Normal Cerebral Perfusion Pressure Research Articles

Craniectomía descompresiva y compliance intracraneal en el traumatismo craneoencefálico grave pediátrico

ObjectiveTo show the effect of primary decompressive craniectomy on ICP, CPP, and intracranial compliance in a group of pediatric patients who suffered from severe head trauma. DesignDescriptive study. FrameworkPediatric intensive care. PatientsPediatric patients who underwent primary decompressive craniectomy due to severe head trauma, admitted to the pediatric intensive care unit of the “Roberto Rodríguez Fernandez” general teaching hospital in Morón, Ciego de Avila, Cuba between January 2003 and December 2017. ResultsDiffuse brain injury Grade IV, was the most frequent tomographic diagnosis at admission 18 (60%), with a predominance of shifts greater than 6mm in 24 cases (80%) and absent cisterns 15 (50%). Eighteen cases (60%) had normal ICP for their age after craniectomy, 20 (66.7%) cases showed normal cerebral perfusion pressure. There was a correlation between normal ICP and normal intracranial compliances. The pulse wave amplitude was used as a neuromonitoring method and qualitative representation of compliances. Twenty-two cases survived (73.3%), 18 (60%) of them without sequelae. Eight cases died (26.7%). ConclusionsPrimary DC was useful for the control of ICP and maintenance of CPP in the management of pediatric patients with severe TBI in the present study. The favorable effect of the procedure for the increase of intracranial compliance has been verified.

Effects of surgical position on cerebral oxygen saturation and its regulation

Background Regional cerebral oxygen saturation (rSO2) is an important parameter to evaluate cerebral perfusion, brain metabolism, brain oxygen supply and demand, and to prevent postoperative neurological complications. Cerebral perfusion and rSO2 vary with different surgical positions. Objective This article reviews the characteristics and underlying mechanisms of the relationship between rSO2 values and surgical positions, and the clinical practices in preventing intraoperative brain ischemia and hypoxia in patients with different surgical positions. This review aims to provide an insight for the prevention of neurological complications associated with general anesthesia. Content Real-time quantification of oxygen supply and consumption is essential in operative monitoring. Insufficient blood and oxygen supply in the brain during operation may result in ischemia, hypoxia, and even postoperative cognitive dysfunction, depression and stroke. Monitoring rSO2 and maintaining it in normal ranges can prevent these postoperative complications. The rSO2 decreases in some surgical positions, including beach chair position, prone position, lateral position, and Trendelenburg position. In these situations, efforts should be made to maintain normal cerebral perfusion pressure and to improve lung ventilation. Trend Using near infrared spectroscopy to monitor rSO2 is valuable to efficiently recognize the adverse effects of altered surgical positions on cerebral oxygen supply, and to timely make efforts to prevent postoperative complications. Key words: Cerebral oxygen saturation; Surgical position; Anesthesia management

Pediatric traumatic brain injury—a review of management strategies

Management of traumatic brain injury (TBI) in children varies due to differing physician practices and availability of resources. Optimizing treatment to meet the physiologic demands of the wounded brain is crucial to achieve maximal recovery and minimize secondary injury. This review aims to discuss and update the different aspects of acute care in a child with TBI. A literature search for relevant original and review articles was carried out via PubMed. Relevant literatures from adult studies were included where there was a lack of pediatric data. Case reports and non-English articles were excluded. Acute airway management with carefully chosen sedative agents, appropriate ventilation and hyperosmolar therapy strategies are targeted at maintaining normal cerebral perfusion pressure (CPP). The goal of temperature control and glycemic control is to maintain normal ranges to optimize outcomes. Decisions for neuroimaging and initiation of anticonvulsants are weighed against potential complications. Achieving a beneficial neurological outcome for pediatric patients with TBI depends on effective management from the onset of injury. More high quality collaborative prospective research is required to develop individualized management strategies for our pediatric TBI patients in the acute setting.

