Measuring Cerebral Oxygenation During Normobaric Hyperoxia: A Comparison of Tissue Microprobes, Near-Infrared Spectroscopy, and Jugular Venous Oximetry in Head Injury

McLeod, Andrew; Igielman, Farrell; Elwell, Clare E.; Cope, M; Smith, Martin

doi:10.1213/01.ane.0000072541.57132.ba

Cited by 77 publications

(57 citation statements)

References 30 publications

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“…Hamamatsu NIRO devices have been shown to track changes in cerebral tissue oxygenation accurately in comparison to measurements of cerebral tissue oxygen tension and jugular venous oxygen saturation (Al-Rawi et al 2001;McLeod et al 2003). Optodes were placed bilaterally, high on the forehead, 4 cm apart, and secured with adhesive tape (Ulrich et al 2014 (Kitabatake et al 1983), and spirometry (EasyOne; NDD, Zurich, Switzerland) was performed (Miller et al 2005).…”

Section: Measurementsmentioning

confidence: 99%

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Furian

Latshang

Aeschbacher

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study?Cerebral hypoxia impairs cognitive function and exercise performance and may result in brain damage. Residents at high altitude, in particular those with high-altitude pulmonary hypertension, are prone to hypoxaemia due to the exposure to reduced barometric pressure and impaired pulmonary gas exchange. Whether highlanders have a reduced cerebral oxygenation has not been studied. r What is the main finding and its importance?We found that despite a reduced arterial oxygen saturation, healthy highlanders and even those with pulmonary hypertension have a similar cerebral oxygenation to healthy lowlanders, suggesting that compensatory mechanisms protect long-term residents at high altitude from cerebral hypoxia.High-altitude pulmonary hypertension (HAPH), a chronic altitude-related illness, causes hypoxaemia and impaired exercise performance. We evaluated the hypothesis that haemodynamic limitation and hypoxaemia in patients with HAPH are associated with impaired cerebral tissue oxygenation (CTO) compared with healthy highlanders (HH) and lowlanders (LL). We studied 36 highlanders with HAPH and 54 HH at an altitude of 3250 m, and 34 LL at 760 m. Mean(±SD) pulmonary artery pressures were 34(±3), 22(±5) and 16(±4) mmHg, respectively (P < 0.05, all comparisons). The CTO was monitored by near-infrared spectroscopy along with pulse oximetry (peripheral arterial oxygen saturation, S pO 2 ) during quiet breathing of room air (RA) and oxygen for 20 min each, and during hyperventilation with RA and oxygen, respectively. In HAPH, HH and LL breathing RA, S pO 2 was 88(±4), 92(±2) and 95(±2)%, respectively (P < 0.001, all comparisons), and CTO was similar in the three groups, at 68(±3), 68(±4) and 69(±4)%, respectively (n.s., all comparisons). Breathing oxygen increased S pO 2 and CTO significantly more in HAPH than in HH and LL. Hyperventilation (RA) did not reduce CTO in HAPH but did in HH and LL; hyperventilation (oxygen) increased CTO in HAPH only. Highlanders with and without HAPH studied at 3250 m had a similar CTO to healthy lowlanders at 760 m even though highlanders were hypoxaemic. The physiological response to hyperoxia and hypocapnia assessed by cerebral near-infrared spectroscopy suggests that healthy highlanders and even highlanders with HAPH effectively maintain an adequate CTO. This

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Section: Measurementsmentioning

confidence: 99%

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Furian

Latshang

Aeschbacher

et al. 2015

Experimental Physiology

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“…This may be particularly valid for the immature brain in which specific features of redox biochemistry and physiology set the stage for increased susceptibility to oxidative stress [3,4] . Moreover, the employment of partial pressure of brain tissue oxygen monitoring and the application of raising fraction of inspired oxygen in the management of TBI patients might enhance oxidative stress [5][6][7][8] . With this in mind, the current review is specifically focused on (1) potential sources of TBI-induced oxidative stress in the immature brain and (2) enzymatic and nonenzymatic antioxidant protection mechanisms.…”

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confidence: 99%

Oxidative Stress in Immature Brain after Traumatic Brain Injury

Bayır¹,

Kochanek²,

Kagan³

2006

Dev Neurosci

124

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High oxygen demand along with the abundance of readily oxidizable substrates yielding productive oxidative metabolism are required for the normal function of the brain. This necessitates the existence of the complex and multicomponent antioxidant system in the brain for protection against oxidative damage. However, during development, individual components of the antioxidant system are not equally expressed and not always sufficient to fulfill their tasks in a coordinated way. As a result, the developing brain may be more vulnerable to oxidative insults than the adult brain. Traumatic brain injury is one of the damaging acute impacts that challenge the brain antioxidant reserves by exposing them to a number of decompartmentalized prooxidant molecules. This review focuses on the sources and assessment of oxidative stress and the link between oxidative stress and cell death pathways in the immature brain after experimental and clinical traumatic brain injury.

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“…The NIRO 300 has also recently ................................................................................................................................................................................................................... Ó 2002 Blackwell Publishing Ltd been released but its predecessor, the NIRO 500, has similarly been compared with jugular venous oximetry and measurements of brain tissue pO 2 [28] and also with the INVOS 3100 [3,27]. There are few published studies to validate TOI as an independent monitor of cerebral oxygenation [29] but the recent report demonstrating high sensitivity and specificity for intracranial changes is likely to stimulate interest in its use in the clinical setting [21].…”

Section: Discussionmentioning

confidence: 99%

A comparison of cerebral oxygenation as measured by the NIRO 300 and the INVOS 5100 Near‐Infrared Spectrophotometers

Broadhead²,

et al. 2002

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SummaryIn this study cerebral oxygenation was measured using the NIRO 300 and the INVOS 5100 spectrophotometers in 10 healthy adult volunteers, exposed to varying degrees of hyperoxia and hypoxia. The results showed similar baseline values for tissue oxygenation index and regional cerebral oxygen saturation with mean (SD) values being 64.9% (5.1) and 62.3% (6.0), respectively. The overall bias was -2.1%, with the INVOS 5100 under-reading cerebral oxygenation compared to the NIRO 300, with limits of agreement of ±14.7%. Both monitors demonstrated similar changes in response to hyperoxia and hypocapnia (coefficient of variance for F I O 2 0.45 ¼ 10.0%, F I O 2 1.0 ¼ 10.1%, hypocapnia ¼ 14.5%). The reasons for the bias and variability may relate to differences in the methodological approaches of the two monitors. The correlation between the monitors in response to changes in cerebral oxygenation implies that they may be useful as trend monitors in clinical practice.

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Measuring Cerebral Oxygenation During Normobaric Hyperoxia: A Comparison of Tissue Microprobes, Near-Infrared Spectroscopy, and Jugular Venous Oximetry in Head Injury

Cited by 77 publications

References 30 publications

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Cerebral oxygenation in highlanders with and without high‐altitude pulmonary hypertension

Oxidative Stress in Immature Brain after Traumatic Brain Injury

A comparison of cerebral oxygenation as measured by the NIRO 300 and the INVOS 5100 Near‐Infrared Spectrophotometers

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