Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler flow velocity is optimal?

Background

Cerebral autoregulation assessed using transcranial Doppler (TCD) mean flow velocity (FV) in response to various physiological challenges is predictive of outcome after traumatic brain injury (TBI). Systolic and diastolic FV have been explored in other diseases. This study aims to evaluate the systolic, mean and diastolic FV for monitoring autoregulation and predicting outcome after TBI.

Methods

300 head-injured patients with blood pressure (ABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), and FV recordings were studied. Autoregulation was calculated as a correlation of slow changes in diastolic, mean and systolic components of FV with CPP (Dx, Mx, Sx, respectively) and ABP (Dxa, Mxa, Sxa, respectively) from 30 consecutive 10?s averaged values. The relationship with age, severity of injury, and dichotomized 6?months outcome was examined.

Results

Association with outcome was significant for Mx and Sx. For favorable/unfavorable and death/survival outcomes Sx showed the strongest association (F?=?20.11; P?=?0.00001 and F?=?13.10; P?=?0.0003, respectively). Similarly, indices derived from ABP demonstrated the highest discriminatory value when systolic FV was used (F?=?12.49; P?=?0.0005 and F?=?5.32; P?=?0.02, respectively). Indices derived from diastolic FV demonstrated significant differences (when calculated using CPP) only when comparing between fatal and non-fatal outcome.

Conclusions

Systolic flow indices (Sx and Sxa) demonstrated a stronger association with outcome than the mean flow indices (Mx and Mxa), irrespective of whether CPP or ABP was used for calculation.     

Should the Neurointensive Care Management of Traumatic Brain Injury Patients be Individualized According to Autoregulation Status and Injury Subtype?

Introduction

The status of autoregulation is an important prognostic factor in traumatic brain injury (TBI), and is important to consider in the management of TBI patients. Pressure reactivity index (PRx) is a measure of autoregulation that has been thoroughly studied, but little is known about its variation in different subtypes of TBI. In this study, we examined the impact of PRx and cerebral perfusion pressure (CPP) on outcome in different TBI subtypes.

Methods

107 patients were retrospectively studied. Data on PRx, CPP, and outcome were collected from our database. The first CT scan was classified according to the Marshall classification system. Patients were assigned to “diffuse” (Marshall class: diffuse-1, diffuse-2, and diffuse-3) or “focal” (Marshall class: diffuse-4, evacuated mass lesion, and non-evacuated mass lesion) groups. 2 × 2 tables were constructed calculating the proportions of favorable/unfavorable outcome at different combinations of PRx and CPP.

Results

Low PRx was significantly associated with favorable outcome in the combined group (p = 0.002) and the diffuse group (p = 0.04), but not in the focal group (p = 0.06). In the focal group higher CPP values were associated with worse outcome (p = 0.02). In diffuse injury patients with disturbed autoregulation (PRx >0.1), CPP >70 mmHg was associated with better outcome (p = 0.03).

Conclusion

TBI patients with diffuse injury may differ from those with mass lesions. In the latter higher levels of CPP may be harmful, possibly due to BBB disruption. In TBI patients with diffuse injury and disturbed autoregulation higher levels of CPP may be beneficial.     

ICP Versus Laser Doppler Cerebrovascular Reactivity Indices to Assess Brain Autoregulatory Capacity

Background

To explore the relationship between various autoregulatory indices in order to determine which approximate small vessel/microvascular (MV) autoregulatory capacity most accurately.

