Continuous Electroencephalography (cEEG) Changes Precede Clinical Changes in a Case of Progressive Cerebral Edema

Background

Continuous electroencephalogram (cEEG) is tightly linked to cerebral metabolism and is sensitive to cerebral ischemia and hypoxia. The severity of cerebral ischemia can be seen on cEEG as changes in morphology, amplitude, or frequency, and cEEG may detect neuronal dysfunction at a reversible stage.

Methods

Case report and imaging.

Results

We present a case of focal cerebral edema with changes seen on cEEG 24 h before clinical signs of increased intracranial pressure. cEEG showed developing asymmetry in the left hemisphere followed by burst suppression. The right hemisphere showed similar progression to burst suppression. Complete suppression of both hemispheres was noted 6 h before clinical signs of herniation. Computed tomography (CT) head confirmed a large left parietal intracerebral hematoma with mass effect.

Conclusions

cEEG has applications in monitoring cerebral dysfunction in addition to detecting seizure activity in the intensive care unit. It may serve a vital role in multi-modality monitoring for early recognition of neurological complications from brain injuries that may not be noticed clinically, which is paramount to early intervention.     

DESTINY-S: Attitudes of Physicians Toward Disability and Treatment in Malignant MCA Infarction

Background

Decompressive hemicraniectomy (DHC) reduces mortality and improves outcome after malignant middle cerebral artery (MCA) infarction but leaves a high number of survivors severely disabled. Attitudes among physicians toward the degree of disability that is considered acceptable and the impact of aphasia may play a major role in treatment decisions.

Methods

DESTINY-S is a multicenter, international, cross-sectional survey among 1,860 physicians potentially involved in the treatment of malignant MCA infarction. Questions concerned the grade of disability, the hemisphere of the stroke, and the preferred treatment for malignant MCA infarction.

Results

mRS scores of 3 or better were considered acceptable by the majority of respondents (79.3 %). Only few considered a mRS score of 5 still acceptable (5.8 %). A mRS score of 4 was considered acceptable by 38.0 %. Involved hemisphere (dominant vs. non-dominant) was considered a major clinical symptom influencing treatment decisions in 47.7 % of respondents, also reflected by significantly different rates for DHC as preferred treatment in dominant versus non-dominant hemispheric infarction (46.9 vs. 72.9 %). Significant differences in acceptable disability and treatment decisions were found among geographic regions, medical specialties, and respondents with different work experiences.

Conclusion

Little consensus exists among physicians regarding acceptable outcome and therapeutic management after malignant MCA infarction, and physician’s recommendations do not correlate with available evidence. We advocate for a decision-making process that balances scientific evidence, patient preference, and clinical expertise.     

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

Background

The neurological wake-up test (NWT) is used to monitor the level of consciousness in patients with traumatic brain injury (TBI). However, it requires interruption of sedation and may elicit a stress response. We evaluated the effects of the NWT using cerebral microdialysis (MD), brain tissue oxygenation (Pb_tiO₂), jugular venous oxygen saturation (SjvO₂), and/or arterial-venous difference (AVD) for glucose, lactate, and oxygen in patients with severe TBI.

Methods

Seventeen intubated TBI patients (age 16–74 years) were sedated using continuous propofol infusion. All patients received intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring in addition to MD, Pb_tiO₂ and/or SjvO₂. Up to 10 days post-injury, ICP, CPP, Pb_tiO₂ (51 NWTs), MD (49 NWTs), and/or SjvO₂ (18 NWTs) levels during propofol sedation (baseline) and NWT were compared. MD was evaluated at a flow rate of 1.0 μL/min (28 NWTs) or the routine 0.3 μL/min rate (21 NWTs).

Results

The NWT increased ICP and CPP levels (p < 0.05). Compared to baseline, interstitial levels of glucose, lactate, pyruvate, glutamate, glycerol, and the lactate/pyruvate ratio were unaltered by the NWT. Pathological SjvO₂ (<50 % or >71 %; n = 2 NWTs) and Pb_tiO₂ (<10 mmHg; n = 3 NWTs) values were rare at baseline and did not change following NWT. Finally, the NWT did not alter the AVD of glucose, lactate, or oxygen.

Conclusions

The NWT-induced stress response resulted in increased ICP and CPP levels although it did not negatively alter focal neurochemistry or cerebral oxygenation in TBI patients.     

