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Introduction: Neurocritical care focuses on the care of critically ill patients with an acute neurologic disorder and has grown significantly in the past few years. However, there is a lack of data that describe the scope of practice of neurointensivists and epidemiological data on the types of patients and treatments used in neurocritical care units worldwide. To address these issues, we designed a multicenter, international, point-prevalence, cross-sectional, prospective, observational, non-interventional study in the setting of neurocritical care (PRINCE Study)., Methods: In this manuscript, we analyzed data from the initial phase of the study that included registration, hospital, and intensive care unit (ICU) organizations. We present here descriptive statistics to summarize data from the registration case report form. We performed the Kruskal-Wallis test followed by the Dunn procedure to test for differences in practices among world regions., Results: We analyzed information submitted by 257 participating sites from 47 countries. The majority of those sites, 119 (46.3%), were in North America, 44 (17.2%) in Europe, 34 (13.3%) in Asia, 9 (3.5%) in the Middle East, 34 (13.3%) in Latin America, and 14 (5.5%) in Oceania. Most ICUs are from academic institutions (73.4%) located in large urban centers (44% > 1 million inhabitants). We found significant differences in hospital and ICU organization, resource allocation, and use of patient management protocols. The highest nursing/patient ratio was in Oceania (100% 1:1). Dedicated Advanced Practiced Providers are mostly present in North America (73.7%) and are uncommon in Oceania (7.7%) and the Middle East (0%). The presence of dedicated respiratory therapist is common in North America (85%), Middle East (85%), and Latin America (84%) but less common in Europe (26%) and Oceania (7.7%). The presence of dedicated pharmacist is highest in North America (89%) and Oceania (85%) and least common in Latin America (38%). The majority of respondents reported having a dedicated neuro-ICU (67% overall; highest in North America: 82%; and lowest in Oceania: 14%)., Conclusion: The PRINCE Study results suggest that there is significant variability in the delivery of neurocritical care. The study also shows it is feasible to undertake international collaborations to gather global data about the practice of neurocritical care.

Background: Neurocritical care is devoted to the care of critically ill patients with acute neurological or neurosurgical emergencies. There is limited information regarding epidemiological data, disease characteristics, variability of clinical care, and in-hospital mortality of neurocritically ill patients worldwide. We addressed these issues in the Point PRevalence In Neurocritical CarE (PRINCE) study, a prospective, cross-sectional, observational study., Methods: We recruited patients from various intensive care units (ICUs) admitted on a pre-specified date, and the investigators recorded specific clinical care activities they performed on the subjects during their first 7 days of admission or discharge (whichever came first) from their ICUs and at hospital discharge. In this manuscript, we analyzed the final data set of the study that included patient admission characteristics, disease type and severity, ICU resources, ICU and hospital length of stay, and in-hospital mortality. We present descriptive statistics to summarize data from the case report form. We tested differences between geographically grouped data using parametric and nonparametric testing as appropriate. We used a multivariable logistic regression model to evaluate factors associated with in-hospital mortality., Results: We analyzed data from 1545 patients admitted to 147 participating sites from 31 countries of which most were from North America (69%, N = 1063). Globally, there was variability in patient characteristics, admission diagnosis, ICU treatment team and resource allocation, and in-hospital mortality. Seventy-three percent of the participating centers were academic, and the most common admitting diagnosis was subarachnoid hemorrhage (13%). The majority of patients were male (59%), a half of whom had at least two comorbidities, and median Glasgow Coma Scale (GCS) of 13. Factors associated with in-hospital mortality included age (OR 1.03; 95% CI, 1.02 to 1.04); lower GCS (OR 1.20; 95% CI, 1.14 to 1.16 for every point reduction in GCS); pupillary reactivity (OR 1.8; 95% CI, 1.09 to 3.23 for bilateral unreactive pupils); admission source (emergency room versus direct admission [OR 2.2; 95% CI, 1.3 to 3.75]; admission from a general ward versus direct admission [OR 5.85; 95% CI, 2.75 to 12.45; and admission from another ICU versus direct admission [OR 3.34; 95% CI, 1.27 to 8.8]); and the absence of a dedicated neurocritical care unit (NCCU) (OR 1.7; 95% CI, 1.04 to 2.47)., Conclusion: PRINCE is the first study to evaluate care patterns of neurocritical patients worldwide. The data suggest that there is a wide variability in clinical care resources and patient characteristics. Neurological severity of illness and the absence of a dedicated NCCU are independent predictors of in-patient mortality.

Background: Multimodality monitoring is used frequently to guide care of patients with severe acute brain injury. The aim of this study was to examine the safety and reliability of multimodality monitoring., Methods: From a prospective observational database at a Level I trauma center, 501 patients, including 300 men and 201 women (mean age 58 ± 39 years) were identified retrospectively. Each patient received a triple-lumen bolt and 3 monitors: intracranial pressure, brain temperature, and brain oxygen. Intensive care unit and hospital records were examined to identify complications, reasons for device replacement, malfunction and infection. Head computed tomography (CT) scans performed before and after the monitors were inserted were examined for evidence of monitor-related adverse effects., Results: A total of 696 triple-lumen bolts were placed. Median duration of monitoring was 78.88 hours (interquartile range, 33.0-133.2 hours). Bilateral monitors were inserted in 22 (3.16%) patients. Ten (1.43%) monitors were replaced to allow magnetic resonance imaging, and 40 (5.74%) monitors were replaced to facilitate additional cranial surgery. Of 35 (5.02%) monitors that were replaced because they were thought to not be functioning properly, 19 (54.29%) were subsequently found to be functioning normally. Follow-up CT scans were compared with CT scans obtained before insertion of monitors; 9 (2.13%) small contusions and 10 (2.36%) extra-axial hematomas associated with the devices were identified. Based on the CT findings, the hematomas were thought to be associated with the insertion technique rather than the device; 4 hematomas required treatment. Twenty-two (3.16%) devices were incorrectly placed (e.g., the probe was in an infarct or an already existing contusion). Only 1 associated infection was identified., Conclusions: Placement of intracranial monitors for multimodality neuromonitoring using a triple-lumen bolt appears to be safe. The complication rate is similar to published complication rates for single-lumen bolts and single monitors., (Copyright © 2019. Published by Elsevier Inc.)

