Cerebral autoregulation following head injury.

OBJECT: The goal of this study was to examine the relationship between cerebral autoregulation, intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP) after head injury by using transcranial Doppler (TCD) ultrasonography. METHODS: Using ICP monitoring and TCD ultrasonography, the authors previously investigated whether the response of flow velocity (FV) in the middle cerebral artery to spontaneous variations in ABP or CPP provides reliable information about cerebral autoregulatory reserve. In the present study, this method was validated in 187 head-injured patients who were sedated and receiving mechanical ventilation. Waveforms of ICP, ABP, and FV were recorded over intervals lasting 20 to 120 minutes. Time-averaged mean FV and CPP were determined. The correlation coefficient index between FV and CPP (the mean index of autoregulation [Mx]) was calculated over 4-minute epochs and averaged for each investigation. The distribution of averaged mean FV values converged with the shape of the autoregulatory curve, indicating lower (CPP < 55 mm Hg) and upper (CPP > 105 mm Hg) thresholds of autoregulation. The relationship between the Mx and either the CPP or ABP was depicted as a U-shaped curve. Autoregulation was disturbed in the presence of intracranial hypertension (ICP > or = 25 mm Hg) and when mean ABP was too low (ABP < 75 mm Hg) or too high (ABP > 125 mm Hg). Disturbed autoregulation (p < 0.005) and higher ICP (p < 0.005) occurred more often in patients with unfavorable outcomes than in those with favorable outcomes. CONCLUSIONS: Autoregulation not only is impaired when associated with a high ICP or low ABP, but it can also be disturbed by too high a CPP. The Mx can be used to guide intensive care therapy when CPP-oriented protocols are used.     

Dynamic cerebral autoregulation: should intracranial pressure be taken into account?

Summary Background. Although the inclusion of cerebral perfusion pressure (CPP) is a standard feature in static testing of autoregulation after head injury, controversy surrounds the use of CPP versus arterial blood pressure (ABP) in dynamic tests. The aim of our project was to assess the discrepancies between methods of dynamic autoregulation testing based on CPP or ABP, and study possible differences in their prognostic value. Method. Intermittent recordings of intracranial pressure (ICP), ABP and middle cerebral artery blood flow velocity (FV) waveforms were made in 151 anaesthetised and ventilated adult head injured patients as part of their required care. Indices of dynamic autoregulation were calculated as a moving correlation coefficient of 60 samples (total time 3 min) of 6 s mean values of FV and ABP (Mxa) or FV and CPP (Mx). Values of Mx and Mxa were averaged over multiple recordings in each patient and correlated with outcome at 6 months post injury. Findings. Association between Mx and Mxa was moderately strong (r ² = 0.73). However, limit of 95% accordance between both indices was ±0.32. Mxa was significantly greater than Mx (0.22 ± 0.22 versus 0.062 ± 0.28; p < 0.000001). The difference between Mx and Mxa decreased with impairment of autoregulation (r = −0.39; p < 0.000001). Mean value of Mx showed a significant difference between dichotomized outcome groups (better autoregulation in patients with favourable than unfavourable outcome), while Mxa did not. Conclusions. Although relatively similar in a large group of patients, the differences between these two methods of assessment of dynamic autoregulation may be considerable in individual cases. When ICP is monitored, CPP rather than ABP should be included in the calculation of the autoregulatory index.     

Asymmetry of pressure autoregulation after traumatic brain injury

OBJECT: The aim of this study was to assess the asymmetry of autoregulation between the left and right sides of the brain by using bilateral transcranial Doppler ultrasonography in a cohort of patients with head injuries. METHODS: Ninety-six patients with head injuries comprised the study population. All significant intracranial mass lesions were promptly removed. The patients were given medications to induce sedation and paralysis, and artificial ventilation. Arterial blood pressure (ABP) and intracranial pressure (ICP) were monitored in an invasive manner. A strategy based on the patient's cerebral perfusion pressure (CPP = ABP - ICP) was applied: CPP was maintained at a level higher than 70 mm Hg and ICP at a level lower than 25 mm Hg. The left and right middle cerebral arteries were insonated daily, and bilateral flow velocities (FVs) were recorded. The correlation coefficient between the CPP and FV, termed Mx, was calculated and time-averaged over each recording period on both sides. An Mx close to 1 signified that slow fluctuations in CPP produced synchronized slow changes in FV, indicating a defective autoregulation. An Mx close to 0 indicated preserved autoregulation. Computerized tomography scans in all patients were reviewed; the side on which the major brain lesion was located was noted and the extent of the midline shift was determined. Outcome was measured 6 months after discharge. The left-right difference in the Mx between the hemispheres was significantly higher in patients who died than in those who survived (0.16 +/- 0.04 compared with 0.08 +/- 0.01; p = 0.04). The left-right difference in the Mx was correlated with a midline shift (r = -0.42; p = 0.03). Autoregulation was worse on the side of the brain where the lesion was located (p < 0.035). CONCLUSIONS: The left-right difference in autoregulation is significantly associated with a fatal outcome. Autoregulation in the brain is worse on the side ipsilateral to the lesion and on the side of expansion in cases in which there is a midline shift.     