Utility of Transcranial Doppler in Estimating Cerebral Perfusion Pressure in Traumatic Brain Injury: A Prospective Observational Trial

Abstract Title Utility of transcranial Doppler (TCD) in estimating cerebral perfusion pressure (eCPP) in traumatic brain injury—a prospective observational trial. Aim To validate the utility of a noninvasive technique of eCPP estimation using transcranial Doppler (TCD). Materials and Methods Eighteen patients with severe traumatic brain injury (TBI) requiring intracranial pressure (ICP) monitoring as per the Brain Trauma Foundation guidelines were prospectively recruited for the study. ICP was measured in all patients using an intraventricular catheter. Mean arterial pressure (MAP) was recorded from an intra-arterial catheter. Cerebral perfusion pressure (CPP) was calculated as the difference between MAP and ICP. Middle cerebral blood flow velocities were recorded using TCD, and CPP was estimated from the middle cerebral artery (MCA) flow velocities (eCPP) using the formula eCPP = (MAP × end diastolic velocity [EDV]/mean velocity [MV]) + 14. Total 185 simultaneous readings of CPP and eCPP were available for analysis. Reliability statistics between CPP and eCPP were computed to calculate the intraclass correlation (ICC). Results The average CPP measured using intraventricular catheter was 73.2 (+/−12.4), and the mean estimated eCPP was 76.7 (+/−10.9). We found a very good Pearson's correlation between CPP and eCPP (r = 0.743) with a Cronbach's α of 0.843. In 86.2% of examinations, the estimation error of measuring CPP was within 10 mm Hg, and in 93.1% examinations, it was within 15 mm Hg. Conclusion eCPP estimated using TCD can serve as reliable noninvasive alternative in situations in which ICP monitoring is not available, even in moderate or mild head injury.

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

Continuous monitoring of cerebral autoregulation is considered clinically useful due to its ability to warn against brain ischemic insults, which may translate to a relationship with adverse outcome. It is typically performed using the pressure reactivity index (PRx) based on mean arterial pressure and intracranial pressure. A new ORx index based on brain tissue oxygenation and cerebral perfusion pressure (CPP) has been proposed that similarly allows for evaluation of cerebrovascular reactivity. Conflicting results exist concerning its clinical utility. Retrospective analysis was performed in 85 patients with traumatic brain injury (TBI). ORx was calculated using three time windows of 5, 20, and 60min. Correlation coefficients and individual "optimal CPP" (CPPopt) were calculated using both PRx and ORx, and relation to patient outcome investigated. Correlation coefficients for all comparisons between PRx and ORx indicated poor association between these indices (range from -0.04 to 0.07). PRx was significantly lower in patients with good outcome (p=0.01), while none of the ORx indices proved to be significantly different in the two outcome groups. Higher mortality related to average CPP<CPPopt was found regardless of which index was used to calculate CPPopt. In the TBI setting, ORx does not appear to correlate with vascular pressure reactivity as assessed with PRx. Its potential use for individualizing CPP thresholds remains unclear.

Experimental animal study of cerebral oxygen metabolism changes during the process of brain death