Methods

Utilizing a retrospective cohort of traumatic brain injury patients (N = 41) with: transcranial Doppler (TCD), intracranial pressure (ICP) and cortical laser Doppler flowmetry (LDF), we calculated various continuous indices of autoregulation and cerebrovascular responsiveness: A. ICP derived [pressure reactivity index (PRx)—correlation between ICP and mean arterial pressure (MAP), PAx—correlation between pulse amplitude of ICP (AMP) and MAP, RAC—correlation between AMP and cerebral perfusion pressure (CPP)], B. TCD derived (Mx—correlation between mean flow velocity (FVm) and CPP, Mx_a—correlation between FVm and MAP, Sx—correlation between systolic flow velocity (FVs) and CPP, Sx_a—correlation between FVs and MAP, Dx—correlation between diastolic flow index (FVd) and CPP, Dx_a—correlation between FVd and MAP], and LDF derived (Lx—correlation between LDF cerebral blood flow [CBF] and CPP, Lx_a—correlation between LDF-CBF and MAP). We assessed the relationship between these indices via Pearson correlation, Friedman test, principal component analysis (PCA), agglomerative hierarchal clustering (AHC), and k-means cluster analysis (KMCA).

Results

LDF-based autoregulatory index (Lx) was most associated with TCD-based Mx/Mx_a and Dx/Dx_a across Pearson correlation, PCA, AHC, and KMCA. Lx was only remotely associated with ICP-based indices (PRx, PAx, RAC). TCD-based Sx/Sx_a was more closely associated with ICP-derived PRx, PAx and RAC. This indicates that vascular-derived indices of autoregulatory capacity (i.e., TCD and LDF based) covary, with Sx/Sx_a being the exception, whereas indices of cerebrovascular reactivity derived from pulsatile CBV (i.e., ICP indices) appear to not be closely related to those of vascular origin.

Conclusions

Transcranial Doppler Mx is the most closely associated with LDF-based Lx/Lx_a. Both Sx/Sx-a and the ICP-derived indices appear to be dissociated with LDF-based cerebrovascular reactivity, leaving Mx/Mx-a as a better surrogate for the assessment of cortical small vessel/MV cerebrovascular reactivity. Sx/Sx_a cocluster/covary with ICP-derived indices, as seen in our previous work.

     

Temporal changes in cerebral tissue oxygenation with cerebrovascular pressure reactivity in severe traumatic brain injury

Objective

To investigate the temporal relationship between cerebrovascular pressure reactivity and brain tissue oxygenation in patients with severe head injury.

Methods

In 40 patients, brain tissue oxygenation and intracranial pressure were monitored. Time‐averaged values for intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain tissue oxygenation (PtiO₂) were computed. The pressure reactivity index (PRx) was calculated. The mean values of the variables were obtained at the 6‐h and 72‐h post‐injury time points, and the difference between the two time points for each of the variables was denoted as delta (δ).

Results

Of the 40 patients, 32 were survivors and 8 were non‐survivors. Statistically significant differences were present between these two groups with regard to δMAP (p = 0.013), ICP at 6 h (p = 0.027), CPP at 72 h (p = 0.018), δCPP (p = 0.033), PRx at 6 h (p = 0.029), PRx at 72 h (p = 0.002), PtiO₂ at 72 h (p<0.0005) and δPtiO₂ (p = 0.023) values, reflecting an improvement with time in survivors and a deterioration with time in non‐survivors. In non‐survivors, the magnitude of change in PtiO₂ and CPP with time correlated in a negative linear fashion (p = 0.042 and 0.029, respectively) with the change in PRx with time, whereas no such relationship was seen in survivors.

