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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.

Introduction: Subarachnoid hemorrhage (SAH) mortality is decreasing, but data on functional outcomes over time is lacking. Methods: We created trends of good (Glasgow Outcomes Scale [GOS] of 4 or 5) and optimal (GOS of 5) functional outcomes and mortality (GOS of 1) using linear regression in 15 SAH trials and registries from 1982 to 2014. Models adjusted for age, sex, history of hypertension, World Federation of Neurological Surgeons grade, Fisher grade, aneurysm size, location, and repair modality, and whether data was from a clinical trial or registry. Analyses were repeated separately for the clinical trials and registries. Missing data were handled with multiple imputation. Results: Overall, 13,343 SAH patients were included. 9,524 (71%) patients had good functional outcome, while 1,608 (12%) died. There was a 0.6% adjusted improvement (95% confidence interval [CI]: 0.5% to 0.7%; p Conclusions: SAH morbidity and mortality decreased from the 1980s to 2010s. This data can be helpful for researchers planning trials, clinicians discussing expected outcomes with patients and family members, and healthcare administrators planning resource utilization.

INTRODUCTION Telemedicine has been available for more than 20 years and is playing an increasing role in clinical care. However, few studies have evaluated the value of telemedicine in neurosurgical consultations and in guiding neurosurgical care. METHODS In this prospective observational study, we examined our experience with emergency video telemedicine consultations for neurosurgical patients at a rural hospital system. Our system uses secure and HIPAA-compliant video conferencing to connect providers and patients to a remote neurosurgery consultant, and operates one out of two days. RESULTS During a ten-month period, 229 neurosurgical telemedicine consultations were performed. Two-thirds of the patients had intracranial pathology, 28% had spinal pathology and 3% of the consults were for patients who returned after care at our institution or required clearance for another procedure. Five patients required transfer within the hospital system and 12 out of the hospital system for a higher level of care (total 7.4%). Patients that required transfer most frequently had intracranial pathology (70%). The number of patients transferred out was less than in the year before telemedicine was available. CONCLUSION Telemedicine consultation for neurosurgery is feasible for a variety of neurosurgical pathologies, improves patient access to neurosurgery expertise, and facilitates appropriate transfers to a higher level of care when required. Our findings are especially relevant in light of the COVID-19 pandemic, which has highlighted the importance of delivering quality medical care when physical patient contact is not possible.

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.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.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).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.

To work toward the goal of building healthier lives, free of cardiovascular diseases and stroke, the American Heart Association (AHA) and American Stroke Association (ASA) have developed a multifaceted strategy for improving the quality of care for stroke. A key feature of this strategy is the development of professional guidelines for evidence-based stroke care. Recommendations are provided for acute management, primary and secondary prevention, rehabilitation, stroke systems of care, and other domains of stroke care.1–4 The strength of the evidence supporting these recommendations is given, according to a specified grading system. For many aspects of care, there is widespread consensus that the intervention is beneficial, usually supported by strong scientific evidence including randomized controlled trials. Professional guidelines improve the delivery of evidence-based care; however, despite these guidelines, gaps between best evidence-based practice and actual practice persist.5 To close these gaps in quality of care, several organizations have developed systems to allow practitioners and healthcare organizations such as hospitals to quantify the quality of their care through performance measures. A performance measure is defined by the Agency for Healthcare Research and Quality as a “mechanism for assessing the degree to which a provider competently and safely delivers the appropriate clinical services to the patient within the optimal time period.”6 The AHA and American College of Cardiology Foundation have additionally suggested that performance measures should be based on the highest level of supportive evidence and have the greatest impact on health outcomes.7 Performance measures, in addition to supporting quality improvement activities, are specifically suitable for public reporting, external comparisons, and possibly pay-for-performance programs. As steward of the professional guidelines for stroke care, with a large group of volunteer expert clinicians with expertise in guideline creation and performance measurement, the AHA/ASA is uniquely positioned to develop high-quality …

