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Introduction: In hypoxic ischemic brain injury (HIBI), increased intracranial pressure (ICP) can ensue from cerebral edema stemming from cytotoxic and vasogenic mechanisms. Downstream sequelae of restricted cerebral blood flow lead to neurologic braindeath. There is limited data characterizing the temporal trends and patterns of ICP and compliance in human HIBI patients., Methods: Patients underwent invasive ICP monitoring with a parenchymal probe (Camino) and were managed with a tier-based management algorithm for elevated ICP. Data pertaining to mean arterial pressure (MAP), ICP, brain tissue oxygenation (PbtO 2 ), end tidal carbon dioxide (ETCO 2 ), core body temperature and RAP (moving correlation coefficient between mean ICP and its mean pulse amplitude) as a measure of intracranial compliance were recorded in the ICM + software. Data pertaining to ICP lowering interventions was also collected., Results: Ten patients were included with a median age of 47 (range 20-71) and seven were male (7/10). The mean ICP was 14 mmHg (SD 11) and time of ICP> 20 mmHg was 22% (range 0-100). The mean MAP, ETCO 2 and temperature were 89 mmHg (SD 13), 31 mmHg (SD 7), 35.7 °C (SD 0.9), respectively. The mean RAP was 0.58 (SD 0.34) and time of RAP > 0.4 was 78% (range 57-97). There were no significant relationships between ETCO 2 and temperature with ICP., Conclusions: In our cohort, HIBI was characterized by normal ICP but with limited intracranial compliance. However, significant in between patient heterogeneity exists with respect to temporal patterns of intracranial pressure - volume relationships in HIBI., Trial Registration: clinicaltrials.gov (NCT03609333)., (Crown Copyright © 2019. Published by Elsevier B.V. All rights reserved.)

Multimodal neuromonitoring in the management of traumatic brain injury (TBI) enables clinicians to make individualized management decisions to prevent secondary ischemic brain injury. Traditionally, neuromonitoring in TBI patients has consisted of a combination of clinical examination, neuroimaging and intracranial pressure monitoring. Unfortunately, each of these modalities has its limitations and although pragmatic, this simplistic approach has failed to demonstrate improved outcomes, likely owing to an inability to consider the underlying heterogeneity of various injury patterns. As neurocritical care has evolved, so has our understanding of underlying disease pathophysiology and patient specific considerations. Recent additions to the multimodal neuromonitoring platform include measures of cerebrovascular autoregulation, brain tissue oxygenation, microdialysis and continuous electroencephalography. The implementation of neurocritical care teams to manage patients with advanced brain injury has led to improved outcomes. Herein, we present a narrative review of the recent advances in multimodal neuromonitoring and highlight the utility of dedicated neurocritical care., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: In many neurological diseases, intracranial pressure (ICP) is elevated and needs to be actively managed. ICP is typically measured with an invasive transducer, which carries risks. Non-invasive techniques for monitoring ICP (nICP) have been developed. The aim of this study was to compare three different methods of transcranial Doppler (TCD) assessment of nICP in an animal model of acute intracranial hypertension., Methods: In 28 rabbits, ICP was increased to 70-80 mmHg by infusion of Hartmann's solution into the lumbar subarachnoid space. Doppler flow velocity in the basilar artery was recorded. nICP was assessed through three different methods: Gosling's pulsatility index PI (gPI), Aaslid's method (AaICP), and a method based on diastolic blood flow velocity (FVdICP)., Results: We found a significant correlation between nICP and ICP when all infusion experiments were combined (FVdICP: r = 0.77, AaICP: r = 0.53, gPI: r = 0.54). The ability to distinguish between raised and 'normal' values of ICP was greatest for FVdICP (AUC 0.90 at ICP >40 mmHg). When infusion experiments were considered independently, FVdICP demonstrated again the strongest correlation between changes in ICP and changes in nICP (mean r = 0.85)., Conclusions: TCD-based methods of nICP monitoring are better at detecting changes of ICP occurring in time, rather than absolute prediction of ICP as a number. Of the studied methods of nICP, the method based on FVd is best to discriminate between raised and 'normal' ICP and to monitor relative changes of ICP.

