Early brain metabolic disturbances associated with delayed cerebral ischemia in patients with severe subarachnoid hemorrhage.

Delayed cerebral ischemia (DCI) is a devastating complication of aneurysmal subarachnoid hemorrhage (ASAH) causing brain infarction and disability. Cerebral microdialysis (CMD) monitoring is a focal technique that may detect DCI-related neurochemical changes as an advance warning. We conducted retrospective analyses from 44 poor-grade ASAH patients and analyzed glucose, lactate, pyruvate, and glutamate concentrations in control patients without DCI (n = 19), and in patients with DCI whose CMD probe was located within (n = 17) or outside (n = 8) a new infarct. When monitored from within a lesion, DCI was preceded by a decrease in glucose and a surge in glutamate, accompanied by increases in lactate/pyruvate and lactate/glucose ratios whereas these parameters remained stable in control patients. When CMD monitoring was performed outside the lesion, the glutamate surge was absent, but glucose and L/G ratio were still significantly altered. Overall, glucose and L/G ratio were significant biomarkers of DCI (se96.0, spe73.7-68.4). Glucose and L/G predicted DCI 67 h before CT detection of a new infarct. The pathogenesis of DCI therefore induces early metabolic disturbances that can be detected by CMD as an advance warning. Glucose and L/G could provide a trigger for initiating further examination or therapy, earlier than when guided by other monitoring techniques.

Incidence of Burnout Syndrome among Anesthesiologists and Intensivists in France: The REPAR Study.

BACKGROUND: Burnout syndrome (BOS) impacts health workers and has become a real public health issue. The primary objective of this observational study was to re-evaluate the incidence of BOS among anesthesiologists and intensivists (AI) in France, ten years after the SESMAT study, a French Physician Health Survey carried out among burnout salaried AI. The secondary objective was to investigate risks factors. METHODS: The REPAR survey is an observational study carried in France among AI, residents, and seniors, whatever their main mode of practice, in the framework of a self-questionnaire distributed on the Internet from 11 April 2018 to 1 July 2018. BOS was assessed using the Copenhagen Burnout Inventory (CBI). A score above 50% on two of the dimensions (personal burnout and work-related burnout) indicated BOS, as a main criterion. In order to investigate risks factors, questions were about sociodemographic characteristics, professional and extraprofessional environments, personality and mood using the Major Depression Inventory (MDI). A significance threshold of p < 0.05 was retained. RESULTS: Among 1519 questionnaires received, 1500 completed questionnaires were analyzed. There were 775 men (52%) and 721 women (48%), aged 23 to 74 years. Among those, 24% suffered from BOS, 9% showed depressive symptoms (MDI > 25) and 35% were considering changing jobs or stopping their studies. There was no significant difference with the SESMAT study for the general BOS score. After multivariate analysis, 12 variables were significantly associated with the main criterion. CONCLUSIONS: Ten years after the SESMAT study, the incidence of BOS in AI has not decreased in the largest cohort of AI studied to date in France.

Road traffic accident-related thoracic trauma: Epidemiology, injury pattern, outcome, and impact on mortality-A multicenter observational study.