Association between dynamic cerebral autoregulation and mortality in severe head injury

The objective of the study was to test the hypothesis that dynamic cerebral pressure-autoregulation is associated with the outcome of patients with severe head injury and to derive optimal criteria for future studies on the predictive value of autoregulation indices. Repeated measurements were performed on 32 patients with severe head injury. Arterial blood pressure (ABP) was measured continuously with an intravascular catheter, intracranial pressure (ICP) was recorded with a subdural semiconductor transducer and cerebral blood flow velocity (CBFV) was measured with Doppler ultrasound in the middle cerebral artery. Transfer function analysis was performed on mean beat-to-beat values, using ABP or CBFV as input variables and CBFV or ICP as the output variables. A dynamic index of autoregulation (ARI) ranging between 0 and 9 was extracted from the CBFV step response for a change in ABP. No significant differences between survivors and non-survivors were found due to mean values of ICP, ABP, CPP, CBFV, pCO2, GCS, age or heart rate. The transfer functions between ABP-ICP and CBFV-ICP did not show any significant differences either. The median [lower, upper quartiles] ARI was significantly lower for non-survivors compared with survivors [4.8 (0.0, 5.9) v. 6.9 (5.9, 7.4), p= 0.004]. The correlation between ARI and GOS was also significant (r=0.464, p=0.011). Cohen's coefficient was optimal for a threshold of ARI= 5.86 (kappa 0.51, p=0.0036), leading to a sensitivity for death of 75%, specificity=76.5%, odds ratio =9.75 and overall precision = 75.8%. The difference in ARI values between survivors and non-survivors persisted when results were adjusted for GCS (p = 0.028). A similar analysis for the Marshall CT scale did not reach significance (p = 0.072). A logistic regression analysis confirmed that apart from the ARI, no other variables had a significant contribution to predict outcome. In this group of patients, death following severe head injury could not be explained by traditional indices of risk, but was strongly correlated to indices of dynamic cerebral pressure-autoregulation extracted by means of transfer function analysis. Future studies using a prospective design are needed to validate the predictive value of the ARI index, as estimated by transfer function analysis, in relation to death and other unfavourable outcomes.     

Dynamic autoregulatory response after severe head injury

OBJECT: The purpose of this study was to evaluate the extent and timing of impairment of cerebral pressure autoregulation after severe head injury. METHODS: In a prospective study of 122 patients with severe head trauma (median Glasgow Coma Scale Score 6), dynamic tests of pressure autoregulation were performed every 12 hours during the first 5 days postinjury and daily during the next 5 days. The autoregulatory index ([ARI] normal value 5 +/- 1.1) was calculated for each test. The changes in the ARI over time were examined and compared with other physiological variables. The ARI averaged 2.8 +/- 1.9 during the first 12 hours postinjury, and continued to decrease to a nadir of 1.7 +/- 1.1 at 36 to 48 hours postinjury. At this nadir, in 87% of the patients the value was less than 2.8. This continued deterioration in the ARI during the first 36 to 48 hours postinjury occurred despite an increase in cerebral blood flow ([CBF], p < 0.05) and in middle cerebral artery blood flow velocity ([BFV], p < 0.001), and could not be explained by changes in cerebral perfusion pressure, end-tidal CO2, or cerebral metabolic rate of O2. A marked decrease in cerebrovascular resistance ([CVR], p < 0.001) accompanied this deterioration in the ARI. Patients with a relatively higher BFV on Day 1 had a lower CVR (p < 0.05) and more impaired pressure autoregulation than those with a lower BFV. CONCLUSIONS: The inability of cerebral vessels to regulate CBF normally may play a role in the vulnerability of the injured brain to secondary ischemic insults. These studies indicate that this vulnerability continues and even increases beyond the first 24 hours postinjury. Local factors affecting cerebrovascular tone may be responsible for these findings.     