Background: Red blood cell (RBC) transfusion is associated with inconsistent changes in brain tissue oxygenation (PbO2). Previous studies have failed to consider alterations in cerebral autoregulation. Our objective was to investigate the effect of RBC transfusion on cerebral autoregulation, as measured by pressure reactivity index (PRx)., Methods: Retrospective analysis of 28 severe traumatic brain injury (TBI) patients from a prospective registry between 2007 and 2014. We recorded hemoglobin (Hb) concentration, intracranial pressure, PbO2, cerebral perfusion pressure, PRx, and cerebral lactate/pyruvate ratio for 6 h before and after RBC transfusion. We also recorded body temperature, PaO2, PCO2, pH, and fraction of inspired oxygen. Subgroups of normoxia (PbO2 >20 mmHg) and hypoxia (PbO2 <20 mmHg) prior to transfusion were defined a priori., Results: The median age was 36 years [interquartile range (IQR) 27-49], 32% were female. The median admission Glasgow Coma score was 5 (IQR 4-9) and injury severity score was 16 (IQR 9-21). Overall, mean Hb concentration [80 g/L (SD 7) to 89 g/L (SD 8), p < 0.001] and PbO2 increased [23.5 mmHg (SD 8) to 25.0 mmHg (SD 9), p = 0.033] following transfusion. PRx increased post-transfusion [0.028 (SD 0.29) to 0.11 (SD 0.24), p = 0.034], indicating worsening cerebrovascular pressure reactivity. In patients with mean PbO2 >20 mmHg pre-transfusion (n = 20), the PRx increased significantly [-0.052 (SD 0.24) to 0.079 (SD 0.22), p = 0.007] but did not change in patients with PbO2 <20 mmHg: PRx [0.22 (SD 0.34) to 0.18 (SD 0.30), p = 0.36]., Conclusion: RBC transfusion in severe TBI patients results in worsening PRx, indicating impaired cerebral autoregulation.

Background: Increased blood glucose and impaired pressure reactivity (PRx) after traumatic brain injury (TBI) are both known to correlate with unfavorable patient outcome. However, the relationship between these two variables is unknown., Methods: To test the hypothesis that increased blood glucose leads to increased PRx, we retrospectively analyzed data from 86 traumatic brain injured patients admitted to the Neurocritical Care Unit. Data analyzed included arterial glucose concentration, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and end-tidal CO2. PRx was calculated as the moving correlation coefficient between averaged (10 seconds) arterial blood pressure and ICP. One arterial glucose concentration and one time-aligned PRx value were obtained for each patient, during each day until the fifth day after ictus., Results: Mean arterial glucose concentrations during the first 5 days since ictus were positively correlated with mean PRx (Pearson correlation coefficient = 0.25, p = 0.02). The correlation was strongest on the first day after injury (Pearson correlation coefficient = 0.47, p = 0.008)., Conclusion: Our preliminary findings indicate that increased blood glucose may impair cerebrovascular reactivity, potentially contributing to a mechanistic link between increased blood glucose and poorer outcome after TBI.

Purpose: The aims of this study are to assess adherence to the Brain Trauma Foundation (BTF) cerebral perfusion pressure (CPP) guidelines and to determine if adherence is associated with mortality in patients who have a severe traumatic brain injury., Materials and Methods: Retrospective cohort study of 127 patients admitted to one intensive care unit between 2006 and 2012. Adherence to BTF guidelines was measured as the time that the CPP was within 50 to 70 mm Hg divided by the total time of CPP monitoring (CPP time index)., Results: The percentage of time that the CPP was within the recommended range was 31.6% (SD, 22.2); CPP was greater than 70 mm Hg for 63.9% (SD, 26.2) of the time and less than 50 mm Hg for 4.5% of the time (SD, 16.3). After adjustment for covariates, CPP time index (between 50 and 70 mm Hg) was not associated with hospital mortality (odds ratio [OR], 1.2; 95% confidence interval [CI], 0.98-1.6; P= .079). The time indices for CPP ≥70 and <50 mm Hg were associated with decreased (OR, 0.66; 95%CI, 0.52-0.82; P< .0001) and increased (OR, 9.9; 95% CI, 1.4-69.6; P= .021) mortality, respectively., Conclusion: Cerebral perfusion pressure was greater than 70 mm Hg for most of the time. This level of CPP was associated with decreased hospital mortality., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Purpose: Assess the relationship between optic nerve sheath diameter (ONSD) measured on bedside portable computed tomography (CT) scans and simultaneously measured intracranial pressure (ICP) in patients with severe traumatic brain injury., Methods: Retrospective cohort study of 57 patients admitted between 2009 and 2013. Linear and logistic regression were used to model the correlation and discrimination between ONSD and ICP or intracranial hypertension, respectively., Results: The cohort had a mean age of 40 years (SD 16) and a median admission Glasgow coma score of 7 (IQR 4-10). The between-rater agreement by intraclass coefficient was 0.89 (95 % CI 0.83-0.93, P < 0.001). The mean ONSD was 6.7 mm (SD 0.75) and the mean ICP during CT was 21.3 mmHg (SD 8.4). Using linear regression, there was a strong correlation between ICP and ONSD (r = 0.74, P < 0.001). ONSD had an area under the curve to discriminate elevated ICP (≥20 mmHg vs. <20 mmHg) of 0.83 (95 % CI 0.73-0.94). Using a cutoff of 6.0 mm, ONSD had a sensitivity of 97 %, specificity of 42 %, positive predictive value of 67 %, and a negative predictive value of 92 %. Comparing linear regression models, ONSD was a much stronger predictor of ICP (R(2) of 0.56) compared to other CT features (R(2) of 0.21)., Conclusions: Simultaneous measurement of ONSD on CT and ICP were strongly correlated and ONSD was discriminative for intracranial hypertension. ONSD was much more predictive of ICP than other CT features. There was excellent agreement between raters in measuring ONSD.

