Abstract

The brain tissue partial oxygen pressure (PbtO2) and near-infrared spectroscopy (NIRS) neuromonitoring are frequently compared in the management of acute moderate and severe traumatic brain injury patients; however, the relationship between their respective output parameters flows from the complex pathogenesis of tissue respiration after brain trauma. NIRS neuromonitoring overcomes certain limitations related to the heterogeneity of the pathology across the brain that cannot be adequately addressed by local-sample invasive neuromonitoring (e.g., PbtO2 neuromonitoring, microdialysis), and it allows clinicians to assess parameters that cannot otherwise be scanned. The anatomical co-registration of an NIRS signal with axial imaging (e.g., computerized tomography scan) enhances the optical signal, which can be changed by the anatomy of the lesions and the significance of the radiological assessment. These arguments led us to conclude that rather than aiming to substitute PbtO2 with tissue saturation, multiple types of NIRS should be included via multimodal systemic- and neuro-monitoring, whose values then are incorporated into biosignatures linked to patient status and prognosis. Discussion on the abnormalities in tissue respiration due to brain trauma and how they affect the PbtO2 and NIRS neuromonitoring is given.

Highlights

  • Introduction distributed under the terms andCurrently, there is no disease-modifying treatment for the primary brain injuries sustained following a traumatic event

  • We argue that the values reported by the intracranial monitoring of PbtO2 are not completely representative of the brain tissue respiration

  • The O2 diffuses across the blood–brain barrier (BBB) in its gaseous form driven by the differences in partial oxygen pressure between the plasma and interstitial tissue [13]

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Summary

Tissue Respiration

The passage of oxygen (O2 ) from vessels into the cells comprises multiple steps in different volumes (e.g., intracellular erythrocytes, plasma, interstitial tissue, intracellular brain cells) and is influenced by multiple physiological factors (e.g., cerebral blood flow, capillary density, concentration of hemoglobin (Hb), O2 affinity for Hb) [11]. The pathogenesis of brain trauma may alter the mechanisms that regulate these steps

Oxygen Forms in the Blood and Oxygen Diffusion
Hemoglobin and Oxygen–Hemoglobin Dissociation Curve
Reduction in Hematocrit Along the Microcirculation
Plasma Gap
Cerebral Blood Flow Autoregulation
Tissue Respiration in Traumatic Brain Injury
Reduction of Circulatory Oxygen Delivery Capacity
Reduction of Cerebral Blood Flow
Reduction of Hematocrit
Response to Therapeutic Hyperoxia
Metabolic Dysfunction
Microcirculatory Dysfunction
Anatomical Damage to the Vessels in the Microcirculation
Reduction of Vascular Density in the Microcirculation
Abnormalities in the Microcirculatory Reactivity to the Metabolic Status
Hydrogen Concentration
Carbon Dioxide Concentration
Chloride Concentration
Temperature
Intracranial Tissue Partial Oxygen Pressure and Near-Infrared Spectroscopy
The Interstitial Tissue Partial Oxygen Pressure Is an Average of Different
Reduction in Oxygen Diffusion and Oxygen-Carrying Capacity
Right-Shift of the Oxygen–Hemoglobin Dissociation Curve
Different Tissue Statuses Across the Brain Can Influence the Values Reported
Tissue Partial Oxygen Pressure Neuromonitoring
Near-Infrared Spectroscopy Neuromonitoring
Biosignatures
Multimodal Monitoring
Tissue Partial Oxygen Pressure and Near-Infrared Spectroscopy Neuromonitoring
Different Types of Near-Infrared Spectroscopy
Contrast-Enhanced Near-Infrared Spectroscopy
Diffuse Optical Tomography
Computerized Tomography and Magnetic Resonance Imaging
Microdialysis
Mean Arterial Pressure and Intracranial Pressure Monitoring
Arterial Blood Gas Analysis
Blood Sampling
Conclusions
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