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.Randomized prospective clinical trial.Ten ICUs in the United States.One hundred nineteen severe traumatic brain injury patients.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.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; p0.0001). 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.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 and Purpose— To address the increasing need to counsel patients about treatment indications for unruptured intracranial aneurysms (UIA), we endeavored to develop a consensus on assessment of UIAs among a group of specialists from diverse fields involved in research and treatment of UIAs. Methods— After composition of the research group, a Delphi consensus was initiated to identify and rate all features, which may be relevant to assess UIAs and their treatment by using ranking scales and analysis of inter-rater agreement (IRA) for each factor. IRA was categorized as very high, high, moderate, or low. Results— Ultimately, 39 specialists from 4 specialties agreed (high or very high IRAs) on the following key factors for or against UIA treatment decisions: (1) patient age, life expectancy, and comorbid diseases; (2) previous subarachnoid hemorrhage from a different aneurysm, family history for UIA or subarachnoid hemorrhage, nicotine use; (3) UIA size, location, and lobulation; (4) UIA growth or de novo formation on serial imaging; (5) clinical symptoms (cranial nerve deficit, mass effect, and thromboembolic events from UIAs); and (6) risk factors for UIA treatment (patient age and life expectancy, UIA size, and estimated risk of treatment). However, IRAs for features rated with low relevance were also generally low, which underlined the existing controversy about the natural history of UIAs. Conclusions— Our results highlight that neurovascular specialists currently consider many features as important when evaluating UIAs but also highlight that the appreciation of natural history of UIAs remains uncertain, even within a group of highly informed individuals.

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. 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. Data from 64 patients were analyzed (12 were lost to follow-up). There were 530 episodes of compromised PbtO2 (

Background Placement of an external ventricular drain (EVD) is a commonly performed and often lifesaving procedure. Although hemorrhage is one of the commonest complications associated with the procedure, ventricular catheter-induced vascular injury is rarely reported. Objective To describe 9 cases of EVD-related vascular trauma: 7 arteriovenous fistulas and 2 traumatic aneurysms. Methods During a 3-year period, 299 patients had EVDs placed. Eight patients (2.75%), 3 male and 5 female (mean age, 48 ± 20 years), developed vascular lesions associated with EVDs. Six patients developed arteriovenous fistulas and 2 patients developed a traumatic aneurysm. The arterial feeders of 5 superficial draining fistulas arose from the middle meningeal artery, and the arterial feeder of a deep-draining fistula originated from a lenticulostriate artery. One traumatic aneurysm arose from a distal branch of the anterior cerebral artery, and the second from a branch of the superficial temporal artery. Four of the superficial fistulas were treated with transarterial embolization. Results Two superficial fistulas and the deep-draining fistula resolved spontaneously after EVD removal. The intracranial aneurysm was embolized with Onyx18, and the superficial temporal artery aneurysm was managed conservatively. There were no hemorrhages associated with any of these vascular lesions and no complications after treatment. Conclusion Our data suggest that iatrogenic vascular trauma associated with EVD insertions (2.75%) may be more common than is currently appreciated. Endovascular treatment is effective and may be necessary when these lesions do not resolve spontaneously.

Jehovah's Witnesses (JW) are a Christian faith with1 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.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.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 value7 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.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.

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 Despite the morbidity and mortality of subarachnoid hemorrhage (SAH), the average volume of a typical hemorrhage is not well defined. Animal models of SAH often do not accurately mimic the human disease process. Objective The purpose of this study is to estimate the average SAH volume, allowing standardization of animal models of the disease. Methods We performed a MEDLINE search of SAH volume and erythrocyte counts in human cerebrospinal fluid as well as for volumes of blood used in animal injection models of SAH, from 1956 to 2010. We polled members of the American Association of Neurological Surgeons (AANS) for estimates of typical SAH volume. Using quantitative data from the literature, we calculated the total volume of SAH as equal to the volume of blood clotted in basal cisterns plus the volume of dispersed blood in cerebrospinal fluid. The results of the AANS poll confirmed our estimates. Results The human literature yielded 322 publications and animal literature, 237 studies. Four quantitative human studies reported blood clot volumes ranging from 0.2 to 170 mL, with a mean of ∼20 mL. There was only one quantitative study reporting cerebrospinal fluid red blood cell counts from serial lumbar puncture after SAH. Dispersed blood volume ranged from 2.9 to 45.9 mL, and we used the mean of 15 mL for our calculation. Therefore, total volume of SAH equals 35 mL. The AANS poll yielded 176 responses, ranging from 2 to 350 mL, with a mean of 33.9 ± 4.4 mL. Conclusions Based on our estimate of total SAH volume of 35 mL, animal injection models may now become standardized for more accurate portrayal of the human disease process.

