Cerebrovascular Pressure Reactivity Index Research Articles

Cerebrovascular Pressure Reactivity Has a Strong and Independent Association With Outcome in Children With Severe Traumatic Brain Injury.

To examine cerebrovascular pressure reactivity index (PRx) in a large cohort of children with severe traumatic brain injury (sTBI) in association with physiologic variables and outcome. Retrospective observational cohort study. Red Cross War Memorial Children's Hospital in Cape Town, South Africa. Pediatric (≤ 14 yr old) sTBI patients with intracranial pressure (ICP) monitoring (postresuscitation Glasgow Coma Score [Glasgow Coma Scale (GCS)] of ≤ 8). Data were analyzed from ICM+ files sampled at 100Hz. PRx (a mathematical indicator of pressure reactivity) was calculated as a moving correlation coefficient between ICP and mean arterial pressure (MAP) as previously described. Associations between PRx, age, GCS, ICP, MAP, and cerebral perfusion pressure (CPP) were examined with summary measures and correlation analysis using high-frequency data. Associations between PRx and mortality/outcome were examined with multivariable logistic regression analysis and the prognostic ability of PRx with receiver operating characteristic (ROCs) curves. The dataset included over 1.7 million minutes (28,634 hr) of MAP and ICP data in 196 children. The series mortality was 10.7% (21/196), and unfavorable outcome 29.6% (58/196). PRx had a moderate positive correlation with ICP ( r = 0.44; p < 0.001), a moderate negative correlation with CPP ( r = -0.43; p < 0.001), and a weak negative correlation with MAP ( r = -0.21; p = 0.004). PRx was consistently higher in patients with poor outcome and had a strong, independent association with mortality (ROC area under the curve = 0.91). A PRx threshold of 0.25 showed the best predictive ability for mortality. This is the largest cohort of children with PRx analysis of cerebrovascular reactivity to date. PRx had a strong association with outcome that was independent of ICP, CPP, GCS, and age. The data suggest that impaired autoregulation is an independent factor associated with poor outcome and may be useful in directing clinical care.

Cerebrovascular pressure reactivity and intracranial pressure are associated with neurologic outcome after hypoxic-ischemic brain injury

AimWe evaluated the association of physiological parameters measured by intracranial multimodality neuromonitoring with neurologic outcome in a consecutive series of patients with hypoxic-ischemic brain injury (HIBI). MethodsWe retrospectively identified all patients with HIBI who underwent combined invasive intracranial pressure (ICP) and brain tissue oxygen (PbtO2) monitoring over a 3 year period. Cerebrovascular pressure reactivity index (PRx) was calculated continuously as a surrogate of cerebral autoregulation. Favorable outcome was defined as recovery of consciousness (Glasgow Coma Scale motor score = 6). Differences in mean ICP, PRx and PbtO2 for the entire monitoring period across outcomes were measured. Logistic regression and area under receiver operating characteristic (AUROC) curve were used to assess the association of each monitoring parameter with neurologic outcome. ResultsWe analyzed data from 36 patients. Most (89%) had an antecedent sudden cardiac arrest. Favorable outcome occurred in 8 (22%) patients. ICP and PRx were higher in patients with unfavorable outcome (ICP: 26 ± 4.1 mmHg vs 7.5 ± 2 mmHg, p = 0.0002; PRx: 0.51 ± 0.05 vs 0.11 ± 0.05, p < 0.0001). There was no significant difference in PbtO2 between groups (unfavorable: 20 ± 2.4 mmHg vs favorable: 25 ± 1.5 mmHg, p = 0.12). Both ICP (AUROC 0.84, 95%CI 0.72–0.98, p = 0.003) and PRx (AUROC 0.94, 95%CI 0.85–1, p = 0.0002) discriminated between favorable and unfavorable outcome, in contrast to PbtO2, (AUROC 0.59, 95%CI 0.39–0.78, p = 0.52). ICP > 15 mmHg, PRx > 0.2, and PbtO2 < 18 mmHg had sensitivity/specificity of 68%/100%, 89%/88%, and 40%/100% respectively for discriminating outcomes. ConclusionCerebrovascular pressure reactivity and intracranial pressure appear to be associated with neurologic outcome in patients with HIBI.

Novel index for predicting mortality during the first 24 hours after traumatic brain injury.

