Cerebral Perfusion Pressure Levels Research Articles

Changes in neurovascular coupling with cerebral perfusion pressure indicate a link to cerebral autoregulation

Cerebral autoregulation ensures a stable average blood supply to brain tissue across steady state cerebral perfusion pressure (CPP) levels. Neurovascular coupling, in turn, relies on sufficient blood flow to meet neuronal demands during activation. These mechanisms break down in pathologies where extreme levels of CPP can cause dysregulation in cerebral blood flow. Here, we experimentally tested the influence of changes in CPP on neurovascular coupling in a hydrocephalus-type non-human primate model (n = 3). We recorded local neural and vascular evoked responses to a checkerboard visual stimulus, non-invasively, using electroencephalography and near-infrared spectroscopy respectively. The evoked signals showed changes in various waveform features in the visual evoked potentials and the hemodynamic responses, with CPP. We further used these signals to fit for a hemodynamic response function (HRF) to describe neurovascular coupling. We estimated n = 26 distinct HRFs at a subset of CPP values ranging from 40–120 mmHg across all subjects. The HRFs, when compared to a subject dependent healthy baseline (CPP 70–90 mmHg) HRF, showed significant changes in shape with increasing CPP (ρCPP = −0.55, p-valueCPP = 0.0049). Our study provides preliminary experimental evidence on the relationship between neurovascular coupling and CPP changes, especially when beyond the limits of static autoregulation.

A novel wireless optical technique for quantitative evaluation of cerebral perfusion pressure in a fluid percussion animal model of traumatic brain injury.

Cerebral perfusion pressure (CPP) calculated by mean arterial pressure (MAP) minus intracranial pressure (ICP) is related to blood flow into the brain and reflects cerebral ischemia and oxygenation indirectly. Near-infrared spectroscopy (NIRS) can assess cerebral ischemia and hypoxia non-invasively and has been widely used in neuroscience. However, the correlation between CPP and NIRS, and its potential application in traumatic brain injury, has seldom been investigated. We used a novel wireless NIRS system and commercial ICP and MAP devices to assess the trauma to rat brains using different impact intensity. The relationship between CPP and NIRS parameters with increasing impact strength were investigated. The results showed that changes in CPP (∆CPP), oxy-hemoglobin {∆[HbO2]}, total-hemoglobin {∆[HbT]}, and deoxy-hemoglobin were inversely proportional to the increase in impact intensity, and the correlations between ∆CPP, NIRS parameters {∆[HbO2], and ∆[HbT]} were significant. The NIRS system can assess cerebral ischemia and oxygenation non-invasively and changes of HbO2 and HbT may be used as reference parameters to assess the level of CPP in an animal model of traumatic brain injury.

Safety of apnea testing for the diagnosis of brain death: a comprehensive study on neuromonitoring data and blood gas analysis.

Here, we studied the safety of apnea testing (AT) for the determination of brain death with regard to intracranial pressure (ICP), cerebral perfusion and arterial blood gas parameters. We hypothesized that ICP only increases when cerebral perfusion pressure (CPP) remains positive during AT. A total of 34 patients who fulfilled brain death criteria were identified by chart review (2009-2017). We analysed ICP, CPP and mean arterial pressure (MAP) prior to AT, during AT and after AT, as well as arterial pH, paCO2 , paO2 and arterial O2 saturation at the start and end of AT. Intracranial pressure was 87.9±17.7mmHg (mean±SD) prior to AT, 89.9±17.2mmHg during AT and 86.4±15.2mmHg after AT (P=0.9). CPP was -6.9±12.8mmHg prior to AT, -7.1±13.7mmHg during AT and -8.6±13.0mmHg after AT (P=0.98), respectively. MAP was 82.9±14.6mmHg prior to AT, 84.7±13.9mmHg during AT and 79.7±9.6mmHg after AT (P=0.57), respectively. A total of 10 patients had positive CPP (8.6±4.3mmHg), but ICP did not increase during AT. Arterial pH decreased from 7.43±0.06 to 7.22±0.06 (P<0.05), paCO2 increased from 38.6±4.2 to 69.6±8.0mmHg (P<0.05), paO2 decreased from 416.3±113.4 to 289.2±146.5mmHg (P<0.05), and O2 saturation was stable at 99.8±0.4% and 98.2±3.2% (P=0.39). Apnea testing had no detrimental effect on ICP, CPP, MAP or oxygenation, regardless of the presence of an initially positive CPP. The lack of further ICP elevations is presumably explained by critical closing pressures above individual CPP levels during AT.

