Noninvasive Assessment Of Cerebral Oxygenation Research Articles

Invasive and noninvasive assessment of cerebral oxygenation in patients with severe traumatic brain injury

The aim of this study is to investigate the relationship between invasive brain tissue oxygen pressure (PbrO(2)) and noninvasive regional transcranial oxygen saturation (rSO(2)) in 22 stable patients with severe traumatic brain injury (TBI) during a 16 h period. This was a prospective, observational study carried out in the Neurocritical Care Unit of a level 1 trauma center in a teaching hospital. A total of 41,809 paired records for neuromonitoring variables were analyzed and compared. A direct and independent correlation between rSO(2) and PbrO(2) was confirmed through adjusted [beta coefficient and (95% confidence interval, CI) = 0.36 (0.35-0.37)] and logistic [PbrO(2) >or=15 mmHg, as a dependent variable; adjusted odds ratio (AOR) and (95% CI) = 1.11 (1.10-1.12)] regression analyses. A receiver-operating characteristic (ROC) curve demonstrated that rSO(2) had low accuracy for detecting moderate (PbrO(2) <or=15 mmHg) intracerebral hypoxia [area under curve (AUC) = 0.62], with the likelihood ratio for a positive test (LR+) = 1.2 for an optimal cutoff of rSO(2) <or=70%. In contrast, the ROC analysis showed that rSO(2) was moderately accurate for detecting severe (PbrO(2) <or=12 mmHg) intracerebral hypoxemia (AUC = 0.82; LR+ = 5.3) for an optimal cutoff of rSO(2) <or=60%. In patients with severe TBI, PbrO(2) and rSO(2) were directly and significantly related. Severe intracerebral hypoxia was better detected by rSO(2) than was moderate intracerebral hypoxia. However, the diagnostic accuracy of rSO(2) was limited, and this measure should not be considered a substitute for routine PbrO(2) monitoring.

Time-resolved optical imager for assessment of cerebral oxygenation

A time-resolved optical instrument allowing for noninvasive assessment of cerebral oxygenation is presented. The instrument is equipped with picosecond diode lasers, fast photodetectors, and time-correlated single photon counting electronics. This technology enables depth-resolved estimation of changes in absorption and, in consequence, assessment of changes in hemoglobin concentrations in the brain cortex. Changes in oxyhemoglobin (HbO(2)) and deoxyhemoglobin (Hb) can be evaluated selectively in extra- and intracerebral tissue compartments using the moments of distributions of times of flight of photons measured at two wavelengths in the near-infrared region. The combination of the data acquired from multiple sources and detectors located on the surface of the head with the depth-resolved analysis, based on the moments, enables imaging of cortex oxygenation. Results of the tests on physical phantoms as well as in vivo validation of the instrument during the motor stimulation experiment are presented.

Microvascular Plasticity and Experimental Heart Failure

Angiogenesis is an essential process in adulthood during wound healing and restoration of blood flow to injured tissues. Angiogenesis is regulated by a very sensitive interplay of growth factors and inhibitors; their imbalance can lead to very diverse diseases. Excessive angiogenesis is involved in malignant, diabetic retinopathy and inflammatory disorders (eg, rheumatoid arthritis, psoriasis, atherosclerosis). Conversely, insufficient angiogenesis may underlie conditions such as ischemic heart diseases, stroke, hypertension, and diabetes. Hence, during the evolution of these degenerative pathologies, inadequate blood vessel growth and insufficient microvascular density leads to poor circulation and tissue suffering or, ultimately, necrosis and death.1 In several physiological conditions, such as muscular exercise training and detraining, acclimatization to altitude, and aging, an adaptation of the microvascular network structure and function to new conditions has been reported.2,3 Interestingly, there is a close link between cerebral angiogenesis and learning; during cognitive decline in relation to senescence or degenerative cerebral diseases, microvascular density is decreased in specific cerebral areas. Specifically, there is a striking relationship between the capillary density, the cerebral tissue blood flow, the local glucose use, and other measures of neuronal signaling, such as the NA+/K+ ATPase (reviewed in Reference 4). Therefore, microvascular plasticity, defined as the ability of the arteriole and capillary network to adapt to the metabolic local conditions by proangiogenesis or antiangiogenesis processes, likely plays a key role in many tissue homeostatic processes. In hypertension, the role of microcirculation (arteriolar and capillary) is of particular importance in increasing periph-eral resistance …

Noninvasive assessment of cerebral oxygenation during high altitude trekking in the Nepal Himalayas (2850–5600 m)

Mountain trekking is significantly increasing in popularity. Hypoxia seems to play a key role in the pathogenesis of acute mountain sickness (AMS). The purpose of this study was to investigate regional cerebral (rSO2) and peripheral (SaO2) oxygen saturation for the first time, during 22 days high altitude trekking (measurement points: 3450, 4450, 4750, 5050 and 2850 m) in the Khumbu region of Nepal with near infrared spectroscopy and pulse oximetry. We examined 17 healthy volunteers 19–65 years old (8 female, 9 male; mean age ± SD, 46.1 ± 13.1 years). RSO2 and SaO were significantly (p < 0.001, ANOVA, Tukey test) decreased at high altitudes (4450, 4750 and 50502m). The decrease in cerebral oxygen saturation was more pronounced at higher altitudes than in the periphery (rSO2/SaO = 0.56 at 5050 m). At higher altitudes (> 4450 m), two subjects showed reversible symptoms of AMS. The present data indicates that acute reduction in rSO2 values might be a primary cause of AMS, however, further studies and analysis are necessary to correlate our findings with cerebral symptom scores.

