Cerebrovascular pressure reactivity and brain tissue oxygen monitoring provide complementary information regarding the lower and upper limits of cerebral blood flow control in traumatic brain injury: a CAnadian High Resolution-TBI (CAHR-TBI) cohort study

Abstract

Background Brain tissue oxygen tension (PbtO2) and cerebrovascular pressure reactivity monitoring have emerged as potential modalities to individualize care in moderate and severe traumatic brain injury (TBI). The relationship between these modalities has had limited exploration. The aim of this study was to examine the relationship between PbtO2 and cerebral perfusion pressure (CPP) and how this relationship is modified by the state of cerebrovascular pressure reactivity. Methods A retrospective multi-institution cohort study utilizing prospectively collected high-resolution physiologic data from the CAnadian High Resolution-TBI (CAHR-TBI) Research Collaborative database collected between 2011 and 2021 was performed. Included in the study were critically ill TBI patients with intracranial pressure (ICP), arterial blood pressure (ABP), and PbtO2 monitoring treated in any one of three CAHR-TBI affiliated adult intensive care units (ICU). The outcome of interest was how PbtO2 and CPP are related over a cohort of TBI patients and how this relationship is modified by the state of cerebrovascular reactivity, as determined using the pressure reactivity index (PRx). Results A total of 77 patients met the study inclusion criteria with a total of 377,744 min of physiologic data available for the analysis. PbtO2 produced a triphasic curve when plotted against CPP like previous population-based plots of cerebral blood flow (CBF) versus CPP. The triphasic curve included a plateau region flanked by regions of relative ischemia (hypoxia) and hyperemia (hyperoxia). The plateau region shortened when cerebrovascular pressure reactivity was disrupted compared to when it was intact. Conclusions In this exploratory analysis of a multi-institution high-resolution physiology TBI database, PbtO2 seems to have a triphasic relationship with CPP, over the entire cohort. The CPP range over which the plateau exists is modified by the state of cerebrovascular reactivity. This indicates that in critically ill TBI patients admitted to ICU, PbtO2 may be reflective of CBF.

Prognostic value of near-infrared spectroscopy regional oxygen saturation and cerebrovascular reactivity index in acute traumatic neural injury: a CAnadian High-Resolution Traumatic Brain Injury (CAHR-TBI) Cohort Study

“…A key takeaway from this study is that rSO 2 as a raw absolute parameter provides little, if any prognostic value in the ICU. This is consistent with recent studies that found high-resolution rSO 2 signals to have differing statistical properties to more established monitoring modalities in moderate-to-severe TBI including brain tissue oxygenation (PbtO 2 ), CPP, and ICP, as well as various measures of CVR [ 47 , 48 ]. It should be noted that in alternative settings, such as intraoperative monitoring, change in rSO 2 is viewed as a more reliable metric of cerebral hypoxia and ischemic risk [ 49 , 50 ].…”

Effect of Increasing Blood Pressure on Brain Tissue Oxygenation in Adults After Severe Traumatic Brain Injury*

“…Although ICP either did not change or decrease in this group, we attributed PbtO 2 deterioration to MAP augmentation. Further, MAP augmentation, when Pa co 2 increases and cerebral autoregulation is impaired, may increase ICP and decrease PbtO 2 (11). Among PbtO 2 responder group 3, where baseline PbtO 2 was low and improved to a normal threshold, one MAP challenge test resulted in ICP increasing from 15 mm Hg to 20 mm Hg when cerebral autoregulation was impaired.…”

Neuromonitoring in neurocritical care for traumatic brain injury in the Thai context

“…The important knowledge is the identification of factors that affect CBF, such as CPP, autoregulation status, and arterial partial pressure of oxygen and carbon dioxide. To prevent sequelae of elevated ICP (herniation syndrome such as uncal ,central transtentorial, subfalcine and tonsillar herniation and cerebral ischemia and hypoxia comprised decreased in CPP and brain oxygen delivery) is to perform neuro-monitoring that classified into monitor in driving pressure (ICP and CPP), CBF (Transcranial Doppler (TCD) ultrasound for detect local and regional blood flow), brain oxygen delivery (Jugular venous oxygen satura- tion (Sjvo 2 ), Near-infrared spectroscopy (NIRS) and Brain tissue oxygenation (PbtO 2 ), cerebral metabolism (CMD to measure cerebral lactate-pyruvate ratio, cerebral lactate and glucose) and central nervous system function (EEG and electrophysiology study) that recommend threshold level in Table 4 [6][7][8][9][10][11]24] and the diagram of the neuromonitoring strategy in traumatic brain injury in Figure 2.…”

“…CeOx has been cleared by the United States Food and Drug Administration for monitoring regional cerebral oxygen saturation [4], and cerebral deoxygenation (rSO 2 below 55%) has been shown to correlate with a variety of adverse systemic complications and multi-organ failure, for example, renal failure, overall well-being, prolonged ventilation, cortical dysfunction, cerebral hypoxia, and low cardiac output syndromes. Many studies [1,7,12,16] showed that CeOx with NIRS correlated with CPP estimation, the Glasgow Outcome Score Scale, and mortality in patients with severe TBI, and NIRS has the capability to provide an early warning of cerebral ischemia and infarction. These impacts of continuous monitoring showed the above correlations between regional cerebral saturation and systemic outcomes, and most of the intraoperative measures taken to optimize cerebral rSO 2 and oxygen delivery potentially affect systemic perfusion (e.g., alterations in PaCO 2 , cardiac output, arterial blood pressure, etc.).…”