To reproduce a stable animal model of brain death in pigs, observe the change regularity of cerebral oxygen metabolism during the process of brain death, and to evaluate the significance and value of cerebral oxygen metabolism parameters for the diagnosis of brain death. Twelve landrace pigs were used to create the brain death models using modified method of increasing epidural intracranial pressure (ICP). The mean arterial pressure (MAP) and ICP were monitored continuously during the process. The pigs were divided into four groups according to cerebral perfusion pressure (CPP) decreasing degree during brain death, namely CPP normal group and CPP decreasing 0%-30%, 30%-70%, and 70%-100% groups. Blood gas analysis of the external carotid artery and internal jugular vein were monitored discontinuously. The changes in cerebral oxygen metabolism parameters, including external carotid artery-internal jugular vein bulb oxygen content difference (AJDO2), internal jugular bulb-external carotid artery carbon dioxide partial pressure difference (DPCO2) and DPCO2/AJDO2 ratio, were observed. Brain death model were successfully reproduced in 12 experimental pigs. With MAP and ICP monitoring, the models at different stages of CPP could be repeatedly induced. The levels of AJDO2 and DPCO2 were increased gradually and then decreased, while the ratio of DPCO2/AJDO2 was constantly increased with the decrease of CPP. The level of AJDO2 in CPP decreasing 0%-30% group was significantly higher than that in CPP normal group [(5.86±1.21)% vs. (3.92±0.64)%], the levels of DPCO2 in CPP decreasing 0%-30% and CPP decreasing 30%-70% groups were significantly higher than those in CPP normal group [mmHg (1 mmHg = 0.133 kPa): 10.33±1.83, 11.48±2.32 vs. 6.11±1.43], and the ratios of DPCO2/AJDO2 in CPP decreasing 30%-70% and CPP decreasing 70%-100% groups were significantly higher than those in CPP normal group and CPP decreasing 0%-30% group (2.81±0.53, 4.12±1.07 vs. 1.57±0.64, 1.62±0.81). All the differences above were statistically significant (all P < 0.05). With the decrease of CPP, cerebral oxygen metabolism showed a regular change during brain death. DPCO2 combined with DPCO2/AJDO2 is a reliable blood gas analysis index indicating intracranial hypoperfusion, which has certain reference value for the determination of brain death.

Safety and efficacy of combined epidural/general anesthesia during major abdominal surgery in patients with increased intracranial pressure: a cohort study

BackgroundThe increased intracranial pressure can significantly complicate the perioperative period in major abdominal surgery, increasing the risk of complications, the length of recovery from the surgery, worsening the outcome. Epidural anesthesia has become a routine component of abdominal surgery, but its use in patients with increased intracranial pressure remains controversial. The goal of the study was to evaluate the safety and efficacy of epidural anesthesia, according to monitoring of intracranial pressure in patients with increased intracranial pressure.MethodsThe study includes 65 surgical patients who were routinely undergone the major abdominal surgery under combined epidural/general anesthesia. Depending on the initial ICP all patients were divided into 2 groups: 1 (N group) - patients with the normal intracranial pressure (≤12 mm Hg, n = 35) and 2 (E group) – patients with the elevated intracranial pressure (ICP > 12 mm Hg, n = 30). During the surgery we evaluated ICP, blood pressure, cerebral perfusion pressure (CPP). The parameters of recovery from anesthesia and the effectiveness of postoperative analgesia were also assessed.ResultsIn N group ICP remained stable. In E group ICP decreased during anesthesia, the overall decline was 40 % at the end of the operation (from 15 to 9 mm Hg (P <0.05)). The correction of MAP with vasopressors to maintain normal CPP was required mainly in patients with increased ICP (70 % vs. 45 %, p <0.05). CPP declined by 19 % in N group. In E group the CPP reduction was 23 %, and then it remained stable at 60 mm Hg. No significant differences in time of the recovery of consciousness, effectiveness of postoperative analgesia and complications between patients with initially normal levels of ICP and patients with ICH were noted.ConclusionsThe combination of general and epidural anesthesia is safe and effective in patients with increased intracranial pressure undergoing elective abdominal surgery under the condition of maintaining the arterial pressure. Its use is not associated with the increase in intracranial pressure during the anesthesia, but it needs an intraoperative monitoring of ICP in order to prevent CPP reduction.

Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. University laboratory. Male Sprague-Dawley rats. At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (Δ intracranial pressure/Δ mean arterial pressure) and induced cerebrovascular reactivity (Δ cerebral blood flow/Δ mean arterial pressure). At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.

Paradoxical reduction of cerebral blood flow after acetazolamide loading: a hemodynamic and metabolic study with (15)O PET.

