22 research outputs found
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Clinical Applications of Neuromonitoring Following Acute Brain Injury
Various invasive and non-invasive cranial monitoring techniques can be applied clinically to describe the extent to which cerebral hemodynamics and subsequently, patient outcome, have been impacted following acute brain injury (ABI).
This Ph.D. thesis examines both prospective and retrospective patient data in both neurocritical and general intensive care patients. Thirty neurotrauma patients and forty general intensive care patients with neurological complications were prospectively monitored after ABI. Retrospective patient data was harvested from a database of 1,023 traumatic brain injury (TBI) patients with invasive intracranial pressure (ICP), arterial blood pressure (ABP), and transcranial Doppler ultrasonography (TCD) recordings. Data analysis focused on ICP microsensor accuracy, compensatory reserve, the pulsatility of brain signals (ICP and TCD), and cerebral arterial blood volume (CaBV) based on TCD. The main results are summarized below:
I. Intracranial hypertension has a profound negative influence on cerebrovascular parameters and patient outcome.
II. ICP microsensor accuracy is limited, with an average error of approximately ± 6.0 mm Hg.
III. ICP weighted with the compensatory reserve better predicts outcome than mean ICP alone.
IV. ICP and TCD pulsatility are functions of mean ICP and cerebral perfusion pressure (CPP).
V. Continuous blood flow forward (CFF) and pulsatile blood flow forward (PFF) models can approximate CaBV with derived TCD signals; CFF best models TCD pulsatility.
VI. The pressure reactivity index (PRx) and the pulse amplitude index (PAx) can be estimated non-invasively using slow waves of TCD estimated by CaBV with similar outcome-predictive power.
VII. Multi-parametric TCD-based monitoring of general intensive care patients is clinically feasible; the joint estimation of autoregulation, dysautonomia, non-invasive ICP, and critical closing pressure is possible.
The culmination of these projects should have an impact on current monitoring practices in ABI patients, emphasizing the continued validation and refinement of TCD methodology in clinical neurosciences
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Critical Closing Pressure During Controlled Increase in Intracranial Pressure - Comparison of Three Methods
Critical closing pressure (CrCP) is the arterial blood pressure (ABP) threshold, below which small arterial vessels collapse and cerebral blood flow ceases. Here we aim to compare three methods for CrCPestimation in scenario of a controlled increase in intracranial pressure (ICP), induced by infusion tests performed in patients with suspected normal pressure hydrocephalus (NPH). METHODS: Computer recordings of directly-measured ICP, ABP and transcranial Doppler cerebral blood flow velocity (CBFV), from 37 NPH patients undergoing infusion tests, were retrospectively analyzed. The CrCP was calculated with three methods: one with the first harmonics ratio of the pulse waveforms of ABP and CBFV (CrCPA) and two methods based on a model of cerebrovascular impedance, as functions of both cerebral perfusion pressure (CrCPinv), and of ABP (CrCPninv). CONCLUSION: All methods give similar results in response to ICP changes. In the case of individual CrCP measurements for each patient, CrCPA may provide negative, non-physiological values. Invasive critical closing pressure is most sensitive to variations in ICP and CPP and can be used as an indicator of the cerebrospinal and the cerebrovascular system status during infusion tests.This study was partially supported by the statutory fund of the Mossakowski Medical Research Centre Polish Academy of Sciences and Institute of Electronic Systems, Warsaw University of Technology. Katarzyna Kaczmarska was also supported by the European Union in the framework of the European Social Fund through the Warsaw University of Technology Development Programme
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Critical thresholds for intracranial pressure vary over time in non-craniectomised traumatic brain injury patients.