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.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.We studied 103 patients monitored with ICP and Pbto(2) for24 hours. Durations of BH (Pbto(2)15 mm Hg), ICP20 mm Hg, and CPP60 mm Hg were calculated with linear interpolation, and their associations with outcome within 30 days were analyzed.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).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.

This summary of the last session of the First Neurocritical Care Research Conference reviews the discussions about research priorities in neurocritical care. The first presentation reviewed current projects funded by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health and potential models to follow including an independent Neurocritical Care Network or the creation of such a network with the goal of collaborating with already existing ones. Experienced neurointensivists then presented their views on the most common and important research questions that need to be answered and investigated in the field. Finally, utility of clinical registries was discussed emphasizing their importance as hypothesis generators. During the group discussion, interests in comparative effectiveness research, the use of physiological endpoints from monitoring and alternate trial design were expressed.

Background Obesity has been associated with compromised tissue oxygenation and reduced organ perfusion. The brain is critically dependent on oxygen delivery, and reduced brain tissue oxygen tension (PbtO2) may result in poor outcome after brain injury. We tested the hypothesis that obesity is associated with compromised PbtO2 after severe brain injury. Methods Patients with severe brain injury (GCS score ≤ 8) who underwent continuous PbtO2 monitoring were retrospectively identified from a prospective single-center database. Patients, were classified by body mass index (BMI = weight (kg)/m2) and were included if they were obese (BMI ≥ 30) or non-obese (BMI =

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.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 was20 mmHg (and the inverse) were calculated.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.Seizures were neither associated with a PbtO(2) value of20 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.

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.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 as20 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.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 (p0.05).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.

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.We examined the association between lung function and brain tissue oxygen tension (PbtO2) in patients with severe TBI.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.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 ratio300 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 ratio100], 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 (PbtO220 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21-3.77; P.01).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 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.

Object 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 (PbtO2) and death after aneurysmal SAH. Methods Forty-six patients, including 34 women and 12 men (Glasgow Coma Scale Score ≤ 8 and median age 58.5 years) who underwent PbtO2 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 PbtO2 targets. The relationship between PbtO2 and 1-month survival was examined. Results Data were available from 5424 hours of PbtO2 monitoring. For the entire cohort the mean ICP, CPP, and PbtO2 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 PbtO2 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 PbtO2 (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 PbtO2 was stratified according to CPP level, survivors had higher PbtO2 levels. Following logistic regression, the number of episodes of compromised PbtO2 (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. Conclusions Patient deaths after SAH may be associated with a lower mean PbtO2 and longer periods of compromised cerebral oxygenation than in survivors. This knowledge may be used to help direct therapy.

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) ≤ 90 mmHg, Glasgow Coma Scale (GCS) ≤ 8, ICP ≥ 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.

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.One hundred and twenty-six patients (Glasgow coma scaleor = 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.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.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.

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.

One of the missions of the Neurocritical Care Society (NCS) is to foster clinical, experimental, and outcomes research focused on developing innovative and cost-effective medical and surgical interventions for acute neurological disorders. To achieve this mission, NCS created a research committee. This committee organized the Neurocritical Care Research Conference. The most important outcome of the First Neurocritical Care Research Conference (September 2009) was the creation of the Neurocritical Care Research Network (NCRN) [1]. Following the success of that first endeavor, the Second Neurocritical Care Research Conference took place in Houston, TX May 18–20, 2012. This symposium was funded by NINDS (1R13NS077610-01, P.I. Jose I. Suarez), Baylor St. Luke’s Medical Center (Neuroscience Center) in Houston, and the Integra Foundation and endorsed by the Baylor College of Medicine (BCM) and the NCS. The overall goal of this interdisciplinary scientific gathering was to bring together a diverse group of academic scientists and physicians with a common interest in understanding and advancing research in multimodality monitoring in neurocritical care diseases, in large part because monitoring patient disease and care is a fundamental aspect of neurocritical care. The need for the design of adequate clinical studies to test these monitoring techniques was addressed in the context of the recently created NCRN to facilitate collaboration and patient enrollment. In addition, this conference provided a unique opportunity for trainees, junior faculty, and other scientists to interact with investigators in the field of neurocritical care. The conference opened with a discussion on new approaches to multifaceted therapeutic bundles in neurocritical care followed by five scientific sessions: (1) Global Brain Monitoring in the Neurocritical Care Unit; (2) Regional Brain Monitoring in the Neurocritical Care Unit; (3) Data Collection and Interpretation; (4) Conventional Clinical Trial Design of Multimodality Monitoring; and (5) Alternative Clinical Trial Design. The meeting had 158 registrants and 135 attendees. This represents a 26 % increase in attendance compared to our first research conference. Attendees came from all parts of the world including the United States, Canada, Latin America, Europe, Japan, India, and the Middle East. We had lively and interesting discussions throughout the meeting. The conference was successful and well received with 94 % stating that it was fair and balanced. At the end of the meeting, there was consensus on two major points: (1) we need a common language to describe the technology available and the information it provides to pursue further research to advance the field and (2) technology alone will not impact upon clinical outcome without specific interventions and pathways that can modify and ameliorate the biochemical cascade unleashed by brain insults. Two projects have since evolved from the Second Neurocritical Care Research Conference: (1) the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care, a collaboration between the NCS, the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, and the Latin & Jose I. Suarez jisuarez@bcm.edu