Paradoxical reduction of cerebral blood flow (CBF) after administration of the vasodilator acetazolamide is the most severe stage of cerebrovascular reactivity failure and is often associated with an increased oxygen extraction fraction (OEF). In this study, we aimed to reveal the mechanism underlying this phenomenon by focusing on the ratio of CBF to cerebral blood volume (CBV) as a marker of regional cerebral perfusion pressure (CPP). In 37 patients with unilateral internal carotid or middle cerebral arterial (MCA) steno-occlusive disease and 8 normal controls, the baseline CBF (CBF(b)), CBV, OEF, cerebral oxygen metabolic rate (CMRO2), and CBF after acetazolamide loading in the anterior and posterior MCA territories were measured by (15)O positron emission tomography. Paradoxical CBF reduction was found in 28 of 74 regions (18 of 37 patients) in the ipsilateral hemisphere. High CBF(b) (> 47.6 mL/100 mL/min, n = 7) was associated with normal CBF(b)/CBV, increased CBV, decreased OEF, and normal CMRO2. Low CBF(b) (< 31.8 mL/100 mL/min, n = 9) was associated with decreased CBF(b)/CBV, increased CBV, increased OEF, and decreased CMRO2. These findings demonstrated that paradoxical CBF reduction is not always associated with reduction of CPP, but partly includes high-CBF(b) regions with normal CPP, which has not been described in previous studies.

Detection of Cerebral Compromise With Multimodality Monitoring in Patients With Subarachnoid Hemorrhage

Studies in traumatic brain injury suggest that monitoring techniques such as brain tissue oxygen (P(BTO₂)) and cerebral microdialysis may complement conventional intracranial pressure (ICP) and cerebral perfusion pressure (CPP) measurements. In this study of poor-grade (Hunt and Hess grade IV and V) subarachnoid hemorrhage (SAH) patients, we examined the prevalence of brain hypoxia and brain energy dysfunction in the presence of normal and abnormal ICP and CPP. SAH patients who underwent multimodal neuromonitoring and cerebral microdialysis were studied. We examined the frequency of brain hypoxia and energy dysfunction in different ICP and CPP ranges and the relationship between P(BTO₂) and the lactate/pyruvate ratio (LPR). A total of 2394 samples from 19 patients were analyzed. There were 149 samples with severe brain hypoxia (P(BTO₂) ≤10 mm Hg) and 347 samples with brain energy dysfunction (LPR >40). The sensitivities of abnormal ICP or CPP for elevated LPR and reduced P(BTO₂) were poor (21.2% at best), and the LPR or P(BTO₂) was abnormal in many instances when ICP or CPP was normal. Severe brain hypoxia was often associated with an LPR greater than 40 (86% of samples). In contrast, mild brain hypoxia (≤20 mm Hg) and severe brain hypoxia were observed in only 53% and 36% of samples with brain energy dysfunction, respectively. Our data demonstrate that ICP and CPP monitoring may not always detect episodes of cerebral compromise in SAH patients. Our data suggest that several complementary monitors may be needed to optimize the care of poor-grade SAH patients.

CT Perfusion Evidence of Early Global Cerebral Hypoperfusion After Aneurysmal Subarachnoid Hemorrhage with Cardiac Arrest

Cardiac arrest and aneurysmal subarachnoid hemorrhage both cause sudden, severe cerebral hypoperfusion at ictus. Animal studies indicate that the resultant microvascular dysfunction and cerebral perfusion abnormalities are important determinants of the associated cerebral injury in both conditions. Although this suggests that perfusion imaging might be a useful tool for prognostication in patients with these conditions, this hypothesis has not been thoroughly investigated in humans. Case report. A 49-year-old man developed cardiac arrest upon rupture of an intracranial aneurysm. When he arrived at our institution 10 h later, he was comatose, had neurogenic hyperventilation, absent corneal reflexes, and continuous multifocal myoclonus. Despite normal intracranial pressure, normal cerebral perfusion pressure, normal flow in the proximal cerebral arteries on CT angiography, and a lack of diffuse cerebral edema, CT perfusion imaging performed 12 h after ictus showed severe, diffuse hypoperfusion. After the development of refractory intracranial hypertension, physiologic support was withdrawn and the patient died. Early global cerebral hypoperfusion can be demonstrated by CT perfusion imaging after cardiac arrest associated with high-grade aneurysmal subarachnoid hemorrhage and may be indicative of poor neurologic outcome. CT perfusion should be investigated as a prognostic tool in these conditions.

