Sumnermcgregor2536

The intracranial pressure (ICP)-volume relationship contains important information for diagnosing hydrocephalus and other space-occupying pathologies. We aimed to design a new parameter which quantifies the relationship and can be calculated from overnight recordings.The new parameter, the respiratory amplitude quotient (RAQ), characterizes the modulation of the pulse amplitude by the respiratory wave in the ICP time course. RAQ is defined as the ratio of the amplitude of the respiratory wave in the ICP signal to the amplitude of the respiration-induced wave in the course of the heartbeat-dependent pulse amplitude.We tested RAQ on synthetically generated ICP waveforms and found a mean difference of less then 0.5% between the calculated values of RAQ and the theoretically determined values. We further extracted RAQ from datasets obtained by overnight recording in hydrocephalus patients with a stenosis of the aqueduct and a comparison group finding a significant difference between the RAQ values of either group.Intracranial pressure (ICP) signals are often contaminated by artefacts and segments of missing values. Some of these artefacts can be observed as very high and short spikes with a physiologically impossible high slope. The presence of these spikes reduces the accuracy of pattern recognition techniques. Thus, we propose a modified empirical mode decomposition (EMD) method for spike removal in raw ICP signals. The EMD breaks down the signal into 16 intrinsic mode functions (IMFs), combines the first 4 to localize spikes using adaptive thresholding, and then either removes or imputes the identified ICP spikes.We present the application of a new method for non-invasive cerebral perfusion pressure estimation (spectral nCPP or nCPPs) accounting for changes in transcranial Doppler-derived pulsatile cerebral blood volume. Primarily, we analysed cases in which CPP was changing (delta [∆],magnitude of changes]) (1) rise during vasopressor-induced augmentation of ABP (N = 16); and (2) spontaneous changes in intracranial pressure (ICP) during plateau waves (N = 14). Secondarily, we assessed nCPPs in a larger cohort in which CPP presented a wider range of values. The average correlation in the time domain between CPP and nCPPs for patients undergoing an induced rise in arterial blood pressure (ABP) was 0.95 ± 0.07. For the greater traumatic brain injury (TBI) cohort, this correlation was 0.63 ± 0.37. ∆ correlations between mean values of CPP and nCPPs were 0.73 (p = 0.002) and 0.78 (p less then 0.001) respectively for induced rise in ABP and ICP plateau wave cohorts. The area under the curve (AUC) for ∆CPP was of 0.71 with a 95% confidence interval of 0.54-0.88. To detect low CPP, AUC was 0.817 with a 95% confidence interval of 0.79-0.85. nCPPs can reliably identify changes in direct CPP across time and the magnitude of these changes in absolute values. The ability to detect changes in CPP is reasonable but stronger for detecting low CPP, ≤70 mmHg.

Neuromonitoring analysis for intracerebral hemorrhage (ICH) is still rare, especially regarding vascular reactivity patterns. Our goal was to analyze neuromonitoring data and 28-day mortality for ICH patients.

Neuromonitoring records were retrospectively reviewed from a cohort of ICH patients admitted to a neurocritical care unit between 2013 and 2016. Variables considered were intracranial pressure (ICP), cerebral perfusion pressure (CPP), optimal CPP, and pressure reactivity index (PRx), as well as ICP dose, PRx dose, and time percentage above critical value (T%abv). Information regarding demographics, surgical drainage, external ventricular drain placement, and 28-day mortality was recorded. Statistical analysis was performed using the t-test and Kaplan-Meier curves.

Forty-six patients were analyzed, with a mean of 263±173h of signal records and a median length of stay in the intensive care unit of 22 (interquartile range of 13) days. The mean age was 62.6±11.8years old, and 24 (52%) of the patients were male. Patients who died within 28day (37.0%) had significantly higher mean ICP, PRx, ICP dose, PRx dose, and T%abv. Although their mean ICP was under 20mmHg, they presented PRx>0.25, indicating impaired cerebrovascular reactivity (0.30±0.26). Also, patients with PRx>0.25 had a lower survival rate, with a proportion of 14% at 28days, as opposed to 85% of those with PRx<0.25 (p<0.001).

The data suggest that autoregulation indexes are associated with 28-day mortality for ICH patients.

The data suggest that autoregulation indexes are associated with 28-day mortality for ICH patients.

Pressure reactivity index (PRx)-cerebral perfusion pressure (CPP) relationships over a given time period can be used to detect a value of CPP at which PRx shows the best autoregulation (optimal CPP, or CPPopt). Algorithms for continuous assessment of CPPopt in traumatic brain injury (TBI) patients reached the desired high yield with a multi-window approach (CPPopt_MA). However, the calculations were tested on retrospective manually cleaned datasets. Moreover, CPPopt false-positive values can be generated from non-physiological variations of intracranial pressure (ICP) and arterial blood pressure (ABP). Therefore, the algorithm robustness was improved, making it suitable for prospective bedside application (COGiTATE trial).

To validate the CPPopt revised algorithm in a large single-centre retrospective cohort of TBI patients.

840 TBI patients were included. CPPopt yield, stability and ability to discriminate outcome groups were compared to CPPopt_MA and the Brain Trauma Foundation (BTF) guideline reference.