Time spent with impaired autoregulation is linked with outcome in severe infant/paediatric traumatic brain injury.

It could be shown in traumatic brain injury (TBI) in adults that the functional status of cerebrovascular autoregulation (AR), determined by the pressure reactivity index (PRx), correlates to and even predicts outcome. We investigated PRx, cerebral perfusion pressure (CPP) and intracranial pressure (ICP) and their correlation to outcome in severe infant and paediatric TBI. Seventeen patients (range, 1day to 14years) with severe TBI (median GCS at presentation, 4) underwent long-term computerised ICP and mean arterial pressure (MAP) monitoring using dedicated software to determine CPP and PRx and optimal CPP (CPP level where PRx shows best autoregulation) continuously. Outcome was determined at discharge and at follow-up using the Glasgow Outcome Scale. Favourable outcome was reached in eight patients, unfavourable outcome in seven patients. Two patients died. Nine patients underwent decompressive craniectomy to control ICP during Intensive Care Unit treatment. When dichotomised to outcome, no significant difference was found for overall ICP, CPP and PRx. The time with severely impaired AR (PRx>0.2) was significantly longer for patients with unfavourable outcome (64h vs 6h, p=0.001). Continuously impaired AR of ≥24h and age<1year was associated to unfavourable outcome. Children with favourable outcome spent the entire monitoring time at or above the optimal CPP. Integrity of AR has a similar role for outcome after TBI in the paediatric population as in adults. The amount of time spent with deranged AR seems to be associated with outcome; a factor especially critical for infant patients. The results of this preliminary study need to be validated in the future.

Novel Noninvasive Method of Cerebrovascular Blood Volume Assessment Using Brain Bioimpedance.

Cerebrovascular autoregulation (CAR) is the ability of vessels to modulate their tone in response to changes in pressure. As an auto-protective mechanism, CAR is critical in preventing secondary brain injury post-trauma. Monitoring of changes in cerebral blood volume might be valuable in evaluating CAR and response to various therapies. In this study, we utilized an ocular-brain bioimpedance interface to assess real time changes in cerebral blood volume in response to a number of physiological challenges. We hypothesize that changes in brain bioimpedance (dz) would track changes in cerebral blood volume. Anesthetized animals were instrumented for monitoring of intracranial pressure (ICP), mean arterial blood pressure, cerebral perfusion pressure (CPP) and cerebral blood flow (CBF). Bioimpedance was monitored continuously through electrocardiographic electrodes placed over the eyelids. Interventions such as hyperventilation, vasopressor administration, creation of an epidural hematoma, and systemic hemorrhage were used to manipulate levels of ICP, CPP, and CBF. The dz correlated with changes in ICP, CPP, and CBF (r = -0.72 to -0.88, p < 0.0001). The receiver operating characteristic for dz at different thresholds of CPP and CBF showed high impedance performance with area under the curve between 0.80-1.00 (p < 0.003) and sensitivity and specificity varying between 83%-100% and 70%-100%, respectively. Our preliminary tests show that brain bioimpedance as measured through the ocular-brain interface tracks changes in CPP and CBF with high precision and may prove to be valuable in the future in assessing changes in cerebral blood volume and CAR.

Superior Sagittal Sinus Obstruction by Giant Meningiomas: Is Total Removal Feasible?

To present our experience with microsurgical technique for patients with giant meningiomas (maximum diameter ≥7 cm) that obstruct the superior sagittal sinus (SSS). All patients who were preoperatively diagnosed (between 2010 and 2014) with giant meningiomas involving the SSS in Ward 10 at the Neurosurgery Department of Beijing Tiantan Hospital were enrolled in this study. Patient charts, imaging findings, and outcomes were examined. The study included 6 male and 4 female patients with a mean age of 46.8 ± 10.7 years. The tumor sizes varied from 7 to 12 cm (mean, 8.8 ± 2.0 cm). All patients underwent customized craniotomies, and aggressive surgery for resection of the invaded SSS was performed. Simpson grade I removals were achieved in all cases. No cases of perioperative mortality occurred. Three patients required cranioplasty as a result of a decompressive craniectomy that was performed during the primary surgery. Histologic examinations showed 1 malignant and 9 benign meningiomas. During the follow-up period (mean, 29.0 ± 9.7 months), recurrence/progression occurred in 1 patient, and 1 patient was lost to follow-up. The recent Karnofsky Performance Score was 80 ± 32.3 and was improved in 5 patients and stabilized in 3 patients. In addition, 7 patients lived independently. The rigorous preservation of cortical veins, draining veins, and eloquent areas should be implemented during the resection of large tumors that obstruct the SSS. Suitable individualized approaches associated with full exposure and low cerebral perfusion pressure levels after surgery are critical for favorable results, and the reconstruction of the SSS may not be necessary.

