Development and validation of a multiwavelength spatial domain near-infrared oximeter to detect cerebral hypoxia-ischemia

2006 ◽  
Vol 11 (6) ◽  
pp. 064022 ◽  
Author(s):  
Lindsey A. Nelson ◽  
John C. McCann ◽  
Andres W. Loepke ◽  
Jun Wu ◽  
Baruch Ben Dor ◽  
...  
2002 ◽  
Vol 22 (3) ◽  
pp. 335-341 ◽  
Author(s):  
C. Dean Kurth ◽  
Warren J. Levy ◽  
John McCann

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 (Sco2) in terms of EEG, brain ATP, and lactate concentrations, and compared these values with CBF and sagittal sinus oxygen saturation (Svo2). Sixty anesthetized piglets were equipped with near-infrared spectroscopy, EEG, laser-Doppler flowmetry, and a sagittal sinus catheter. After baseline, Sco2 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 Sco2, CBF, and Svo2 thresholds for abnormal EEG, ATP, and lactate findings. Baseline Sco2 was 68 + 5%. The Sco2 thresholds for increased lactate, minor and major EEG change, and decreased ATP were 44 ± 1%, 42 ± 5%, 37 ± 1%, and 33 ± 1%. The Sco2 correlated linearly with Svo2 (r = 0.98) and CBF (r = 0.89), with corresponding Svo2 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 Sco2 33% to 44%, a range that is well below baseline Sco2 of 68%, suggesting a buffer between normal and dysfunction that also exists for CBF and Svo2.


PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107192 ◽  
Author(s):  
Cuicui Xie ◽  
Kai Zhou ◽  
Xiaoyang Wang ◽  
Klas Blomgren ◽  
Changlian Zhu

2007 ◽  
Vol 412 (2) ◽  
pp. 114-117 ◽  
Author(s):  
John C. Ashton ◽  
Rosanna M.A. Rahman ◽  
Shiva M. Nair ◽  
Brad A. Sutherland ◽  
Michelle Glass ◽  
...  

2017 ◽  
Vol 4 (10) ◽  
pp. 722-738 ◽  
Author(s):  
Rafael Galindo ◽  
Marianne Banks Greenberg ◽  
Toshiyuki Araki ◽  
Yo Sasaki ◽  
Nehali Mehta ◽  
...  

Author(s):  
Shigeki Imaizumi ◽  
Teiji Tominaga ◽  
Hiroshi Uenohara ◽  
Hiroyuki Kinouchi ◽  
Takashi Yoshimoto ◽  
...  

2018 ◽  
Vol 70 (1) ◽  
pp. 56-66 ◽  
Author(s):  
Gabriella Koning ◽  
Ellinor Lyngfelt ◽  
Pernilla Svedin ◽  
Anna‐Lena Leverin ◽  
Masako Jinnai ◽  
...  

2006 ◽  
Vol 100 (3) ◽  
pp. 850-857 ◽  
Author(s):  
Kenneth M. Tichauer ◽  
Derek W. Brown ◽  
Jennifer Hadway ◽  
Ting-Yim Lee ◽  
Keith St. Lawrence

Impaired oxidative metabolism following hypoxia-ischemia (HI) is believed to be an early indicator of delayed brain injury. The cerebral metabolic rate of oxygen (CMRO2) can be measured by combining near-infrared spectroscopy (NIRS) measurements of cerebral blood flow (CBF) and cerebral deoxy-hemoglobin concentration. The ability of NIRS to measure changes in CMRO2 following HI was investigated in newborn piglets. Nine piglets were subjected to 30 min of HI by occluding both carotid arteries and reducing the fraction of inspired oxygen to 8%. An additional nine piglets served as sham-operated controls. Measurements of CBF, oxygen extraction fraction (OEF), and CMRO2 were obtained at baseline and at 6 h after the HI insult. Of the three parameters, only CMRO2 showed a persistent and significant change after HI. Five minutes after reoxygenation, there was a 28 ± 12% (mean ± SE) decrease in CMRO2, a 72 ± 50% increase in CBF, and a 56 ± 19% decrease in OEF compared with baseline ( P < 0.05). By 30 min postinsult and for the remainder of the study, there were no significant differences in CBF and OEF between control and insult groups, whereas CMRO2 remained depressed throughout the 6-h postinsult period. This study demonstrates that NIRS can measure decreases in CMRO2 caused by HI. The results highlight the potential for NIRS to be used in the neonatal intensive care unit to detect delayed brain damage.


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