Intracranial hypertension: what additional information can be derived from ICP waveform after head injury?

Summary Objective. Although intracranial hypertension is one of the important prognostic factors after head injury, increased intracranial pressure (ICP) may also be observed in patients with favourable outcome. We have studied whether the value of ICP monitoring can be augmented by indices describing cerebrovascular pressure-reactivity and pressure-volume compensatory reserve derived from ICP and arterial blood pressure (ABP) waveforms.Method. 96 patients with intracranial hypertension were studied retrospectively: 57 with fatal outcome and 39 with favourable outcome. ABP and ICP waveforms were recorded. Indices of cerebrovascular reactivity (PRx) and cerebrospinal compensatory reserve (RAP) were calculated as moving correlation coefficients between slow waves of ABP and ICP, and between slow waves of ICP pulse amplitude and mean ICP, respectively. The magnitude of slow waves was derived using ICP low-pass spectral filtration.Results. The most significant difference was found in the magnitude of slow waves that was persistently higher in patients with a favourable outcome (p<0.00004). In patients who died ICP was significantly higher (p<0.0001) and cerebrovascular pressure-reactivity (described by PRx) was compromised (p<0.024). In the same patients, pressure-volume compensatory reserve showed a gradual deterioration over time with a sudden drop of RAP when ICP started to rise, suggesting an overlapping disruption of the vasomotor response.Conclusion. Indices derived from ICP waveform analysis can be helpful for the interpretation of progressive intracranial hypertension in patients after brain trauma.     

Assessment of Critical Closing Pressure in the Cerebral Circulation as a Measure of Cerebrovascular Tone

Critical closing pressure (CCP) calculated from the blood flow velocity (FV) and arterial blood pressure (ABP) waveforms has been previously reported to be useful in the assessment of the dynamics of cerebral circulation. We investigated the relationship between CCP and intracranial pressure (ICP) and cerebrovascular tone in a model of intracranial hypertension in 22 anaesthetised New Zealand White rabbits during manipulations of arterial CO2, ABP and vasodilatation caused by hypoxia. Recordings were made of FV in the basilar artery, ABP and ICP during subarachnoid infusion of saline. During infusion ICP and CCP were significantly correlated (R=0.68; p<0.001), but the magnitude of increase in ICP and CCP during infusion were not correlated to each other. Linear regression between the difference: CCP-ICP (representing a factor due to vasogenic tone) and cerebral perfusion pressure (CPP=ABP-ICP) was highly significant (R=-0.87; p<0.01). Generally, CCP decreased significantly (p<0.05) with hypercarbia, arterial hypotension and after and post-hypoxia and the difference: CCP-ICP decreased consistently after each vasodilatatory manoeuvre studied. Our data confirmed the linear relationship between CCP and ICP, and between the difference: CCP-ICP and cerebrovascular tone. However, because the magnitude of increase in ICP was not correlated to magnitude of change in CCP, CCP cannot be use for detection of increasing ICP quantitatively.     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Characterization of cerebrovascular reactivity after craniectomy for acute brain injury

Analysis of slow waves in arterial blood pressure (ABP) and intracranial pressure (ICP) has been used as an index to describe cerebrovascular pressure-reactivity. It has been previously demonstrated that the pressure-reactivity index (PRx) can be used to reflect global cerebrovascular reactivity with changes in ABP. A positive PRx signifies a positive association between ABP and ICP, indicating a non-reactive vascular bed, while a negative PRx is reflective of intact cerebral autoregulation, where ABP waves provoke inversely correlated waves in ICP. To date, there has been no characterization of pressure-reactivity following decompressive craniectomy. In this prospective observational study, 33 patients who underwent surgery for acute brain injury with mass lesions for which the bone flap was left out were studied. The PRx was calculated as a moving correlation coefficient between 30 consecutive samples of values of ICP and ABP averaged for a period of 10 s. The time profiles of mean PRx values at 6-hourly intervals were analysed and compared with that in seven patients treated by medical therapy alone. The initial mean PRx 6 h after surgery was positive, indicative of disturbed pressure-reactivity. With time, PRx trended towards a more negative value, suggestive of an improving cerebrovascular autoregulatory reserve. The mean PRx 24 h after surgery was 0.28 (+/-0.26), while the mean PRx 72 h after surgery was 0.15 (+/-0.25) (p = 0.012). In contrast, the mean PRx in patients that were not decompressed did not change significantly with time (p = 0.357). Surgery in acute brain injury for which the bone flap is left out in anticipation of raised intracranial pressure in the postoperative period leads to an improved PRx as compared with controls. Craniectomy in this situation may have a contribution to the restoration of disturbed cerebrovascular pressure-reactivity.     