Quantitative EEG Correlates of Low Cerebral Perfusion in Severe Stroke

Continuous EEG provides the unique possibility to monitor neuronal function non-invasively. In our pilot study, we evaluated EEG spectral power during spontaneous drops in cerebral perfusion pressure (CPP) in deeply sedated and mechanically ventilated patients with severe stroke. We aimed to identify parameters that may be used for continuous monitoring even in patients with a burst-suppression baseline EEG pattern. Twenty ventilated and sedated patients with severe hemorrhagic or ischemic stroke underwent continuous EEG monitoring with synchronous CPP recording. EEG monitoring duration was 83.9 hours on average per patient. Spectral power of EEG during drops of CPP was compared with epochs during normal CPP under the same levels of sedation. We found a significant decrease in faster EEG activity (3.5-20.7 Hz) during phases of low CPP (unaffected hemisphere P < 0.01, affected hemisphere P < 0.01, both P < 0.01). Despite considerable changes in baseline activity due to deep sedation and severe brain injury, we found evidence for disturbed neuronal function during drops in CPP. Thus, continuous EEG monitoring may add clinically relevant information on neuronal function in the setting of multimodality brain monitoring. Further studies are needed to implement real-time data analysis in the ICU setting.

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

The methods for continuous assessment of cerebral autoregulation using correlation, phase shift, or transmission (either in time- or frequency-domain) were introduced a decade ago. They express dynamic relationships between slow waves of transcranial Doppler (TCD), blood flow velocity (FV) and cerebral perfusion pressure (CPP), or arterial pressure (ABP). We review a methodology and clinical application of indices useful for monitoring cerebral autoregulation and pressure-reactivity in various scenarios of neuro-critical care. Poor autoregulation and loss of pressure-reactivity are independent predictors of fatal outcome following head injury. Autoregulation is impaired by too low or too high CPP when compared to autoregulation with normal CPP (usually between 60 and 85 mmHg; and these limits are highly individual). Hemispheric asymmetry of the bi-laterally assessed autoregulation has been associated with asymmetry of CT scan findings: autoregulation was found to be worse ipsilateral to contusion or lateralized edema causing midline shift. The pressure-reactivity (PRx index) correlated with a state of low CBF and CMRO2 revealed using PET studies. The PRx is easier to monitor over prolonged periods of time than the TCD-based indices as it does not require fixation of external probes. Continuous monitoring with the PRx can be used to direct CPP-oriented therapy by determining the optimal CPP for pressure-reactivity. Autoregulation indices are able to reflect transient changes of autoregulation, as seen during plateau waves of ICP. However, minute-to-minute assessment of autoregulation has a poor signal-to-noise ratio. Averaging across time (30 min) or by combining with other relevant parameters improves the accuracy. MYTHS: It is debatable whether the TCD-based indices in head injured patients can be calculated using ABP instead of CPP. Thresholds for functional and disturbed autoregulation dramatically depends on arterial tension of CO2--therefore, comparison between patients cannot be performed without comparing their PaCO2. The TCD pulsatility index cannot accurately detect the lower limit of autoregulation. MISSING LINKS: We still do not know whether autoregulation-oriented therapy can be understood as a consensus between CPP-directed protocols and the Lund-concept. What are the links between endothelial function and autoregulation indices? Can autoregulation after head injury be improved with statins or EPO, as in subarachnoid hemorrhage? In conclusion, monitoring cerebral autoregulation can be used in a variety of clinical scenarios and may be helpful in delineating optimal therapeutic strategies.