✓ 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.

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). 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. 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

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.

When a new technology is introduced it is important to empower the bedside practitioner with a resource tool that outlines the purpose, placement procedure, technology application guidelines, and interventions associated with that new technology. This promotes product and patient safety and successful implementation of the new technology. Continued evaluation of bedside clinical practice and the technology used in the care and treatment of the severe brain injured patient can lead to improvements in management and in technology design. Future clinical research initiatives exploring the impact of new technology will enable us to discover cost-effective treatments and interventions that will improve the outcome for a person with traumatic brain injury, a condition that devastates hundreds of thousands of Americans each year.

Objective: We endeavored to develop an unruptured intracranial aneurysm (UIA) treatment score (UIATS) model that includes and quantifies key factors involved in clinical decision-making in the management of UIAs and to assess agreement for this model among specialists in UIA management and research. Methods: An international multidisciplinary (neurosurgery, neuroradiology, neurology, clinical epidemiology) group of 69 specialists was convened to develop and validate the UIATS model using a Delphi consensus. For internal (39 panel members involved in identification of relevant features) and external validation (30 independent external reviewers), 30 selected UIA cases were used to analyze agreement with UIATS management recommendations based on a 5-point Likert scale (5 indicating strong agreement). Interrater agreement (IRA) was assessed with standardized coefficients of dispersion (vr*) (vr* 5 0 indicating excellent agreement and vr* 5 1 indicating poor agreement). Results: The UIATS accounts for 29 key factors in UIA management. Agreement with UIATS (mean Likert scores) was 4.2 (95% confidence interval [CI] 4.1–4.3) per reviewer for both reviewer cohorts; agreement per case was 4.3 (95% CI 4.1–4.4) for panel members and 4.5 (95% CI 4.3–4.6) for external reviewers (p 5 0.017). Mean Likert scores were 4.2 (95% CI 4.1–4.3) for interventional reviewers (n 5 56) and 4.1 (95% CI 3.9–4.4) for noninterventional reviewers (n 5 12) (p 5 0.290). Overall IRA (vr*) for both cohorts was 0.026 (95% CI 0.019–0.033). Conclusions: This novel UIA decision guidance study captures an excellent consensus among highly informed individuals on UIA management, irrespective of their underlying specialty. Clinicians can use the UIATS as a comprehensive mechanism for indicating how a large group of specialists might manage an individual patient with a UIA. Neurology® 2015;85:881–889

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. 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. 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. 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: 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.

Anaemia is common among patients in the neurocritical care unit (NCCU) and is thought to exacerbate brain injury. However, the optimal haemoglobin (Hgb) level still remains to be elucidated for traumatic brain injury (TBI), subarachnoid haemorrhage (SAH) and acute ischaemic stroke (AIS). This review outlines recent studies about anaemia and the effects of red blood cell transfusion (RBCT) on outcome in TBI, SAH and AIS patients admitted to the NCCU.Patients with severe SAH, AIS and TBI often develop anaemia and require RBCT. In general critical care, a restrictive RBCT strategy (Hgb ~7 g/dl) is preferable in patients without serious cardiac disease. In severe TBI, AIS and SAH, both anaemia and RBCT may negatively influence clinical outcome. However, the appropriate RBCT trigger remains unclear and there is great variance in how these patients are transfused. There is evidence from PET and microdialysis studies in humans that RBCT can favourably influence brain metabolism and oxygenation. This correction of hypoxia or altered metabolism rather than anaemia may be of greater importance.Results from general critical care should not be extrapolated to all patients with acute brain injury. Transfusion is not risk free, but RBCT use needs to be considered also in terms of potential benefit.