Objectives: The goal for this project was to develop a comprehensive set of common data elements (CDEs), data definitions, case report forms and guidelines for use in unruptured intracranial aneurysm (UIA) and subarachnoid hemorrhage (SAH) clinical research, as part of a new joint effort between the National Institute of Neurological Disorders and Stroke (NINDS) and the National Library of Medicine of the US National Institutes of Health. These UIA and SAH CDEs will join several other neurological disease-specific CDEs that have already been developed and are available for use by research investigators., Methods: A Working Group (WG) divided into eight sub-groups and a Steering Committee comprised of international UIA and SAH experts reviewed existing NINDS CDEs and instruments, created new elements when needed and provided recommendations for UIA and SAH clinical research. The recommendations were compiled, internally reviewed by the entire UIA and SAH WG and posted online for 6 weeks for external public comments. The UIA and SAH WG and the NINDS CDE team reviewed the final version before posting the SAH Version 1.0 CDE recommendations., Results: The NINDS UIA and SAH CDEs and supporting documents are publicly available on the NINDS CDE ( https://www.commondataelements.ninds.nih.gov/#page=Default ) and NIH Repository ( https://cde.nlm.nih.gov/home ) websites. The recommendations are organized into domains including Participant Characteristics and Outcomes and Endpoints., Conclusion: Dissemination and widespread use of CDEs can facilitate UIA and SAH clinical research and clinical trial design, data sharing, and analyses of observational retrospective and prospective data. It is vital to maintain an international and multidisciplinary collaboration to ensure that these CDEs are implemented and updated when new information becomes available.

Objectives: A relationship between reduced brain tissue oxygenation and poor outcome following severe traumatic brain injury has been reported in observational studies. We designed a Phase II trial to assess whether a neurocritical care management protocol could improve brain tissue oxygenation levels in patients with severe traumatic brain injury and the feasibility of a Phase III efficacy study., Design: Randomized prospective clinical trial., Setting: Ten ICUs in the United States., Patients: One hundred nineteen severe traumatic brain injury patients., Interventions: Patients were randomized to treatment protocol based on intracranial pressure plus brain tissue oxygenation monitoring versus intracranial pressure monitoring alone. Brain tissue oxygenation data were recorded in the intracranial pressure -only group in blinded fashion. Tiered interventions in each arm were specified and impact on intracranial pressure and brain tissue oxygenation measured. Monitors were removed if values were normal for 48 hours consecutively, or after 5 days. Outcome was measured at 6 months using the Glasgow Outcome Scale-Extended., Measurements and Main Results: A management protocol based on brain tissue oxygenation and intracranial pressure monitoring reduced the proportion of time with brain tissue hypoxia after severe traumatic brain injury (0.45 in intracranial pressure-only group and 0.16 in intracranial pressure plus brain tissue oxygenation group; p < 0.0001). Intracranial pressure control was similar in both groups. Safety and feasibility of the tiered treatment protocol were confirmed. There were no procedure-related complications. Treatment of secondary injury after severe traumatic brain injury based on brain tissue oxygenation and intracranial pressure values was consistent with reduced mortality and increased proportions of patients with good recovery compared with intracranial pressure-only management; however, the study was not powered for clinical efficacy., Conclusions: Management of severe traumatic brain injury informed by multimodal intracranial pressure and brain tissue oxygenation monitoring reduced brain tissue hypoxia with a trend toward lower mortality and more favorable outcomes than intracranial pressure-only treatment. A Phase III randomized trial to assess impact on neurologic outcome of intracranial pressure plus brain tissue oxygenation-directed treatment of severe traumatic brain injury is warranted.

Background: Jehovah's Witnesses (JW) are a Christian faith with >1 million members in the United States who do not accept autologous blood transfusions. The optimal management of these patients undergoing neurosurgical procedures is not well defined. Here, we examined the feasibility and safety of JW undergoing neurosurgery in a blood management program., Study Design and Methods: Sixty-eight JW patients including 23 men and 45 women (mean age 53 ± 12 years) who underwent a variety of cranial (n = 19) and spinal (n = 49) neurosurgical procedures during a 5-year period were identified retrospectively and their hospital charts, anesthetic records, and operative reports reviewed. A concurrent cohort of sex-, age-, and procedure-matched non-JW controls also was identified., Results: Among JW patients, a cell-saving system was used in 27 cases, with blood retransfused in 13 cases. Lactated Ringers solution was used extensively intraoperatively; albumin was given to 15 patients. The median decrease in hemoglobin was 2.1 g/dL. One patient had a postoperative hemoglobin value <7 g/dL. One patient returned to the operating room to revise a lumbar pedicle screw, and one patient had postoperative seizures. No cardiopulmonary complications, sepsis, pneumonia, or wound infection were observed. Compared with the matched control group, similar outcome results were observed. Blood loss and operative time also were similar in JW patients and controls., Conclusions: Neurosurgical procedures in Jehovah's Witnesses are feasible, safe, and have similar outcomes to patients willing to accept transfusion when managed within a multidisciplinary blood-management program., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Regional multimodality monitoring has evolved over the last several years as a tool to understand the mechanisms of brain injury and brain function at the cellular level. Multimodality monitoring offers an important augmentation to the clinical exam and is especially useful in comatose neurocritical care patients. Cerebral microdialysis, brain tissue oxygen monitoring, and cerebral blood flow monitoring all offer insight into permutations in brain chemistry and function that occur in the context of brain injury. These tools may allow for development of individual therapeutic strategies that are mechanistically driven and goal-directed. We present a summary of the discussions that took place during the Second Neurocritical Care Research Conference regarding regional brain monitoring.

Multi-modal monitoring has become an integral part of neurointensive care. However, our approach is at this time neither standardized nor backed by data from randomized controlled trials. The goal of the second Neurocritical Care Research Conference was to discuss research priorities in multi-modal monitoring, what research tools are available, as well as the latest advances in clinical trial design. This section of the meeting was focused on how such a trial should be designed so as to maximize yield and avoid mistakes of the past.

Neurocritical care involves the care of highly complex patients with combinations of physiologic derangements in the brain and in extracranial organs. The level of evidence underpinning treatment recommendations remains low due to a multitude of reasons including an incomplete understanding of the involved physiology; lack of good quality, prospective, standardized data; and the limited success of conventional randomized controlled trials. Comparative effectiveness research can provide alternative perspectives and methods to enhance knowledge and evidence within the field of neurocritical care; these include large international collaborations for generation and maintenance of high quality data, statistical methods that incorporate heterogeneity and individualize outcome prediction, and finally advanced bioinformatics that integrate large amounts of variable-source data into patient-specific phenotypes and trajectories.