Conclusion

The severity of brain tissue oxygenation derangement correlates with increasing cerebrovascular dysautoregulation in patients succumbing to severe head injury, supporting the utility of PRx as a monitoring variable and the rationale for a target‐driven approach to head injury management.Cerebral ischaemia is a critical contributory factor to secondary brain injury after trauma. In the presence of an unstable cerebral perfusion pressure (CPP), the autoregulatory cerebrovascular reactivity attempts to maintain an adequate cerebral blood flow. Increasing CPP may result in raised or lowered intracranial pressure (ICP), depending on whether cerebral autoregulation is preserved. Rosner et al¹ have described how increases in CPP within the autoregulatory range lead to compensatory vasoconstriction to maintain a stable cerebral blood flow. In so doing, cerebral blood volume and thus ICP levels fall. However, outside of these autoregulatory limits, a pressure‐passive scenario exists where increases in CPP lead to vasodilatation and a rise in ICP. Investigators have defined an index comparing arterial blood pressure (ABP) and ICP to quantify this relationship between CPP and ICP, known as the pressure reactivity index (PRx).^2,3 If a rise in ABP (and hence CPP) leads to a parallel increase in ICP, a good correlation exists, and the PRx is positive. However, in the face of intact cerebral autoregulatory capacity, vasoconstriction in the face of rising CPP leads to a drop in ICP, and hence PRx approaches zero or takes a negative value. Measurement of PRx could thus form the basis for target‐driven management, as ABP can be manipulated.Clinical studies on patients with head injury have shown the feasibility of continuous monitoring of local brain tissue oxygenation (PtiO₂) as a variable for cerebral oxygenation.^4,5,6 Despite the limitations of such a local method of measurement, PtiO₂ indicates global cerebral oxygenation when the monitoring is carried out in a relatively uninjured part of the brain.⁶ The presence of autoregulation disturbance could conceivably lead to disturbance in oxygen tension in the tissue of interest by virtue of blood flow metabolism uncoupling as PtiO₂ reflects the net balance between oxygen supply and demand at the tissue level.⁷We hypothesised that a worsening PRx indicative of increasing dysautoregulation during the temporal course of monitoring is related to mortality, and this may arise from specific patterns of change in various physiological variables including PtiO₂.     

Brain Tissue Oxygenation and Cerebral Perfusion Pressure Thresholds of Ischemia in a Standardized Pig Brain Death Model

Background

Neurointensive care of traumatic brain injury (TBI) patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted protocols. Monitoring brain tissue oxygenation (B_tipO₂) is of considerable clinical interest, but the exact threshold level of ischemia has been difficult to establish due to the complexity of the clinical situation. The objective of this study was to use the Neurovent-PTO (NV) probe, and to define critical cerebral oxygenation- and CPP threshold levels of cerebral ischemia in a standardized brain death model caused by increasing the ICP in pig. Ischemia was defined by a severe increase of cerebral microdialysis (MD) lactate/pyruvate ratio (L/P ratio?>?30).

Methods

B_tipO₂, L/P ratio, Glucose, Glutamate, Glycerol and CPP were recorded using NV and MD probes during gradual increase of ICP by inflation of an epidural balloon catheter with saline until brain death was achieved.

Results

Baseline level of B_tipO₂ was 22.9?±?6.2?mmHg, the L/P ratio 17.7?±?6.1 and CPP 73?±?17?mmHg. B_tipO₂ and CPP decreased when intracranial volume was added. The L/P ratio increased above its ischemic levels, (>30) when CPP decreased below 30?mmHg and B_tipO₂ to <10?mmHg.

Conclusions

A severe increase of ICP leading to CPP below 30?mmHg and B_tipO₂ below 10?mmHg is associated with an increase of the L/P ratio, thus seems to be critical thresholds for cerebral ischemia under these conditions.     

Critical Thresholds for Cerebrovascular Reactivity After Traumatic Brain Injury

Introduction

Pressure-reactivity index (PRx) is a useful tool in brain monitoring of trauma patients, but the question remains about its critical values. Using our TBI database, we identified the thresholds for PRx and other monitored parameters that maximize the statistical difference between death/survival and favorable/unfavorable outcomes. We also investigated how these thresholds depend on clinical factors such as age, gender and initial GCS.

Methods

A total of 459 patients from our database were eligible. Tables of 2?×?2 format were created grouping patients according to survival/death or favorable/unfavorable outcomes and varying thresholds for PRx, ICP and CPP. Pearson??s chi square was calculated, and the thresholds returning the highest score were assumed to have the best discriminative value. The same procedure was repeated after division according to clinical factors.

