Normothermic central hypovolemia tolerance reflects hyperthermic tolerance

Purpose

To test the hypothesis that those who are highly tolerant to lower body negative pressure (LBNP) while normothermic are also highly tolerant to this challenge while hyperthermic.

Methods

Sixty pairs of normothermic and hyperthermic LBNP tests to pre-syncope were evaluated. LBNP tolerance was quantified via the cumulative stress index (CSI), which is calculated as the sum of the product of the LBNP level and the duration of each level until test termination (i.e., 20 mmHg × 3 min + 30 mmHg × 3 min, etc.). CSI was compared between normothermic and hyperthermic trials. Internal and skin temperatures, heart rate, and arterial pressure were measured throughout.

Results

Hyperthermia reduced (P < 0.001) CSI from 997 ± 437 to 303 ± 213 mmHg min. There was a positive correlation between normothermic and hyperthermic LBNP tolerance (R ² = 0.38; P < 0.001). As a secondary analysis, the 20 trials with the highest LBNP tolerance while normothermic were identified (indicated as the HIGH group; CSI 1,467 ± 356 mmHg min), as were the 20 trials with the lowest normothermic tolerance (indicated as the LOW group; CSI 565 ± 166 mmHg min; P < 0.001 between groups). While hyperthermia unanimously reduced CSI in both HIGH and LOW groups, in this hyperthermic condition CSI was ~threefold higher in the HIGH group (474 ± 226 mmHg min) relative to the LOW group (160 ± 115 mmHg min; P < 0.001).

Conclusions

LBNP tolerance while hyperthermic is related to normothermic tolerance and, associated with this finding, those who have a high LBNP tolerance while normothermic remain relatively tolerant when hyperthermic.     

Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Objective

Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP).

Methods

Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS + 20 mmHg LBNP (HS_LBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V _mean). Cerebrovascular responses were calculated from the slope of the change in MCA V _mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide ( \( {\text{PET}}_{{{\text{CO}}_{ 2} }} \) ) during rebreathing.

Results

MCA V _mean was similar in HS (55 ± 19 cm s^?1) and HS_LBNP (52 ± 16 cm s^?1), and both values were reduced relative to NT (66 ± 20 cm s^?1), yet the rise in MCA V _mean per Torr increase in \( {\text{PET}}_{{{\text{CO}}_{ 2} }} \) during rebreathing was similar in each condition (NT: 2.5 ± 0.6 cm s^?1 Torr^?1; HS: 2.4 ± 0.8 cm s^?1 Torr^?1; HS_LBNP: 2.1 ± 1.1 cm s^?1 Torr^?1). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1 ± 0.65 cm s^?1 mmHg^?1100 Torr^?1; HS: 2.4 ± 0.8 cm s^?1 mmHg^?1 100 Torr^?1; HS_LBNP: 2.0 ± 1.0 cm s^?1 mmHg^?1 100 Torr^?1).

Interpretations

These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.     

Continuous Optical Monitoring of Cerebral Hemodynamics During Head-of-Bed Manipulation in Brain-Injured Adults

Introduction

Head-of-bed manipulation is commonly performed in the neurocritical care unit to optimize cerebral blood flow (CBF), but its effects on CBF are rarely measured. This pilot study employs a novel, non-invasive instrument combining two techniques, diffuse correlation spectroscopy (DCS) for measurement of CBF and near-infrared spectroscopy (NIRS) for measurement of cerebral oxy- and deoxy-hemoglobin concentrations, to monitor patients during head-of-bed lowering.

Methods

Ten brain-injured patients and ten control subjects were monitored continuously with DCS and NIRS while the head-of-bed was positioned first at 30° and then at 0°. Relative CBF (rCBF) and concurrent changes in oxy- (ΔHbO₂), deoxy- (ΔHb), and total-hemoglobin concentrations (ΔTHC) from left/right frontal cortices were monitored for 5 min at each position. Patient and control response differences were assessed.

Results

rCBF, ΔHbO₂, and ΔTHC responses to head lowering differed significantly between brain-injured patients and healthy controls (P < 0.02). For patients, rCBF changes were heterogeneous, with no net change observed in the group average (0.3 ± 28.2 %, P = 0.938). rCBF increased in controls (18.6 ± 9.4 %, P < 0.001). ΔHbO₂, ΔHb, and ΔTHC increased with head lowering in both groups, but to a larger degree in brain-injured patients. rCBF correlated moderately with changes in cerebral perfusion pressure (R = 0.40, P < 0.001), but not intracranial pressure.

