Andrea Lavinio

Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury

Objectives: We have sought to develop an automated methodology for the continuous updating of optimal cerebral perfusion pressure (CPPopt) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascular pressure reactivity. We then validated the CPPopt algorithm by determining the association between outcome and the deviation of actual CPP from CPPopt. Design: Retrospective analysis of prospectively collected data. Setting: Neurosciences critical care unit of a university hospital. Patients: A total of 327 traumatic head-injury patients admitted between 2003 and 2009 with continuous monitoring of arterial blood pressure and intracranial pressure. Measurements and Main Results: Arterial blood pressure, intracranial pressure, and CPP were continuously recorded, and pressure reactivity index was calculated online. Outcome was assessed at 6 months. An automated curve fitting method was applied to determine CPP at the minimum value for pressure reactivity index (CPPopt). A time trend of CPPopt was created using a moving 4-hr window, updated every minute. Identification of CPPopt was, on average, feasible during 55% of the whole recording period. Patient outcome correlated with the continuously updated difference between median CPP and CPPopt (chi-square = 45, p < .001; outcome dichotomized into fatal and nonfatal). Mortality was associated with relative “hypoperfusion” (CPP < CPPopt), severe disability with “hyperperfusion” (CPP > CPPopt), and favorable outcome was associated with smaller deviations of CPP from the individualized CPPopt. While deviations from global target CPP values of 60 mm Hg and 70 mm Hg were also related to outcome, these relationships were less robust. Conclusions: Real-time CPPopt could be identified during the recording time of majority of the patients. Patients with a median CPP close to CPPopt were more likely to have a favorable outcome than those in whom median CPP was widely different from CPPopt. Deviations from individualized CPPopt were more predictive of outcome than deviations from a common target CPP. CPP management to optimize cerebrovascular pressure reactivity should be the subject of future clinical trial in severe traumatic head-injury patients.

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

OBJECT 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. METHODS 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. RESULTS 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. CONCLUSIONS 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.

An Assessment of Dynamic Autoregulation from Spontaneous Fluctuations of Cerebral Blood Flow Velocity: A Comparison of Two Models, Index of Autoregulation and Mean Flow Index

BACKGROUND:Various methods of assessment of cerebral autoregulation, using spontaneous slow fluctuations of blood flow velocity (FV), arterial blood pressure, and cerebral perfusion pressure, have been used in clinical practice. We studied the association between the dynamic index of autoregulation (ARI) and time correlation index (mean flow index, Mx) in a group of patients after head injury. METHODS:Fifty head-injured patients of an average age of 31 yr, sedated, paralyzed, and ventilated (mild hypocapnia) with continuous monitoring of arterial blood pressure and intracranial pressure were studied. Cerebral blood FV was monitored daily for 3 days after injury during periods that were free from interventions (e.g., suctioning). Digitally recorded data were analyzed retrospectively. ARI was calculated as a coefficient graded from 0 (absence of autoregulation) to 9 (strongest autoregulation), describing a dynamic model of autoregulation. Mx was calculated as the correlation coefficient between 40 consecutive 6-s averages of FV and cerebral perfusion pressure and then averaged over the whole recording period. ARI and Mx values, assessed during the first 3 days after injury, were averaged for each patient. RESULTS:ARI and Mx showed moderately strong mutual linear relationship with correlation r = −0.62; P = 0.0001. Both indices correlated with outcome, indicating worse autoregulation in patients achieving unfavorable outcome. CONCLUSION:ARI and Mx agree relatively well in head-injured patients. Autoregulation affects outcome after head injury.

Magnetic field interactions in adjustable hydrocephalus shunts.