Results

In all patients, we found that PRx had different thresholds for survival (0.25) and for favorable outcome (0.05). Thresholds of 70?mmHg for CPP and 22?mmHg for ICP were identified for both survival and favorable outcomes. The ICP threshold for favorable outcome was lower (18?mmHg) in females and patients older than 55?years. In logistic regression models, independent variables associating with mortality and unfavorable outcome were age, GCS, ICP and PRx.

Conclusion

The prognostic role of PRx is confirmed but with a lower threshold of 0.05 for favorable outcome than for survival (0.25). Results for ICP are in line with current guidelines. However, the lower value in elderly and in females suggests increased vulnerability to intracranial hypertension in these groups.     

A Continuous Correlation Between Intracranial Pressure and Cerebral Blood Flow Velocity Reflects Cerebral Autoregulation Impairment During Intracranial Pressure Plateau Waves

Background

In the healthy brain, small oscillations in intracranial pressure (ICP) occur synchronously with those in cerebral blood volume (CBV), cerebrovascular resistance, and consequently cerebral blood flow velocity (CBFV). Previous work has shown that the usual synchrony between ICP and CBFV is lost during intracranial hypertension. Moreover, a continuously computed measure of the ICP/CBFV association (Fix index) was a more sensitive predictor of outcome after traumatic brain injury (TBI) than a measure of autoregulation (Mx index). In the current study we computed Fix during ICP plateau waves, to observe its behavior during a defined period of cerebrovascular vasodilatation.

Methods

Twenty-nine recordings of arterial blood pressure (ABP), ICP, and CBFV taken during ICP plateau waves were obtained from the Addenbrooke’s hospital TBI database. Raw data was filtered prior to computing Mx and Fix according to previously published methods. Analyzed data was segmented into three phases (pre, peak, and post), and a median value of each parameter was stored for analysis.

Results

ICP increased from a median of 22–44 mmHg before falling to 19 mmHg. Both Mx and Fix responded to the increase in ICP, with Mx trending toward +1, while Fix trended toward ?1. Mx and Fix correlated significantly (Spearman’s R = ?0.89, p < 0.000001), however, Fix spanned a greater range than Mx. A plot of Mx and Fix against CPP showed a plateau (Mx) or trough (Fix) consistent with a zone of “optimal CPP”.

Conclusions

The Fix index can identify complete loss of cerebral autoregulation as the point at which the normally positive CBF/CBV correlation is reversed. Both CBF and CBV can be monitored noninvasively using near-infrared spectroscopy (NIRS), suggesting that a noninvasive method of monitoring autoregulation using only NIRS may be possible.     

Further Controversies About Brain Tissue Oxygenation Pressure-Reactivity After Traumatic Brain Injury

Background

Continuous monitoring of cerebral autoregulation is considered clinically useful due to its ability to warn against brain ischemic insults, which may translate to a relationship with adverse outcome. It is typically performed using the pressure reactivity index (PRx) based on mean arterial pressure and intracranial pressure. A new ORx index based on brain tissue oxygenation and cerebral perfusion pressure (CPP) has been proposed that similarly allows for evaluation of cerebrovascular reactivity. Conflicting results exist concerning its clinical utility.

Methods

Retrospective analysis was performed in 85 patients with traumatic brain injury (TBI). ORx was calculated using three time windows of 5, 20, and 60 min. Correlation coefficients and individual “optimal CPP” (CPP_opt) were calculated using both PRx and ORx, and relation to patient outcome investigated.

Results

Correlation coefficients for all comparisons between PRx and ORx indicated poor association between these indices (range from ?0.04 to 0.07). PRx was significantly lower in patients with good outcome (p = 0.01), while none of the ORx indices proved to be significantly different in the two outcome groups. Higher mortality related to average CPP < CPP_opt was found regardless of which index was used to calculate CPP_opt.

Conclusion

In the TBI setting, ORx does not appear to correlate with vascular pressure reactivity as assessed with PRx. Its potential use for individualizing CPP thresholds remains unclear.