Effective methods of monitoring the status of patients with neurological injuries began with non-invasive observations and evolved during the past several decades to include more invasive monitoring tools and physiologic measures. The monitoring paradigm continues to evolve, this time back toward the use of less invasive tools. In parallel, the science of monitoring began with the global assessment of the patient's neurological condition, evolved to focus on regional monitoring techniques, and with the advent of enhanced computing capabilities is now moving back to focus on global monitoring. The purpose of this session of the Second Neurocritical Care Research Conference was to collaboratively develop a comprehensive understanding of the state of the science for global brain monitoring and to identify research priorities for intracranial pressure monitoring, neuroimaging, and neuro-electrophysiology monitoring.

Background: Subarachnoid hemorrhage (SAH) is a devastating disease. Nimodipine is the only medical treatment shown to improve outcome of SAH patients. Human albumin (ALB) may exert neuroprotection in SAH. However, current usage of ALB in SAH is not known. We conducted an international survey of clinicians involved in the care of SAH patients to determine current practice of ALB administration in SAH., Methods: We constructed a 27-question survey. Our sampling frame consisted of neurointensivists, general intensivists, neurocritical care nurses, critical care pharmacists, and neurosurgeons. The survey was available from 11/15/2012 to 12/15/2012. We performed mostly descriptive statistical analysis., Results: We obtained 362 responses from a diverse range of world regions. Most respondents were intensivist physicians (88 %), who worked in academic institutions (73.5 %) with a bed capacity >500 (64.1 %) and an established institutional management protocol for SAH patients (70.2 %). Most respondents (83.5 %) indicated that their institutions do not incorporate ALB in their protocol, but half of them (45.9 %) indicated using ALB outside it. ALB administration is influenced by several factors: geographic variation (more common among US respondents); institutions with a dedicated neuroICU; and availability of SAH management protocol. Most respondents (75 %) indicated that a clinical trial to test the efficacy of ALB in SAH is needed., Conclusions: In this survey we found that ALB administration in SAH patients is common and influenced by several factors. Majority of respondents support a randomized clinical trial to determine the safety and efficacy of ALB administration in SAH patients.

Background: Brain oxygen (PbtO2) monitoring can help guide care of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients. The relationship between PbtO2-directed therapy and long-term outcome is unclear. We hypothesized that responsiveness to PbtO2-directed interventions is associated with outcome., Methods: Seventy-six aSAH patients who underwent PbtO2 monitoring were included. Long-term outcome [Glasgow Outcome Score-Extended (GOS-E) and modified Rankin Scale (mRS)] was ascertained using the social security death database and structured telephone interviews. Univariate and multivariate regression were used to identify variables that correlated with outcome., Results: Data from 64 patients were analyzed (12 were lost to follow-up). There were 530 episodes of compromised PbtO2 (<20 mmHg) during a total of 7,174 h of monitor time treated with 1,052 interventions. Forty-two patients (66 %) survived to discharge. Median follow-up was 8.5 months (range 0.1-87). At most recent follow-up 35 (55 %) patients were alive, and 28 (44 %) had a favorable outcome (mRS ≤3). In multivariate ordinal regression analysis, only age and response to PbtO2-directed intervention correlated significantly with outcome. Increased age was associated with worse outcome (coeff. 0.8, 95 % CI 0.3-1.3, p = 0.003), and response to PbtO2-directed intervention was associated with improved outcome (coeff. -2.12, 95 % CI -4.0 to -0.26, p = 0.03). Patients with favorable outcomes had a 70 % mean rate of response to PbtO2-directed interventions whereas patients with poor outcomes had a 45 % response rate (p = 0.005)., Conclusions: Response to PbtO2-directed intervention is associated with improved long-term functional outcome in aSAH patients.

Background: Our objective was to determine whether there is variability in the foundational literature and across centers in how mean arterial blood pressure is measured to calculate cerebral perfusion pressure., Methods: We reviewed foundational literature and sent an e-mail survey to members of the Neurocritical Care Society., Results: Of 32 articles reporting cerebral perfusion pressure data, the reference point for mean arterial blood pressure was identified in 16: 10 heart and 6 midbrain. The overall survey response rate was 14.3%. Responses from 31 of 34 (91%) United Council for Neurologic Subspecialties fellowship-accredited Neurointensive Care Units indicated the reference point was most often the heart (74%), followed by the midbrain (16%). Conflicting answers were received from 10%., Conclusions: There is substantive heterogeneity in both research reports and clinical practice in how mean arterial blood pressure is measured to determine cerebral perfusion pressure.

Despite more than 30 years of clinical use, questions remain about the safety of xenon gas in Xenon-CT cerebral blood flow (XeCTCBF) studies. In particular, xenon's effect on brain oxygen (PbtO2) in comatose patients is not well defined. Our objective was to assess the effect of a 4.5-min inhalation of 28 % stable xenon on several physiologic variables, including intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO2 in comatose patients (Glasgow Coma Scale [GCS] ≤ 8). Thirty-seven comatose patients who underwent 73 XeCTCBF studies were identified retrospectively from a prospective observational database. Changes in MAP, HR, SaO2, EtCO2, ICP, CPP, and PbtO2 measured at the start of xenon administration and every minute for 5 min thereafter were assessed. The maximum change in each variable also was determined for each scan to tabulate clinically relevant changes. Statistically, but not clinically significant changes in MAP, HR, and EtCO2 were seen. Xenon had no effect on ICP, and a small, but clinically insignificant decrease in CPP and PbtO2, was observed. There was a varied response to xenon in most measured variables. Clinically significant changes in each were infrequent, and readily reversed with the cessation of the gas. We conclude that xenon does not appear to have a clinically significant effect on ICP, CPP, and PbtO2 and so appears safe to evaluate cerebral blood flow in comatose patients.

