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.     

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.     

Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Background

Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP.

Methods

A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003?C2009) with continuous ABP and ICP monitoring.

Results

PAx was worse in patients who died compared to those who survived (?0.04?±?0.15 vs. ?0.16?±?0.15, ??²?=?28, p?2?=?6, p?=?0.01).

Conclusions

PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.     

Transcranial Doppler Monitoring of Intracranial Pressure Plateau Waves

Background

Transcranial Doppler (TCD) has been used to estimate ICP noninvasively (nICP); however, its accuracy varies depending on different types of intracranial hypertension. Given the high specificity of TCD to detect cerebrovascular events, this study aimed to compare four TCD-based nICP methods during plateau waves of ICP.

Methods

A total of 36 plateau waves were identified in 27 patients (traumatic brain injury) with TCD, ICP, and ABP simultaneous recordings. The nICP methods were based on: (1) interaction between flow velocity (FV) and ABP using a “black-box” mathematical model (nICP_BB); (2) diastolic FV (nICP_FV _d ); (3) critical closing pressure (nICP_CrCP), and (4) pulsatility index (nICP_PI). Analyses focused on relative changes in time domain between ICP and noninvasive estimators during plateau waves and the magnitude of changes (? between baseline and plateau) in real ICP and its estimators. A ROC analysis for an ICP threshold of 35 mmHg was performed.

Results

In time domain, nICP_PI, nICP_BB, and nICP_CrCP presented similar correlations: 0.80 ± 0.24, 0.78 ± 0.15, and 0.78 ± 0.30, respectively. nICP_FV _d presented a weaker correlation (R = 0.62 ± 0.46). Correlations between ?ICP and ?nICP were better represented by nICP_CrCP and BB, R = 0.48, 0.44 (p < 0.05), respectively. nICP_FV _d and PI presented nonsignificant ? correlations. ROC analysis showed moderate to good areas under the curve for all methods: nICP_BB, 0.82; nICP_FV _d , 0.77; nICP_CrCP, 0.79; and nICP_PI, 0.81.

Conclusions

Changes of ICP in time domain during plateau waves were replicated by nICP methods with strong correlations. In addition, the methods presented high performance for detection of intracranial hypertension. However, absolute accuracy for noninvasive ICP assessment using TCD is still low and requires further improvement.

     

Pressures,Flow, and Brain Oxygenation During Plateau Waves of Intracranial Pressure

Background

Plateau waves are common in traumatic brain injury. They constitute abrupt increases of intracranial pressure (ICP) above 40 mmHg associated with a decrease in cerebral perfusion pressure (CPP). The aim of this study was to describe plateau waves characteristics with multimodal brain monitoring in head injured patients admitted in neurocritical care.

Methods

Prospective observational study in 18 multiple trauma patients with head injury admitted to Neurocritical Care Unit of Hospital Sao Joao in Porto. Multimodal systemic and brain monitoring of primary variables [heart rate, arterial blood pressure, ICP, CPP, pulse amplitude, end tidal CO₂, brain temperature, brain tissue oxygenation pressure, cerebral oximetry (CO) with transcutaneous near-infrared spectroscopy and cerebral blood flow (CBF)] and secondary variables related to cerebral compensatory reserve and cerebrovascular reactivity were supported by dedicated software ICM+ (www.neurosurg.cam.ac.uk/icmplus). The compiled data were analyzed in patients who developed plateau waves.

Results

In this study we identified 59 plateau waves that occurred in 44 % of the patients (8/18). During plateau waves CBF, cerebrovascular resistance, CO, and brain tissue oxygenation decreased. The duration and magnitude of plateau waves were greater in patients with working cerebrovascular reactivity. After the end of plateau wave, a hyperemic response was recorded in 64 % of cases with increase in CBF and brain oxygenation. The magnitude of hyperemia was associated with better autoregulation status and low oxygenation levels at baseline.

Conclusions

Multimodal brain monitoring facilitates identification and understanding of intrinsic vascular brain phenomenon, such as plateau waves, and may help the adequate management of acute head injury at bed side.     