The correlation between brain near-infrared spectroscopy and cerebral blood flow in piglets with intracranial hypertension.

Cerebral perfusion pressure (CPP) is used as a surrogate for measurement of cerebral blood flow (CBF) but its determination requires that intracranial pressure be directly measured. Near-infrared spectroscopy (NIRS) can noninvasively measure tissue oxygenation. We hypothesized that NIRS would correlate well with CBF, with cerebral metabolism of oxygen (CMRO2) and glucose and with lactate production as CPP was reduced. Seven anesthetized piglets were subjected to reductions in CPP to 60, 50, 40, 30, and 20 mmHg by infusing an artificial cerebral spinal fluid into the lateral ventricle of the brain. After a period of equilibration, NIRS over the left temporal cortex and regional CBF (microspheres) were measured at each CPP level as well as arterial and internal jugular PaO2 , glucose, and lactate. CMRO2 and glucose consumption and lactate production were calculated by standard formulae. NIRS correlated very well (P < 0.05) with CBF in the left temporal cortex [mean r (95% CI) = 0.95 (0.91-0.99)] and with left hemispheric CMRO2 [0.94 (0.90-0.98)], glucose consumption [0.87 (0.76-0.97)], and lactate production [0.89 (0.81-0.97)]. The correlation of NIRS with CBF was slightly better (P < 0.05) than that of CPP with CBF [0.89 (0.84-0.94)]. In this model of global cerebral hypertension, NIRS correlated well with CBF and measures of cerebral metabolism, and might be useful as a surrogate for CPP. Further studies are warranted to determine if NIRS is associated with these variables in focal cerebral injury.

Clinical and Physiological Events That Contribute to the Success Rate of Finding "Optimal" Cerebral Perfusion Pressure in Severe Brain Trauma Patients.

Recently, a concept of an individually targeted level of cerebral perfusion pressure that aims to restore impaired cerebral vasoreactivity has been advocated after traumatic brain injury. The relationship between cerebral perfusion pressure and pressure reactivity index normally is supposed to have a U-shape with its minimum interpreted as the value of "optimal" cerebral perfusion pressure. The aim of this study is to investigate the relation between the absence of the optimal cerebral perfusion pressure curve and physiological variables, clinical factors, and interventions. Retrospective analysis of prospectively collected data. Neurocritical care units in two university centers. Between May 2012 and December 2013, a total of 48 traumatic brain injury patients were studied with real-time annotation of predefined clinical events. None. All patients had continuous monitoring of arterial blood pressure, intracranial pressure, and cerebral perfusion pressure, with real-time calculations of pressure reactivity index and optimal cerebral perfusion pressure using ICM+ software (Cambridge Enterprise, University of Cambridge, Cambridge, UK). Selected clinical events were inserted on a daily basis, including changes in physiological variables, sedativeanalgesic drugs, vasoactive drugs, and medical/surgical therapies for intracranial hypertension. The collected data were divided into 4-hour periods, with the primary outcome being absence of the optimal cerebral perfusion pressure curve. For every period, mean values (± SDs) of arterial blood pressure, intracranial pressure, pressure reactivity index, and other physiological variables were calculated; clinical events were organized using predefined scales. In 28% of all 1,561 periods, an optimal cerebral perfusion pressure curve was absent. A generalized linear mixed model with binary logistic regression was fitted. Absence of slow arterial blood pressure waves (odds ratio, 2.7; p < 0.001), higher pressure reactivity index values (odds ratio, 2.9; p < 0.001), lower amount of sedative-analgesic drugs (odds ratio, 1.9; p = 0.03), higher vasoactive medication dose (odds ratio, 3.2; p = 0.02), no administration of maintenance neuromuscular blockers (odds ratio, 1.7; p < 0.01), and following decompressive craniectomy (odds ratio, 1.8; p < 0.01) were independently associated with optimal cerebral perfusion pressure curve absence. This study identified six factors that were independently associated with absence of optimal cerebral perfusion pressure curves.