BACKGROUND: Intracranial pressure (ICP)- and cerebral perfusion pressure (CPP)-guided therapy is central to neurocritical care for traumatic brain injury (TBI) patients. We sought to identify time-dependent critical thresholds for mortality and unfavourable outcome for ICP and CPP in non-craniectomised TBI patients. METHODS: This is a retrospective cohort study of 355 patients with moderate-to-severe TBI who received ICP monitoring and were managed without decompressive craniectomy in a tertiary hospital neurocritical care unit. Patients were grouped in 2 × 2 tables according to survival/death or favourable/unfavourable outcomes at 6 months and serial thresholds of mean ICP and CPP, using increments of 0.1 and 0.5 mmHg respectively. Sequential chi-square analysis was performed, and the thresholds yielding the highest chi-square test statistic were taken as having the best discriminative value for outcome. This process was repeated over monitoring periods of 1, 3, 5 and 7 days and for each day of recording to establish time-dependent thresholds. The same analysis was performed for age and sex subgroups. RESULTS: Global ICP thresholds were 21.3 and 20.5 mmHg for mortality and unfavourable outcome respectively (p < 0.001). After the first day of ICP monitoring, ICP thresholds fell to between 15 and 20 mmHg and remained significant (p < 0.05). Significant time-dependent CPP thresholds for mortality or unfavourable outcome were often not identified, and no identifiable trends were produced. CONCLUSION: Critical ICP thresholds in non-craniectomised TBI patients vary with time and fall below established ICP targets after the first day of monitoring
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Validation of Pressure Reactivity and Pulse Amplitude Indices against the Lower Limit of Autoregulation, Part I: Experimental Intracranial Hypertension.
The purpose of this study was to provide validation of intracranial pressure (ICP) derived continuous indices of cerebrovascular reactivity against the lower limit of autoregulation (LLA). Utilizing an intracranial hypertension model within white New Zealand rabbits, ICP, transcranial Doppler (TCD), laser Doppler flowmetry (LDF), and arterial blood pressure were recorded. Data were retrospectively analyzed in a cohort of 12 rabbits with adequate signals for interrogating the LLA. We derived continuous indices of cerebrovascular reactivity: PRx (correlation between ICP and mean arterial pressure [MAP]), PAx (correlation between pulse amplitude of ICP [AMP] and MAP), and Lx (correlation between LDF-based cerebral blood flow [CBF] and cerebral perfusion pressure [CPP]). LLA was derived via piecewise linear regression of CPP versus LDF or CPP versus systolic flow velocity (FVs) plots. We then produced error bar plots for PRx, PAx, and Lx against 2.5 mm Hg bins of CPP, to display the relationship between these indices and the LLA. We compared the CPP values at clinically relevant thresholds of PRx and PAx, to the CPP defined at the LLA. Receiver operating curve (ROC) analysis was performed for each index across the LLA using 2.5 mm Hg bins for CPP. The mean LLA was 51.5 ± 8.2 mm Hg. PRx and PAx error bar plots demonstrate that each index correlates with the LLA, becoming progressively more positive below the LLA. Similarly, CPP values at clinically relevant thresholds of PRx and PAx were not statistically different from the CPP derived at the LLA. Finally, ROC analysis indicated that PRx and PAx predicted the LAA, with areas under the curve (AUCs) of 0.795 (95% confidence interval [CI]: 0.731-0.857, p < 0.0001) and 0.703 (95% CI: 0.631-0.775, p < 0.0001), respectively. Both PRx and PAx generally agree with LLA within this experimental model of intracranial hypertension. Further analysis of clinically used indices of autoregulation across the LLA within pure arterial hypotension models is required
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Validation of non-invasive cerebrovascular pressure reactivity and pulse amplitude reactivity indices in traumatic brain injury