Background and Purpose— Lactate is central for the regulation of brain metabolism and is an alternative substrate to glucose after injury. Brain lactate metabolism in patients with subarachnoid hemorrhage has not been fully elucidated. Methods— Thirty-one subarachnoid hemorrhage patients monitored with cerebral microdialysis (CMD) and brain oxygen (PbtO 2 ) were studied. Samples with elevated CMD lactate (>4 mmol/L) were matched to PbtO 2 and CMD pyruvate and categorized as hypoxic (PbtO 2 119 μmol/L) versus nonhyperglycolytic. Results— Median per patient samples with elevated CMD lactate was 54% (interquartile range, 11%–80%). Lactate elevations were more often attributable to cerebral hyperglycolysis (78%; interquartile range, 5%–98%) than brain hypoxia (11%; interquartile range, 4%–75%). Mortality was associated with increased percentage of samples with elevated lactate and brain hypoxia (28% [interquartile range 9%–95%] in nonsurvivors versus 9% [interquartile range 3%–17%] in survivors; P =0.02) and lower percentage of elevated lactate and cerebral hyperglycolysis (13% [interquartile range, 1%–87%] versus 88% [interquartile range, 27%–99%]; P =0.07). Cerebral hyperglycolytic lactate production predicted good 6-month outcome (odds ratio for modified Rankin Scale score, 0–3 1.49; CI, 1.08–2.05; P =0.016), whereas increased lactate with brain hypoxia was associated with a reduced likelihood of good outcome (OR, 0.78; CI, 0.59–1.03; P =0.08). Conclusions— Brain lactate is frequently elevated in subarachnoid hemorrhage patients, predominantly because of hyperglycolysis rather than hypoxia. A pattern of increased cerebral hyperglycolytic lactate was associated with good long-term recovery. Our data suggest that lactate may be used as an aerobic substrate by the injured human brain.

Ornithine transcarbamylase deficiency (OTCD) is the most common of the urea cycle disorders and results in an accumulation of ammonia and its metabolites. Excess ammonia in the brain is metabolized to glutamine, which increases intracellular osmolarity and contributes to cytotoxic edema. We report a case of a woman heterozygous for OTCD who developed acute hyperammonemic encephalopathy and increased intracranial pressure (ICP). Despite hemodialysis, protein restriction, and administration of pharmacologic nitrogen scavengers, she developed progressive cerebral edema and increased ICP that was refractory to maximal medical management. She underwent a bifrontal decompressive craniectomy resulting in resolution of her intracranial hypertension. Aggressive multimodality management of the patient coupled with bifrontal decompressive hemicraniectomy was a life-saving measure, offering the patient a reasonable outcome. At 6 month follow-up she had moderate disability on the Glasgow Outcome Score associated with cognitive difficulties.

Objective: In this study, available medical literature were reviewed to determine whether brain hypoxia as measured by brain tissue oxygen (Bto 2 ) 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 BtO 2 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 Bto 2 monitor, 3) brain hypoxia defined as Bto 2 15 or 30 minutes, 4) 6-month outcome data, and 5) clear reporting of patient outcome associated with Bto 2 . For the analysis, each selected article had to have adequate data to determine odds ratios (ORs) and confidence intervals (Cls). 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 ≤8). Brain hypoxia was identified in 71 (47%) of these patients. Among the patients with brain hypoxia, 52 (73%) had unfavorable outcome including 39 (55%) who died. In the absence of brain hypoxia, 34 (43%) patients had an unfavorable outcome, including 17 (22%) who died. Overall brain hypoxia (Bto 2 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 Bto 2 probe, only two adverse events were reported. Conclusion: Summary results indicate that brain hypoxia (