Background: Brain tissue oxygen (PbtO(2)) monitors are utilized in a threshold-based fashion, triggering actions based on the presumption of tissue compromise when PbtO(2) is less than 20 mmHg. Some early published practice guidelines suggest that seizure is a potential culprit when PbtO(2) crosses this threshold; evidence for this is not well defined., Methods: Data were collected manually as part of a prospective observational database. PbtO(2) monitors and continuous electroencephalogram (cEEG) were placed by clinical protocol in aneurysmal subarachnoid hemorrhage (aSAH) or traumatic brain injury (TBI) patients with a Glasgow Coma Scale (GCS) ≤ 8. Eight patients with discrete seizures during an overlapping monitored period were identified. Probability of seizure when PbtO(2) value was <20 mmHg (and the inverse) were calculated., Results: There were 343 distinct seizure episodes and 1797 PbtO(2) measurements. 8.9% of seizures were followed by a PbtO(2) value below 20 mmHg. Of all observed low PbtO(2) values, 3.8% were associated with seizure. Seizure length did not influence PbtO(2). Two patients with the highest number of seizures developed low PbtO(2) values post-seizure., Conclusions: Seizures were neither associated with a PbtO(2) value of <20 mmHg nor associated with a drop in PbtO(2) value across a clinically significant threshold. However, we cannot rule out the existence of any relationship between PbtO(2) and seizure with this limited data set. Prospective research using electronically recorded data is required to more effectively examine the relationship between PbtO(2) and seizure.

Background: Brain hypoxia (BH) can aggravate outcome after severe traumatic brain injury (TBI). Whether BH or reduced brain oxygen (Pbto(2)) is an independent outcome predictor or a marker of disease severity is not fully elucidated., Objective: To analyze the relationship between Pbto(2), intracranial pressure (ICP), and cerebral perfusion pressure (CPP) and to examine whether BH correlates with worse outcome independently of ICP and CPP., Methods: We studied 103 patients monitored with ICP and Pbto(2) for > 24 hours. Durations of BH (Pbto(2) < 15 mm Hg), ICP > 20 mm Hg, and CPP < 60 mm Hg were calculated with linear interpolation, and their associations with outcome within 30 days were analyzed., Results: Duration of BH was longer in patients with unfavorable (Glasgow Outcome Scale score, 1-3) than in those with favorable (Glasgow Outcome Scale, 4-5) outcome (8.3 ± 15.9 vs 1.7 ± 3.7 hours; P < .01). In patients with intracranial hypertension, those with BH had fewer favorable outcomes (46%) than those without (81%; P < .01); similarly, patients with low CPP and BH were less likely to have favorable outcome than those with low CPP but normal Pbto(2) (39% vs 83%; P < .01). After ICP, CPP, age, Glasgow Coma Scale score, Marshall computed tomography grade, and Acute Physiology and Chronic Health Evaluation II score were controlled for, BH was independently associated with poor prognosis (adjusted odds ratio for favorable outcome, 0.89 per hour of BH; 95% confidence interval, 0.79-0.99; P = .04)., Conclusion: Brain hypoxia is associated with poor short-term outcome after severe traumatic brain injury independently of elevated ICP, low CPP, and injury severity. Pbto(2) may be an important therapeutic target after severe traumatic brain injury.

Background: 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., Objective: 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., Methods: 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)., Results: 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., Conclusion: 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.

Background: Brain tissue oxygenation (PbtO2)-guided management facilitates treatment of reduced PbtO2 episodes potentially conferring survival and outcome advantages in severe traumatic brain injury (TBI). To date, the nature and effectiveness of commonly used interventions in correcting compromised PbtO2 in TBI remains unclear. We sought to identify the most common interventions used in episodes of compromised PbtO2 and to analyze which were effective., Methods: A retrospective 7-year review of consecutive severe TBI patients with a PbtO2 monitor was conducted in a Level I trauma center's intensive care unit or neurosurgical registry. Episodes of compromised PbtO2 (defined as <20 mm Hg for 0.25-4 hours) were identified, and clinical interventions conducted during these episodes were analyzed. Response to treatment was gauged on how rapidly (ΔT) PbtO2 normalized (>20 mm Hg) and how great the PbtO2 increase was (ΔPbtO2). Intracranial pressure (ΔICP) and cerebral perfusion pressure (ΔCPP) also were examined for these episodes., Results: Six hundred twenty-five episodes of reduced PbtO2 were identified in 92 patients. Patient characteristics were: age 41.2 years, 77.2% men, and Injury Severity Score and head or neck Abbreviated Injury Scale score of 34.0 ± 9.2 and 4.9 ± 0.4, respectively. Five interventions: narcotics or sedation, pressors, repositioning, FIO2/PEEP increases, and combined sedation or narcotics + pressors were the most commonly used strategies. Increasing the number of interventions resulted in worsening the time to PbtO2 correction. Triple combinations resulted in the lowest ΔICP and dual combinations in the highest ΔCPP (p < 0.05)., Conclusion: Clinicians use a limited number of interventions when correcting compromised PbtO2. Using strategies employing many interventions administered closely together may be less effective in correcting PbO2, ICP, and CPP deficits. Some PbtO2 deficits may be self-limited., (Copyright © 2011 by Lippincott Williams & Wilkins)

Background: Pulmonary complications are frequently observed after severe traumatic brain injury (TBI), but little is known about the consequences of lung injury on brain tissue oxygenation and metabolism., Objective: We examined the association between lung function and brain tissue oxygen tension (PbtO2) in patients with severe TBI., Methods: We analyzed data from 78 patients with severe, nonpenetrating TBI who underwent continuous PbtO2 and intracranial pressure monitoring. Acute lung injury was defined by the presence of pulmonary infiltrates with a PaO2/FiO2 (PF) ratio less than 300 and the absence of left ventricular failure. A total of 587 simultaneous measurements of PbtO2 and PF ratio were examined using longitudinal data analysis., Results: PbtO2 correlated strongly with PaO2 and PF ratio (P < .05) independent of PaCO2, brain temperature, cerebral perfusion pressure, and hemoglobin. Acute lung injury was associated with lower PbtO2 (34.6 +/- 13.8 mm Hg at PF ratio >300 vs 30.2 +/- 10.8 mm Hg [PF ratio 200-300], 28.9 +/- 9.8 mm Hg [PF ratio 100-199], and 21.1 +/- 7.4 mm Hg [PF ratio <100], all P values <.01). After adjusting for intracranial pressure, Marshall computed tomography score, and APACHE II (Acute Physiology and Chronic Health Evaluation) score, acute lung injury was an independent risk factor for compromised PbtO2 (PbtO2 <20 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21-3.77; P < .01)., Conclusion: After severe TBI, PbtO2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO2, independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.