Malignant MCA territory infarction in the pediatric population: subgroup analysis of the Greater Cincinnati/Northern Kentucky Stroke Study

Purpose

Malignant middle cerebral artery (MCA) infarctions are thought to be rare in children. In a recent hospital-based study, only 1.3 % of pediatric ischemic strokes were malignant MCA infarctions. However, population-based rates have not been published. We performed subgroup analysis of a population-based study to determine the rate of malignant MCA infarctions in children.

Methods

In 2005 and 2010, all ischemic stroke-related emergency visits and hospital admissions among the 1.3 million residents of the five-county Greater Cincinnati/Northern Kentucky area were ascertained. Cases that occurred in patients 18 years and younger were reviewed in detail, and corresponding clinical and neuroimaging findings were recorded. Infarctions were considered malignant if they involved 50 % or more of the MCA territory and resulted in cerebral edema and mass effect.

Results

In 2005, eight pediatric ischemic strokes occurred in the study population, none of which were malignant infarctions. In 2010, there were also eight ischemic strokes. Of these, two malignant MCA infarctions were identified: (1) a 7-year-old boy who underwent hemicraniectomy and survived with moderate disability at 30 days and (2) a 17-year-old girl with significant prestroke disability who was not offered hemicraniectomy and died following withdrawal of care. Thus, among 16 children over 2 years, there were two malignant MCA infarctions (12.5 %, 95 % CI 0–29).

Conclusions

Malignant MCA infarctions in children may not be as rare as previously thought. Given the significant survival and functional outcome benefit conferred by hemicraniectomy in adults, future studies focusing on its potential role in pediatric patients are warranted.     

Systemic Glucose and Brain Energy Metabolism after Subarachnoid Hemorrhage

Background

Brain energy metabolic crisis (MC) and lactate–pyruvate ratio (LPR) elevations have been linked to poor outcome in comatose patients. We sought to determine if MC and LPR elevations after subarachnoid hemorrhage (SAH) are associated with acute reductions in serum glucose.

Methods

Twenty-eight consecutive comatose SAH patients that underwent multimodality monitoring with intracranial pressure and microdialysis were studied. MC was defined as lactate/pyruvate ratio (LPR) ≥ 40 and brain glucose < 0.7 mmol/l. Time-series data were analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes.

Results

Multimodality monitoring included 3,178 h of observation (mean 114 ± 65 h per patient). In exploratory analysis, serum glucose significantly decreased from 8.2 ± 1.8 mmol/l (148 mg/dl) 2 h before to 6.9 ± 1.9 mmol/l (124 mg/dl) at the onset of MC (P < 0.001). Reductions in serum glucose of 25% or more were significantly associated with new onset MC (adjusted odds ratio [OR] 3.6, 95% confidence interval [CI] 2.2–6.0). Acute reductions in serum glucose of 25% or more were also significantly associated with an LPR rise of 25% or more (adjusted OR 1.6, 95% CI 1.1–2.4). All analyses were adjusted for significant covariates including Glasgow Coma Scale and cerebral perfusion pressure.

Conclusions

Acute reductions in serum glucose, even to levels within the normal range, may be associated with brain energy metabolic crisis and LPR elevation in poor-grade SAH patients.     

Bone Flap Necrosis After Decompressive Hemicraniectomy for Malignant Middle Cerebral Artery Infarction

Background

Autologous bone flap reinsertion follows as a second surgical intervention after decompressive craniectomy in patients with malignant middle cerebral artery (MCA) infarction. In addition to surgery-related short-term complications, aseptic resorption of the reimplanted bone flap is a possible long-term problem which has not yet been sufficiently elucidated in these patients.

Methods

A total of 109 patients who had undergone decompressive hemicraniectomy for malignant MCA infarction in our institution between September 1994 and December 2011 were included in the study. Clinical and radiological findings were retrieved retrospectively. Aseptic bone necrosis was classified into two categories based on computer tomographic features.

Results

A total of 76 patients received their own cryoconserved bone flap (mean age 54.34 ± 10.73 years; 49 males). The overall short-term complication rate was 9.2 %. Bone flap necrosis occurred in 26 patients (22.8 %) with 7 flaps showing signs of surgically relevant type II necrosis after a median time of 14 months (interquartile range [IQR] 4–22).