     

Relationship of Vascular Wall Tension and Autoregulation Following Traumatic Brain Injury

Background

The vascular wall tension (WT) of small cerebral vessels can be quantitatively estimated through the concept of critical closing pressure (CrCP), which denotes the lower limit of arterial blood pressure (ABP), below which small cerebral arterial vessels collapse and blood flow ceases. WT can be expressed as the difference between CrCP and intracranial pressure (ICP) and represent active vasomotor tone. In this study, we investigated the association of WT and CrCP with autoregulation and outcome of a large group of patients after traumatic brain injury (TBI).

Methods

We retrospectively analysed recordings of ABP, ICP and transcranial Doppler (TCD) blood flow velocity from 280 TBI patients (median age: 29 years; interquartile range: 20–43). CrCP and WT were calculated using the cerebrovascular impedance methodology. Autoregulation was assessed based on TCD-based indices, Mx and ARI.

Results

Low values of WT were found to be associated with an impaired autoregulatory capacity, signified by its correlation to FV-based indices Mx (R = ?0.138; p = 0.021) and ARI (R = 0.118; p = 0.048). No relationship could be established between CrCP and any of the autoregulatory indices. Neither CrCP nor WT was found to correlate with outcome.

Conclusions

Impaired autoregulation was found to be associated with a lower WT supporting the role of vasoparalysis in the loss of autoregulatory capacity. In contrast, no links between CrCP and autoregulation could be identified.     

Association between intracranial,arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

Abstract

Objective: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation.

Methods: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1–14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording.

Results: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p ≤ 0.04, multiple regression analysis). Correlations between intracranial and arterial pulse pressure amplitudes were weakly related to PRx (Pearson's correlation coefficient: 0.16; p=0.01), but were not related to the indices of cerebral autoregulation Mx (Pearson's correlation coefficient: 0.07) and Sx (Pearson's correlation coefficient: 0.04).

Conclusions: In this cohort of pressure recordings, we found no evidence of a correlation between intracranial and arterial blood pressure amplitudes. The correlation appeared not to be related to the state of cerebral autoregulation, although a weak correlation was found with pressure reactivity index PRx.     

Hypertonic Saline Reduces Intracranial Hypertension in the Presence of High Serum and Cerebrospinal Fluid Osmolalities

Background

Osmotherapy has been the cornerstone in the management of patients with elevated intracranial pressure (ICP) following traumatic brain injury (TBI). Several studies have demonstrated that hypertonic saline (HTS) is a safe and effective osmotherapy agent. This study evaluated the effectiveness of HTS in reducing intracranial hypertension in the presence of a wide range of serum and cerebrospinal fluid (CSF) osmolalities.

Methods

Forty-two doses of 23.4% saline boluses for treatment of refractory intracranial hypertension were reviewed retrospectively. Thirty milliliters of 23.4% NaCl was infused over 15?min for intracranial hypertension, defined as ICP?>20?mmHg. The CSF and serum osmolalities from frozen stored samples were measured with an osmometer. The values of serum sodium, hourly ICP, blood urea nitrogen (BUN), and creatinine were obtained directly from the medical records.

Results

The serum and CSF osmolalities correlated very closely to serum sodium (r?>?0.9, P?P?320 as it was at???320.

Conclusion

This study demonstrates that 23.4% HTS bolus is effective for the reduction of elevated ICP in patients with severe TBI even in the presence of high serum and CSF osmolalities.     

Critical Closing Pressure During Intracranial Pressure Plateau Waves

Background

Critical closing pressure (CCP) denotes a threshold of arterial blood pressure (ABP) below which brain vessels collapse and cerebral blood flow ceases. Theoretically, CCP is the sum of intracranial pressure (ICP) and arterial wall tension (WT). The aim of this study is to describe the behavior of CCP and WT during spontaneous increases of ICP, termed plateau waves, in order to quantify ischemic risk.