Conclusion

DCS/NIRS detected differences in CBF and oxygenation responses of brain-injured patients versus controls during head-of-bed manipulation. This pilot study supports the feasibility of continuous bedside measurement of cerebrovascular hemodynamics with DCS/NIRS and provides the rationale for further investigation in larger cohorts.     

Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

Introduction

Hemorrhage is accompanied by baroreflex-mediated tachycardia and vasoconstriction. The difference between baseline and maximum responses is defined as the heart rate (HR) and vasoconstrictor ??reserve??.

Objective

To test the hypothesis that higher HR and vasoconstrictor reserves in subjects with high tolerance (HT) to central hypovolemia is associated with greater reserve for sympathoexcitation and vagal withdrawal compared with low tolerant (LT) subjects.

Methods

R?CR intervals (RRI), systolic arterial pressure (SAP), estimated stroke volume, and muscle sympathetic nerve activity (MSNA) were measured during lower body negative pressure (LBNP) designed to induce pre-syncope. Subjects with tolerance ??60?mmHg LBNP were classified as LT (n?=?22) while subjects who tolerated LBNP levels >60?mmHg were classified as HT (n?=?56). Spontaneous cardiac baroreflex sensitivity (BRS) was assessed via RRI-SAP down?Cdown sequences.

Results

HR reserve in HT subjects (+52?±?2?bpm) was twofold greater (P?P?=?0.04) than that of the LT group (+1.9?±?0.3?pru). HT subjects demonstrated greater (P????0.03) BRS reserve (?14.2?±?1.8?ms/mmHg) and MSNA reserve (+41?±?2 bursts/min) compared with LT subjects (?7.4?±?1.7?ms/mmHg and +26?±?7?bursts/min).

Interpretation

Our data support the hypothesis that greater physiological reserve capacity for tachycardia and vasoconstriction related to high tolerance to central hypovolemia is associated with greater reserves for sympathoexcitation and cardiac vagal withdrawal.     

Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury

Background

To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury.

Methods

Continuous monitoring of the partial pressure of brain tissue oxygen (P_brO₂), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of P_brO₂ to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings.

Results

Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. P_brO₂ increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = ?0.33, P = 0.32, respectively.

Conclusions

The results suggest a strong link between cerebrovascular pressure reactivity and the brain’s ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.     

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Background

Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after subarachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypothermia on Doppler blood flow velocity after SAH.

Methods

In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFV_MCA) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFV_MCA was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming.

Results

Hypothermia was induced on average 5 days after SAH (range 1–12) and maintained for 144 h (range 29–270). After hypothermia induction, MFV_MCA decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFV_MCA further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypothermia, MFV_MCA remained unchanged after rewarming (65.6 ± 32.1 vs 70.3 ± 36.8 cm/s; p = 0.219). However, patients treated with hypothermia alone showed an increase in MFV_MCA after rewarming (p = 0.016).

Conclusion

Therapeutic hypothermia after SAH decreases Doppler blood flow velocity in both intracranial hypertension and DCI cases. The results can be the effect of hypothermia-related mechanisms or resolving cerebral vasospasm during prolonged hypothermia.     

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.     

Impact of Baseline Weight on Smoking Cessation and Weight Gain in Quitlines

Background

The use and effectiveness of tobacco quitlines by weight is still unknown.

Purpose

This study aims to determine if baseline weight is associated with treatment engagement, cessation, or weight gain following quitline treatment.

Methods

Quitline participants (n?=?595) were surveyed at baseline, 3 and 6 months.

Results

Baseline weight was not associated with treatment engagement. In unadjusted analyses, overweight smokers reported higher quit rates and were more likely to gain weight after quitting than obese or normal weight smokers. At 3 months, 40 % of overweight vs. 25 % of normal weight or obese smokers quit smoking (p?=?0.01); 42 % of overweight, 32 % of normal weight, and 33 % of obese quitters gained weight (p?=?0.05). After adjusting for covariates, weight was not significantly related to cessation (approaching significance at 6 months, p?=?0.06) or weight gain.