Noninvasive assessment of cerebral oxygenation during acclimation to hypobaric hypoxia.

Factors regulating cerebral tissue PO2 (PtO2) are complex. With the increased use of clinical PtO2 monitors, it has become important to elucidate these mechanisms. The authors are investigating a new methodology (electron paramagnetic resonance oximetry) for use in monitoring cerebral PtO2 in awake animals over time courses of weeks. The authors used this to study cerebral PtO2 in rats during chronic acclimation to hypoxia predicting that such acclimation would cause an increase in PtO2 because of increases that occur in capillary density and oxygen carrying capacity. The average PtO2 between 7 and 21 days was increased by 228% over controls.

Does Hypothermia Prevent Cerebral Ischaemia during Cardiopulmonary Bypass?

It is believed that moderate hypothermia (25–32°C) during cardiopulmonary bypass provides cerebral protection by reducing the cerebral metabolic rate (CMRO2). Nevertheless episodes of ischaemia do occur and thus it has been suggested that cerebral oxygenation should be monitored by jugular venous oximetry. However, this technique is cumbersome and invasive. Near infrared spectroscopy (NIRS) provides a non-invasive assessment of cerebral oxygenation and this was used together with continuous Jugular venous oximetry in 21 patients undergoing hypothermic cardiopulmonary bypass. During the hypothermic period, jugular venous oximetry indicated reduced oxygen extraction consistent with a reduction in CMRO2 (Increase from 61 ± 2.5% to 74 ± 2.5%). In contrast, near infrared spectroscopy demonstrated increased oxygen extraction (HbO2 − 11.5 ± 1 μM. HHb + 3.2 ± 0.3 μM) and a fall in the cerebral concentration of oxidized cytochrome oxidase (– 1.7 ± 0.3 μM) indicating ischaemia. These results suggest that cerebral ischaemia occurs during hypothermic cardiopulmonary bypass with a spurious rise in jugular venous oxygen saturation, which represents arterio-venous shunting. Thus if hypothermia does facilitate cerebral protection it does not appear to be a direct result of a reduction in CMRO2 and oxygen requirement.

Does hypothermia prevent cerebral ischaemia during cardiopulmonary bypass?

It is believed that moderate hypothermia (25–32°C) during cardiopulmonary bypass provides cerebral protection by reducing the cerebral metabolic rate (CMRO 2). Nevertheless episodes of ischaemia do occur and thus it has been suggested that cerebral oxygenation should be monitored by jugular venous oximetry. However, this technique is cumbersome and invasive. Near infrared spectroscopy (NIRS) provides a non-invasive assessment of cerebral oxygenation and this was used together with continuous jugular venous oximetry in 21 patients undergoing hypothermic cardiopulmonary bypass. During the hypothermic period, jugular venous oximetry indicated reduced oxygen extraction consistent with a reduction in CMRO 2 (increase from 61±2.5% to 74±2.5%). In contrast, near infrared spectroscopy demonstrated increased oxygen extraction (HbO 2 −11.5±1 μM, HHb +3.2±0.3 μM) and a fall in the cerebral concentration of oxidized cytochrome oxidase (−1.7±0.3 μM) indicating ischaemia. These results suggest that cerebral ischaemia occurs during hypothermic cardiopulmonary bypass with a spurious rise in jugular venous oxygen saturation, which represents arterio-venous shunting. Thus if hypothermia does facilitate cerebral protection it does not appear to be a direct result of a reduction in CMRO 2 and oxygen requirement.

Validation in Volunteers of a Near-Infrared Spectroscope for Monitoring Brain Oxygenation In Vivo

Cerebral oximeters based on near-infrared spectroscopy may provide a continuous, noninvasive assessment of cerebral oxygenation. We evaluated a prototype cerebral oximeter (Invos 3100; Somanetics, Troy, MI) in 22 conscious, healthy volunteers breathing hypoxic gas mixtures. Using the first 12 subjects (training group), we developed an algorithm based on the mathematic relationship that converts detected light from the field surveyed by the probe to cerebral hemoglobin oxygen saturation (CSfO2). To develop the algorithm, we correlated the oximeter result with the estimated combined brain hemoglobin oxygen saturation (CScombO2, where CScombO2 = SaO2 x 0.25 + SjO2 x 0.75 and SjO2 = jugular venous saturation). We then validated the algorithm in the remaining 10 volunteers (validation group). A close association (r2 = 0.798-0.987 for individuals in the training group and r2 = 0.794-0.992 for individuals in the validation group) existed between CSfO2 and CScombO2. We conclude that continuous monitoring with cerebral oximetry may accurately recognize decreasing cerebral hemoglobin oxygen saturation produced by systemic hypoxemia.

O112 A novel method for the non-invasive assessment of cerebral oxygenation during CPR

O112 A novel method for the non-invasive assessment of cerebral oxygenation during CPR