Conclusions

There is a noticeable complication rate in patients undergoing bone flap reinsertion after hemicraniectomy due to malignant MCA infarction. Aseptic bone necrosis represents a significant complication during long-term follow-up. The pathophysiological mechanisms remain unclear and more efforts should be undertaken to understand and possibly prevent this complication in these patients.     

Infarct Volume After Hyperacute Infusion of Hypertonic Saline in a Rat Model of Acute Embolic Stroke

Introduction

Hypertonic saline (HS) can treat cerebral edema arising from a number of pathologic conditions. However, physicians are reluctant to use it during the first 24 h after stroke because of experimental evidence that it increases infarct volume when administered early after reperfusion. Here, we determined the effect of HS on infarct size in an embolic clot model without planned reperfusion.

Methods

A clot was injected into the internal carotid artery of male Wistar rats to reduce perfusion in the middle cerebral artery territory to less than 40 % of baseline, as monitored by laser-Doppler flowmetry. After 25 min, rats were randomized to receive 10 mL/kg of 7.5 % HS (50:50 chloride:acetate) or normal saline (NS) followed by a 0.5 mL/h infusion of the same solution for 22 h.

Results

Infarct volume was similar between NS and HS groups (in mm³: cortex 102 ± 65 mm³ vs. 93 ± 49 mm³, p = 0.72; caudoputamenal complex 15 ± 9 mm³ vs. 21 ± 14, p = 0.22; total hemisphere 119 ± 76 mm³ vs. 114 ± 62, p = 0.88, respectively). Percent water content was unchanged in the infarcted hemisphere (NS 81.6 ± 1.5 %; HS 80.7 ± 1.3 %, p = 0.16), whereas the HS-treated contralateral hemisphere was significantly dehydrated (NS 79.4 ± 0.8 %; HS 77.5 ± 0.8 %, p < 0.01).

Conclusions

HS reduced contralateral hemispheric water content but did not affect ipsilateral brain water content when compared to NS. Infarct volume was unaffected by HS administration at all evaluated locations.     

Evaluation of a New Brain Tissue Probe for Intracranial Pressure,Temperature, and Cerebral Blood Flow Monitoring in Patients with Aneurysmal Subarachnoid Hemorrhage

Objective

To evaluate an intraparenchymal probe for intracranial pressure (ICP) and temperature (TEMP) monitoring as well as determination of cerebral hemodynamics using a near-infrared spectroscopy (NIRS) and indocyanine green (ICG) dye dilution method (NIRS-ICP probe).

Methods

The NIRS-ICP probe was applied after aneurysmal subarachnoid hemorrhage if multimodal monitoring was established due to poor neurological condition. ICP and TEMP values were obtained from ventricular catheters and systemic temperature sensors. Repeated NIRS-ICG measurements (2 injections within 30 min) were performed daily for determination of cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time of ICG (mttICG). Secondary neurologic dysfunction was defined as brain tissue oxygen tension <20 mmHg and/or lactate/pyruvate ratio >35 obtained from cerebral probing.

Results

A total of 128 NIRS-ICG measurements were performed in ten patients. The correlation coefficients between ICP and TEMP values obtained with the NIRS-ICP probe and values from routine monitoring were r = 0.72 and r = 0.96, respectively. The mean values were 30.3 ± 13.6 ml/100 g/min for CBF, 3.3 ± 1.2 ml/100 g for CBV, and 6.8 ± 1.6 s for mttICG. The coefficients of variation from repeated NIRS-ICG measurements were 10.9 % for CBF, 11.7 % for CBV, and 3.8 % for mttICG. The sensitivity for detection of secondary neurologic dysfunction was 85 % and the specificity 83 % using a CBF-threshold of 25 ml/100 g/min.

Conclusion

Multimodal monitoring using the NIRS-ICP probe is feasible with high reproducibility of measurement values and the ability to detect secondary neurologic dysfunction. No safety concerns exist for the routine clinical use of the NIRS-ICP probe.

     

Risk of Venous Thromboembolism in Patients with Large Hemispheric Infarction Undergoing Decompressive Hemicraniectomy

Background

Deep-venous thrombosis (DVT) and pulmonary embolism (PE) are major causes of morbidity and mortality in patients with acute ischemic stroke. This study is the first to examine the risk of venous thromboembolism in patients with large hemispheric infarction undergoing decompressive hemicraniectomy.