Background: The impact of osmotic therapies on brain oxygen has not been extensively studied in humans. We examined the effects on brain tissue oxygen tension (PbtO(2)) of mannitol and hypertonic saline (HTS) in patients with severe traumatic brain injury (TBI) and refractory intracranial hypertension., Methods: 12 consecutive patients with severe TBI who underwent intracranial pressure (ICP) and PbtO(2) monitoring were studied. Patients were treated with mannitol (25%, 0.75 g/kg) for episodes of elevated ICP (>20 mm Hg) or HTS (7.5%, 250 ml) if ICP was not controlled with mannitol. PbtO(2), ICP, mean arterial pressure, cerebral perfusion pressure (CPP), central venous pressure and cardiac output were monitored continuously., Results: 42 episodes of intracranial hypertension, treated with mannitol (n = 28 boluses) or HTS (n = 14 boluses), were analysed. HTS treatment was associated with an increase in PbtO(2) (from baseline 28.3 (13.8) mm Hg to 34.9 (18.2) mm Hg at 30 min, 37.0 (17.6) mm Hg at 60 min and 41.4 (17.7) mm Hg at 120 min; all p<0.01) while mannitol did not affect PbtO(2) (baseline 30.4 (11.4) vs 28.7 (13.5) vs 28.4 (10.6) vs 27.5 (9.9) mm Hg; all p>0.1). Compared with mannitol, HTS was associated with lower ICP and higher CPP and cardiac output., Conclusions: In patients with severe TBI and elevated ICP refractory to previous mannitol treatment, 7.5% hypertonic saline administered as second tier therapy is associated with a significant increase in brain oxygenation, and improved cerebral and systemic haemodynamics.

Objective: In this study, available medical literature were reviewed to determine whether brain hypoxia as measured by brain tissue oxygen (Bto2) levels is associated with increased risk of poor outcome after traumatic brain injury (TBI). A secondary objective was to examine the safety profile of a direct BtO2 probe. DATA SOURCE AND EXTRACTION: Clinical studies published between 1993 and 2008 were identified from electronic databases, Index Medicus, bibliographies of pertinent articles, and expert consultation. The following inclusion criteria were applied for outcome analysis: 1) more than 10 patients described, 2) use of a direct Bto2 monitor, 3) brain hypoxia defined as Bto2 <10 mm Hg for >15 or 30 minutes, 4) 6-month outcome data, and 5) clear reporting of patient outcome associated with Bto2. For the analysis, each selected article had to have adequate data to determine odds ratios (ORs) and confidence intervals (CIs). Thirteen studies met the initial inclusion criteria and three were included in the final outcome analysis. Safety data were abstracted from any report where it was mentioned., Data Synthesis: The three studies included 150 evaluable patients with severe TBI (Glasgow Coma Scale 15 minutes) was associated with worse outcome (OR 4.0; 95% CI 1.9-8.2) and increased mortality (OR 4.6; 95% CI 2.2-9.6). We reviewed published safety data; in 292 patients monitored with a Bto2 probe, only two adverse events were reported., Conclusion: Summary results indicate that brain hypoxia (<10 mm Hg) is associated with worse outcome after severe TBI and that Bto2 probes are safe. These results imply that treating patients to increase Bto2 may improve outcome after severe TBI. This question will require further study.

Objective: Barbiturate-induced coma can be used in patients to treat intractable intracranial hypertension when other therapies, such as osmotic therapy and sedation, have failed. Despite control of intracranial pressure, cerebral infarction may still occur in some patients, and the effect of barbiturates on outcome remains uncertain. In this study, we examined the relationship between barbiturate infusion and brain tissue oxygen (PbtO2)., Methods: Ten volume-resuscitated brain-injured patients who were treated with pentobarbital infusion for intracranial hypertension and underwent PbtO2 monitoring were studied in a neurosurgical intensive care unit at a university-based Level I trauma center. PbtO2, intracranial pressure (ICP), mean arterial pressure, cerebral perfusion pressure (CPP), and brain temperature were continuously monitored and compared in settings in which barbiturates were or were not administered., Results: Data were available from 1595 hours of PbtO2 monitoring. When pentobarbital administration began, the mean ICP, CPP, and PbtO2 were 18 +/- 10, 72 +/- 18, and 28 +/- 12 mm Hg, respectively. During the 3 hours before barbiturate infusion, the maximum ICP was 24 +/- 13 mm Hg and the minimum CPP was 65 +/- 20 mm Hg. In the majority of patients (70%), we observed an increase in PbtO2 associated with pentobarbital infusion. Within this group, logistic regression analysis demonstrated that a higher likelihood of compromised brain oxygen (PbtO2 < 20 mm Hg) was associated with a decrease in pentobarbital dose after controlling for ICP and other physiological parameters (P < 0.001). In the remaining 3 patients, pentobarbital was associated with lower PbtO2 levels. These patients had higher ICP, lower CPP, and later initiation of barbiturates compared with patients whose PbtO2 increased., Conclusion: Our preliminary findings suggest that pentobarbital administered for intractable intracranial hypertension is associated with a significant and independent increase in PbtO2 in the majority of patients. However, in some patients with more compromised brain physiology, pentobarbital may have a negative effect on PbtO2, particularly if administered late. Larger studies are needed to examine the relationship between barbiturates and cerebral oxygenation in brain-injured patients with refractory intracranial hypertension and to determine whether PbtO2 responses can help guide therapy.

Background: The objective of this study is to examine the utility of acetazolamide TCD ultrasound in the evaluation of MCA collateral blood flow reserve in patients with carotid occlusive disease., Methods: Acetazolamide TCD and cerebral angiography were performed for 28 carotid territories in 14 patients with carotid occlusive disease. The percentage change in mean blood flow velocity and PI in the MCA was measured before and after 1 g of acetazolamide was administered. The carotid territories were divided into groups according their angiographic findings: (1) mild/moderate (<70%) vs severe (> or =70%) extracranial carotid artery stenosis, and (2) active collateral blood flow to the MCA territory vs no collateral blood flow to the MCA., Results: After acetazolamide injection, the percentage increase in mean MCA velocity for mild/moderate vs severe carotid artery stenosis was 43% +/- 10% and 19% +/- 6%, respectively, indicating less collateral blood flow reserve in patients with severe stenosis (P = .04). The percentage decrease in the PI for MCA territories with vs without angiographic evidence of collateral blood flow was 4.6% +/- 4% and 16% +/- 3%, respectively (P = .04), indicating an exhausted vascular reserve in patients with evidence of active collateral blood flow on angiography., Conclusions: A decrease in the PI after acetazolamide administration represents a safe and noninvasive indicator of limited collateral blood flow reserve to the MCA territory ipsilateral to an extracranial carotid stenosis. Further study into the role acetazolamide TCD has in the preoperative evaluation of these patients, including threshold values, is warranted.