OBJECT Exposing patients with ventricular shunts to magnetic fields and MR imaging procedures poses a significant risk of unintentional changes in shunt settings. Shunt valves can also generate considerable imaging artifacts. The purpose of this study was to determine the magnetic field safety and MR imaging compatibility of 5 adjustable models of hydrocephalus shunts. METHODS The Codman Hakim (regular and with SiphonGuard), Miethke ProGAV, Medtronic Strata, Sophysa Sophy and Polaris programmable valves were tested in a low-intensity magnetic field, and then translational attraction (TA), magnetic torque (MT), and volume of artifacts on T1-weighted spin echo (SE) and gradient echo (GE) pulse sequences in a 3-T MR imaging unit were measured. RESULTS The ProGAV and Polaris valves were immune to unintentional reprogramming by magnetic fields up to 3 T. Other valves randomly changed settings, starting from the intensity of field: Sophy valve 24 mT, Strata valve 30 mT, and both Codman Hakim programmable valves from 42 mT. Shunt performances in the 3-T MR imaging unit are reported in the order of compatibility: 1) Codman Hakim regular, TA = 0.005 N, MT = 0.000 Nm, GE = 30 cm(3), SE = 2 cm(3); 2) Miethke ProGAV, TA = 0.001 N, MT = 1.4 x 10(3) Nm, GE = 231 cm(3), SE = 13 cm(3); 3) Codman Hakim with SiphonGuard, TA = 0.005 N, MT = 2.3 x 10(3) Nm, GE = 233 cm(3), SE = 19 cm(3); 4) Medtronic Strata, TA = 0.27 N, MT = 18.0 x 10(3) Nm, GE = 484 cm(3), SE = 86 cm(3); 5) Sophysa Sophy, TA = 0.82 N, MT = 38.9 x 10(3) Nm, GE = 758 cm(3), SE = 72 cm(3); and 6) Sophysa Polaris, TA = 0.80 N, MT = 39.6 x 10(3) Nm, GE = 954 cm(3), SE = 100 cm(3). CONCLUSIONS All valves, with the exception of the Polaris and ProGAV models, are prone to unintentional reprogramming when exposed to heterogeneous magnetic fields stronger than 40 mT. All tested valves can be considered safe for 3-T MR imaging. All valves generated a distortion of the MR image, especially the GE sequences.

The monitoring of relative changes in compartmental compliances of brain

The study aimed to develop a computational method for assessing relative changes in compartmental compliances within the brain: the arterial bed and the cerebrospinal space. The method utilizes the relationship between pulsatile components in the arterial blood volume, arterial blood pressure (ABP) and intracranial pressure (ICP). It was verified by using clinical recordings of intracranial pressure plateau waves, when massive vasodilatation accompanying plateau waves produces changes in brain compliances of the arterial bed (C(a)) and compliance of the cerebrospinal space (C(i)). Ten patients admitted after head injury with a median Glasgow Coma Score of 6 were studied retrospectively. ABP was directly monitored from the radial artery. Changes in the cerebral arterial blood volume were assessed using Transcranial Doppler (TCD) ultrasonography by digital integration of inflow blood velocity. During plateau waves, ICP increased (P = 0.001), CPP decreased (P = 0.001), ABP remained constant (P = 0.532), blood flow velocity decreased (P = 0.001). Calculated compliance of the arterial bed C(a) increased significantly (P = 0.001); compliance of the CSF space C(i) decreased (P = 0.001). We concluded that the method allows for continuous monitoring of relative changes in brain compartmental compliances. Plateau waves affect the balance between vascular and CSF compartments, which is reflected by the inverse change of compliance of the cerebral arterial bed and global compliance of the CSF space.

Intracranial pressure: why we monitor it, how to monitor it, what to do with the number and what's the future?