Critical closing pressure determined with a model of cerebrovascular impedance

Critical closing pressure (CCP) is the arterial blood pressure (ABP) at which brain vessels collapse and cerebral blood flow (CBF) ceases. Using the concept of impedance to CBF, CCP can be expressed with brain-monitoring parameters: cerebral perfusion pressure (CPP), ABP, blood flow velocity (FV), and heart rate. The novel multiparameter method (CCPm) was compared with traditional transcranial Doppler (TCD) calculations of CCP (CCP1). Digital recordings of ABP, intracranial pressure (ICP), and TCD-based FV from previously published studies of 29 New Zealand White rabbits were reanalyzed. Overall, CCP1 and CCPm showed correlation across wide ranges of ABP, ICP, and PaCO2 (R=0.93, P<0.001). Three physiological perturbations were studied: increase in ICP (n=29) causing both CCP1 and CCPm to increase (P<0.001 for both); reduction of ABP (n=10) resulting in decrease of CCP1 (P=0.006) and CCPm (P=0.002); and controlled increase of PaCO2 (n=8) to hypercapnic levels, which decreased CCP1 and CCPm, albeit insignificantly (P=0.123 and P=0.306 respectively), caused by a spontaneous significant increase in ABP (P=0.025). Multiparameter mathematical model of critical closing pressure explains the relationship of CCP on brain-monitoring variables, allowing the estimation of CCP during cases such as hypercapnia-induced hyperemia, where traditional calculations, like CCP1, often reach negative non-physiological values.     

Effect of Early Physiotherapy on Intracranial Pressure and Cerebral Perfusion Pressure

Background

Physiotherapy plays an important role in the therapy of patients with acute cerebral diseases. Studies concerning the effects of physiotherapy on intracerebral pressure (ICP) and cerebral perfusion pressure (CPP) are, however, rare.

Methods

An observational study was performed on critically ill patients who were receiving ICP measurements and who were treated with passive range of motion (PROM) on our neuro-intensive care unit. ICP, CPP, mean arterial pressure (MAP) and heart rate were recorded continuously every minute, beginning 15 min before, during (26 min) and 15 min after treatment with PROM. Patients with mean ICP <15 mmHg (Group 1) and patients with mean ICP ≥15 mmHg (Group 2) before physiotherapy were analyzed separately.

Results

Overall there were 84 patients (f:m = 1:1) with 298 treatments units, 224 in Group 1 and 74 in Group 2, respectively. Mean ICP before treatment was 11.5 ± 5.1 mmHg, with a significant decrease of 1 mmHg during therapy (p = 2.0e–10). This was also true for Group 1 (baseline ICP 9.4 ± 3.7 mmHg, decrease of 0.7 mmHg, p = 3.8e–6) and Group 2 (baseline ICP 18.1 ± 2.7 mmHg, decrease of 2 mmHg, p = 3.7e–6). However, a persistent ICP reduction after therapy was seen only in Group 2. There were no significant differences between mean CPP and MAP comparing ICP before and after PROM in all groups. No adverse side effects of PROM were observed.

Conclusions

Physiotherapy with PROM can be used safely in patients with acute neurological diseases, even if ICP is elevated before therapy.     

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.

     

Comparison of Non-invasive and Invasive Arterial Blood Pressure Measurement for Assessment of Dynamic Cerebral Autoregulation

Background

There is a growing interest in measuring cerebral autoregulation in patients with acute brain injury. Non-invasive finger photo-plethysmography (Finapres) is the method of choice to relate arterial blood pressure to changes in cerebral blood flow. Among acutely ill patients, however, peripheral vasoconstriction often limits the use of Finapres requiring direct intravascular blood pressure measurement. We evaluated how these two different forms of blood pressure monitoring affect the parameters of dynamic cerebral autoregulation (DCA).

Methods

We performed 37 simultaneous recordings of BP and cerebral blood flow velocity in 15 patients with acute brain injury. DCA was estimated in the frequency domain using transfer function analysis to calculate phase shift, gain, and coherence. In addition the mean velocity index (Mx) was calculated for assessment of DCA in the time domain.