Object: The goal of this paper was to examine the relationship between methods of acute clinical assessment and measures of secondary cerebral insults in severe traumatic brain injury in children., Methods: Patients who underwent intracranial pressure (ICP), cerebral perfusion pressure (CPP), and brain oxygenation (PbtO(2)) monitoring and who had an initial Glasgow Coma Scale score, Pediatric Trauma Score, Pediatric Index of Mortality 2 score, and CT classification were evaluated. The relationship between these acute clinical scores and secondary cerebral insult measures, including ICP, CPP, PbtO(2), and systemic hypoxia were evaluated using univariate and multivariate analysis., Results: The authors found significant associations between individual acute clinical scores and select physiological markers of secondary injury. However, there was a large amount of variability in these results, and none of the scores evaluated predicted each and every insult. Furthermore, a number of physiological measures were not predicted by any of the scores., Conclusions: Although they may guide initial treatment, grading systems used to classify initial injury severity appear to have a limited value in predicting who is at risk for secondary cerebral insults.

Objective: Most physicians rely on conventional treatment targets for intracranial pressure, cerebral perfusion pressure, systemic oxygenation, and hemoglobin to direct management of traumatic brain injury (TBI) in children. In this study, we used brain tissue oxygen tension (PbtO2) monitoring to examine the association between PbtO2 values and outcome in pediatric severe TBI and to determine the incidence of compromised PbtO2 in patients for whom acceptable treatment targets had been achieved., Methods: In this prospective observational study, 26 children with severe TBI and a median postresuscitation Glasgow Coma Scale score of 5 were managed with continuous PbtO2 monitoring. The relationships between outcome and the 6-hour period of lowest PbtO2 values and the length of time that PbtO2 was less than 20, 15, 10, and 5 mmHg were examined. The incidence of reduced PbtO2 for each threshold was evaluated where the following targets were met: intracranial pressure less than 20 mmHg, cerebral perfusion pressure greater than 50 mmHg, arterial oxygen tension greater than 60 mmHg (and peripheral oxygen saturation > 90%), and hemoglobin greater than 8 g/dl., Results: There was a significant association between poor outcome and the 6-hour period of lowest PbtO2 and length of time that PbtO2 was less than 15 and 10 mmHg. Multiple logistic regression analysis showed that low PbtO2 had an independent association with poor outcome. Despite achieving the management targets described above, 80% of patients experienced one or more episodes of compromised PbtO2 (< 20 mmHg), and almost one-third experienced episodes of brain hypoxia (PbtO2 < 10 mmHg)., Conclusion: Reduced PbtO2 is associated with poor outcome in pediatric severe TBI. In addition, many patients experience episodes of compromised PbtO2 despite achieving acceptable treatment targets.

Hypertonic saline (HTS) may decrease intracranial pressure (ICP) in severe traumatic brain injury (STBI) and effectively resuscitates hypotensive patients. No data exist on institutional standardization of HTS for hypotensive patients with STBI. It remains unclear how HTS affects brain tissue oxygenation (PbtO2) in STBI. We hypothesized HTS could be safely standardized in patients with STBI and would lower ICP while improving cerebral perfusion pressure (CPP) and PbtO2. Under institutional guidelines in a Level I trauma center, 12 hypotensive STBI intensive care unit subjects received HTS. Inclusion criteria included mean arterial pressure (MAP) < or = 90 mmHg, Glasgow Coma Scale (GCS) < or = 8, ICP > or = 20 mmHg, and serum [Na+] <155 mEq/L. All patients underwent ICP monitoring. Hemodynamics, CPP, ICP, and PbtO2 data were collected before and hourly for 6 hours after HTS infusion. Guideline criteria compliance was greater than 95 per cent. No major complications occurred. Mean ICP levels dropped by 45 per cent (P < 0.01) and this drop persisted for 6 hours. CPP levels increased by 20 per cent (P < 0.05). PbtO2 remained persistently elevated for all time points after HTS infusion. Institutional use of HTS in STBI can be safely implemented in a center caring for neurotrauma patients. HTS infusion in hypotensive STBI reduces ICP and raises CPP. Brain tissue oxygenation tends to improve after HTS infusion.

Objective: Angiographic cerebral vasospasm occurs in approximately 70% of patients hospitalized after aneurysmal subarachnoid hemorrhage (SAH) and is associated with poor outcome. In this study, we examined whether or not cerebral circulation time (CCT) measured with digital subtraction angiography was associated with angiographic vasospasm., Methods: Patients who underwent cerebral angiography within 24 hours of SAH were analyzed. Contrast dye transit time from the arterial to the venous phase was measured to obtain CCT (supraclinoid internal carotid artery to parietal cortical veins) and microvascular CCT (cortical middle cerebral artery to parietal cortical veins). Patients with ruptured anterior circulation aneurysms and vasospasm on follow-up angiography (Group A) were compared with patients with SAH without vasospasm (Group B) and with normal control subjects (Group C)., Results: There were 20 patients in Group A (mean age, 51 +/- 13 yr), 17 patients in Group B (56 +/- 12 yr), and 98 patients in Group C (52 +/- 12 yr). CCT in patients in Group A (7.7 +/- 1.9 s) was significantly longer than those in Groups B (6.6 +/- 1.2 s; P = 0.005) and C (5.9 +/- 1 s; P < 0.001). Microvascular CCT in patients in Group A (7.1 +/- 1.8 s) was significantly longer than those in Groups B (6.1 +/- 1.2 s; P = 0.003) and C (5.4 +/- 0.9 s; P < 0.001)., Conclusion: Prolonged CCT, a measurement of increased small vessel resistance, can be identified within 24 hours after SAH and is associated with subsequent angiographic vasospasm. These results suggest that microcirculation changes may be involved in vasospasm.