Funder: University of CambridgeAbstract: Background: Two transcranial Doppler (TCD) estimators of cerebral arterial blood volume (CaBV) coexist: continuous outflow of arterial blood outside the cranium through a low-pulsatile venous system (continuous flow forward, CFF) and pulsatile outflow through regulating arterioles (pulsatile flow forward, PFF). We calculated non-invasive equivalents of the pressure reactivity index (PRx) and the pulse amplitude index PAx with slow waves of mean CaBV and its pulse amplitude. Methods: About 273 individual TBI patients were retrospectively reviewed. PRx is the correlation coefficient between 30 samples of 10-second averages of ICP and mean ABP. PAx is the correlation coefficient between 30 samples of 10-second averages of the amplitude of ICP (AMP, derived from Fourier analysis of the raw full waveform ICP tracing) and mean ABP. nPRx is calculated with CaBV instead of ICP and nPAx with the pulse amplitude of CaBV instead of AMP (calculated using both the CFF and PFF models). All reactivity indices were additionally compared with Glasgow Outcome Score (GOS) to verify potential outcome-predictive strength. Results: When correlated, slow waves of ICP demonstrated good coherence between slow waves in CaBV (>0.75); slow waves of AMP showed good coherence with slow waves of the pulse amplitude of CaBV (>0.67) in both the CFF and PFF models. nPRx was moderately correlated with PRx (R = 0.42 for CFF and R = 0.38 for PFF; p < 0.0001). nPAx correlated with PAx with slightly better strength (R = 0.56 for CFF and R = 0.41 for PFF; p < 0.0001). nPAx_CFF showed the strongest association with outcomes. Conclusions: Non-invasive estimators (nPRx and nPAx) are associated with their invasive counterparts and can provide meaningful associations with outcome after TBI. The CFF model is slightly superior to the PFF model
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Validation of non-invasive cerebrovascular pressure reactivity and pulse amplitude reactivity indices in traumatic brain injury
Funder: University of CambridgeAbstract: Background: Two transcranial Doppler (TCD) estimators of cerebral arterial blood volume (CaBV) coexist: continuous outflow of arterial blood outside the cranium through a low-pulsatile venous system (continuous flow forward, CFF) and pulsatile outflow through regulating arterioles (pulsatile flow forward, PFF). We calculated non-invasive equivalents of the pressure reactivity index (PRx) and the pulse amplitude index PAx with slow waves of mean CaBV and its pulse amplitude. Methods: About 273 individual TBI patients were retrospectively reviewed. PRx is the correlation coefficient between 30 samples of 10-second averages of ICP and mean ABP. PAx is the correlation coefficient between 30 samples of 10-second averages of the amplitude of ICP (AMP, derived from Fourier analysis of the raw full waveform ICP tracing) and mean ABP. nPRx is calculated with CaBV instead of ICP and nPAx with the pulse amplitude of CaBV instead of AMP (calculated using both the CFF and PFF models). All reactivity indices were additionally compared with Glasgow Outcome Score (GOS) to verify potential outcome-predictive strength. Results: When correlated, slow waves of ICP demonstrated good coherence between slow waves in CaBV (>0.75); slow waves of AMP showed good coherence with slow waves of the pulse amplitude of CaBV (>0.67) in both the CFF and PFF models. nPRx was moderately correlated with PRx (R = 0.42 for CFF and R = 0.38 for PFF; p < 0.0001). nPAx correlated with PAx with slightly better strength (R = 0.56 for CFF and R = 0.41 for PFF; p < 0.0001). nPAx_CFF showed the strongest association with outcomes. Conclusions: Non-invasive estimators (nPRx and nPAx) are associated with their invasive counterparts and can provide meaningful associations with outcome after TBI. The CFF model is slightly superior to the PFF model
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Relationship Between Brain Pulsatility and Cerebral Perfusion Pressure: Replicated Validation Using Different Drivers of CPP Change.