Conclusions

In the first quitline study of this kind, we found no consistent patterns of association between baseline weight and treatment engagement, cessation, or weight gain.     

Relationship of Vascular Wall Tension and Autoregulation Following Traumatic Brain Injury

Background

The vascular wall tension (WT) of small cerebral vessels can be quantitatively estimated through the concept of critical closing pressure (CrCP), which denotes the lower limit of arterial blood pressure (ABP), below which small cerebral arterial vessels collapse and blood flow ceases. WT can be expressed as the difference between CrCP and intracranial pressure (ICP) and represent active vasomotor tone. In this study, we investigated the association of WT and CrCP with autoregulation and outcome of a large group of patients after traumatic brain injury (TBI).

Methods

We retrospectively analysed recordings of ABP, ICP and transcranial Doppler (TCD) blood flow velocity from 280 TBI patients (median age: 29 years; interquartile range: 20–43). CrCP and WT were calculated using the cerebrovascular impedance methodology. Autoregulation was assessed based on TCD-based indices, Mx and ARI.

Results

Low values of WT were found to be associated with an impaired autoregulatory capacity, signified by its correlation to FV-based indices Mx (R = ?0.138; p = 0.021) and ARI (R = 0.118; p = 0.048). No relationship could be established between CrCP and any of the autoregulatory indices. Neither CrCP nor WT was found to correlate with outcome.

Conclusions

Impaired autoregulation was found to be associated with a lower WT supporting the role of vasoparalysis in the loss of autoregulatory capacity. In contrast, no links between CrCP and autoregulation could be identified.     

The Prognostic Value of Brain Extracellular Fluid Nitric Oxide Metabolites After Traumatic Brain Injury

Background

Nitric oxide (NO) is a compound with both protective and damaging effects on neurons. Quantification of NO metabolites in humans is limited by sample contamination with blood. In vivo cerebral microdialysis may offer an alternative approach as sampling of extracellular fluid (ECF) adjacent to neurons becomes possible. We investigate the prognostic value of brain ECF NO metabolites in patients with traumatic brain injury (TBI).

Methods

A prospective case cohort of 195 ECF samples collected from 11 cases over 4 days following TBI was collected. Nitrate and nitrite concentrations ([NO _x ]) were quantified using a vanadium-based colorimetric assay.

Results

Early ECF [NO _x ] (<48 h post TBI) were significantly higher in non-survivors (median 59.2 μmol/l, n = 7) compared to survivors (23.3 μmol/l, n = 4) (P = 0.04). Late (48–96 h) ECF [NO _x ] remained higher in non-survivors (47.9 μmol/l) compared to survivors (23.0 μmol/l) but this was not significant (P = 0.29). Receiver operator characteristic analysis shows an optimized cutoff level for ECF [NO _x ] of 26.5 μmol/l measured <48 h post TBI for predicting non-survival (sensitivity 100%, specificity 75%).

Conclusion

Early ECF NO _x concentrations are of prognostic value after TBI. ECF NO _x may be a useful biomarker for treatment trials targeted at nitric oxide metabolism.     

Early Predictors of Prolonged Stay in a Critical Care Unit Following Aneurysmal Subarachnoid Hemorrhage

Background

Aneurysmal subarachnoid hemorrhage (aSAH) is a neurologic emergency that typically warrants initial monitoring in a critical care setting. The aim of this study is to identify clinical and radiologic features on admission that predict a protracted critical care admission following aSAH.

Methods

Exploratory posthoc analysis was performed on the 413 patients enrolled in Clazosentan to Overcome Neurological iSChemia and Infarction OccUrring after Subarachnoid hemorrhage (CONSCIOUS-1), a prospective randomized control trial of clazosentan for the prevention of vasospasm after aSAH. The association between potential clinical and radiographic covariates, and the length of stay (LOS) in a critical care unit after aSAH was determined using a Cox proportional hazards model. Covariates with a significance level of p < 0.20, on univariate analysis, were entered into a multivariate forward conditional analysis to identify independent predictors of prolonged LOS.