Adherence to guidelines for management of cerebral perfusion pressure and outcome in patients who have severe traumatic brain injury

PurposeThe aims of this study are to assess adherence to the Brain Trauma Foundation (BTF) cerebral perfusion pressure (CPP) guidelines and to determine if adherence is associated with mortality in patients who have a severe traumatic brain injury. Materials and methodsRetrospective cohort study of 127 patients admitted to one intensive care unit between 2006 and 2012. Adherence to BTF guidelines was measured as the time that the CPP was within 50 to 70 mm Hg divided by the total time of CPP monitoring (CPP time index). ResultsThe percentage of time that the CPP was within the recommended range was 31.6% (SD, 22.2); CPP was greater than 70 mm Hg for 63.9% (SD, 26.2) of the time and less than 50 mm Hg for 4.5% of the time (SD, 16.3). After adjustment for covariates, CPP time index (between 50 and 70 mm Hg) was not associated with hospital mortality (odds ratio [OR], 1.2; 95% confidence interval [CI], 0.98-1.6; P= .079). The time indices for CPP ≥70 and <50 mm Hg were associated with decreased (OR, 0.66; 95%CI, 0.52-0.82; P< .0001) and increased (OR, 9.9; 95% CI, 1.4-69.6; P= .021) mortality, respectively. ConclusionCerebral perfusion pressure was greater than 70 mm Hg for most of the time. This level of CPP was associated with decreased hospital mortality.

Brain tissue oxygenation and cerebral metabolic patterns in focal and diffuse traumatic brain injury.

Introduction: Neurointensive care of traumatic brain injury (TBI) patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted protocols. There are reasons to believe that knowledge of brain tissue oxygenation (BtipO2) would add information with the potential of improving patient outcome. The aim of this study was to examine BtipO2 and cerebral metabolism using the Neurovent-PTO probe and cerebral microdialysis (MD) in TBI patients.Methods: Twenty-three severe TBI patients with monitoring of physiological parameters, ICP, CPP, BtipO2, and MD for biomarkers of energy metabolism (glucose, lactate, and pyruvate) and cellular distress (glutamate, glycerol) were included. Patients were grouped according to injury type (focal/diffuse) and placement of the Neurovent-PTO probe and MD catheter (injured/non-injured hemisphere).Results: We observed different patterns in BtipO2 and MD biomarkers in diffuse and focal injury where placement of the probe also influenced the results (ipsilateral/contralateral). In all groups, despite fairly normal levels of ICP and CPP, increased MD levels of glutamate, glycerol, or the L/P ratio were observed at BtipO2 <5 mmHg, indicating increased vulnerability of the brain at this level.Conclusion: Monitoring of BtipO2 adds important information in addition to traditional ICP and CPP surveillance. Because of the different metabolic responses to very low BtipO2 in the individual patient groups we submit that brain tissue oximetry is a complementary tool rather than an alternative to MD monitoring.

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

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. 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. 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). 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.

Quelle pression de perfusion cérébrale après traumatisme crânien chez l’enfant ?

The management of cerebral perfusion pressure (CPP) is the one of the main preoccupation for the care of paediatric traumatic brain injury (TBI). The physiology of cerebral autoregulation, CO2 vasoreactivity, cerebral metabolism changes with age as well as the brain compliance. Low CPP leads to high morbidity and mortality in pediatric TBI. The recent guidelines for the management of CPP for the paediatric TBI indicate a CPP threshold 40–50mmHg (infants for the lower and adolescent for the upper). But we must consider the importance of age-related differences in the arterial pressure and CPP. The best CPP is the one that allows to avoid cerebral ischaemia and oedema. In this way, the adaptation of optimal CPP must be individual. To assess this objective, interesting tools are available. Transcranial Doppler can be used to determine the best level of CPP. Other indicators can predict the impairment of autoregulation like pressure reactivity index (PRx) taking into consideration the respective changes in ICP and CPP. Measurement of brain tissue oxygen partial pressure is an other tool that can be used to determine the optimal CPP.