Methods

The study population included 95 consecutive patients with a large hemispheric infarction who underwent decompressive hemicraniectomy between 2006 and 2014 at our institution. All patients received prophylactic unfractionated heparin and intermittent compression devices (SCD). Patients were systematically screened for DVT at 5-day interval using Duplex ultrasound. PE was diagnosed on chest CT angiography.

Results

Mean age was 57 ± 12 years; mean BMI was 28.3 ± 7.4 kg/m². 30.5 % of patients had infarction in the dominant hemisphere and 69.5 % in the non-dominant hemisphere. The mean NIHSS score was 16.0 ± 5 at admission. The mean length of stay was 22 ± 17 days. 35 % of patients developed a DVT including 27 % who developed above-knee DVT and required placement of an inferior vena cava filter. In multivariable analysis, predictors of DVT were an NIHSS ≥ 17 (p = 0.007), seizures (p = 0.003), hypertension (p = 0.03), and increasing length of stay (p = 0.01). The proportion of patients who developed PE was 13 %. In multivariate analysis, BMI ≥ 30 predicted PE (p = 0.05).

Conclusions

The rate of DVT and PE is remarkably high in patients with large hemispheric infarction undergoing decompressive hemicraniectomy despite prophylactic measures. We recommend routine screening for DVT in this population. Interventions beyond the standard prophylactic measures may be necessary in this high-risk group.

     

Brain Tissue Oxygenation and Cerebral Perfusion Pressure Thresholds of Ischemia in a Standardized Pig Brain Death Model

Background

Neurointensive care of traumatic brain injury (TBI) patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted protocols. Monitoring brain tissue oxygenation (B_tipO₂) is of considerable clinical interest, but the exact threshold level of ischemia has been difficult to establish due to the complexity of the clinical situation. The objective of this study was to use the Neurovent-PTO (NV) probe, and to define critical cerebral oxygenation- and CPP threshold levels of cerebral ischemia in a standardized brain death model caused by increasing the ICP in pig. Ischemia was defined by a severe increase of cerebral microdialysis (MD) lactate/pyruvate ratio (L/P ratio?>?30).

Methods

B_tipO₂, L/P ratio, Glucose, Glutamate, Glycerol and CPP were recorded using NV and MD probes during gradual increase of ICP by inflation of an epidural balloon catheter with saline until brain death was achieved.

Results

Baseline level of B_tipO₂ was 22.9?±?6.2?mmHg, the L/P ratio 17.7?±?6.1 and CPP 73?±?17?mmHg. B_tipO₂ and CPP decreased when intracranial volume was added. The L/P ratio increased above its ischemic levels, (>30) when CPP decreased below 30?mmHg and B_tipO₂ to <10?mmHg.

Conclusions

A severe increase of ICP leading to CPP below 30?mmHg and B_tipO₂ below 10?mmHg is associated with an increase of the L/P ratio, thus seems to be critical thresholds for cerebral ischemia under these conditions.     

Reduced Brain/Serum Glucose Ratios Predict Cerebral Metabolic Distress and Mortality After Severe Brain Injury

Background

The brain is dependent on glucose to meet its energy demands. We sought to evaluate the potential importance of impaired glucose transport by assessing the relationship between brain/serum glucose ratios, cerebral metabolic distress, and mortality after severe brain injury.

Methods

We studied 46 consecutive comatose patients with subarachnoid or intracerebral hemorrhage, traumatic brain injury, or cardiac arrest who underwent cerebral microdialysis and intracranial pressure monitoring. Continuous insulin infusion was used to maintain target serum glucose levels of 80–120 mg/dL (4.4–6.7 mmol/L). General linear models of logistic function utilizing generalized estimating equations were used to relate predictors of cerebral metabolic distress (defined as a lactate/pyruvate ratio [LPR] ≥ 40) and mortality.

Results

A total of 5,187 neuromonitoring hours over 300 days were analyzed. Mean serum glucose was 133 mg/dL (7.4 mmol/L). The median brain/serum glucose ratio, calculated hourly, was substantially lower (0.12) than the expected normal ratio of 0.40 (brain 2.0 and serum 5.0 mmol/L). In addition to low cerebral perfusion pressure (P = 0.05) and baseline Glasgow Coma Scale score (P < 0.0001), brain/serum glucose ratios below the median of 0.12 were independently associated with an increased risk of metabolic distress (adjusted OR = 1.4 [1.2–1.7], P < 0.001). Low brain/serum glucose ratios were also independently associated with in-hospital mortality (adjusted OR = 6.7 [1.2–38.9], P < 0.03) in addition to Glasgow Coma Scale scores (P = 0.029).