Results

The mean LOS was 12.6 ± 10.6 days. On multivariate analysis, age (hazard ratio [HR] 1.01, 95 % confidence interval [CI] 1.00–1.02; p = 0.032), a history of hypertension (HR 1.30, CI 1.01–1.67; p = 0.045), and a World Federation of Neurosurgical Societies Score of IV–V on admission (HR 1.38, CI 1.05–1.81; p = 0.02) were the clinical features associated with a greater critical care LOS following aSAH. Intracerebral hemorrhage (HR 1.50, CI 1.03–2.21; p = 0.004) and increasing intraventricular clot burden (HR 1.08, CI 1.03–1.14; p = 0.037) on admission computed tomography were the radiologic features associated with prolonged LOS.

Conclusions

We have identified several early risk factors associated with a prolonged critical care stay following aSAH.     

Does Prone Positioning Increase Intracranial Pressure? A Retrospective Analysis of Patients with Acute Brain Injury and Acute Respiratory Failure

Purpose

The objective of our trial was to obtain more comprehensive data on the risks and benefits of kinetic therapy in intensive care patients with intracerebral pathology.

Methods

Standardized data of prone positioning in our NeuroIntensive Care Unit were collected from 2007 onward. A post hoc analysis of all available data was undertaken, with special consideration given to values of intracranial pressure (ICP), cerebral perfusion pressure (CPP) and oxygenation in correlation to prone (PP), or supine positioning (SP) of patients. Cases were considered eligible if kinetic therapy and ICP were documented. Prone positioning was performed in a 135° position for 8 h per treatment unit.

Results

A total of 115 patients treated with prone positioning from 2007 to 2013 were identified in our medical records. Of these, 29 patients received ICP monitoring. Overall, 119 treatment units of prone positioning with a mean duration of 2.5 days per patient were performed. The mean baseline ICP in SP was 9.5 ± 5.9 mmHg and was increased significantly during PP (p < 0.0001). There was no significant difference between CPP in SP (82 ± 14.5 mmHg) compared to PP (p > 0.05). ICP values >20 mmHg occurred more often during PP than SP (p < 0.0001) and were associated with significantly more episodes of decreased CPP <70 mmHg (p < 0.0022). The mean paO₂/FiO₂ ratio (P/F ratio) was increased significantly in prone positioning of patients (p < 0.0001).

Conclusions

The analyzed data allow a more precise understanding of changes in ICP and oxygenation during prone positioning in patients with acute brain injury and almost normal baseline ICP. Our study shows a moderate, yet significant elevation of ICP during prone positioning. However, the achieved increase of oxygenation by far exceeded the changes in ICP. It is evident that continuous monitoring of cerebral pressure is required in this patient group.     

Bedside Diagnosis of Mitochondrial Dysfunction After Malignant Middle Cerebral Artery Infarction

Background

The study explores whether the cerebral biochemical pattern in patients treated with hemicraniectomy after large middle cerebral artery infarcts reflects ongoing ischemia or non-ischemic mitochondrial dysfunction.

Methods

The study includes 44 patients treated with decompressive hemicraniectomy (DCH) due to malignant middle cerebral artery infarctions. Chemical variables related to energy metabolism obtained by microdialysis were analyzed in the infarcted tissue and in the contralateral hemisphere from the time of DCH until 96 h after DCH.

Results

Reperfusion of the infarcted tissue was documented in a previous report. Cerebral lactate/pyruvate ratio (L/P) and lactate were significantly elevated in the infarcted tissue compared to the non-infarcted hemisphere (p < 0.05). From 12 to 96 h after DCH the pyruvate level was significantly higher in the infarcted tissue than in the non-infarcted hemisphere (p < 0.05).

Conclusion

After a prolonged period of ischemia and subsequent reperfusion, cerebral tissue shows signs of protracted mitochondrial dysfunction, characterized by a marked increase in cerebral lactate level with a normal or increased cerebral pyruvate level resulting in an increased LP-ratio. This biochemical pattern contrasts to cerebral ischemia, which is characterized by a marked decrease in cerebral pyruvate. The study supports the hypothesis that it is possible to diagnose cerebral mitochondrial dysfunction and to separate it from cerebral ischemia by microdialysis and bed-side biochemical analysis.     