Failure of cerebral autoregulation and subsequent hypoperfusion is common during the acute phase of traumatic brain injury (TBI). The cerebrovascular pressure-reactivity index (PRx) indirectly reflects cerebral autoregulation and has been used to derive optimal cerebral perfusion pressure (CPP). This study provides a method for the use of a combination of PRx, CPP, and intracranial pressure (ICP) to better evaluate the extent of cerebral hypoperfusion during the first 24 hours after TBI, allowing for a more accurate prediction of mortality risk. Continuous ICP and arterial blood pressure (ABP) signals acquired from 295 TBI patients during the first 24 hours after admission were retrospectively analyzed. The CPP at the lowest PRx was determined as the optimal CPP (CPPopt). The duration of a severe hypoperfusion event (dHP) was defined as the cumulative time that the PRx was > 0.2 and the CPP was < 70 mm Hg with the addition of intracranial hypertension (ICP > 20 or > 22 mm Hg). The outcome was determined as 6-month mortality. The cumulative duration of PRx > 0.2 and CPP < 70 mm Hg exhibited a significant association with mortality (p < 0.001). When utilized with basic clinical information available during the first 24 hours after admission (i.e., Glasgow Coma Scale score, age, and mean ICP), a dHP > 25 minutes yielded a significant predictive capacity for mortality (p < 0.05, area under the curve [AUC] = 0.75). The parameter was particularly predictive of mortality for patients with a mean ICP > 20 or > 22 mm Hg (AUC = 0.81 and 0.87, respectively). A short duration (25 minutes) of severe hypoperfusion, evaluated as lowered CPP during worsened cerebrovascular reactivity during the 1st day after TBI, is highly indicative of mortality.

Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation.

In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying "one" autoregulation-guided cerebral perfusion pressure target-called "cerebral perfusion pressure optimal". We investigated whether a cerebral perfusion pressure autoregulation range-which uses a continuous estimation of the "lower" and "upper" cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with pressure reactivity index)-has prognostic value. Single-center retrospective analysis of prospectively collected data. The neurocritical care unit at a tertiary academic medical center. Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol. None. Cerebral perfusion pressure-pressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this "U-shaped curve" crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001). Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical.

Systemic, local, and imaging biomarkers of brain injury: more needed, and better use of those already established?

Much progress has been made over the past two decades in the treatment of severe acute brain injury, including traumatic brain injury and subarachnoid hemorrhage, resulting in a higher proportion of patients surviving with better outcomes. This has arisen from a combination of factors. These include improvements in procedures at the scene (pre-hospital) and in the hospital emergency department, advances in neuromonitoring in the intensive care unit, both continuously at the bedside and intermittently in scans, evolution and refinement of protocol-driven therapy for better management of patients, and advances in surgical procedures and rehabilitation. Nevertheless, many patients still experience varying degrees of long-term disabilities post-injury with consequent demands on carers and resources, and there is room for improvement. Biomarkers are a key aspect of neuromonitoring. A broad definition of a biomarker is any observable feature that can be used to inform on the state of the patient, e.g., a molecular species, a feature on a scan, or a monitoring characteristic, e.g., cerebrovascular pressure reactivity index. Biomarkers are usually quantitative measures, which can be utilized in diagnosis and monitoring of response to treatment. They are thus crucial to the development of therapies and may be utilized as surrogate endpoints in Phase II clinical trials. To date, there is no specific drug treatment for acute brain injury, and many seemingly promising agents emerging from pre-clinical animal models have failed in clinical trials. Large Phase III studies of clinical outcomes are costly, consuming time and resources. It is therefore important that adequate Phase II clinical studies with informative surrogate endpoints are performed employing appropriate biomarkers. In this article, we review some of the available systemic, local, and imaging biomarkers and technologies relevant in acute brain injury patients, and highlight gaps in the current state of knowledge.

Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury

To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury. Continuous monitoring of the partial pressure of brain tissue oxygen (PbrO2), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of PbrO2 to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings. Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. PbrO2 increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = -0.33, P = 0.32, respectively. The results suggest a strong link between cerebrovascular pressure reactivity and the brain's ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.