Conclusions

Reduced brain/serum glucose ratios, consistent with impaired glucose transport across the blood brain barrier, are associated with cerebral metabolic distress and increased mortality after severe brain injury.     

Impact of Methamphetamine on Regional Metabolism and Cerebral Blood Flow After Traumatic Brain Injury

Background

Substance abuse is a frequent comorbid condition among patients with traumatic brain injury (TBI), but little is known about its potential additive or interactive effects on tissue injury or recovery from TBI. This study aims to evaluate changes in regional metabolism and cerebral perfusion in subjects who used methamphetamine (METH) prior to sustaining a TBI. We hypothesized that METH use would decrease pericontusional cerebral perfusion and markers of neuronal metabolism, in TBI patients compared to those without METH use.

Methods

This is a single center prospective observational study. Adults with moderate and severe TBI were included. MRI scanning was performed on a 3 Tesla scanner. MP-RAGE and FLAIR sequences as well as Metabolite spectra of NAA and lactate in pericontusional and contralateral voxels identified on the MP-RAGE scans. A spiral-based FAIR sequence was used for the acquisition of cerebral blood flow (CBF) maps. Regional CBF images were analyzed using ImageJ open source software. Pericontusional and contralateral CBF, NAA, and lactate were assessed in the entire cohort and in the METH and non-METH groups.

Results

Seventeen subjects completed the MR studies. Analysis of entire cohort: pericontusional NAA concentrations (5.81 ± 2.0 mM/kg) were 12 % lower compared to the contralateral NAA (6.98 ± 1.2 mM/kg; p = 0.03). Lactate concentrations and CBF were not significantly different between the two regions; however, regional CBF was equally reduced in the two regions. Subgroup analysis: 41 % of subjects tested positive for METH. The mean age, Glasgow Coma Scale, and time to scan did not differ between groups. The two subject groups also had similar regional NAA and lactate. Pericontusional CBF was 60 % lower in the METH users than the non-users, p = 0.04; contralateral CBF did not differ between the groups.

Conclusion

This small study demonstrates that tissue metabolism is regionally heterogeneous after TBI and pericontusional perfusion was significantly reduced in the METH subgroup.     

Cerebral Ischemia and Neurogenesis: A Two-time Comparison

Background

This study compares the effect of mild and severe cerebral ischemia on neuronal damage and neurogenesis.

Methods

Sixteen Sprague–Dawley rats, anesthetized with 0.8 vol% halothane in O₂/air, were subjected to forebrain ischemia by bilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure = 40 mmHg) for 8 (mild) or 13 (severe) min. Four non-ischemic animals were investigated as naïve controls. Bromodeoxyuridine (50 mg/kg), a marker of new cells, was administrated for seven consecutive postischemic days. After 28 days, animals were perfused with 4% paraformaldehyde and the brains were sliced. Histopathological damage of the hippocampus and the volume of the dentate gyrus were assessed by HE-staining. With immunohistochemistry BrdU-positve cells were detected in the dentate gyrus. The amount of new generated neurons was identified by double-immunofluorescence-staining of BrdU and neuronal marker (NeuN).

Results

In the CA-1 region of the hippocampus, mild ischemia induced damage up to 10% (HE-index 0.8 ± 1.2) and severe ischemia up to 50% (HE-index 2.1 ± 1.4). There was no histopathological damage in naïve control animals. The amount of new neurons was increased by 250% after mild insult and by 160% after severe insult compared to the naïve control animals.

Conclusions

These data indicate that histopathological damage depends on the severity of the ischemic insult and that forebrain ischemia activates generation of new neurons. A mild ischemic challenge appears to be a more potent neurogenic stimulus than severe ischemia. The new neurons survive at least 28 days. This may relate to delayed histopathological and functional recovery after cerebral ischemia.     

Successful Management of Refractory Intracranial Hypertension from Acute Hyperammonemic Encephalopathy in a Woman with Ornithine Transcarbamylase Deficiency

Background

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.

Methods

We report a case of a woman heterozygous for OTCD who developed acute hyperammonemic encephalopathy and increased intracranial pressure (ICP).

Results

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.

Conclusion

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.     

Left Ventricular Dysfunction and Cerebral Infarction from Vasospasm After Subarachnoid Hemorrhage

Background

Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH.