The Neurological Wake-up Test Does not Alter Cerebral Energy Metabolism and Oxygenation in Patients with Severe Traumatic Brain Injury

The neurological wake-up test (NWT) is used to monitor the level of consciousness in patients with traumatic brain injury (TBI). However, it requires interruption of sedation and may elicit a stress response. We evaluated the effects of the NWT using cerebral microdialysis (MD), brain tissue oxygenation (PbtiO2), jugular venous oxygen saturation (SjvO2), and/or arterial-venous difference (AVD) for glucose, lactate, and oxygen in patients with severe TBI. Seventeen intubated TBI patients (age 16-74 years) were sedated using continuous propofol infusion. All patients received intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring in addition to MD, PbtiO2 and/or SjvO2. Up to 10 days post-injury, ICP, CPP, PbtiO2 (51 NWTs), MD (49 NWTs), and/or SjvO2 (18 NWTs) levels during propofol sedation (baseline) and NWT were compared. MD was evaluated at a flow rate of 1.0 μL/min (28 NWTs) or the routine 0.3 μL/min rate (21 NWTs). The NWT increased ICP and CPP levels (p < 0.05). Compared to baseline, interstitial levels of glucose, lactate, pyruvate, glutamate, glycerol, and the lactate/pyruvate ratio were unaltered by the NWT. Pathological SjvO2 (<50 % or >71 %; n = 2 NWTs) and PbtiO2 (<10 mmHg; n = 3 NWTs) values were rare at baseline and did not change following NWT. Finally, the NWT did not alter the AVD of glucose, lactate, or oxygen. The NWT-induced stress response resulted in increased ICP and CPP levels although it did not negatively alter focal neurochemistry or cerebral oxygenation in TBI patients.

Guiding value of brain tissue oxygenation plus intracranial pressure monitoring in severe traumatic brain injury patients

To elucidate the effectiveness of brain tissue oxygenation (PbtO2) plus intracranial pressure (ICP) monitoring and targeted therapy in patients of severe traumatic brain injury (TBI). A total of 46 patients with severe TBI (Glasgow coma scale, GCS scale ≤ 8) admitted at Jiangyin People's Hospital from June 2009 to June 2012 were divided randomly into 2 groups and evaluated prospectively.Patients undergoing ICP plus PbtO2 monitoring were compared with controls with ICP monitoring alone.Therapies of both patient groups were attempted to maintain an ICP < 20 mm Hg and a cerebral perfusion pressure (CPP) ≥ 60 mm Hg.Among those with PbtO2 monitoring, oxygenation was maintained at a level of ≥ 20 mm Hg.The scores of Glasgow outcome scale (GOS) were compared between two groups at Month 6 post-injury. The mean daily ICP and CPP levels were similar in each group.The mortality rate was 21.7% in patients with ICP monitoring alone and the favorable outcome rate was 47.8%.However, those receiving combined management had a significantly reduced mortality rate of 8.7% and good outcome rate of 65.2% (P < 0.05). The combined use of both ICP and PbtO2 may be associated with reduced mortality and improved outcome in patients with severe TBI.

Clinical significant and changes of brain tissue partial pressure of oxygen in the course of mild hypothermia with severe traumatic brain injury

Objective To investigate clinical significant and changes of brain tissue partial pressure of oxygen (Pbt O2 ) in the course of mild hypothermia treatment (MHT) of severe traumatic brain injury (sTBI).Methods There were 38 sTBI cases with mild hypothermia treatment in the course.Pbt O2,intracranial pressure (ICP),jugularn venous oxygen saturation (SjvO2 ),and cerebral perfusion pressure (CPP) were continuously monitored for analyzing the correlations insides,and clinical outcomes were valued using the Glasgow Outcome Scale score (GOSs).Results Of 38 patients with sTBI,increasing PbtO2,Sjv O2,CPP and decreasing ICP were found obviously from the begin of MHT. There was negative linear correlation between PbtO2 and ICP.Otherwise,there was positive linear correlation between PbtO2 and SjvO2.Monitoring process which CPP and Sjv O2 levels were under normal circumstances,there were still a large proportion of patients with low PbtO2 situation after MHT.Conclusions Continuous monitoring of PbtO2 can reflect the condition of regional cerebral oxygen metabolism and guide treatment and predicting outcome. Key words: Traumatic brain injury; Mild hypothermia; Brain tissue partial pressure of oxygen

Abstract 22: Increased Cerebral Perfusion Pressure Delays the Microvascular Shunting and Tissue Hypoxia in the Rat Brain at High ICP in a Time Dependent Manner