The Values of Cerebrovascular Pressure Reactivity and Brain Tissue Oxygen Pressure Reactivity in Experimental Anhepatic Liver Failure

We investigated in a porcine model of anhepatic acute liver failure (ALF), the value of two parameters describing cerebrovascular autoregulatory capacity, pressure reactivity index (PRx) and brain tissue oxygen pressure reactivity (ORx), regarding their power to predict the development of intracranial hypertension. In six pigs, hepatectomy was performed. Only one animal was sham operated. All animals received neuromonitoring including arterial blood pressure, intracranial pressure (ICP), and brain tissue partial oxygen pressure (P(br)O(2)). The average time of neuromonitoring was 31.0h. Cerebral perfusion pressures (CPP), cerebrovascular pressure reactivity index (PRx) and brain tissue oxygen reactivity index (ORx) were calculated. Perioperative disturbance of AR improved within 4h after surgery. From 6 to 16h post hepatectomy, ICP did slowly increase by 4mmHg from baseline; CPP remained stable around 40mmHg. PRx and ORx, however, indicated in this period a progressive loss of AR, reflected in a decrease of P(br)O(2) despite unchanged CPP. Beyond 16h, ICP rose quickly. At CPP levels below 35mmHg, P(br)O(2) fell to ischemic levels. The loss of cerebrovascular autoregulatory capacity, indicated by a rise of PRx and ORx precedes the final crisis of uncontrollable intracranial hypertension in this animal model by hours. During this phase cerebral blood flow, as reflected in tissue oxygenation, deteriorates despite unchanged CPP. Monitoring of AR during ALF therefore seems to carry the power to identify a risk for development of critical CBF and intracranial hypertension.

Interaction between brain chemistry and physiology after traumatic brain injury: impact of autoregulation and microdialysis catheter location.

Bedside monitoring of cerebral metabolism in traumatic brain injury (TBI) with microdialysis is gaining wider clinical acceptance. The objective of this study was to examine the relationship between the fundamental physiological neuromonitoring modalities intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygen (P(bt)O(2)), and cerebrovascular pressure reactivity index (PRx), and cerebral chemistry assessed with microdialysis, with particular focus on the lactate/pyruvate (LP) ratio as a marker of energy metabolism. Prospectively collected observational neuromonitoring data from 97 patients with TBI, requiring neurointensive care management and invasive cerebral monitoring, were analyzed. A linear mixed model analysis was used to account for individual patient differences. Perilesional tissue chemistry exhibited a significant independent relationship with ICP, P(bt)O(2) and CPP thresholds, with increasing LP ratio in response to decrease in P(bt)O(2) and CPP, and increase in ICP. The relationship between CPP and chemistry depended upon the state of PRx. Within the studied physiological range, tissue chemistry only changed in response to increasing ICP or drop in P(bt)O(2)<1.33 kPa (10 mmHg). In agreement with previous studies, significantly higher levels of cerebral lactate (p<0.001), glycerol (p=0.013), LP ratio (p<0.001) and lactate/glucose (LG) ratio (p=0.003) were found in perilesional tissue, compared to "normal" brain tissue (Mann-Whitney test). These differences remained significant following adjustment for the influences of other important physiological parameters (ICP, CPP, P(bt)O(2), P(bt)CO(2), PRx, and brain temperature; mixed linear model), suggesting that they may reflect inherent tissue properties related to the initial injury. Despite inherent biochemical differences between less-injured brain and "perilesional" cerebral tissue, both tissue types exhibited relationships between established physiological variables and biochemistry. Decreases in perfusion and oxygenation were associated with deteriorating neurochemistry and these effects were more pronounced in perilesional tissue and when cerebrovascular reactivity was impaired.

Cerebral extracellular chemistry and outcome following traumatic brain injury: a microdialysis study of 223 patients.

Secondary insults can adversely influence outcome following severe traumatic brain injury. Monitoring of cerebral extracellular chemistry with microdialysis has the potential for early detection of metabolic derangements associated with such events. The objective of this study was to determine the relationship between the fundamental biochemical markers and neurological outcome in a large cohort of patients with traumatic brain injury. Prospectively collected observational neuromonitoring data from 223 patients were analysed. Monitoring modalities included digitally recorded intracranial pressure, cerebral perfusion pressure, cerebrovascular pressure reactivity index and microdialysis markers glucose, lactate, pyruvate, glutamate, glycerol and the lactate/pyruvate ratio. Outcome was assessed using the Glasgow Outcome Scale at 6 months post-injury. Patient-averaged values of parameters were used in statistical analysis, which included univariate non-parametric methods and multivariate logistic regression. Monitoring with microdialysis commenced on median (interquartile range) Day 1 (1-2) from injury and median (interquartile range) duration of monitoring was 4 (2-7) days. Averaged over the total monitoring period levels of glutamate (P = 0.048), lactate/pyruvate ratio (P = 0.044), intracranial pressure (P = 0.006) and cerebrovascular pressure reactivity index (P = 0.01) were significantly higher in patients who died. During the initial 72 h of monitoring, median glycerol levels were also higher in the mortality group (P = 0.014) and median lactate/pyruvate ratio (P = 0.026) and lactate (P = 0.033) levels were significantly lower in patients with favourable outcome. In a multivariate logistic regression model (P < 0.0001), which employed data averaged over the whole monitoring period, significant independent positive predictors of mortality were glucose (P = 0.024), lactate/pyruvate ratio (P = 0.016), intracranial pressure (P = 0.029), cerebrovascular pressure reactivity index (P = 0.036) and age (P = 0.003), while pyruvate was a significant independent negative predictor of mortality (P = 0.004). The results of this study suggest that extracellular metabolic markers are independently associated with outcome following traumatic brain injury. Whether treatment-related improvement in biochemistry translates into better outcome remains to be established.