Methods

To calculate CCP, we used a recently introduced multi-parameter method (CCPm) which is based on the modulus of cerebrovascular impedance. CCP is derived from cerebral perfusion pressure, ABP, transcranial Doppler estimators of cerebrovascular resistance and compliance, and heart rate. Arterial WT was estimated as CCPm-ICP. The clinical data included recordings of ABP, ICP, and transcranial Doppler-based blood flow velocity from 38 events of ICP plateau waves, recorded in 20 patients after head injury.

Results

Overall, CCPm increased significantly from 51.89 ± 8.76 mmHg at baseline ICP to 63.31 ± 10.83 mmHg at the top of the plateau waves (mean ± SD; p < 0.001). Cerebral arterial WT decreased significantly during plateau waves by 34.3 % (p < 0.001), confirming their vasodilatatory origin. CCPm did not exhibit the non-physiologic negative values that have been seen with traditional methods for calculation, therefore rendered a more plausible estimation of CCP.

Conclusions

Rising CCP during plateau waves increases the probability of cerebral vascular collapse and zero flow when the difference: ABP–CCP (the “collapsing margin”) becomes zero or negative.     

Effect of Percutaneous Tracheostomy on Intracerebral Pressure and Perfusion Pressure in Patients with Acute Cerebral Dysfunction (TIP Trial): An Observational Study

Background

Bedside percutaneous tracheostomy (PT) is very commonly used for patients who require prolonged mechanical ventilation. The effect of tracheostomy on intracranial pressure (ICP) is currently a subject of controversy. The aim of our study is to clarify the relation between PT and its effect on ICP and cerebral perfusion pressure.

Methods

38 patients on our intensive care unit were included prospectively in an observational study. We examined mean values of HF, SpO₂, ICP, CPP, and MAP for changes over five different phases of the procedure using paired Mann?CWhitney U tests. A p value of <0.05 was considered significant. p values were Bonferroni corrected for multiple testing.

Results

PT was performed on 38 patients (f?=?19, m?=?19; mean?=?56?years). Median ICP before intervention was 9?mmHg. During positioning of the patient, ICP had risen to 14, during bronchoscopy to 16, and during tracheostomy to 18?mmHg, all being significantly higher than baseline level. Monitoring of MAP showed a significant increase to 101?mmHg only during tracheostomy. SpO₂ and HF did not show any significant changes. Mean duration of positioning, bronchoscopy and tracheostomy was 19, 10, and 17?min. 8 patients received osmotherapy due to a rise of ICP of more than 30?mmHg.

Conclusion

PT only leads to a significant rise of ICP during the procedure. Nevertheless, therapy of ICP is necessary in some patients. From our point of view, therefore, tracheostomy should only be performed under continuous monitoring of ICP and CPP in patients with severe cerebral dysfunctions and critically elevated ICP.     

Association between intracranial, arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

OBJECTIVE: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation. METHODS: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1-14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording. RESULTS: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p 相似文献   

Intraoperative blood loss during decompressive craniectomy for intractable intracranial hypertension after severe traumatic brain injury in children

Purpose

There are no data available on the risk of intraoperative bleeding during decompressive craniectomy (DC) after traumatic brain injury (TBI) in children. The objectives of this study were to assess the risk of intraoperative bleeding during DC for intractable intracranial hypertension after TBI, to identify potential factors associated with the risk of bleeding during DC, and to assess the impact of DC on systemic and cerebral hemodynamics and on coagulation.

Methods

Twelve children were identified as having undergone DC after TBI from April 2009 to June 2013 in our center. Subjects were allocated into two groups according to the percentage of blood loss (IBL) during the intraoperative period (<or ≥50 % of the estimated blood volume (EBV)).

Results

The median IBL during DC was 49 [17–349] % of the EBV. Children with an IBL?≥?50 % of EBV had higher preoperative intracranial pressure (ICP) (p?=?0.03) and international normalized ratio (INR) (p?=?0.02) than those with an IBL?<?50 % of EBV. DC induced significant decreases in ICP (p?=?0.0005), mean arterial pressure (p?=?0.01), and a significant increase in norepinephrine flow rate (p?=?0.04) between the immediate pre- and postoperative periods.