BACKGROUND: Determination of relationships between transcranial Doppler (TCD)-based spectral pulsatility index (sPI) and pulse amplitude (AMP) of intracranial pressure (ICP) in 2 groups of severe traumatic brain injury (TBI) patients (a) displaying plateau waves and (b) with unstable mean arterial pressure (MAP). METHODS: We retrospectively reviewed patients with severe TBI and continuous TCD monitoring displaying either plateau waves or unstable MAP from 1992 to 1998. We utilized linear and nonlinear regression techniques to describe both cohorts: cerebral perfusion pressure (CPP) versus AMP, CPP versus sPI, mean ICP versus ICP AMP, mean ICP versus sPI, and AMP versus sPI. RESULTS: Nonlinear regression techniques were employed to analyze the relationships with CPP. In plateau wave and unstable MAP patients, CPP versus sPI displayed an inverse nonlinear relationship (R 2 = 0.820 vs. R 2 = 0.610, respectively), with the CPP versus sPI relationship best modeled by the following function in both cases: PI = a + (b/CPP). Similarly, in both groups, CPP versus AMP displayed an inverse nonlinear relationship (R 2 = 0.610 vs. R 2 = 0.360, respectively). Positive linear correlations were displayed in both the plateau wave and unstable MAP cohorts between: ICP versus AMP, ICP versus sPI, AMP versus sPI. CONCLUSIONS: There is an inverse relationship through nonlinear regression between CPP versus AMP and CPP versus sPI display. This provides evidence to support a previously-proposed model of TCD pulsatility index. ICP shows a positive linear correlation with AMP and sPI, which is also established between AMP and sPI
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Validation of non-invasive cerebrovascular pressure reactivity and pulse amplitude reactivity indices in traumatic brain injury
Funder: University of CambridgeAbstract: Background: Two transcranial Doppler (TCD) estimators of cerebral arterial blood volume (CaBV) coexist: continuous outflow of arterial blood outside the cranium through a low-pulsatile venous system (continuous flow forward, CFF) and pulsatile outflow through regulating arterioles (pulsatile flow forward, PFF). We calculated non-invasive equivalents of the pressure reactivity index (PRx) and the pulse amplitude index PAx with slow waves of mean CaBV and its pulse amplitude. Methods: About 273 individual TBI patients were retrospectively reviewed. PRx is the correlation coefficient between 30 samples of 10-second averages of ICP and mean ABP. PAx is the correlation coefficient between 30 samples of 10-second averages of the amplitude of ICP (AMP, derived from Fourier analysis of the raw full waveform ICP tracing) and mean ABP. nPRx is calculated with CaBV instead of ICP and nPAx with the pulse amplitude of CaBV instead of AMP (calculated using both the CFF and PFF models). All reactivity indices were additionally compared with Glasgow Outcome Score (GOS) to verify potential outcome-predictive strength. Results: When correlated, slow waves of ICP demonstrated good coherence between slow waves in CaBV (>0.75); slow waves of AMP showed good coherence with slow waves of the pulse amplitude of CaBV (>0.67) in both the CFF and PFF models. nPRx was moderately correlated with PRx (R = 0.42 for CFF and R = 0.38 for PFF; p < 0.0001). nPAx correlated with PAx with slightly better strength (R = 0.56 for CFF and R = 0.41 for PFF; p < 0.0001). nPAx_CFF showed the strongest association with outcomes. Conclusions: Non-invasive estimators (nPRx and nPAx) are associated with their invasive counterparts and can provide meaningful associations with outcome after TBI. The CFF model is slightly superior to the PFF model
Pressure Autoregulation Measurement Techniques in Adult Traumatic Brain Injury, Part I: A Scoping Review of Intermittent/Semi-Intermittent Methods.