Integration of Brain Signals in Multimodal Bedside Monitoring After Traumatic Brain Injury

Background: During the last decade, with the development of on-line monitoring and waveform analysis, inte- gration of brain signals has increasingly been used in patients with traumatic brain injury (TBI) to guide clinical manage- ment and predict outcome. Objective: The goal of this review is to describe current methodology for brain signal integration in TBI patients focusing on 'reactivity indices'. Methods: We reviewed selected techniques to monitor patients in the acute phase of TBI using the comparison and inte- gration of different physiological signals. The autoregulation indices, Mx and Mxa were defined as the moving correla- tion between cerebral blood flow velocities (CBFV) and cerebral perfusion pressure (CPP) or arterial blood pressure (ABP), respectively. The cerebrovascular pressure reactivity index PRx was defined as the moving correlation coefficient between ABP and intracranial pressure (ICP). The oxygen reactivity index, Orx, was defined as the moving correlation co- efficient between brain tissue oxygenation and CPP. Finally, Tox was defined as the moving correlation coefficient be- tween brain tissue oxygenation measured by Near Infrared Spectroscopy (NIRS) and ABP. Results: Both Mx > 0.3 and Mxa > 0.45 as well as an asymmetry of Mx between both hemispheres of the brain in the acute phase were associated with poor outcome. PRx may be used to determine the individual optimal CPP and is also a powerful and independent predictor of outcome. Orx showed conflicting results and more studies are need to determine its role in the acute setting of TBI. Studies concerning the role of NIRS in the acute phase of TBI are ongoing. Conclusion: Multimodal neuromonitoring (MNM) is useful in the neuroICU as it provides valuable insights into the pathophysiological mechanisms occurring in the acute phase of TBI. Furthermore, indices obtained with MNM have been shown to be strong predictors of outcome. Further studies combining current and emergent techniques such as NIRS em- phasize on the ability for MNM to continuously evolve.

Autoregulation and brain metabolism in the perihematomal region of spontaneous intracerebral hemorrhage: An observational pilot study

The metabolic and hemodynamic processes in the edema surrounding spontaneous, supratentorial intracerebral hemorrhage (ICH) are poorly understood. Specifically, the local metabolic effects of autoregulatory failure have not been described previously. In the current observational pilot study, microdialysis and brain tissue oxygenation probes (P brO 2) were placed in the perihemorrhagic edema using neuronavigation in five non-surgically treated patients with deep ICH. The cerebrovascular pressure reactivity index (PRx, moving correlation between mean arterial and intracranial pressure) and P brO 2 reactivity index (ORx, correlation between P brO 2 and cerebral perfusion pressure) were used to characterize cerebral autoregulation. While all five patients had ORx values indicative for severely disturbed autoregulation, assessment of PRx only in one patient was consistent with sustained failure of cerebrovascular reactivity. This patient at the same time had the worst metabolic parameters and the poorest tissue oxygenation. We conclude that multimodality monitoring in the perihemorrhagic penumbra is feasible. A study in a larger population is needed to clarify the relationship between PRx and ORx in ICH patients, the local metabolic effects of autoregulatory failure and its relation to brain edema formation and clinical outcome.