Purpose of review The review touches upon the current physiopathological concepts relating to the field of intracranial pressure (ICP) monitoring and offers an up-to-date overview of the ICP monitoring technologies and of the signal-analysis techniques relevant to clinical practice. Recent findings Improved ICP probes, antibiotic-impregnated ventricular catheters and multimodality, computerized systems allow ICP monitoring and individualized optimization of brain physiology. Noninvasive technologies for ICP and cerebral perfusion pressure assessment are being tested in the clinical arena. Computerized morphological analysis of the ICP pulse-waveform can provide an indicator of global cerebral perfusion. Summary Current recommendations for the management of traumatic brain injury indicate ICP monitoring in patients who remain comatose after resuscitation if the admission computed tomography scan reveals intracranial abnormalities such as haematomas, contusions and cerebral oedema. The most reliable methods of ICP monitoring are ventricular catheters and intraparenchymal systems. A growing number of these devices are being safely placed by neurointensivists. The consensus is to treat ICP exceeding the 20 mmHg threshold, and to target cerebral perfusion pressure between 50 and 70 mmHg. Recent evidence suggests that such thresholds should be optimized based on multimodality monitoring and individual brain physiology. Noninvasive ICP estimation using transcranial Doppler can have a role as a screening tool in patients with low to intermediate risk of developing intracranial hypertension. However, the technology remains insufficiently accurate and too cumbersome for continuous ICP monitoring.

Is There a Direct Link Between Cerebrovascular Activity and Cerebrospinal Fluid Pressure-Volume Compensation?

Background and Purpose— Cerebral blood flow is coupled to brain metabolism by means of active modulation of cerebrovascular resistance. This homeostatic vasogenic activity is reflected in slow waves of cerebral blood flow velocities (FV) which can also be detected in intracranial pressure (ICP). However, effects of increased ICP on the modulation of cerebral blood flow are still poorly understood. This study focused on the question whether ICP has an independent impact on slow waves of FV within the normal cerebral perfusion pressures range. Methods— Twenty patients presenting with communicating hydrocephalus underwent a diagnostic intraventricular constant-flow infusion test. Blood flow velocities in the middle cerebral artery and posterior cerebral arteries were measured using Transcranial Doppler. Pulsatility index, FV variability of slow vasogenic waves (3 to 9 bpm), ICP, and arterial blood pressure were simultaneously monitored. Results— During the test, ICP increased from a baseline of 11 (6) mm Hg to a plateau value of 21 (6) mm Hg (P=0.00005). Although the infusion did not induce significant changes in cerebral perfusion pressures, FV, pulsatility index, or index of autoregulation, the magnitude of FV vasogenic waves at plateau became inversely correlated to ICP (middle cerebral artery: r=−0.58, P<0.01; posterior cerebral arteries: r=−0.54, P<0.01). Conclusions— This study shows that even moderately increased ICP can limit the modulation of cerebral blood flow in both vascular territories within the autoregulatory range of cerebral perfusion pressures. The exhaustion of cerebrospinal fluid volume buffering reserve during infusion studies elicits a direct interaction between the cerebrospinal fluid space and the cerebrovascular compartment.

Noninvasive Evaluation of Dynamic Cerebrovascular Autoregulation Using Finapres Plethysmograph and Transcranial Doppler

Background and Purpose— Mx is an index of cerebrovascular autoregulation. It is calculated as the correlation coefficient between slow spontaneous fluctuations of cerebral perfusion pressure (cerebral perfusion pressure=arterial blood pressure−intracranial pressure) and cerebral blood flow velocity. Mx can be estimated noninvasively (nMxa) with the use of a finger plethysmograph arterial blood pressure measurement instead of an invasive cerebral perfusion pressure measurement. We investigated the agreement between nMxa and the previously validated index Mx. Methods— The study included 10 head-injured adults. Intracranial pressure was monitored with a parenchymal probe. Arterial blood pressure was monitored simultaneously with an arterial catheter and with the Finapres plethysmograph. Flow velocity in the middle cerebral artery was measured bilaterally with transcranial Doppler. Mx and nMxa were computed in both hemispheres, and asymmetry of autoregulation was calculated. Results— Ninety-six measures of Mx and nMxa were obtained (48 for each side) in 10 patients. Mx correlated with nMxa (R=0.755, P<0.001; 95% agreement=±0.36; bias=0.01). Asymmetry in autoregulation assessed with Mx correlated significantly with asymmetry estimated with nMxa (R=0.857, P<0.0001; 95% agreement=±0.26; bias=−0.03). Conclusions— The noninvasive index of autoregulation nMxa correlates with Mx and is sensitive enough to detect autoregulation asymmetry. nMxa is proposed as a practical tool to assess cerebral autoregulation in patients who do not require invasive monitoring.