Brain oxygen tension and outcome in patients with aneurysmal subarachnoid hemorrhage

Poor outcome is common after aneurysmal subarachnoid hemorrhage (SAH). Clinical studies suggest that cerebral hypoxia after traumatic brain injury is associated with poor outcome. In this study we examined the relationship between brain oxygen tension (PbtO(2)) and death after aneurysmal SAH. Forty-six patients, including 34 women and 12 men (Glasgow Coma Scale Score < or = 8 and median age 58.5 years) who underwent PbtO(2) monitoring were studied prospectively during a 2-year period in a neurosurgical intensive care unit at a University Level I Trauma Center. Brain oxygen tension, intracranial pressure (ICP), mean arterial pressure, cerebral perfusion pressure (CPP), and brain temperature were continuously monitored, and treatment was directed toward ICP, CPP, and PbtO(2) targets. The relationship between PbtO(2) and 1-month survival was examined. Data were available from 5424 hours of PbtO(2) monitoring. For the entire cohort the mean ICP, CPP, and PbtO(2) were 13.85 +/- 2.40, 84.05 +/- 3.41, and 30.79 +/- 1.91 mm Hg, respectively. Twenty-five patients died (54%). The mean daily PbtO(2) was higher in survivors than nonsurvivors (33.94 +/- 2.74 vs 28.14 +/- 2.59 mm Hg; p = 0.05). In addition, survivors had significantly shorter episodes of compromised PbtO(2) (defined as 15-25 mm Hg) than nonsurvivors (125.85 +/- 15.44 vs 271.14 +/- 55.23 minutes; p < 0.01). Intracranial pressure was similar in survivors and nonsurvivors. In contrast, the average CPP was significantly lower in nonsurvivors than survivors (76.96 +/- 5.50 vs 92.49 +/- 2.75 mm Hg; p = 0.01). When PbtO(2) was stratified according to CPP level, survivors had higher PbtO(2) levels. Following logistic regression, the number of episodes of compromised PbtO(2) (odds ratio 1.1, 95% confidence interval 1.003-1.2) and number of episodes of cerebral hypoxia (< 15 mm Hg; odds ratio 1.3, 95% confidence interval 1.0-1.7) were more frequent in those who died. Patient deaths after SAH may be associated with a lower mean PbtO(2) and longer periods of compromised cerebral oxygenation than in survivors. This knowledge may be used to help direct therapy.

The relationship between the intracranial pressure–volume index and cerebral autoregulation

The pressure-volume index (PVI) can be used to assess the cerebrospinal fluid dynamics and intracranial elastance in critically ill brain injured patients. The dependency of PVI on the state of cerebral autoregulation within the physiologic range of cerebral perfusion pressure (CPP) can be described by mathematical models that account for changes in cerebral blood volume during PVI testing. This relationship has never been verified clinically using direct PVI measurement and independent cerebral autoregulation assessment. PVI and cerebral autoregulation were prospectively assessed in a cohort of 19 comatose patients admitted to an academic intensive care unit in Brescia, Italy. None. PVI was measured injecting a fixed volume of 2 ml of 0.9% sodium chloride solution into the cerebral ventricles through an intraventricular catheter. Cerebral autoregulation was assessed using transcranial Doppler transient hyperaemic response (THR) test. Fifty-nine PVI assessments and 59 THR tests were performed. Mean PVI was 20.0 (SD 10.2) millilitres in sessions when autoregulation was intact (THR test >or=1.1) and 31.6 (8.8) millilitres in sessions with defective autoregulation (THR test <1.1) (DeltaPVI = 11.7 ml, 95% CI = 4.7-19.3 ml; P = 0.002). Intracranial pressure, CPP and brain CT findings were not significantly different between the measurements with intact and disturbed autoregulation. Cerebral autoregulation status can affect PVI estimation despite a normal CPP. PVI measurement may overestimate the tolerance of the intracranial system to volume loads in patients with disturbed cerebral autoregulation.