Different Indices to Assess Cerebrovascular Autoregulation Have Different Dynamic Properties

With great interest I have read the article by Radolovich et al. [1], published in the June 2009 issue of Neurocritical Care. In that article, the authors have calculated the index of brain tissue oxygen pressure reactivity ORx from spontaneous fluctuations of cerebral perfusion pressure (CPP) and the partial pressure of brain tissue oxygen (PbrO2) from continuous monitoring of these parameters in the first 24 h after probe insertion in n = 32 head injured patients. ORx is a previously introduced index for continuous bedside assessment of cerebrovascular autoregulation [2]. Furthermore, they have analyzed ORx in relation to PbrO2, CPP, the cerebrovascular pressure reactivity index (PRx), and PRx-based optimal cerebral perfusion pressure (CPPOPT) and did not reveal any significant relationships. The study is in some aspects similar to our own previously published work, but the authors’ conclusions differ somewhat from ours [2]. I think that some of the authors’ findings and their methodological approach require further discussion and I would like to propose a few remarks.

Continuous monitoring of carbon dioxide reactivity in traumatic brain injury

The objective is to study the relationship between end-tidal carbon dioxide (EtCO2) and cerebrovascular pressure reactivity in traumatic brain injury (TBI). Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between the mean intracranial pressure (ICP) and mean arterial blood pressure. A negative or zero value reflects a normally reactive vascular bed whereas positive values reflect passive, non-reactive vessels. This index correlates significantly with outcome after TBI [1]. Carbon dioxide affects the cerebral vascular response. Our aim is to identify the optimal EtCO2, at which PRx reaches its lowest value.

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between mean intracranial pressure (ICP) and mean arterial blood pressure. The authors analyzed a database consisting of 398 patients with head injuries who underwent continuous monitoring of cerebrovascular pressure reactivity. In 298 patients, the PRx was compared with a transcranial Doppler ultrasonography assessment of cerebrovascular autoregulation (the mean index [Mx]), in 17 patients with the PET-assessed static rate of autoregulation, and in 22 patients with the cerebral metabolic rate for O(2). Patient outcome was assessed 6 months after injury. There was a positive and significant association between the PRx and Mx (R(2) = 0.36, p < 0.001) and with the static rate of autoregulation (R(2) = 0.31, p = 0.02). A PRx > 0.35 was associated with a high mortality rate (> 50%). The PRx showed significant deterioration in refractory intracranial hypertension, was correlated with outcome, and was able to differentiate patients with good outcome, moderate disability, severe disability, and death. The graph of PRx compared with cerebral perfusion pressure (CPP) indicated a U-shaped curve, suggesting that too low and too high CPP was associated with a disturbance in pressure reactivity. Such an optimal CPP was confirmed in individual cases and a greater difference between current and optimal CPP was associated with worse outcome (for patients who, on average, were treated below optimal CPP [R(2) = 0.53, p < 0.001] and for patients whose mean CPP was above optimal CPP [R(2) = -0.40, p < 0.05]). Following decompressive craniectomy, pressure reactivity initially worsened (median -0.03 [interquartile range -0.13 to 0.06] to 0.14 [interquartile range 0.12-0.22]; p < 0.01) and improved in the later postoperative course. After therapeutic hypothermia, in 17 (70.8%) of 24 patients in whom rewarming exceeded the brain temperature threshold of 37 degrees C, ICP remained stable, but the average PRx increased to 0.32 (p < 0.0001), indicating significant derangement in cerebrovascular reactivity. The PRx is a secondary index derived from changes in ICP and arterial blood pressure and can be used as a surrogate marker of cerebrovascular impairment. In view of an autoregulation-guided CPP therapy, a continuous determination of a PRx is feasible, but its value has to be evaluated in a prospective controlled trial.

Cerebral oxygenation, vascular reactivity, and neurochemistry following decompressive craniectomy for severe traumatic brain injury

This study addresses the changes in brain oxygenation, cerebrovascular reactivity, and cerebral neurochemistry in patients following decompressive craniectomy for the control of elevated intracranial pressure (ICP) after severe traumatic brain injury (TBI). Sixteen consecutive patients with isolated TBI and elevated ICP, who were refractory to maximal medical therapy, underwent decompressive craniectomy over a 1-year period. Thirteen patients were male and 3 were female. The mean age of the patients was 38 years and the median Glasgow Coma Scale score on admission was 5. RESULTS Six months following TBI, 11 patients had a poor outcome (Group 1, Glasgow Outcome Scale [GOS] Score 1-3), whereas the remaining 5 patients had a favorable outcome (Group 2, GOS Score 4 or 5). Decompressive craniectomy resulted in a significant reduction (p < 0.001) in the mean ICP and cerebrovascular pressure reactivity index to autoregulatory values (< 0.3) in both groups of patients. There was a significant improvement in brain tissue oxygenation (PbtO(2)) in Group 2 patients from 3 to 17 mm Hg and an 85% reduction in episodes of cerebral ischemia. In addition, the durations of abnormal PbtO(2) and biochemical indices were significantly reduced in Group 2 patients after decompressive craniectomy, but there was no improvement in the biochemical indices in Group 1 patients despite surgery. Decompressive craniectomy, when used appropriately in protocol-driven intensive care regimens for the treatment of recalcitrant elevated ICP, is associated with a return of abnormal metabolic parameters to normal values in patients with eventually favorable outcomes.