Cessation of Diastolic Cerebral Blood Flow Velocity: The Role of Critical Closing Pressure

Background

Reducing cerebral perfusion pressure (CPP) below the lower limit of autoregulation (LLA) causes cerebral blood flow (CBF) to become pressure passive. Further reductions in CPP can cause cessation of CBF during diastole. We hypothesized that zero diastolic flow velocity (FV) occurs when diastolic blood pressure becomes less than the critical closing pressure (CrCP).

Methods

We retrospectively analyzed studies of 34 rabbits with CPP below the LLA, induced with pharmacologic sympathectomy (N = 23) or cerebrospinal fluid infusion (N = 11). Basilar artery blood FV and cortical Laser Doppler Flow (LDF) were monitored. CrCP was trended using a model of cerebrovascular impedance. The diastolic closing margin (DCM) was monitored as the difference between diastolic blood pressure and CrCP. LDF was recorded for DCM values greater than and less than zero.

Results

Arterial hypotension caused a reduction of CrCP (p < 0.001), consistent with decreased wall tension (p < 0.001) and a drop in intracranial pressure (ICP; p = 0.004). Cerebrospinal infusion caused an increase of CrCP (p = 0.002) accounted for by increasing ICP (p < 0.001). The DCM was compromised by either arterial hypotension or intracranial hypertension (p < 0.001 for both). When the DCM reached zero, diastolic FV ceased for a short period during each heart cycle (R = 0.426, p < 0.001). CBF pressure passivity accelerated when DCM decreased below zero (from 1.51 ± 0.51 to 2.17 ± 1.17 % ΔLDF/ΔmmHg; mean ± SD; p = 0.010).

Conclusions

The disappearance of diastolic CBF below LLA can be explained by DCM reaching zero or negative values. Below this point the decrease in CBF accelerates with further decrements of CPP.     

Energy expenditure in obesity associated with craniopharyngioma

Background and purpose

Obesity is a common yet incompletely understood complication of childhood craniopharyngioma. We hypothesized that craniopharyngioma is associated with specific defects in energy balance compared to obese control children.

Methods

Eleven craniopharyngioma patients were recruited for a study on body composition and energy balance. Eight subjects were obese. The obese craniopharyngioma patients had a mean age (±SD) of 11.2?±?1.7 years. The average body mass index z score was 2.33 (±0.32). A previously studied group of obese children (BMI z score 2.46?±?0.46) served as controls. Resting energy expenditure (REE) was determined by indirect calorimetry and body composition by dual energy X-ray absorptiometry in all children.

Results

Obese craniopharyngioma patient subjects had increased mean (±standard error) fat-free mass compared to obese controls (57%?±?0.88 % vs 50.0%?±?0.87%, p?=?0.02). The obese craniopharyngioma patients had a 17% lower REE compared to values expected from the World Health Organization equation (1,541?±?112.6 vs 1,809?±?151.8 kcal; p?=?0.01). In contrast, the obese control children had measured REE within 1% of predicted (1,647?±?33.2 vs. 1,652?±?40.2; p?=?0.8). In a linear regression model, REE remained significantly lower than predicted after controlling for FFM.

Conclusions

Lower REE may be a factor contributing to obesity in children with craniopharyngioma. Further study is needed into the mechanisms for reduced energy expenditure in patients with craniopharyngioma.     

Secondary Peaks of S100B in Serum Relate to Subsequent Radiological Pathology in Traumatic Brain Injury

Introduction

Patients suffering from severe traumatic brain injury (TBI) often develop secondary brain lesions that may worsen outcome. S100B, a biomarker of brain damage, has been shown to increase in response to secondary cerebral deterioration. The aim of this study was to analyze the occurrence of secondary increases in serum levels of S100B and their relation to potential subsequent radiological pathology present on CT/MRI-scans.

Methods

Retrospective study from a trauma level 1 hospital, neuro-intensive care unit. 250 patients suffering from TBI were included. Inclusion required a minimum of two radiological examinations and at least three serum samples of S100B, with at least one >48 h after trauma.

Results

Secondary pathological findings on CT/MRI, present in 39 % (n = 98) of the patients, were highly correlated to secondary increases of ≥0.05 μg/L S100B (P < 0.0001, pseudo-R ² 0.532). Significance remained also after adjusting for known important TBI predictors. In addition, secondary radiological findings were significantly correlated to outcome (Glasgow Outcome Score, GOS) in uni-(P < 0.0001, pseudo-R ² 0.111) and multivariate analysis. The sensitivity and specificity of detecting later secondary radiological findings was investigated at three S100B cut-off levels: 0.05, 0.1, and 0.5 μg/L. A secondary increase of ≥0.05 μg/L had higher sensitivity (80 %) but lower specificity (89 %), compared with a secondary increase of ≥0.5 μg/L (16 % sensitivity, 98 % specificity), to detect secondary radiological findings.