BACKGROUND: Thoracic trauma is a major cause of death in trauma patients and road traffic accident (RTA)-related thoracic injuries have different characteristics than those with non-RTA related thoracic traumas, but this have been poorly described. The main objective was to investigate the epidemiology, injury pattern and outcome of patients suffering a significant RTA-related thoracic injury. Secondary objective was to investigate the influence of serious thoracic injuries on mortality, compared to other serious injuries. METHODS: We performed a multicenter observational study including patients of the Rhône RTA registry between 1997 and 2016 sustaining a moderate to lethal (Abbreviated Injury Scale, AIS≥2) injury in any body region. A subgroup (AISThorax≥2 group) included those with one or more AIS≥2 thoracic injury. Descriptive statistics were performed for the main outcome and a multivariate logistic regression was computed for our secondary outcome. RESULTS: A total of 176,346 patients were included in the registry and 6,382 (3.6%) sustained a thoracic injury. Among those, median age [IQR] was 41 [25-58] years, and 68.9% were male. The highest incidence of thoracic injuries in female patients was in the 70-79 years age group, while this was observed in the 20-29 years age group among males. Most patients were car occupants (52.3%). Chest wall injuries were the most frequent thoracic injuries (62.1%), 52.4% of which were multiple rib fractures. Trauma brain injuries (TBI) were the most frequent concomitant injuries (29.1%). The frequency of MAISThorax = 2 injuries increased with age while that of MAISThorax = 3 injuries decreased. A total of 16.2% patients died. Serious (AIS≥3) thoracic injuries (OR = 12.4, 95%CI [8.6;18.0]) were strongly associated with mortality but less than were TBI (OR = 27.9, 95%CI [21.3;36.7]). CONCLUSION: Moderate to lethal RTA-related thoracic injuries were rare. Multiple ribs fractures, pulmonary contusions, and sternal fractures were the most frequent anatomical injuries. The incidence, injury pattern and mechanisms greatly vary across age groups.

How should dexmedetomidine and clonidine be prescribed in the critical care setting? / Como a dexmedetomidina e a clonidina devem ser prescritas no ambiente de terapia intensiva?

Cardiac, ventilatory and kidney management in the critical care setting has been optimized over the past decades. Cognition and sedation represent one of the last remaning challenges. As conventional sedation is suboptimal and as the sedation evoked by alpha-2 adrenergic agonists ("cooperative" sedation with dexmedetomidine, clonidine or guanfacine) represents a valuable alternative, this manuscript covers three practical topics for which evidence-based medicine is lacking: a) Switching from conventional to cooperative sedation ("switching"): the short answer is the abrupt withdrawal of conventional sedation, immediate implementation of alpha-2 agonist infusion and the use of "rescue sedation" (midazolam bolus[es]) or "breakthrough sedation" (haloperidol bolus[es]) to stabilize cooperative sedation. b) Switching from conventional to cooperative sedation in unstable patients (e.g., refractory delirium tremens, septic shock, acute respiratory distress syndrome, etc.): to avoid hypotension and bradycardia evoked by sympathetic deactivation, the short answer is to maintain the stroke volume through volume loading, vasopressors and inotropes. c) To avoid these switches and associated difficulties, alpha-2 agonists may be considered first-line sedatives. The short answer is to administer alpha-2 agonists slowly from admission or endotracheal intubation up to stabilized cooperative sedation. The "take home" message is as follows: a) alpha-2 agonists are jointly sympathetic deactivators and sedative agents; b) sympathetic deactivation implies maintaining the stroke volume and iterative assessment of volemia. Evidence-based medicine should document our propositions.

O manejo cardíaco, ventilatório e renal no ambiente de terapia intensiva tem melhorado nas últimas décadas. Cognição e sedação representam dois dos últimos desafios a vencer. Como a sedação convencional não é ideal, e a sedação evocada por agonistas adrenérgicos alfa-2 (sedação "cooperativa" com dexmedetomidina, clonidina ou guanfacina) representa uma alternativa valiosa, este artigo abrange três tópicos práticos para os quais há lacunas na medicina baseada em evidência. O primeiro deles é a mudança de sedação convencional para sedação cooperativa ("mudança"): a resposta curta consiste em retirada abrupta de sedação convencional, implantação imediata de infusão de um agonista alfa-2 e uso de "sedação de resgate" (bolos de midazolam) ou "sedação agressiva" (haloperidol em bolos) para estabilizar a sedação cooperativa. O segundo tópico é a mudança de sedação convencional para sedação cooperativa em pacientes instáveis (por exemplo: delirium tremens refratário, choque séptico, síndrome do desconforto respiratório agudo etc.), pois, para evitar a hipotensão e a bradicardia provocadas por desativadores simpáticos, a resposta curta é manter o volume sistólico por administração de volume, vasopressores e inotrópicos. Por fim, para evitar essas mudanças e dificuldades associadas, os agonistas alfa-2 podem ser sedativos de primeira linha. A resposta curta é administrar agonistas alfa-2 lentamente desde a admissão ou intubação endotraqueal, até estabilização da sedação cooperativa. Dessa forma, conclui-se que os agonistas alfa-2 são, ao mesmo tempo, agentes desativadores simpáticos e sedativos, bem como a desativação simpática implica na manutenção do volume sistólico e na avaliação persistente da volemia. A medicina baseada em evidência deve documentar esta proposta.