Cerebral blood flow at constant cerebral perfusion pressure but changing arterial and intracranial pressure: relationship to autoregulation

Therapeutic agents for reducing raised intracranial pressure (ICP) may do so at the expense of reduced mean arterial pressure (MAP). As a consequence, cerebral perfusion pressure (CPP) = (MAP - ICP) may not improve. It is unknown whether the level of MAP alters cerebral blood flow (CBF) when MAP and ICP change in parallel so that CPP remains constant. This study investigates CBF at a constant CPP but varying levels of MAP and ICP in 12 anaesthetized cats. CBF was studied at three levels of CPP: 60 (n = 4), 50 (n = 4), and 40 mm Hg (n = 4) under conditions of both intact and impaired autoregulation. At CPP levels of 50 and 60 mm Hg, when autoregulation was intact, CBF remained unchanged. With loss of autoregulation, there was a trend for CBF to increase as MAP and ICP were increased in parallel at a CPP of 50 and 60 mm Hg, although the relationship did not achieve statistical significance. Absolute CBF levels were, however, significantly different between the autoregulating and nonautoregulating groups (p <0.001). At a CPP of 40 mm Hg, CBF showed a linear correlation with blood pressure (BP) (r = 0.57, p <0.05). These results demonstrate that when autoregulation is impaired, there is a functional difference between autoregulating and nonautoregulating cerebral vessels despite similar MAP and CPP. These results also show that at a CPP of 40 mm Hg when autoregulation is impaired, CBF depends more on arterial driving pressure than on CPP.     

The continuous assessment of cerebrovascular reactivity: a validation of the method in healthy volunteers.

Using transcranial Doppler ultrasonography, we investigated the moving correlation between slow waves in arterial blood pressure (ABP) and blood flow velocity (FV) at different levels of cerebrovascular vasodilation provoked by changing PETCO2. Fourteen healthy volunteers were examined. The FV in middle cerebral arteries, PETCO2, and ABP were recorded during normocapnia, hypercapnia, and hypocapnia. The moving correlation coefficients between ABP and mean FV (FVm) or systolic FV (FVs) during spontaneous fluctuations in ABP were calculated for 3-min epochs and averaged for each investigation, thus yielding the mean index (Mx) and systolic index (Sx). As a reference method, Aaslid's cuff tests were performed to obtain the rate of regulation (RoR). RoR, Mx, and Sx significantly depended on PETCO2 (analysis of variance, P < 0.00001). At high PETCO2, cerebrovascular reactivity was disturbed as reflected in RoR values of < 0.17/s for all volunteers and increased values of Mx (> 0.4 in 86% of volunteers) and Sx (> 0.2 in 79% of volunteers). Overall, there was a reasonably good correlation of both Mx and Sx with RoR (R2 = 0.65 and 0.58, respectively). IMPLICATIONS: Indices derived from the correlation between spontaneous fluctuations of blood flow velocity wave form and arterial blood pressure may be used for the noninvasive continuous monitoring of cerebrovascular reactivity.     

Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study.