Results

The mean patient age was 58.1 ± 15.9 years, 80 % (n = 12) were women. We found good inter-method agreement between Finapres and direct intravascular measurement using Bland–Altman and correlation analyses. Finapres gives higher values for the efficiency of dynamic CA compared with values derived from radial artery catheter, as indicated by biases in the phase (26.3 ± 11.6° vs. 21.7 ± 10.5°, p = 0.001) and Mx (0.571 ± 0.137 vs. 0.649 ± 0.128, p < 0.001). Gain in the low frequency range did not significantly differ between the two arterial blood pressure methods. The average coherence between CBFV and ABP was higher when BP was measured with arterial catheter for frequencies above 0.05 Hz (0.8 vs. 0.73, p < 0.001).

Conclusion

Overall, both methods yield similar results and can be used for the assessment of DCA. However, there was a small but significant difference for both mean Mx and phase shift, which would need to be adjusted for during monitoring of patients when using both methods. When available, invasive arterial blood pressure monitoring may improve accuracy and thus should be the preferred method for DCA assessment in the ICU.     

Cessation of Diastolic Cerebral Blood Flow Velocity: The Role of Critical Closing Pressure

Background

Reducing cerebral perfusion pressure (CPP) below the lower limit of autoregulation (LLA) causes cerebral blood flow (CBF) to become pressure passive. Further reductions in CPP can cause cessation of CBF during diastole. We hypothesized that zero diastolic flow velocity (FV) occurs when diastolic blood pressure becomes less than the critical closing pressure (CrCP).

Methods

We retrospectively analyzed studies of 34 rabbits with CPP below the LLA, induced with pharmacologic sympathectomy (N = 23) or cerebrospinal fluid infusion (N = 11). Basilar artery blood FV and cortical Laser Doppler Flow (LDF) were monitored. CrCP was trended using a model of cerebrovascular impedance. The diastolic closing margin (DCM) was monitored as the difference between diastolic blood pressure and CrCP. LDF was recorded for DCM values greater than and less than zero.

Results

Arterial hypotension caused a reduction of CrCP (p < 0.001), consistent with decreased wall tension (p < 0.001) and a drop in intracranial pressure (ICP; p = 0.004). Cerebrospinal infusion caused an increase of CrCP (p = 0.002) accounted for by increasing ICP (p < 0.001). The DCM was compromised by either arterial hypotension or intracranial hypertension (p < 0.001 for both). When the DCM reached zero, diastolic FV ceased for a short period during each heart cycle (R = 0.426, p < 0.001). CBF pressure passivity accelerated when DCM decreased below zero (from 1.51 ± 0.51 to 2.17 ± 1.17 % ΔLDF/ΔmmHg; mean ± SD; p = 0.010).

Conclusions

The disappearance of diastolic CBF below LLA can be explained by DCM reaching zero or negative values. Below this point the decrease in CBF accelerates with further decrements of CPP.     

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.     

Does Prone Positioning Increase Intracranial Pressure? A Retrospective Analysis of Patients with Acute Brain Injury and Acute Respiratory Failure

Purpose

The objective of our trial was to obtain more comprehensive data on the risks and benefits of kinetic therapy in intensive care patients with intracerebral pathology.

Methods

Standardized data of prone positioning in our NeuroIntensive Care Unit were collected from 2007 onward. A post hoc analysis of all available data was undertaken, with special consideration given to values of intracranial pressure (ICP), cerebral perfusion pressure (CPP) and oxygenation in correlation to prone (PP), or supine positioning (SP) of patients. Cases were considered eligible if kinetic therapy and ICP were documented. Prone positioning was performed in a 135° position for 8 h per treatment unit.

Results

A total of 115 patients treated with prone positioning from 2007 to 2013 were identified in our medical records. Of these, 29 patients received ICP monitoring. Overall, 119 treatment units of prone positioning with a mean duration of 2.5 days per patient were performed. The mean baseline ICP in SP was 9.5 ± 5.9 mmHg and was increased significantly during PP (p < 0.0001). There was no significant difference between CPP in SP (82 ± 14.5 mmHg) compared to PP (p > 0.05). ICP values >20 mmHg occurred more often during PP than SP (p < 0.0001) and were associated with significantly more episodes of decreased CPP <70 mmHg (p < 0.0022). The mean paO₂/FiO₂ ratio (P/F ratio) was increased significantly in prone positioning of patients (p < 0.0001).