Objectives: Brain death is a clinical diagnosis often confirmed with supplementary tests. In this study, we examined the relationship between brain death and the partial pressure of brain tissue oxygen (PbtO(2)). We hypothesized that a sustained PbtO(2) of 0 is associated with brain death., Methods: One hundred and twenty-six patients (Glasgow coma scale < or = 8, median age: 50 years) who underwent PbtO(2) monitoring were studied prospectively during a 2 year period in the neurointensive care unit at a university-based level I trauma center. PbtO(2), intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain temperature (BT) were compared before and after the diagnosis of brain death., Results: Six patients (median age: 52 years) experienced brain death. In these patients, PbtO(2) decreased toward 0 mmHg as ICP increased and CPP decreased. PbtO(2) reached 0 only when there was clinical evidence for brain death. During the subsequent 12 hours until the second brain death examination, PbtO(2) remained 0 mmHg and did not respond to oxygen challenge. In addition, TCD examination demonstrated a 'to and fro' pattern consistent with brain death and cerebral circulatory arrest. PbtO(2) of 0 mmHg was observed in five non-brain dead patients. These episodes were transient (>30 minutes) and responded to an oxygen challenge, directed treatment or catheter replacement., Discussion: A sustained (>30 minutes) brain PbtO(2) of 0 is consistent with brain death. We suggest that a sustained 'zero' PbtO(2) may be used to determine when a brain death examination is appropriate in the pharmacologically suppressed patient.

Glioblastoma is the most common primary brain tumor in adults from which about 15,000 patients die each year in the United States. Despite aggressive surgery, radiotherapy and chemotherapy, median survival remains only 1 year. Here we evaluate growth of primary human brain tumor cells in a defined nutrient culture medium (Neuregen) that was optimized for neuron regeneration. We hypothesized that Neuregen would inhibit tumor cell growth because of its ability to inhibit gliosis in rat brain. Tumor tissue was collected from 18 patients including 10 males and 8 females (mean age 60+/-12 years) who underwent craniotomy for newly diagnosed, histologically confirmed brain tumors. The tissue was shipped overnight in Hibernate transport medium. Tumor cells were isolated and plated in Neurobasal/serum or Neuregen on culture plastic. After 1 week, growth in Neuregen was significantly less in 9/10 glioblastoma multiforme cases, 5/5 meningioma cases and 3/3 cases of brain metastasis. Analysis of deficient formulations of Neuregen and formulations to which selected components were added back implicate no single active component. However, individual cases were sensitive to corticosterone, selenium, ethanolamine, fatty acids and/or antioxidants. Therefore, a defined culture medium that promotes neuron regeneration inhibits the growth of human primary glioblastoma, meningioma and metastatic tumor cells in culture. The possible in vivo efficacy of Neuregen for treatment of brain tumor resections remains to be determined.

The authors review literature that challenges the view that vasospasm involving large arteries is the exclusive cause of delayed ischemic neurological deficits (DINDs) following subarachnoid hemorrhage. They discuss alternative mechanisms and review the evidence supporting a potential role for thromboembolism. They conclude that vasospasm and thromboembolism play interrelated and additive roles in the development of DINDs, and that this interaction provides opportunities for novel therapeutic approaches.

Introduction: Intra-arterial papaverine (IAP) is used to treat symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). IAP, however, can increase intracranial pressure (ICP). In this study we examined whether IAP alters brain oxygen (BtO2)., Methods: Poor clinical grade (Hunt & Hess IV or V) SAH patients who underwent continuous ICP and BtO2 monitoring during IAP infusion for symptomatic cerebral vasospasm were evaluated as part of a prospective observational study., Results: Data are available for five patients (median age 58) who received IAP for cerebral vasospasm 4 to 7 days after SAH. In each patient, angiographic vasospasm was improved on postinfusion angiogram. Mean ICP before IAP was 23.04 +/- 1.18 mmHg; it increased immediately after IAP infusion and remained elevated (29.89 +/- 1.18 mmHg; p < 0.05) during IAP and for approximately 10 minutes after IAP ended. Baseline mean arterial pressure (MAP) was 110.55 +/- 1.36 mmHg. During IAP treatment MAP remained stable (110.90 +/- 2.00 mmHg; p = 0.31). Mean BtO2 before IAP was 32.99 +/- 1.45 mmHg. There was a significant BtO2 decrease in all patients during IAP to a mean of 22.96 +/- 2.9 mmHg (p < 0.05). BtO2 returned to baseline within 10 minutes after IAP ended. There was a modest relationship between the ICP increase and BtO2 decrease (R2 = 0.526)., Conclusion: IAP infusion to treat cerebral vasospasm following SAH can increase ICP and reduce BtO2. The IAP-induced reduction in BtO2 may help explain why IAP, although it reverses arterial narrowing, does not improve patient outcome.

Object: An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome., Methods: Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 +/- 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 +/- 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05)., Conclusions: The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

Background: Extraaxial cavernous hemangiomas (cavernomas) are very rare lesions, and less than 20 descriptions of these lesions outside the middle fossa have been reported. In this report, we describe a dural cavernous angioma involving the posterior sagittal sinus and discuss the clinical, radiological, operative, and histological features of this very uncommon lesion., Case Description: A 31-year-old right-handed male presented with headache and decreasing visual acuity. Severe bilateral papilledema was found on fundoscopic examination. Neurological examination demonstrated a minor right temporal field cut. Brain magnetic resonance imaging with contrast demonstrated a 2.5 x 2.5 cm hyperintense enhancing mass in the midline, which was contiguous with the posterior margin of the falx cerebri. The patient underwent a bilateral occipital craniotomy centered on the lesion. The histological features were consistent with cavernous angioma., Conclusion: This report demonstrates that although extra axial cavernomas are quite rare, they must be included in the differential diagnosis of enhancing lesions along the posterior sagittal sinus. The operative removal of these lesions can be quite treacherous and usually requires a careful reapproximation of the patent sinus after lesion excision.

Object: Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2., Methods: Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4+/-10.9 mm Hg. The baseline MABP and CPP were 90+/-20 and 84+/-19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9+/-7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5+/-7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7+/-11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2., Conclusions: Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