OBJECT: Contemporary management of head-injured patients is based on assumptions about CO2 reactivity, pressure autoregulation (PA), and vascular reactivity to pharmacological metabolic suppression. In this study, serial assessments of vasoreactivity of the middle cerebral artery (MCA) were performed using bilateral transcranial Doppler (TCD) ultrasonography. METHODS: Twenty-eight patients (mean age 33 +/- 13 years, median Glasgow Coma Scale score of 7) underwent a total of 61 testing sessions during postinjury Days 0 to 13. The CO2 reactivity (58 studies in 28 patients), PA (51 studies in 23 patients), and metabolic suppression reactivity (35 studies in 16 patients) were quantified for each cerebral hemisphere by measuring changes in MCA velocity in response to transient hyperventilation, arterial blood pressure elevation, or propofol-induced burst suppression, respectively. One or both hemispheres registered below normal vasoreactivity scores in 40%, 69%, and 97% of study sessions for CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.0001), respectively. Intracranial hypertension, classified as intracranial pressure (ICP) greater than 20 mm Hg at the time of testing, was associated with global impairment of CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.05). A low baseline cerebral perfusion pressure (CPP) was also predictive of impaired CO2 reactivity and PA (p < 0.01). Early postinjury hypotension or hypoxia was also associated with impaired CO2 reactivity (p < 0.05), and hemorrhagic brain lesions in or overlying the MCA territory were predictive of impaired metabolic suppression reactivity (p < 0.01). The 6-month Glasgow Outcome Scale score correlated with the overall degree of impaired vasoreactivity (p < 0.05). CONCLUSIONS: During the first 2 weeks after moderate or severe head injury, CO2 reactivity remains relatively intact, PA is variably impaired, and metabolic suppression reactivity remains severely impaired. Elevated ICP appears to affect all three components of vasoreactivity that were tested, whereas other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state of vasoreactivity. Incorporation of TCD ultrasonography-derived vasoreactivity data may facilitate more injury- and time-specific therapies for head-injured patients.     

短期应用高渗盐水对重症蛛网膜下腔出血患者颅内压、脑血流量的影响

目的 探讨23.4%高渗盐水(HTS)对重症蛛网膜下腔出血(SAH)患者颅内压、脑灌注压、脑血流量(CBF)的影响.方法 16例重症SAH患者(GCS≤8分)在颅压升高时接受静脉输注23.4%HTS,监测用药前及用药后30、60、90、120、150、180 min的颅内压(ICP),平均动脉压(MAP),脑灌注压(CPP)及脑血流速度(FV).结果 用药后30 min可见ICP显著降低,同时MAP、CPP及FV显著升高(P<0.05),ICP显著降低可持续180 min,CPP和FV的改善持续约90 min(P<0.05).结论 HTS能显著降低重症SAH患者的ICP,改善脑组织灌注,可用来纠正脑缺血引起的病生理变化.     

Arterio-jugular difference of oxygen and intracranial pressure in comatose, head injured patients. II. Clinical correlations]

The ICP monitoring is currently used in the treatment of the head injured patients in order to avoid dangerous increases of the pressure and critical reduction of cerebral perfusion pressure (CPP). The cerebral blood flow is dependent on the CPP and is kept constant, under normal circumstances, by autoregulation. When autoregulation is impaired or overwhelmed oxygen delivery becomes uncoupled to the metabolic needs of cerebral tissue: in such a condition the rate of oxygen extraction changes and the artero-jugular difference for O2 (AVDO2) reflects this change. The AVDO2 can be used as an estimate of the CBF and can detect a situation of hyperemia (low AVDO2) or ischemia (high AVDO2). In 224 comatose head injured patients the ICP was measured using ventricular or subarachnoid catheters: the CPP was continuously assessed and the outcome was evaluated six months after the trauma. In 45 patients the AVDO2 was studied and the data were corrected for a PaCO2 of 40 mmHg and investigated. The severity of the ICP is decisive for the prognosis and, accordingly, the number of times the CPP is below 60 mmHg plays a major role in the outcome. The mortality rate was 21% for the patients without ICP greater than 20 mmHg and 54% for the patients with severe increases in ICP. The mean values of AVDO2 were low, ranging around 4.6 vol%; only 4 patients showed some temporary evidence of ischemia, as assessed by an AVDO2 greater than 8 vol%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictive value of initial computerized tomography scan, intracranial pressure, and state of autoregulation in patients with traumatic brain injury