Conclusions

DC allows a significant decrease in ICP after severe pediatric TBI but is a surgical procedure at a high risk of bleeding. High ICP and INR during the immediate preoperative period are the main factors associated with increased IBL during DC. Further studies are needed to confirm our results and to assess the impact of the amount of IBL on the postoperative survival and functional outcome.     

Cerebral Critical Closing Pressure: Is the Multiparameter Model Better Suited to Estimate Physiology of Cerebral Hemodynamics?

Background

Cerebral critical closing pressure (CrCP) is the level of arterial blood pressure (ABP) at which small brain vessels close and blood flow stops. This value is always greater than intracranial pressure (ICP). The difference between CrCP and ICP is explained by the tone of the small cerebral vessels (wall tension). CrCP value is used in several dynamic cerebral autoregulation models. However, the different methods for calculation of CrCP show frequent negative values. These findings are viewed as a methodological limitation. We intended to evaluate CrCP in patients with severe traumatic brain injury (TBI) with a new multiparameter impedance-based model and compare it with results found earlier using a transcranial Doppler (TCD)–ABP pulse waveform-based method.

Methods

Twelve severe TBI patients hospitalized during September 2005–May 2007. Ten men, mean age 32 years (16–61). Four had decompressive craniectomies (DC); three presented anisocoria. Patients were monitored with TCD cerebral blood flow velocity (FV), invasive ABP, and ICP. Data were acquired at 50 Hz with an in-house developed data acquisition system. We compared the earlier studied “first harmonic” method (M1) results with results from a new recently developed (M2) “multiparameter method.”

Results

M1: In seven patients CrCP values were negative, reaching ?150 mmHg. M2: All positive values; only one lower than ICP (ICP 60 mmHg/ CrCP 57 mmHg). There was a significant difference between M1 and M2 values (M1 < M2) and between ICP and M2 (M2 > ICP).

Conclusion

M2 results in positive values of CrCP, higher than ICP, and are physiologically interpretable.

     

Early Cerebral Metabolic Crisis After TBI Influences Outcome Despite Adequate Hemodynamic Resuscitation

Background

Optimal resuscitation after traumatic brain injury (TBI) remains uncertain. We hypothesize that cerebral metabolic crisis is frequent despite adequate resuscitation of the TBI patient and that metabolic crisis negatively influences outcome.

Methods

We assessed the effectiveness of a standardized trauma resuscitation protocol in 89 patients with moderate to severe TBI, and determined the frequency of adequate resuscitation. Prospective hourly values of heart rate, blood pressure, pulse oximetry, intracranial pressure (ICP), respiratory rate, jugular venous oximetry, and brain extracellular values of glucose, lactate, pyruvate, glycerol, and glutamate were obtained. The incidence during the initial 72?h after injury of low brain glucose <0.8?mmol/L, elevated lactate/pyruvate ratio (LPR) >25, and metabolic crisis, defined as the simultaneous occurrence of both low glucose and high LPR, were determined for the group.

Results

5 patients were inadequately resuscitated and eight patients had intractable ICP. In patients with successful resuscitation and controlled ICP (n?=?76), within 72?h of trauma, 76?% had low glucose, 93?% had elevated LPR, and 74?% were in metabolic crisis. The duration of metabolic crisis was longer in those patients with unfavorable (GOSe????6) versus favorable (GOSe????7) outcome at 6?months (P?=?0.011). In four multivariate models the burden of metabolic crisis was a powerful independent predictor of poor outcome.

Conclusions

Metabolic crisis occurs frequently after TBI despite adequate resuscitation and controlled ICP, and is a strong independent predictor of poor outcome at 6?months.     

Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury

Background

To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury.

Methods

Continuous monitoring of the partial pressure of brain tissue oxygen (P_brO₂), 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 P_brO₂ 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.

Results

Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. P_brO₂ 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.

Conclusions

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.