Methods

Of the 481 patients enrolled in the University Columbia SAH Outcomes Project between 10/96 and 05/02, we analyzed a subset of 119 patients with at least one echocardiogram, serial transcranial Doppler (TCD) data, and with no prior history of cardiac disease. LV dysfunction was defined as an ejection fraction <40% on echocardiography. Infarction from vasospasm was adjudicated by the study team after comprehensive review of all clinical and imaging data. Functional outcome was assessed at 15 and 90 days with the modified Rankin Scale (mRS).

Results

Eleven percent of patients had LV dysfunction (N = 13). Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles were associated with LV dysfunction (all P < 0.05). Despite a similar frequency of pre-existing hypertension, 0% of patients with LV dysfunction reported taking antihypertensive medication, compared to 35% of those without (P = 0.009). There was a significant association between LV dysfunction and infarction from vasospasm after adjusting for clinical grade, age, and peak TCD flow velocity (P = 0.03). Patients with LV dysfunction also had higher rates of hypotension requiring vasopressors (P = 0.001) and pulmonary edema (P = 0.002). However, there was no association between LV dysfunction and outcome at 14 days after adjustment for established prognostic variables.

Conclusions

LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.     

The Effect of Packed Red Blood Cell Transfusion on Cerebral Oxygenation and Metabolism After Subarachnoid Hemorrhage

Background

Anemia adversely affects cerebral oxygenation and metabolism after subarachnoid hemorrhage (SAH) and is also associated with poor outcome. There is limited evidence to support the use of packed red blood cell (PRBC) transfusion to optimize brain homeostasis after SAH. The aim of this study was to investigate the effect of transfusion on cerebral oxygenation and metabolism in patients with SAH.

Methods

This was a prospective observational study in a neurological intensive care unit of a university hospital. Nineteen transfusions were studied in 15 consecutive patients with SAH that underwent multimodality monitoring (intracranial pressure, brain tissue oxygen, and cerebral microdialysis). Data were collected at baseline and for 12 h after transfusion. The relationship between hemoglobin (Hb) change and lactate/pyruvate ratio (LPR) orbrain tissue oxygen (PbtO₂) was tested using univariate and multivariable analyses.

Results

PRBC transfusion was administered on the median post-bleed day 8. The average Hb concentration at baseline was 8.1 g/dL and increased by 2.2 g/dL after transfusion. PbtO₂ increased between hours 2 and 4 post-transfusion and this increase was maintained until hour 10. LPR did not change significantly during the 12-h monitoring period. After adjusting for SpO₂, cerebral perfusion pressure, and LPR, the change in Hb concentration was independently and positively associated with a change in PbtO₂ (adjusted b estimate = 1.39 [95 % confidence interval 0.09–2.69]; P = 0.04). No relationship between the change in Hb concentration and LPR was found.

Conclusions

PRBC transfusion resulted in PbtO₂ improvement without a clear effect on cerebral metabolism prior to SAH.

     

Outcome of Poor-Grade Subarachnoid Hemorrhage as Determined by Biomarkers of Glucose Cerebral Metabolism

Purpose

The aim of this study was to determine if the measurement of blood biomarkers of glucose cerebral metabolism, performed with retrograde jugular catheter, could predict the outcome of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients.

Methods

This study was conducted in 68 poor-grade aSAH patients. A total of 4,024 blood samples obtained from jugular and radial catheters were analyzed for glucose, lactate, and oxygen content every 8 h for 10 ± 0.5 days. Metabolic ratio (MR) and lactate–oxygen index (LOI) were obtained by ratios using arterio-jugular differences. Functional outcome was evaluated at 12 months with the Glasgow Outcome Scale.

Results

Outcome was unfavorable in 40 patients. In this group of patients, the MR was significantly lower (p < 0.0001) and the LOI was significantly higher (p = 0.0001) than in the group with favorable outcome. The MR cutoff value, below which the patients are likely to have an unfavorable outcome, was determined to be 3.35. More interestingly, the data obtained in this study demonstrated that the patients achieving an unfavorable outcome were distinguished from those with a favorable outcome by having at least three events of MR inferior to 3.35 (sensitivity = 90 %, specificity = 82.1 %). Moreover, in patients who developed cerebral vasospasm, we observed a significant decrease in the MR.

Conclusion

Our data provide additional support to the view that the MR is a reliable marker for predicting the outcome of poor-grade aSAH patients. Prospective studies are needed to confirm its value in multimodal monitoring.     