The purpose of this study was to perform a systematic, scoping review of commonly described intermittent/semi-intermittent autoregulation measurement techniques in adult traumatic brain injury (TBI). Nine separate systematic reviews were conducted for each intermittent technique: computed tomographic perfusion (CTP)/Xenon-CT (Xe-CT), positron emission tomography (PET), magnetic resonance imaging (MRI), arteriovenous difference in oxygen (AVDO2) technique, thigh cuff deflation technique (TCDT), transient hyperemic response test (THRT), orthostatic hypotension test (OHT), mean flow index (Mx), and transfer function autoregulation index (TF-ARI). MEDLINE®, BIOSIS, EMBASE, Global Health, Scopus, Cochrane Library (inception to December 2016), and reference lists of relevant articles were searched. A two tier filter of references was conducted. The total number of articles utilizing each of the nine searched techniques for intermittent/semi-intermittent autoregulation techniques in adult TBI were: CTP/Xe-CT (10), PET (6), MRI (0), AVDO2 (10), ARI-based TCDT (9), THRT (6), OHT (3), Mx (17), and TF-ARI (6). The premise behind all of the intermittent techniques is manipulation of systemic blood pressure/blood volume via either chemical (such as vasopressors) or mechanical (such as thigh cuffs or carotid compression) means. Exceptionally, Mx and TF-ARI are based on spontaneous fluctuations of cerebral perfusion pressure (CPP) or mean arterial pressure (MAP). The method for assessing the cerebral circulation during these manipulations varies, with both imaging-based techniques and TCD utilized. Despite the limited literature for intermittent/semi-intermittent techniques in adult TBI (minus Mx), it is important to acknowledge the availability of such tests. They have provided fundamental insight into human autoregulatory capacity, leading to the development of continuous and more commonly applied techniques in the intensive care unit (ICU). Numerous methods of intermittent/semi-intermittent pressure autoregulation assessment in adult TBI exist, including: CTP/Xe-CT, PET, AVDO2 technique, TCDT-based ARI, THRT, OHT, Mx, and TF-ARI. MRI-based techniques in adult TBI are yet to be described, with the main focus of MRI techniques on metabolic-based cerebrovascular reactivity (CVR) and not pressure-based autoregulation.This work was made possible through salary support through the Cambridge Commonwealth Trust Scholarship, the Royal College of Surgeons of Canada – Harry S. Morton Travelling Fellowship in Surgery, the University of Manitoba Clinician Investigator Program, R. Samuel McLaughlin Research and Education Award, the Manitoba Medical Service Foundation, and the University of Manitoba Faculty of Medicine Dean’s Fellowship Fund.
JD is supported by a Woolf Fisher Scholarship (NZ).
These studies were also supported by National Institute for Healthcare Research (NIHR, UK) through the Acute Brain Injury and Repair theme of the Cambridge NIHR Biomedical Research Centre, an NIHR Senior Investigator Award to DKM. Authors were also supported by a European Union Framework Program 7 grant (CENTER-TBI; Grant Agreement No. 602150
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Do ICP-Derived Parameters Differ in Vegetative State from Other Outcome Groups After Traumatic Brain Injury?
OBJECTIVE: In nearly 1,000 traumatic brain injury (TBI) patients monitored in the years 1992-2014, we identified 18 vegetative state (VS) cases. Our database provided access to continuous computer-recorded signals, which we used to compare primary signals, intracranial pressure (ICP)-derived indices and demographic data between VS patients, patients who survived but who were not VS (S), and patients who died (D). METHOD: Mean values of ICP, arterial blood pressure (ABP) and cerebral perfusion pressure (CPP) from the whole monitoring periods were compared between the different outcome groups. Secondary indices included pressure reactivity index (PRx), the magnitude of slow ICP vasogenic waves, the pulse amplitude of the first harmonic component of the ICP waveform and heart rate (HR). RESULTS: Mean blood pressure was lowest in the VS group-significantly in comparison to those who died (p = 0.02) and almost significantly (p = 0.1) in comparison to the patients who survived. Mean ICP in VS patients was lower than those who died (VS, 13 ± 5 mmHg; D, 22 ± 14 mmHg; p 0.05). The magnitude of slow vasogenic ICP waves was the same in VS patients and those who died, but significantly lower than in those who survived (S, 1.04 ± 0.57 mmHg; VS, 0.74 ± 0.45; p = 0.01). CONCLUSION: Patients who progress to a VS differ from non-VS survivors in displaying decreased power of slow vasogenic waves and from those who die by not experiencing as high a burden of intracranial hypertension