Conclusions

The analyzed data allow a more precise understanding of changes in ICP and oxygenation during prone positioning in patients with acute brain injury and almost normal baseline ICP. Our study shows a moderate, yet significant elevation of ICP during prone positioning. However, the achieved increase of oxygenation by far exceeded the changes in ICP. It is evident that continuous monitoring of cerebral pressure is required in this patient group.     

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.

     

Intracranial Pressure Dose and Outcome in Traumatic Brain Injury

Objective

Detecting and treating elevated intracranial pressure (ICP) is a cornerstone of management in patients with severe traumatic brain injury. The aim of this study was to determine the association between area under the curve measurement of elevated ICP and clinical outcome.

Methods

Single center observational study using prospectively collected data at a University hospital, level one-trauma center. Sixty prospective patients with severe traumatic brain injury were prospectively enrolled over a 2-year period. Intracranial pressure measurements were captured using a real-time automated, high resolution vital signs data recording system. Mortality and functional outcome were assessed at 30 days, 3 and 6 months using Extended Glasgow Outcome Scale.

Results

Increasing elevated intracranial pressure time dose was associated with mortality (OR 1.08; 95 % confidence interval [CI], 1.01–1.15, p = 0.03) and poor functional outcome at 3 (OR 1.04; CI 1.00–1.07, p = 0.03) and 6 months (1.04; CI 1.01–1.08, p = 0.02). However, there was no association between episodic ICP data and outcome.

Conclusions

These results suggest that pressure time dose measurement of intracranial pressure may be used to predict outcome in severe traumatic brain injury and may be a candidate biomarker in this disease.     

Intracranial Pressure Changes During Intrahospital Transports of Neurocritically Ill Patients

Background

Intrahospital transport is associated with a high rate of complications. Investigations of this problem using neuromonitoring remain scarce.

Methods

This is a monocentric, prospective observational study. Patients with severe brain diseases and intracranial pressure (ICP) monitoring were included. Continuous monitoring of ICP, cerebral perfusion pressure (CPP), oxygen saturation (SpO₂), heart rate, and mean arterial pressure was measured during seven different periods of intrahospital transport (baseline for 30 min, I = preparation, II = transport I, III = CT scan, IV = transport II, V = postprocessing, and follow-up for another 30 min). All complications were documented.

Results

Between July 2013 and December 2013, a total number of 56 intrahospital transports of 43 patients were performed from ICU to CT. Data recording was incomplete in six cases. Fifty transports have been taken into account for statistical analysis. Forty-two percent were emergency transports. Mean duration of the procedure was 17′ (preparation), 6′ (transport I), 9′ (CT scan), 6′ (transport II), and 15′ (postprocessing), respectively. Mean ICP at baseline was 8.53 mmHg. Comparing all periods of intrahospital transport and the follow-up period to the baseline showed a significant increase of ICP only during CT scan (15.83 mmHg, p < 0.01), not during the transport to and from the radiology department. An overall complication rate of 36 % (n = 18) was observed. In 26 % (n = 13), additional ICP therapy was necessary due to an elevation of ICP above 20 mmHg.

Conclusion

There is a considerable rate of complications during intrahospital transport of critically ill patients with severe brain diseases, with a significant increase of ICP during transport and CT scan. In one-fifth of all patients, additional therapy was necessary. From our point of view, transport of critically ill patients should only be performed by trained staff and under monitoring of ICP and CPP.

     