CPPopt yield was lower than CPPopt_MA yield (85% and 90%, p<0.001), but, importantly, with increased stability (p<0.0001). The ∆(CPP-CPPopt) could distinguish the mortality and survival outcome (t=-6.7, p<0.0001) with a statistical significance higher than the ∆CPP calculated with the guideline reference (CPP-60) (t=-4.5, p<0.0001).

This study validates, on a large cohort of patients, the new algorithm proposed for prospective use of CPPopt as a CPP target at bedside.

This study validates, on a large cohort of patients, the new algorithm proposed for prospective use of CPPopt as a CPP target at bedside.Intracranial pressure (ICP)-derived indices of cerebrovascular reactivity (e.g., PRx, PAx, and RAC) have been developed to improve understanding of brain status from available neuromonitoring variables. These indices are moving correlation coefficients between slow-wave vasogenic fluctuations in ICP and arterial blood pressure. In this retrospective analysis of neuromonitoring data from 200 patients admitted with moderate/severe traumatic brain injury (TBI), we evaluate the predictive value of CPPopt based on these ICP-derived indices of cerebrovascular reactivity. Valid CPPopt values were obtained in 92.3% (PRx), 86.7% (PAX), and 84.6% (RAC) of the monitoring periods, respectively. In multivariate logistic analysis, a baseline model that includes age, sex, and admission Glasgow Coma Score had an area under the receiver operating curve of 0.762 (P less then 0.0001) for dichotomous outcome prediction (dead vs. good recovery). When adding time/dose of CPP below CPPopt, all multivariate models (based on PRx, PAx, and RAC) predicted the dichotomous outcome measure, but additional value of the prediction was only significantly added by the PRx-based calculations of time spent with CPP below CPPopt and dose of CPP below CPPopt.

The 'optimal' CPP (CPPopt) concept is based on the vascular pressure reactivity index (PRx). The feasibility and effectiveness of CPPopt guided therapy in severe traumatic brain injury (TBI) patients is currently being investigated prospectively in the COGiTATE trial. At the moment there is no clear evidence that certain admission and treatment characteristics are associated with CPPopt availability (yield).

To test the relation between patients' admission and treatment characteristics and the average CPPopt yield.

Retrospective analysis of 230 patients from the CENTER-TBI high-resolution database with intracranial pressure (ICP) measured using an intraparenchymal probe. CPPopt was calculated using the algorithm set for the COGiTATE study. click here CPPopt yield was defined as the percentage of CPP monitored time (%) when CPPopt is available. The variables in the statistical model included age, admission Glasgow Coma Scale (GCS), gender, pupil response, hypoxia and hypotension at the scene, Marshall computed tomography (CT) score, decompressive craniectomy, injury severity score score and 24-h therapeutic intensity level (TIL) score.

The median CPPopt yield was 80.7% (interquartile range 70.9-87.4%). None of the selected variables showed a significant statistical correlation with the CPPopt yield.

In this retrospective multicenter study, none of the selected admission and treatment variables were related to the CPPopt yield.

In this retrospective multicenter study, none of the selected admission and treatment variables were related to the CPPopt yield.The pressure reactivity index (PRx) and the pulse amplitude index (PAx) are invasively determined parameters that are commonly used to describe autoregulation following traumatic brain injury (TBI). Using a transcranial Doppler ultrasound (TCD) technique, it is possible to approximate cerebral arterial blood volume (CaBV) solely from cerebral blood flow velocities, and further, to calculate non-invasive markers of autoregulation. In this brief study, we aimed to investigate whether the estimation of relative CaBV with different models could describe the cerebrovascular reactivity of TBI patients. PRx, PAx and their non-invasive counterparts (nPRx and nPAx) were calculated retrospectively from data collected during the monitoring of TBI patients. CaBV, an essential parameter for the calculation of nPRx and nPAx, was determined with both a continuous flow forward (CFF) model-considering a non-pulsatile blood outflow from the brain-and a pulsatile flow forward (PFF) model, presuming a pulsatile outflow. We found that the estimated CaBV demonstrates good coherence with ICP and that nPRx and nPAx can describe cerebrovascular reactivity similarly to PRx and PAx. Continuous monitoring with TCD is difficult, so the usability of PRx and PAx is limited. However, they might become useful for clinicians in the near future owing to rapid advances in these technologies.The purpose of this study was to investigate the relationship between the development of secondary cerebral ischemia (SCI), intracranial pressure (ICP) and cerebrovascular reactivity (CVR) after traumatic brain injury (TBI).

89 patients with severe TBI with ICP monitoring were studied retrospectively. The mean age was 36.3±4.8years, 53 men, 36 women. The median Glasgow Coma Score (GCS) was 6.2±0.7. The median Injury Severity Score was 38.2±12.5. To specify the degree of impact of changes in ICP and CVR on the SCI progression in TBI patients, logistic regression was performed. Significant p-values were<0.05.

The deterioration of CVR in combination with the severity of ICP has a significant impact on the increase in the prevalence rate of SCI. A logistic regression analysis for a model of SCI dependence on intracranial hypertension and CVR was performed. The results of the analysis showed that CVR was the most significant factor affecting SCI development in TBI.

The development of SCI in severe TBI depends largely on CVR impairment and to a lesser extent on ICP level.