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Introduction: Standard monitoring of severe traumatic brain injury patients (TBI) by intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring fails to recognize episodes of cerebral oxygen desaturation. We found and characterized frequent episodes of desaturation of jugular venous oxygen (SjO2) in the face of normal ICP and CPP. Methods: Fifty six patients with severe TBI had SjO2 and ICP monitors placed. The charts were retrospectively reviewed and all episodes of desaturation were recorded and characterized. Results: Nineteen patients had episodes of desaturation with normal ICP and CPP. The average GCS score was 5.8. 63% of desaturations occurred in the first 24 hours, 17% of desaturations occurred in 24-48 hours, and 20% occurred in 48-72 hours. The depth of desaturation was 50-54% in 50% of instances, 45-49% in 37% of instances, and 40-44% in 13% of in- stances. The duration of the desaturation episodes was less than 10 minutes in 47%, 10-30 minutes in 17%, 30-60 minutes in 23%, and greater than 50 minutes in 13%. Treatment of the desaturation was elevation of FIO2 in all patients, elevation of pCO2 in 15 patients, volume expansion in 9 patients, pressors in 9 patients, and Propofol in 5 patients. Conclusions: The monitoring of severe TBI patients with ICP and CPP alone is insufficient to recognize cerebral oxygen de- saturation episodes in 34% of patients. The monitoring of SjO2 facilitates the recognition and treatment of these episodes.

Magnesium Sulfate Decreases Cerebral Perfusion Pressure in Preeclampsia

Objective: To determine the cerebral hemodynamic effect of magnesium sulfate (MgSO4) in preeclampsia. Design: Prospective observational study. Setting: Tertiary Care Medical Center. Population: Preeclamptic patients (systolic < 160, diastolic < 110 mmHg). Methods: Transcranial Doppler (TCD) of the middle cerebral arteries (MCA) of 15 preeclamptics, before and after IV MgSO4. No vasoactive drugs other than MgSO4 were given. 11 patients with mild range BP (140/90 – 160/110 mmHg) had measurements at baseline, 30 and 120 minutes after MgSO4, and 7 patients with elevated CPP had baseline and 30 minute measurements. Hemodynamic parameters were compared with normative curves. Main Outcome Measures: Mean arterial pressure (MAP), heart rate (HR), cerebral perfusion pressure (CPP), resistance index (RI), resistance area product (RAP), and cerebral flow index (CFI). Results: Eight women had normal baseline CPP, and 11 had normal CFI. 11 had mild preeclampsia range blood pressure and MgSO4 had no significant effect on CPP, CFI, HR, MCA velocities, or RAP but did decrease the MAP in the first 30 minutes (107 +/– 8 to 100+/–9 mmHg; p = 0.035), mainly due to a drop in diastolic pressure (87+/–10 to 82+/– 9 mmHg; p = 0.004). 7 patients with elevated baseline CPP had a significant reduction in CPP, but no change in CFI, after MgSO4. Conclusions: MgSO4 does not significantly effect CPP or CFI in preeclamptics with baseline blood pressure in the mild range, but does significantly reduce CPP in those with high baseline CPP. This may be important in the prevention of hypertensive encephalopathy.

What is the optimal threshold for cerebral perfusion pressure following traumatic brain injury?

Intensive care of the patient with traumatic brain injury centers on control of intracranial pressure and cerebral perfusion pressure (CPP). The optimal CPP by definition delivers an adequate supply of blood and oxygen to meet the metabolic demands of brain tissue. A great deal of controversy exists regarding the optimal CPP value, with disparate studies providing conflicting evidence for the use of supraphysiological CPP values. No study that accurately assesses the efficacy of normal CPP compared with elevated CPP has been performed, but several studies demonstrate that a CPP threshold exists on an individual basis for patients with TBI. The use of brain monitors of cerebral metabolism and oxygen supply may assist the clinician in the selection of the optimal CPP for an individual patient.

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.

Management of cerebral perfusion pressure after traumatic brain injury.

IN 1996, the Brain Trauma Foundation sponsored the development of guidelines for the management of severe traumatic brain injury (TBI). The method used for development of the guidelines was evidence based, and probably the most significant contribution of the guidelines has been to highlight the remarkable lack of class I evidence available for many current management practices. Recently, revisions to the guidelines were published, and little has been changed in the recommendations. 1 From all of the aspects of management that were reviewed for the guidelines, the authors were only able to provide three standards based on class I evidence (randomized clinical trials) and only eight guidelines based on class II evidence (table 1). Furthermore, the randomized clinical trials that have supported the three guideline standards showed ineffectiveness of certain long-standing management practices (prophylactic hyperventilation, steroid administration, prophylactic anticonvulsants) rather than showing that any practices are