Apart from choriocarcinoma, involvement of the central nervous system (CNS) by gynecologic malignancy is rare. A 10-year retrospective review at the University of Washington Medical Center (Seattle, WA) and Swedish Hospital and Medical Center Tumor Registry (Seattle, WA) identified 14 patients with cerebral metastases from ovarian carcinoma. Median age at diagnosis of cerebral metastases was 52.5 years. Median interval from the diagnosis of ovarian carcinoma to the diagnosis of CNS metastases was 14.5 months. Seven patients had received cisplatin therapy before CNS relapse. Seven patients underwent second-look procedures before developing CNS metastases; in three, results were negative. Eight patients had evidence of extraperitoneal spread to other sites at the time of CNS relapse. Clinical manifestations included motor weakness, seizures, headache, confusion, and speech disturbance. All lesions were contrast enhancing on computed tomography (CT) scans and were located in the cerebral hemispheres. Nine patients had single lesions, five of whom underwent surgical resection of the lesion with histologic confirmation of metastases from the primary site. Median survival was 2 months in patients receiving radiation therapy alone and 17 months in patients who received surgery and radiation. Median survival of the entire series was 3 months. The presence of multiple cerebral metastases or evidence of extraperitoneal spread elsewhere in the body was adversely associated with survival. The prognosis of patients with cerebral metastases from ovarian carcinoma appears poor. However, early diagnosis by routine CT scanning followed by surgical resection and radiation may improve overall survival in a select group of patients.

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 (PbtO 2 ). METHODS: Ten volume-resuscitated brain-injured patients who were treated with pentobarbital infusion for intracranial hypertension and underwent PbtO 2 monitoring were studied in a neurosurgical intensive care unit at a university-based Level I trauma center. PbtO 2 , 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 PbtO 2 monitoring. When pentobarbital administration began, the mean ICP, CPP, and PbtO 2 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 PbtO 2 associated with pentobarbital infusion. Within this group, logistic regression analysis demonstrated that a higher likelihood of compromised brain oxygen (PbtO 2 < 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 PbtO 2 levels. These patients had higher ICP, lower CPP, and later initiation of barbiturates compared with patients whose PbtO 2 increased. CONCLUSION: Our preliminary findings suggest that pentobarbital administered for intractable intracranial hypertension is associated with a significant and independent increase in PbtO 2 in the majority of patients. However, in some patients with more compromised brain physiology, pentobarbital may have a negative effect on PbtO 2 , 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 PbtO 2 responses can help guide therapy.

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 (PbtO2) 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, PbtO2, 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.

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, ICPor = 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 (P0.01) and this drop persisted for 6 hours. CPP levels increased by 20 per cent (P0.05). 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.

Vancomycin pharmacokinetics were determined in 25 patients receiving ventriculoperitoneal shunts for hydrocephalus. Computed tomography scan-derived ventricular-brain ratio as an expression of hydrocephalus varied between 9.3% and 15.4% (12.9% +/- 1.7%). One hour prior to surgery each patient received 1 g of vancomycin infused intravenously over 60 minutes. Samples of cerebrospinal fluid and venous blood were obtained 1 hour later and vancomycin levels assayed by fluorescence polarization immunoassay. There were 11 females and 14 males, with a mean age of 44.5 +/- 10.3 years and a mean weight of 72.0 +/- 11.4 kg. All had normal renal function. Levels of vancomycin in the cerebrospinal fluid at 1 hour ranged from 0.1 to 1.5 micrograms/mL (0.9 +/- 0.3). Weight did not affect these values (p greater than 0.1). Simultaneous blood vancomycin levels varied between 9.1 and 38.7 micrograms/mL (22.3 +/- 8.3). Ventricular volume, expressed as the ventricular-brain ratio, did not correlate with cerebrospinal fluid vancomycin levels (p greater than 0.5). There was no significant increase in concentrations of vancomycin in CSF as cerebrospinal fluid protein concentration increased, nor when blood vancomycin concentration was greater than 20 mg/dL (therapeutic range) (p greater than 0.1). No patient had evidence of infection at 6 months follow up. These results indicate minimal cerebrospinal fluid penetrance of vancomycin when administered systemically 1 hour prior to shunt surgery. In addition concentrations of vancomycin in cerebrospinal fluid bear no relationship to weight, ventricular volume, meningeal inflammation, or blood levels in the therapeutic range. The minimum inhibitory concentration of vancomycin for staphylococci is 1.5 to 3.1, and as bactericidal levels of 5 to 8 minimum inhibitory concentration are needed to kill organisms, a combination of both systemic and intraventricular vancomycin may be needed to ensure adequate cerebrospinal fluid and tissue concentration of antibiotic during shunt prophylaxis.