Introduction: Invasive monitoring of cerebral autoregulation using the pressure reactivity index (PRx) allows for the determination of optimal mean arterial pressure (MAPOPT) in hypoxic ischemic brain injury (HIBI) patients following cardiac arrest. However, the utility of non-invasive surrogates to determine MAPOPT has not been addressed. We aimed to determine the agreement between PRx-derived MAPOPT versus MAPOPT determined by the near-infrared spectroscopy (NIRS) based cerebral oximetry index (COx).Methods: Ten HIBI patients were enrolled. PRx-derived MAPOPT, lower (LLA) and upper limits of autoregulation (ULA) were compared against COx-derived MAPOPT, LLA and ULA. Multimodal neuromonitoring included mean arterial pressure, intracranial pressure, brain tissue oxygenation, jugular venous oxygen saturation, and NIRS-derived regional cerebral oxygen saturation.Results: Repeated measures Bland-Altman plots demonstrated limited agreement between MAPOPT derived from COx and PRx (mean bias: 1.4 mmHg; upper limit of agreement: 25.9 mmHg; lower limit of agreement: -23.0 mmHg). Similarly, there was limited agreement between the absolute values of PRx and COx. Mean bias was 0.26 and the upper and lower limits of agreement were 1.05 and -0.53, respectively. Systematic bias was apparent, whereby at low PRx values COx overestimated PRx and at high PRx values, COx underestimated PRx. COx was limited in its ability to determine impaired autoregulation defined by PRx (receiver operator characteristic area under the curve was 0.488).Conclusion: Collectively, we demonstrate that COx-based determination of MAPOPT lacks agreement with MAPOPT derived from PRx. Further research must be done to evaluate the physiologic and clinical efficacy of PRx derived MAPOPT in HIBI. [ABSTRACT FROM AUTHOR]

Objectives: We sought to characterize 1) the difference in the diffusion gradient of cellular oxygen delivery and 2) the presence of diffusion limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as defined by parenchymal brain tissue oxygen tension less than 20 mm Hg versus normoxia (brain tissue oxygen tension > 20 mm Hg).Design: Post hoc subanalysis of a prospective study in hypoxic-ischemic brain injury patients dichotomized into those with brain hypoxia versus normoxia.Setting: Quaternary ICU.Patients: Fourteen adult hypoxic-ischemic brain injury patients after cardiac arrest.Interventions: Patients underwent monitoring with brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen saturation. Data were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterprises, Cambridge, United Kingdom). Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively.Measurements and Main Results: Both the normoxia and hypoxia groups consisted of seven patients. In the normoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm Hg (SD, 9), and 80 mm Hg (SD, 7), respectively. In the hypoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen to brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm Hg (SD, 8), and 72 mm Hg (SD, 6), respectively. There were significant differences in the jugular venous bulb oxygen tension-brain oxygen tension gradient (16 mm Hg [sd, 6] vs 39 mm Hg SD, 11]; p < 0.001) and in the relationship of jugular venous bulb oxygen tension-brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia to hypoxia. Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular venous bulb oxygen tension-brain oxygen tension gradient by 0.36 mm Hg (95% CI, -0.54 to 0.18; p < 0.001) in the normoxia group, but no such relation was demonstrable in the hypoxia group.Conclusions: In hypoxic-ischemic brain injury patients with brain hypoxia, there is an elevation in the jugular venous bulb oxygen tension-brain oxygen tension gradient, which is not modulated by changes in cerebral perfusion pressure. [ABSTRACT FROM AUTHOR]

Aim: Increased intracranial pressure (ICP) in hypoxic ischaemic brain injury (HIBI) can cause secondary ischaemic brain injury and culminate in brain death. Invasive ICP monitoring is limited by associated risks in HIBI patients. We sought to evaluate the agreement between invasive ICP measurements and non-invasive estimators of ICP (nICP) in HIBI patients.Methods: Eligible consecutive adult (age>18) cardiac arrest patients with HIBI were included as part of a single centre prospective interventional study. Invasive ICP monitoring and nICP measurements were undertaken using: a) transcranial Doppler ultrasonography (TCD), b) optic nerve sheet diameter ultrasound (ONSD) and c) jugular venous bulb pressure (JVP). Multiple measurements applied in linear mixed-effects models were considered to obtain the correlation coefficient between ICP and nICP as well as their predictive abilities to detect intracranial hypertension (ICP≥20mm Hg).Results: Eleven patients were included (median age of 47 [range 20-71], 8 males and 3 females). There was a linear relationship between ICP and nICP with ONSD (R=0.53 [p<0.0001]), JVP (R=0.38 [p<0.001]) and TCD (R=0.30 [p<0.01]). The ability to predict intracranial hypertension was highest for ONSD and TCD (area under the receiver operating curve (AUC)=0.96 [95% CI: 0.90-1.00] and AUC=0.91 [95% CI: 0.83-1.00], respectively). JVP presented the weakest prediction ability (AUC=0.75 [95% CI: 0.56-0.94]).Conclusions: ONSD and TCD methods demonstrated agreement with invasively-monitored ICP, suggesting their potential roles in the detection of intracranial hypertension in HIBI after cardiac arrest. [ABSTRACT FROM AUTHOR]