Brain Iron Metabolism and Brain Injury Following Subarachnoid Hemorrhage: iCeFISH-Pilot (CSF Iron in SAH)

Introduction

Iron-mediated oxidative damage has been implicated in the genesis of cerebral vasospasm in animal models of SAH. We sought to explore the relationship between levels of non-protein bound iron in cerebrospinal fluid and the development of brain injury in patients with aneurysmal SAH.

Methods

Patients admitted with aneurysmal subarachnoid hemorrhage to a Neurointensive care unit of an academic, tertiary medical center, with Hunt and Hess grades 2–4 requiring ventriculostomy insertion as part of their clinical management were included in this pilot study. Samples of cerebrospinal fluid (CSF) were obtained on days 1, 3, and 5. A fluorometric assay that relies on an oxidation sensitive probe was used to measure unbound iron, and levels of iron-handling proteins were measured by means of enzyme-linked immunosorbent assays. We prospectively collected and recorded demographic, clinical, and radiological data.

Results

A total of 12 patients were included in this analysis. Median Hunt and Hess score on admission was 3.5 (IQR: 1) and median modified Fisher scale score was 4 (IQR: 1). Seven of 12 patients (58 %) developed delayed cerebral ischemia (DCI). Day 5 non-transferrin bound iron (NTBI) (7.88 ± 1 vs. 3.58 ± 0.8, p = 0.02) and mean NTBI (7.39 ± 0.4 vs. 3.34 + 0.4 p = 0.03) were significantly higher in patients who developed DCI. Mean redox-active iron, as well as day 3 levels of redox-active iron correlated with development of angiographic vasospasm in logistic regression analysis (p = 0.02); while mean redox-active iron and lower levels of ceruloplasmin on days 3, 5, and peak concentration were correlated with development of deep cerebral infarcts.

Conclusions

Our preliminary data indicate a causal relationship between unbound iron and brain injury following SAH and suggest a possible protective role for ceruloplasmin in this setting, particularly in the prevention of cerebral ischemia. Further studies are needed to validate these findings and to probe their clinical significance.     

Cerebral Vasospasm and Delayed Cerebral Ischemia in Intraventricular Hemorrhage

Background

Intracerebral hemorrhage (ICH) with intraventricular extension (IVH) is a devastating disease with a particular high mortality. In some aspects, IVH may resemble subarachnoid hemorrhage. The incidence and role of cerebral vasospasm in ICH with IVH are poorly understood. Here, we aimed to analyze the incidence and relationship of cerebral vasospasm to clinical characteristics, in-hospital mortality, and functional outcome at 3 months in patients suffering ICH with IVH.

Methods

Patients with ICH and IVH treated on a neurological intensive care unit were prospectively enrolled in a single-center observational study. Vasospasm was defined using established ultrasound criteria. Delayed cerebral ischemia (DCI) was defined as a new hypodensity on follow-up cranial CT. Functional outcome at 3 months was assessed using the modified Rankin Scale.

Results

129 patients with ICH and IVH were screened for the study. 62 patients entered the final analysis. The incidence of significant vasospasm was 37 %. A strong trend was found for the association between all cerebral vasospasm and DCI (P = 0.046). Early (up to 48 h) vasospasm was significantly associated with a DCI (P = 0.033). Overall mortality and outcome after 3 months did not differ between the groups.

Conclusion

Cerebral vasospasm seems to be a frequent complication after ICH with IVH and might be associated with DCI. Larger studies are warranted to confirm this hypothesis.     

Endoscopic treatment of convexity arachnoid cysts

Objective

The aim of this study was to investigate the endoscopic treatment of cerebral hemisphere convexity arachnoid cyst.

Methods

Eight cases of hemisphere convexity arachnoid cyst treated with cyst–ventricular or cisternal endoscopic approach in September 2007 to March 2011 were retrospectively recruited. The clinical symptoms, radiological findings, surgical indications, surgical approach, complications, and follow-up studies were analyzed.

Results

All patients showed convexity arachnoid cysts adjacent to the ventricles or cisternal. After treatment, all patients showed decrease in size of the cysts (100 %), with preoperative symptoms disappeared in six patients and improved in two cases. In one case, postoperative subdural effusion was found without symptoms reported.

Conclusion

Endoscopic surgery is ideal for treatment of arachnoid cysts adjacent to the ventricles or cisternal.