporting

confidence: 89%

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

Self Cite

173

192

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show abstract

“…SctO 2 is determined from the ratio of HbO 2 / (HbO 2 þ Hb). Light from the sensor interrogates blood in the microvasculature (i.e., arterioles, venules and capillaries), 31 with the contribution of venous to arterial blood volume at approximately 70-30% ratio. 20,32 Therefore cerebral tissue blood oxygen saturation values are usually below arterial oxygen saturation (i.e.…”

Section: Cerebral Oximetry Backgroundmentioning

confidence: 99%

Validation of a noninvasive neonatal optical cerebral oximeter in veno-venous ECMO patients with a cephalad catheter

2006

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“…This ScO 2 difference between normal and dysfunction is well within NIRS precision (± 5%), affording some luxury in clinical monitoring. In many sick neonates, cerebral hemoglobin oxygenation is at or below the functional ScO 2 threshold, indicating that cerebral hypoxia-ischemia may not be recognized during clinical care (Brun et al, 1997;Tsuji et al, 1998;Watzman et al, 2000;Kurth et al, 2001;Fantini et al, 1999;Springett et al, 2001).…”

Section: Critical Near-infrared Cerebral Oxygen Saturation 339mentioning

confidence: 99%

Near-Infrared Spectroscopy Cerebral Oxygen Saturation Thresholds for Hypoxia–Ischemia in Piglets

Kurth¹,

Levy

McCann

2002

J Cereb Blood Flow Metab

216

135

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Summary:Detection of cerebral hypoxia-ischemia remains problematic in neonates. Near-infrared spectroscopy, a noninvasive bedside technology has potential, although thresholds for cerebral hypoxia-ischemia have not been defined. This study determined hypoxic-ischemic thresholds for cerebral oxygen saturation (ScO 2 ) in terms of EEG, brain ATP, and lactate concentrations, and compared these values with CBF and sagittal sinus oxygen saturation (SvO 2 ). Sixty anesthetized piglets were equipped with near-infrared spectroscopy, EEG, laser-Doppler flowmetry, and a sagittal sinus catheter. After baseline, ScO 2 levels of less than 20%, 20% to 29%, 30% to 39%, 40% to 49%, 50% to 59%, 60% to 79%, or 80% or greater were recorded for 30 minutes of normoxic normocapnia, hypercapnic hyperoxia, or bilateral carotid occlusion with or without arterial hypoxia. Brain ATP and lactate concentrations were measured biochemically. Logistic and linear regression determined the ScO 2, , CBF, and SvO 2 thresholds for abnormal EEG, ATP, and lactate findings. Baseline ScO 2 was 68 + 5%. The ScO 2 thresholds for increased lactate, minor and major EEG change, and decreased ATP were 44 ± 1%, 42 ± 5%, 37 ± 1%, and 33 ± 1%. The ScO 2 correlated linearly with SvO 2 (r ‫ס‬ 0.98) and CBF (r ‫ס‬ 0.89), with corresponding SvO 2 thresholds of 23%, 20%, 13%, and 8%, and CBF thresholds (% baseline) of 56%, 52%, 42%, and 36%. Thus, cerebral hypoxia-ischemia near-infrared spectroscopy thresholds for functional impairment are ScO 2 33% to 44%, a range that is well below baseline ScO 2 of 68%, suggesting a buffer between normal and dysfunction that also exists for CBF and SvO 2 .

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Cerebral oxygen saturation before congenital heart surgery

Cited by 162 publications

References 22 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

Validation of a noninvasive neonatal optical cerebral oximeter in veno-venous ECMO patients with a cephalad catheter

Near-Infrared Spectroscopy Cerebral Oxygen Saturation Thresholds for Hypoxia–Ischemia in Piglets

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