A comparison study of cerebral autoregulation assessed with transcranial Doppler and cortical laser Doppler flowmetry.

Abstract Objectives: We compared autoregulation monitored with cortical laser Doppler flowmetry (LDF) and autoregulation monitored with transcranial Doppler (TCD) in the middle cerebral artery (MCA) to verify the hypothesis that, following brain trauma, cortical vessel autoregulation to intracranial hypertension is different than assessed in the MCA. Methods: Data collected from 29 head injured patients were analysed retrospectively. Arterial blood pressure (ABP), intracranial pressure (ICP), flow velocity (FV) of the MCA and cortical flux (LDF) were monitored. Indices of cortical autoregulation (Lx) and autoregulation of cerebral blood flow in the MCA (Mx) were calculated as a moving correlation coefficient between slow waves of LDF and cerebral perfusion pressure (CPP) (Lx) or FV and CPP (Mx), respectively. Intact autoregulation was indicated by negative values for Lx and Mx; disturbed autoregulation was reflected by positive values. Results: FV and LDF showed a high coherence in the slow wave spectrum of 1–4 cycles/min (mean: 0·79 ± 0·12), indicating that similar information regarding autoregulation is carried by both signals. Mx and Lx correlated in all patients (R=0·43, p=0·02). On average, Lx was significantly higher than Mx; the mean difference was 0·13 ± 0·38 (p=0·032), potentially due to severe intracranial hypertension above 40 mmHg, driving CPP values below 60 mmHg. Conclusion: After traumatic brain injury, cortical autoregulation appears to be worse than autoregulation assessed in the MCA during rising ICP and falling CPP. When CPP is above 60 mmHg, cortical assessed autoregulation is similar to autoregulation assessed in the MCA.

Transient changes in brain tissue oxygen in response to modifications of cerebral perfusion pressure: an observational study.

BACKGROUND: The relative merits of the mechanisms for the maintenance of brain tissue oxygenation (PbtO2) have been much debated. There is a wealth of studies regarding various factors that may determine the absolute value and changes in PbtO2. However, only a few of them analyzed fast (few minutes) and transient behavior of PbtO2 in response to variations (waves) of intracranial pressure (ICP) and cerebral perfusion pressure (CPP). METHODS: This was a retrospective analysis and observational study. PbtO2, arterial blood pressure (ABP), and ICP waveforms were digitally monitored in 23 head-injured patients, admitted to the Neuroscience Critical Care Unit, who were sedated, paralyzed, and ventilated. Computer recordings were retrospectively reviewed. The dynamic changes in PbtO2 in response to transient changes in ABP and ICP were investigated. RESULTS: Several patterns of response to short-lasting arterial hypotension and hypertension, intracranial hypertension, cerebral vasocycling, and cerebral hyperemia were observed and characterized. During the majority of the transient events, PbtO2 generally followed the direction of changes in CPP. Only during episodes of hyperemia, CPP and PbtO2 changed in the opposite direction. Changes in PbtO2 were delayed after dynamic changes in ABP, CPP, and ICP. The CPP-PbtO2 delay during changes provoked by variations in ABP was 35.0 s (range: maximum 827.0 s; minimum 0.0 s) compared with changes induced by variations in ICP of 0.0 s (range: maximum 265.0 s; minimum 0.0 s); the difference was significant at P < 0.0001. CONCLUSIONS: PbtO2 is more than a number; it is rather a waveform following rapid changes in ICP and ABP. We show that PbtO2 generally tracks the direction of CPP irrespective of the state of cerebral autoregulation.