Background: We reported earlier that high intracranial pressure (ICP) in rats is associated with tissue hypoxia and brain edema due to a transition from capillary (CAP) to thoroughfare channel (TFC) non-nutritive shunt flow. Recently we showed that increasing cerebral perfusion pressure (CPP) shifts the transition threshold to a higher ICP. Here we studied the time dependence of the transition to TFC shunt flow at high ICP to determine how long the increased CPP could delay the transition from CAP to TFC shunting Methods: ICP was increased and maintained at 20, 40 or 60 mmHg for three hours by raising an artificial cerebrospinal fluid reservoir connected to a catheter in the cisterna magna while MAP was elevated by i.v. dopamine infusion to keep CPP at 60 or 80 mmHg. Using in vivo 2-photon laser scanning microscopy through a cranial window over the rat parietal cortex, we measured microvascular red blood cells flow velocity (by fluorescein dye) and tissue oxygenation (NADH fluorescence). CAP flow = microvessel flow velocities &lt; 1.0 and TFC shunt flow = microvessel flow velocities &gt;1.0 mm/sec. Doppler flow, rectal and cranial temperatures, ICP, arterial blood pressure and arterial blood gases were monitored. Results: Maintenance of CPP at 60 mmHg even at a moderate ICP of 20 mmHg did not prevent a gradual increase in microvascular shunting and tissue hypoxia over 3 hours. However, a CPP of 80 mmHg prevented the transition from CAP to TFC shunting at an ICP of 20 mmHg ( Fig. 1 , p&lt;0.05). At ICP of 40 and 60 mmHg and CPP of 60 and 80 mmHg there was a gradual decrease in the CAP/TFC ratio (increased microvascular TFC shunting) and rise in NADH with time. However at a CPP of 80 mmHg, the gradual increase occurred at later time points and was less detrimental than at CPP of 60 mmHg ( Fig. 1 , p&lt;0.05). Conclusions: Increasing CPP with raised ICP could prevent the transition from CAP to TFC shunt flow and tissue hypoxia for a duration that depends upon the level of CPP. Thus, the transition to shunt flow at a given raised ICP and sustained CPP is time dependent. Our data suggest that increasing CPP above the clinical guideline of 50 to 60 mmHg may be beneficial at high ICP.

Cerebral perfusion pressure, microdialysis biochemistry and clinical outcome in patients with traumatic brain injury

BackgroundTraumatic Brain Injury (TBI) is a major cause of death and disability. It has been postulated that brain metabolic status, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are related to patients' outcome. The aim of this study was to investigate the relationship between CPP, ICP and microdialysis parameters and clinical outcome in TBIs.ResultsThirty four individuals with severe brain injury hospitalized in an intensive care unit participated in this study. Microdialysis data were collected, along with ICP and CPP values. Glasgow Outcome Scale (GOS) was used to evaluate patient outcome at 6 months after injury. Fifteen patients with a CPP greater than 75 mmHg, L/P ratio lower than 37 and Glycerol concentration lower than 72 mmol/l had an excellent outcome (GOS 4 or 5), as opposed to the remaining 19 patients. No patient with a favorable outcome had a CPP lower than 75 mmHg or Glycerol concentration and L/P ratio greater than 72 mmol/l and 37 respectively. Data regarding L/P ratio and Glycerol concentration were statistically significant at p = 0.05 when patients with favorable and unfavorable outcome were compared. In a logistic regression model adjusted for age, sex and Glasgow Coma Scale on admission, a CPP greater than 75 mmHg was marginally statistically significantly related to outcome at 6 months after injury.ConclusionsPatients with favorable outcome had certain common features in terms of microdialysis parameters and CPP values. An individualized approach regarding CPP levels and cut -off points for Glycerol concentration and L/P ratio are proposed.