Effect of decompressive craniectomy on intracranial pressure and cerebrospinal compensation following traumatic brain injury

Decompressive craniectomy is an advanced treatment option for intracranial pressure (ICP) control in patients with traumatic brain injury. The purpose of this study was to evaluate the effect of decompressive craniectomy on ICP and cerebrospinal compensation both within and beyond the first 24 hours of craniectomy. This study was a retrospective analysis of the physiological parameters from 27 moderately to severely head-injured patients who underwent decompressive craniectomy for progressive brain edema. Of these, 17 patients had undergone prospective digital recording of ICP with estimation of ICP waveform-derived indices. The pressure-volume compensatory reserve (RAP) index and the cerebrovascular pressure reactivity index (PRx) were used to assess those parameters. The values of parameters prior to and during the 72 hours after decompressive craniectomy were included in the analysis. Decompressive craniectomy led to a sustained reduction in median (interquartile range) ICP values (21.2 mm Hg [18.7; 24.2 mm Hg] preoperatively compared with 15.7 mm Hg [12.3; 19.2 mm Hg] postoperatively; p = 0.01). A similar improvement was observed in RAP. A significantly lower mean arterial pressure (MAP) was needed after decompressive craniectomy to maintain optimum cerebral perfusion pressure (CPP) levels, compared with the preoperative period (99.5 mm Hg [96.2; 102.9 mm Hg] compared with 94.2 mm Hg [87.9; 98.9 mm Hg], respectively; p = 0.017). Following decompressive craniectomy, the PRx had positive values in all patients, suggesting acquired derangement in pressure reactivity. In this study, decompressive craniectomy led to a sustained reduction in ICP and improvement in cerebral compliance. Lower MAP levels after decompressive craniectomy are likely to indicate a reduced intensity of treatment. Derangement in cerebrovascular pressure reactivity requires further studies to evaluate its significance and influence on outcome.

Cerebrovascular reactivity during hypothermia and rewarming

Experimental evidence from a murine model of traumatic brain injury (TBI) suggests that hypothermia followed by fast rewarming may damage cerebral microcirculation. The effects of hypothermia and subsequent rewarming on cerebral vasoreactivity in human TBI are unknown. This is a retrospective analysis of data acquired during a prospective, observational neuromonitoring and imaging data collection project. Brain temperature, intracranial pressure (ICP), and cerebrovascular pressure reactivity index (PRx) were continuously monitored. Twenty-four TBI patients with refractory intracranial hypertension were cooled from 36.0 (0.9) to 34.2 (0.5) degrees C [mean (sd), P < 0.0001] in 3.9 (3.7) h. Induction of hypothermia [average duration 40 (45) h] significantly reduced ICP from 23.1 (3.6) to 18.3 (4.8) mm Hg (P < 0.05). Hypothermia did not impair cerebral vasoreactivity as average PRx changed non-significantly from 0.00 (0.21) to -0.01 (0.21). Slow rewarming up to 37.0 degrees C [rate of rewarming, 0.2 (0.2) degrees C h(-1)] did not increase ICP [18.6 (6.2) mm Hg] or PRx [0.06 (0.18)]. However, in 17 (70.1%) out of 24 patients, rewarming exceeded the brain temperature threshold of 37 degrees C. In these patients, the average brain temperature was allowed to increase to 37.8 (0.3) degrees C (P < 0.0001), ICP remained stable at 18.3 (8.0) mm Hg (P = 0.74), but average PRx increased to 0.32 (0.24) (P < 0.0001), indicating significant derangement in cerebrovascular reactivity. After rewarming, PRx correlated independently with brain temperature (R = 0.53; P < 0.05) and brain tissue O2 (R = 0.66; P < 0.01). After moderate hypothermia, rewarming exceeding the 37 degrees C threshold is associated with a significant increase in average PRx, indicating temperature-dependent hyperaemic derangement of cerebrovascular reactivity.