Conclusions

Secondary increases in serum levels of S100B, even as low as ≥0.05 μg/L, beyond 48 h after TBI are strongly correlated to the development of clinically significant secondary radiological findings.     

A Comparative Study of Fractional Anisotropy Measures and ICH Score in Predicting Functional Outcomes After Intracerebral Hemorrhage

Background

Improved prognostication during the acute phase of intracerebral hemorrhage (ICH) could influence goals of care. We investigated the utility of diffusion tensor imaging (DTI)-derived data obtained during the acute phase of ICH in predicting outcome, compared with the ICH score.

Methods

We measured fractional anisotropy (FA) values in 5 slices below the level of the lesion on the affected and unaffected corticospinal tracts (CST) and in the cerebral peduncles (CPs) in 32 patients with supratentorial ICH who had DTI MRI within 4 days after ictus. We calculated the FA ratio (rFA = FA_{affected side}/FA_{unaffected side}), and examined the value of the ICH score and rFA in predicting functional outcome assessed by modified Ranking Scale (mRS) at follow-up, using ROC analyses.

Results

The rFA values at the CPs level, but not the 5 slices below the lesion, were significantly lower in the group with poor functional outcome (defined as mRS > 2) than in those with good functional outcome (0.96 ± 0.14 vs. 0.99 ± 0.08, p = 0.025). The ICH score had greater areas under ROC curve in predicting functional outcome compared to the mean rFA (AUC 0.74 vs. 0.44; p = 0.01 for mRS > 2; and 0.84 vs. 0.40; p < 0.001 for mRS > 3).

Conclusions

The prognostic value of the ICH score surpassed that of DTI-derived data during the acute phase of ICH in this cohort of patients. Prospective and larger studies are needed to validate our findings and to assess the prognostic role of various DTI-derived measures at different times following ICH.     

Intraoperative secondary insults during extracranial surgery in children with traumatic brain injury

Purpose

Data on intraoperative secondary insults in pediatric traumatic brain injury (TBI) are limited.

Methods

We examined intraoperative secondary insults during extracranial surgery in children with moderate-severe TBI and polytrauma and their association with postoperative head computed tomography (CT) scans, intracranial pressure (ICP), and therapeutic intensity level (TIL) scores 24 h after surgery. After IRB approval, we reviewed the records of children <18 years with a Glasgow Coma Scale score <13 who underwent extracranial surgery within 72 h of TBI. Definitions of secondary insults were as follows: systemic hypotension (SBP <70?+?2?×?age or 90 mmHg), cerebral hypotension (cerebral perfusion pressure <40 mmHg), intracranial hypertension (ICP >20 mmHg), hypoxia (oxygen saturation <90 %), hypercarbia (end-tidal CO₂ >45 mmHg), hypocarbia (end-tidal CO₂ <30 mmHg without hypotension and in the absence of intracranial hypertension), hyperglycemia (blood glucose >200 mg/dL), hyperthermia (temperature >38 °C), and hypothermia (temperature <35 °C).

Results

Data from 50 surgeries in 42 patients (median age 15.5 years, 25 males) revealed systemic hypotension during 78 %, hypocarbia during 46 %, and hypercarbia during 25 % surgeries. Intracranial hypertension occurred in 64 % and cerebral hypotension in 18 % surgeries with ICP monitoring (11/50). Hyperglycemia occurred during 17 % of the 29 surgeries with glucose monitoring. Cerebral hypotension and hypoxia were associated with postoperative intracranial hypertension (p?=?0.02 and 0.03, respectively). We did not observe an association between intraoperative secondary insults and postoperative worsening of head CT scan or TIL score.

Conclusions

Intraoperative secondary insults were common during extracranial surgery in pediatric TBI. Intraoperative cerebral hypotension and hypoxia were associated with postoperative intracranial hypertension. Strategies to prevent secondary insults during extracranial surgery in TBI are needed.