Critical closing pressure in cerebrovascular circulation

OBJECTIVE: Cerebral critical closing pressure (CCP) has been defined as an arterial pressure threshold below which arterial vessels collapse. Hypothetically this is equal to intracranial pressure (ICP) plus the contribution from the active tone of cerebral arterial smooth muscle. The correlation of CCP with ICP, cerebral autoregulation, and other clinical and haemodynamic modalities in patients with head injury was evaluated. METHOD: intracranial pressure, arterial blood pressure (ABP) and middle cerebral artery blood flow velocity were recorded daily in ventilated patients. Waveforms were processed to calculate CCP, the transcranial Doppler-derived cerebral autoregulation index (Mx), mean arterial pressure (ABP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). RESULTS: Critical closing pressure reflected the time related changes in ICP during plateau and B waves. Overall correlation between CCP and ICP was mild but significant (R=0.41; p<0.0002). The mean difference between ABP and CCP correlated with CPP (R=0.57, 95% confidence interval (95% CI) for prediction 25 mm Hg). The difference between CCP and ICP, described previously as proportional to arterial wall tension, correlated with the index of cerebral autoregulation Mx (p<0.0002) and CPP (p<0.0001). However, by contrast with the Mx index, CCP-ICP was not significantly correlated with outcome after head injury. CONCLUSION: Critical closing pressure, although sensitive to variations in ICP and CPP, cannot be used as an accurate estimator of these modalities with acceptable confidence intervals. The difference CCP-ICP significantly correlates with cerebral autoregulation, but it lacks the power to predict outcome after head injury.     

Reliability of Optic Nerve Ultrasound for the Evaluation of Patients with Spontaneous Intracranial Hemorrhage

Introduction

The aim of our study is to confirm the reliability of optic nerve ultrasound as a method to detect intracranial hypertension in patients with spontaneous intracranial hemorrhage, to assess the reproducibility of the measurement of the optic nerve sheath diameter (ONSD), and to verify that ONSD changes concurrently with intracranial pressure (ICP) variations.

Methods

Sixty-three adult patients with subarachnoid hemorrhage (n = 34) or primary intracerebral hemorrhage (n = 29) requiring sedation and invasive ICP monitoring were enrolled in a 10-bed multivalent ICU. ONSD was measured 3 mm behind the globe through a 7.5-MHz ultrasound probe. Mean binocular ONSD was used for statistical analysis. ICP values were registered simultaneously to ultrasonography. Twenty-eight ONSDs were measured consecutively by two different observers, and interobserver differences were calculated. Twelve coupled measurements were taken before and within 1 min after cerebrospinal fluid (CSF) drainage to control elevated ICP.

Results

Ninety-four ONSD measurements were analyzed. 5.2 mm proved to be the optimal ONSD cut-off point to predict raised ICP (>20 mmHg) with 93.1% sensitivity (95% CI: 77.2–99%) and 73.85% specificity (95% CI: 61.5–84%). ONSD–ICP correlation coefficient was 0.7042 (95% CI for r = 0.5850–0.7936). The median interobserver ONSD difference was 0.25 mm. CSF drainage to control elevated ICP caused a rapid and significant reduction of ONSD (from 5.89 ± 0.61 to 5 ± 0.33 mm, P < 0.01).

Conclusion

Our investigation confirms the reliability of optic nerve ultrasound as a non-invasive method to detect elevated ICP in intracranial hemorrhage patients. ONSD measurements proved to have a good reproducibility. ONSD changes almost concurrently with CSF pressure variations.     

The Effect of Positive End-Expiratory Pressure on Intracranial Pressure and Cerebral Hemodynamics

Background

Lung protective ventilation has not been evaluated in patients with brain injury. It is unclear whether applying positive end-expiratory pressure (PEEP) adversely affects intracranial pressure (ICP) and cerebral perfusion pressure (CPP). We aimed to evaluate the effect of PEEP on ICP and CPP in a large population of patients with acute brain injury and varying categories of acute lung injury, defined by PaO₂/FiO₂.

Method

Retrospective data were collected from 341 patients with severe acute brain injury admitted to the ICU between 2008 and 2015. These patients experienced a total of 28,644 paired PEEP and ICP observations. Demographic, hemodynamic, physiologic, and ventilator data at the time of the paired PEEP and ICP observations were recorded.

Results

In the adjusted analysis, a statistically significant relationship between PEEP and ICP and PEEP and CPP was found only among observations occurring during periods of severe lung injury. For every centimeter H₂O increase in PEEP, there was a 0.31 mmHg increase in ICP (p = 0.04; 95 % CI [0.07, 0.54]) and a 0.85 mmHg decrease in CPP (p = 0.02; 95 % CI [?1.48, ?0.22]).

Conclusion

Our results suggest that PEEP can be applied safely in patients with acute brain injury as it does not have a clinically significant effect on ICP or CPP. Further prospective studies are required to assess the safety of applying a lung protective ventilation strategy in brain-injured patients with lung injury.