Cerebral Perfusion Pressure Thresholds for Brain Tissue Hypoxia and Metabolic Crisis After Poor-Grade Subarachnoid Hemorrhage

To identify a minimally acceptable cerebral perfusion pressure threshold above which the risks of brain tissue hypoxia (BTH) and oxidative metabolic crisis are reduced for patients with subarachnoid hemorrhage (SAH). We studied 30 poor-grade SAH patients who underwent brain multimodality monitoring (3042 hours). Physiological measures were averaged over 60 minutes for each collected microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio>40 with a brain glucose concentration≤0.7 mmol/L. BTH was defined as PbtO2<20 mm Hg. Outcome was assessed at 3 months with the Modified Rankin Scale. Multivariable analyses adjusting for admission Hunt-Hess grade, intraventricular hemorrhage, systemic glucose, and end-tidal CO2 revealed that cerebral perfusion pressure≤70 mm Hg was significantly associated with an increased risk of BTH (OR, 2.0; 95% CI, 1.2-3.3; P=0.007) and metabolic crisis (OR, 2.1; 95% CI, 1.2-3.7; P=0.007). Death or severe disability at 3 months was significantly associated with metabolic crisis (OR, 5.4; 95% CI, 1.8-16; P=0.002) and BTH (OR, 5.1; 95% CI, 1.2-23; P=0.03) after adjusting for admission Hunt-Hess grade. Metabolic crisis and BTH are associated with mortality and poor functional recovery after SAH. Cerebral perfusion pressure levels<70 mm Hg was associated with metabolic crisis and BTH, and may increase the risk of secondary brain injury in poor-grade SAH patients.

Favorable Outcome in Traumatic Brain Injury Patients With Impaired Cerebral Pressure Autoregulation When Treated at Low Cerebral Perfusion Pressure Levels

Cerebral pressure autoregulation (CPA) is defined as the ability of the brain vasculature to maintain a constant blood flow over a range of different systemic blood pressures by means of contraction and dilatation. To study CPA in relation to physiological parameters, treatment, and outcome in a series of traumatic brain injury patients. In this prospective observational study, 44 male and 14 female patients (age, 15-72 years; mean, 38.7 years; Glasgow Coma Scale score, 4-13; median, 7) were analyzed. Patients were divided into groups on the basis of status of CPA (more pressure active vs more pressure passive) and level of cerebral perfusion pressure (CPP; low vs high CPP). The proportions of favorable outcome in the groups were assessed. Differences in physiological variables in the different groups were analyzed. Patients with more impaired CPA treated at CPP levels below median had a significantly higher proportion of favorable outcome compared with patients with more impaired CPA treated at CPP levels above median. No significant difference in outcome was seen between patients with more intact CPA when divided by level of CPP. In patients with more impaired CPA, CPP<50 mm Hg and CPP<60 mm Hg were associated with favorable outcome, whereas CPP>70 mm Hg and CPP>80 mm Hg were associated with unfavorable outcome. In patients with more intact CPA, no difference in physiological variables was seen between patients with favorable and unfavorable outcomes. Our results support that in traumatic brain injury patients with impaired CPA, CPP should not be elevated.

Effects of cerebrovascular pressure reactivity-guided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury*

To evaluate the concept of a cerebrovascular pressure reactivity-guided optimal cerebral perfusion pressure after traumatic brain injury by analyzing the relationship between optimal cerebral perfusion pressure and brain tissue oxygen. Prospective observational cohort study. Neurosurgical intensive care unit of a university hospital. Thirty-eight patients after head injury. Continuous computerized monitoring of mean arterial pressure, intracranial pressure, and brain tissue oxygen for 5.3 +/- 2.6 days. The index of cerebrovascular pressure reactivity was calculated as a moving correlation coefficient between spontaneous low-frequency fluctuations of mean arterial pressure and intracranial pressure. Optimal cerebral perfusion pressure was defined as the cerebral perfusion pressure level with the lowest average index of cerebrovascular pressure reactivity. Optimal cerebral perfusion pressure could be identified in 32 of 38 patients. Median optimal cerebral perfusion pressure was between 70 and 75 mm Hg (range, 60-100 mm Hg). Below the level of optimal cerebral perfusion pressure, brain tissue oxygen decreased in parallel to cerebral perfusion pressure, whereas brain tissue oxygen reached a plateau above optimal cerebral perfusion pressure. Optimal cerebral perfusion pressure correlated significantly with the cerebral perfusion pressure level, where brain tissue oxygen reached its plateau (r = .79; p < .01). Average brain tissue oxygen at optimal cerebral perfusion pressure was 24.5 +/- 6.0 mm Hg. This study supports the concept of cerebrovascular pressure reactivity-based individual optimal cerebral perfusion pressure. Driving cerebral perfusion pressure in excess of optimal cerebral perfusion pressure does not yield improvements in brain tissue oxygen after head injury and should be avoided, whereas cerebral perfusion pressure below optimal cerebral perfusion pressure may result in secondary cerebral ischemia.