Object: Increased intracranial pressure (ICP) is well known to affect adversely patients with head injury. In contrast, the variables associated with ICP following aneurysmal subarachnoid hemorrhage (SAH) and their impact on outcome have been less intensely studied., Methods: In this retrospective study the authors reviewed a prospective observational database cataloging the treatment details in 433 patients with SAH who had undergone surgical occlusion of an aneurysm as well as ICP monitoring. All 433 patients underwent postoperative ICP monitoring, whereas only 146 (33.7%) underwent both pre- and postoperative ICP monitoring. The mean maximal ICP was 24.9 +/- 17.3 mm Hg (mean +/- standard deviation). During their hospital stay, 234 patients (54%) had elevated ICP (> 20 mm Hg), including 136 of those (48.7%) with a good clinical grade (Hunt and Hess Grades I-III) and 98 (63.6%) of the 154 patients with a poor grade (Hunt and Hess Grades IV and V) on admission. An increased mean maximal ICP was associated with several admission variables: worse Hunt and Hess clinical grade (p < 0.0001), a lower Glasgow Coma Scale (GSC) motor score (p < 0.0001); worse SAH grade based on results of computerized tomography studies (p < 0.0001); intracerebral hemorrhage (p = 0.024); severity of intraventricular hemorrhage (p < 0.0001); and rebleeding (p = 0.0048). Both intraoperative cerebral swelling (p = 0.0017) and postoperative GCS score (p < 0.0001) were significantly associated with a raised ICP. Variables such as patient age, aneurysm size, symptomatic vasospasm, intraoperative aneurysm rupture, and secondary cerebral insults such as hypoxia were not associated with raised ICP. Increased ICP adversely affected outcome: 71.9% of patients with normal ICP demonstrated favorable 6-month outcomes postoperatively, whereas 63.5% of patients with ICP between 20 and 50 mm Hg and 33.3% with ICP greater than 50 mm Hg demonstrated favorable outcomes. Among 21 patients whose raised ICP did not respond to mannitol therapy, all experienced a poor outcome and 95.2% died. Among 145 patients whose elevated ICP responded to mannitol, 66.9% had a favorable outcome and only 20.7% were dead 6 months after surgery (p < 0.0001). According to results of multivariate analysis, however, ICP was not an independent outcome predictor (odds ratio 1.26, 95% confidence interval 0.28-5.68)., Conclusions: Increased ICP is common after SAH, even in patients with a good clinical grade. Elevated ICP post-SAH is associated with a worse patient outcome, particularly if ICP does not respond to treatment. This association, however, may depend more on the overall severity of the SAH than on ICP alone.

Object: Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease., Methods: The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management., Conclusions: All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

Background: Cerebral hypoxia (cerebral cortical oxygenation [Pbro2] < 20 mm Hg) monitored by direct measurement has been shown in animal and small clinical studies to be associated with poor outcome. We present our preliminary results observing Pbro2 in patients with traumatic brain injury (TBI)., Methods: A prospective observational cohort study was performed. Institutional review board approval was obtained. All patients with TBI who required measurement of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and Pbro2 because of a Glasgow Coma Scale score < 8 were enrolled. Data sets (ICP, CPP, Pbro2, positive end-expiratory pressure (PEEP), Pao2, and Paco2) were recorded during routine manipulation. Episodes of cerebral hypoxia were compared with episodes without. Results are displayed as mean +/- SEM; t test, chi2, and Fisher's exact test were used to answer questions of interest., Results: One hundred eighty-one data sets were abstracted from 20 patients. Thirty-five episodes of regional cerebral hypoxia were identified in 14 patients. Compared with episodes of acceptable cerebral oxygenation, episodes of cerebral hypoxia were noted to be associated with a significantly lower mean Pao2 (144 +/- 14 vs. 165 +/- 8; p < 0.01) and higher mean PEEP (8.8 +/- 0.7 vs. 7.1 +/- 0.3; p < 0.01). Mean ICP and CPP measurements were similar between groups. In a univariate analysis, cerebral hypoxic episodes were associated with Pao2 < or = 100 mm Hg (p < 0.01) and PEEP > 5 cm H2O (p < 0.01), but not ICP > 20 mm Hg, CPP < or = 65 mm Hg, or Pac2 < or = 35 mm Hg., Conclusion: Cerebral oxymetry is confirmed safe in the patient with multiple injuries with TBI. Occult cerebral hypoxia is present in the traumatic brain injured patient despite normal traditional measurements of cerebral perfusion. Further research is necessary to determine whether management protocols aimed at the prevention of cerebral cortical hypoxia will affect outcome.

Introduction: Three-dimensional computed tomographic angiography (3-D-CTA) can be used to evaluate cerebrovascular disease. A potential limitation of this technology is obscuration of vascular anatomy by bone. In view of this, we developed a method for bone-free rendering using iterative relative fuzzy connectedness (IRFC) of 3-D-CTA to examine the cerebral vasculature without the intervening cranial base., Methods: 3-D-CTA was obtained in 10 patients with cerebrovascular disease by use of an algorithm based on IRFC. Bone structures were removed and vascular anatomy was isolated with an almost completely automated process. Bone-removed images were rendered via maximum intensity projections, compared with digital subtraction angiography, and evaluated for vascular abnormalities., Results: Compared with digital subtraction angiography, IRFC 3-D-CTA successfully defined the intracranial vascular anatomy in all 10 patients. An aneurysm was identified in 6 patients, bilateral carotid-cavernous fistulae in 1 patient, and no structural abnormalities in the remaining 3 patients., Conclusion: In 3-D-CTA, our preliminary findings suggest that bone obscuration, one of the current limitations of CTA, can be overcome through appropriate computer algorithms. We are now working on improving the computational efficiency of these algorithms to allow routine use of IRFC 3-D-CTA in an interventional or surgical suite.

Study Design: A case of iatrogenic intramedullary contrast injection during a C1-C2 cervical myelography is reported., Objective: To investigate the occurrence of iatrogenic intramedullary contrast injection during a current C1-C2 cervical myelography., Summary of Background Data: Intramedullary injection of contrast is a rare but serious complication of C1-C2 cervical myelography that has not been reported since the widespread use of magnetic resonance imaging and the NASCIS III study protocol., Methods: A 39-year-old woman received an iatrogenic intramedullary contrast injection during a C1-C2 cervical myelography., Results: During the procedure the patient reported right-side face, neck, and arm pain and parethesias. After the procedure, right arm weakness and diffuse hyperreflexia developed. Postmyelography imaging demonstrated intramedullary contrast and cord swelling. High-dose methylprednisolone was administered intravenously and the patient's symptoms improved. The literature and management of this rare complication are reviewed., Conclusions: Intramedullary cord injection is a rare complication of cervical myelography. The mechanism of spinal cord injury appears to involve a combination of physical compression from the injected liquid and neurotoxicity of the contrast material. Iohexol rather than metrizamide should be used when C1-C2 myelography is indicated in patients who are unable to undergo magnetic resonance imaging, or those whose pathology is inadequately demonstrated magnetic resonance imaging alone. In the event of contrast injection into the spinal cord, administration of high-dose methylprednisolone is recommended.

Growing skull fractures (GSF) are rare in adults. We report the case of an adult who was found to have a GSF 50 years after head trauma. This case highlights the need to consider GSFs in the differential diagnosis of adults with intradiploic skull lesions.