OBJECT: The authors explored the relationship between computerized tomography (CT) scan findings and intracranial pressure (ICP) measurements obtained in the first 24 hours of monitoring to identify parameters predicting outcome in patients with severe traumatic brain injury (TBI). METHODS: Intracranial pressure, mean arterial blood pressure, cerebral perfusion pressure (CPP), and pressure reactivity index were measured continuously in 126 patients with severe TBI who were admitted to a neuroscience critical care unit. Mean values in the initial 24 hours of monitoring and in the total period of monitoring were compared with types of injury categorized on the basis of the initial CT scan according to the classification of Marshall, et al., and with Glasgow Outcome Scale scores. The initial CT scan classification correlated significantly but weakly with ICP measured during the first 24 hours of monitoring (p = 0.036) but not with mean ICP over the total time of intensive care. Both midline shift and the ratio of frontal horn diameter to internal diameter correlated with ICP in the first 24 hours (p < 0.007) and with ICP over the total monitoring period (p < 0.03). Outcome score correlated with initial CT scan findings (p = 0.018), ICP over the total monitoring period (p < 0.0023), pressure reactivity over the total monitoring period (p < 0.0002), and pressure reactivity in the first 24 hours (p < 0.0001) but not with ICP in the first 24 hours. Patients with disturbed pressure reactivity in the first 24 hours after injury had a significantly higher mortality rate than patients with intact pressure reactivity (28.6% compared with 9.5%; p < 0.001). CONCLUSIONS: Patients with severe TBI who have early loss of autoregulation have a worse prognosis. Mean ICP values in patients with diffuse TBI cannot be predicted by using the Marshall CT scan classification.     

Cerebral hemodynamic responses to blood pressure manipulation in severely head-injured patients in the presence or absence of intracranial hypertension

The management of cerebral perfusion pressure (CPP) remains a controversial issue in the critical care of severely head-injured patients. Recently, it has been proposed that the state of cerebrovascular autoregulation should determine individual CPP targets. To find optimal perfusion pressure, we pharmacologically manipulated CPP in a range of 51 mm Hg (median; 25th-75th percentile, 48-53 mm Hg) to 108 mm Hg (102-112 mm Hg) on Days 0, 1, and 2 after severe head injury in 13 patients and studied the effects on intracranial pressure (ICP), autoregulation capacity, and brain tissue partial pressure of oxygen. Autoregulation was expressed as a static rate of regulation for 5-mm Hg CPP intervals based on middle cerebral artery flow velocity. When ICP was normal (26 occasions), there were no major changes in the measured variables when CPP was altered from a baseline level of 78 mm Hg (74-83 mm Hg), indicating that the brain was within autoregulation limits. Conversely, when intracranial hypertension was present (11 occasions), CPP reduction to less than 77 mm Hg (73-82 mm Hg) further increased ICP, decreased the static rate of regulation, and decreased brain tissue partial pressure of oxygen, whereas a CPP increase improved these variables, indicating that the brain was operating at the lower limit of autoregulation. We conclude that daily trial manipulation of arterial blood pressure over a wide range can provide information that may be used to optimize CPP management.     

Intérêt du doppler transcrânien dans la prise en charge des traumatisés crâniens graves

Transcranial doppler ultrasonography (TCD) is a non invasive technique for the assessment of cerebral blood flow (CBF). The aim of this prospective study was to evaluate the benefit of TCD for the monitoring of major head trauma patients. Therefore 10 of such patients, aged 17 to 37 years, had a TCD at admission and subsequently at least twice a day. Following data were measured simultaneously at the site of the right and the left middle cerebral arteries : the systolic (SV), diastolic (DV) and mean (MV) blood velocity, the resistance index (RI) of Pourcelot (RI = SV − DV/SV) and the pulsatility index (PI) of Gosling (PI = SV − DV/MV). Simultaneously, the mean intracranial pressure (ICP) obtained with a subarachnoid probe, the PaCO2 and the mean arterial pressure (Pa) were measured. The cerebral perfusion pressure (CPP) was calculated with the formula : CPP = Pa − ICP. A total of 132 measures were analysed. There was a linear relation between RI and CPP (r = 0.566 ; p < 0.001), between RI and ICP (r = 0.822 ; p < 0.001), as well as between PI and CPP (r = 0.563 ; p < 0.001) and between PI and ICP (r = 0.837 ; p < 0.001). In the opposite there was no statistically significant relation between ICP and MV (r = 0.18) nor between CPP and MV (r = 0.23). However, a MV over 100 cm · s⁻¹ was regularly associated with a ICP over 60 mmHg. The close correlation between RI, PI and ICP allows to use RI or PI to estimate ICP. Since this evaluation can be obtained non invasely, this possibility is important for the clinician, despite the lack of correlation between MV and ICP. The measurement of MV provides an estimated value of CBF in patients with steady Pa and steady Paco₂. The TCD allows the allocation of head trauma patients with high ICP or RI into two groups : a first group with a low MV, in which hyperventilation and barbiturates may cause cerebral ischaemia by a further decrease of CBF ; a second group with a normal or increased MV and for which these treatments can be administered. Multimodal monitoring should be used more and more in severely head injured patients, to allow such situations to be identified.     

Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: validation and utility

A moving correlation index (Mx-CPP) of cerebral perfusion pressure (CPP) and mean middle cerebral artery blood flow velocity (CBFV) allows continuous monitoring of dynamic cerebral autoregulation (CA) in patients with severe traumatic brain injury (TBI). In this study we validated Mx-CPP for TBI, examined its prognostic relevance, and assessed its relationship with arterial blood pressure (ABP), CPP, intracranial pressure (ICP), and CBFV. We tested whether using ABP instead of CPP for Mx calculation (Mx-ABP) produces similar results. Mx was calculated for each hemisphere in 37 TBI patients during the first 5 days of treatment. All patients received sedation and analgesia. CPP and bilateral CBFV were recorded, and GOS was estimated at discharge. Both Mx indices were calculated from 10,000 data points sampled at 57.4Hz. Mx-CPP > 0.3 indicates impaired CA; in these patients CPP had a significant positive correlation with CBFV, confirming failure of CA, while in those with Mx < 0.3, CPP was not correlated with CBFV, indicating intact CA. These findings were confirmed for Mx-ABP. We found a significant correlation between impaired CA, indicated by Mx-CPP and Mx-ABP, and poor outcome for TBI patients. ABP, CPP, ICP, and CBFV were not correlated with CA but it must be noted that our average CPP was considerably higher than in other studies. This study confirms the validity of this index to demonstrate CA preservation or failure in TBI. This index is also valid if ABP is used instead of CPP, which eliminates the need for invasive ICP measurements for CA assessment. An unfavorable outcome is associated with early CA failure. Further studies using the Mx-ABP will reveal whether CA improves along with patients' clinical improvement.     

Hemodynamic characterization of intracranial pressure plateau waves in head-injury patients.

OBJECT: Plateau waves of intracranial pressure (ICP) are often recorded during intensive care monitoring of severely head injured patients. They are traditionally interpreted as meaningful secondary brain insults because of the dramatic decrease in cerebral perfusion pressure (CPP). The aim of this study was to investigate both the hemodynamic profile and the clinical consequences of plateau waves. METHODS: One hundred sixty head-injured patients were studied using continuous monitoring of ICP; almost 20% of these patients exhibited plateau waves. In 96 patients arterial pressure, ICP, and transcranial Doppler (TCD) blood flow velocity were studied daily for 20 minutes to 3 hours. Sixteen episodes of plateau waves in eight patients were recorded and analyzed. The dramatic increase in ICP was followed by a profound fall in CPP (by 45%). In contrast, flow velocity fell by only 20%. Autoregulation was documented to be intact both before and after plateau but was disturbed during the wave (p < 0.05). Pressure-volume compensatory reserve was always depleted before the wave. Cerebrovascular resistance decreased during the wave by 60% (p < 0.05) and TCD pulsatility increased (p < 0.05). Plateau waves did not increase the probability of an unfavorable outcome following injury. CONCLUSIONS: The authors have confirmed that the plateau waves are a hemodynamic phenomenon associated with cerebrovascular vasodilation. They are observed in patients with preserved cerebral autoregulation but reduced pressure-volume compensatory reserve.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients.

The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head position in the care of head-injured patients. The effect of 0 degree and 30 degrees head elevation on ICP, CPP, CBF, mean carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30 degrees than at 0 degrees (84.3 +/- 14.5 mm Hg vs. 89.5 +/- 14.6 mm Hg), as was the mean ICP (14.1 +/- 6.7 mm Hg vs. 19.7 +/- 8.3 mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen, arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position. The data indicate that head elevation to 30 degrees significantly reduced ICP in the majority of the 22 patients without reducing CPP or CBF.