Como a dexmedetomidina e a clonidina devem ser prescritas no ambiente de terapia intensiva? / How should dexmedetomidine and clonidine be prescribed in the critical care setting?

RESUMO O manejo cardíaco, ventilatório e renal no ambiente de terapia intensiva tem melhorado nas últimas décadas. Cognição e sedação representam dois dos últimos desafios a vencer. Como a sedação convencional não é ideal, e a sedação evocada por agonistas adrenérgicos alfa-2 (sedação "cooperativa" com dexmedetomidina, clonidina ou guanfacina) representa uma alternativa valiosa, este artigo abrange três tópicos práticos para os quais há lacunas na medicina baseada em evidência. O primeiro deles é a mudança de sedação convencional para sedação cooperativa ("mudança"): a resposta curta consiste em retirada abrupta de sedação convencional, implantação imediata de infusão de um agonista alfa-2 e uso de "sedação de resgate" (bolos de midazolam) ou "sedação agressiva" (haloperidol em bolos) para estabilizar a sedação cooperativa. O segundo tópico é a mudança de sedação convencional para sedação cooperativa em pacientes instáveis (por exemplo: delirium tremens refratário, choque séptico, síndrome do desconforto respiratório agudo etc.), pois, para evitar a hipotensão e a bradicardia provocadas por desativadores simpáticos, a resposta curta é manter o volume sistólico por administração de volume, vasopressores e inotrópicos. Por fim, para evitar essas mudanças e dificuldades associadas, os agonistas alfa-2 podem ser sedativos de primeira linha. A resposta curta é administrar agonistas alfa-2 lentamente desde a admissão ou intubação endotraqueal, até estabilização da sedação cooperativa. Dessa forma, conclui-se que os agonistas alfa-2 são, ao mesmo tempo, agentes desativadores simpáticos e sedativos, bem como a desativação simpática implica na manutenção do volume sistólico e na avaliação persistente da volemia. A medicina baseada em evidência deve documentar esta proposta.

ABSTRACT Cardiac, ventilatory and kidney management in the critical care setting has been optimized over the past decades. Cognition and sedation represent one of the last remaning challenges. As conventional sedation is suboptimal and as the sedation evoked by alpha-2 adrenergic agonists ("cooperative" sedation with dexmedetomidine, clonidine or guanfacine) represents a valuable alternative, this manuscript covers three practical topics for which evidence-based medicine is lacking: a) Switching from conventional to cooperative sedation ("switching"): the short answer is the abrupt withdrawal of conventional sedation, immediate implementation of alpha-2 agonist infusion and the use of "rescue sedation" (midazolam bolus[es]) or "breakthrough sedation" (haloperidol bolus[es]) to stabilize cooperative sedation. b) Switching from conventional to cooperative sedation in unstable patients (e.g., refractory delirium tremens, septic shock, acute respiratory distress syndrome, etc.): to avoid hypotension and bradycardia evoked by sympathetic deactivation, the short answer is to maintain the stroke volume through volume loading, vasopressors and inotropes. c) To avoid these switches and associated difficulties, alpha-2 agonists may be considered first-line sedatives. The short answer is to administer alpha-2 agonists slowly from admission or endotracheal intubation up to stabilized cooperative sedation. The "take home" message is as follows: a) alpha-2 agonists are jointly sympathetic deactivators and sedative agents; b) sympathetic deactivation implies maintaining the stroke volume and iterative assessment of volemia. Evidence-based medicine should document our propositions.

Management of severe traumatic brain injury (first 24hours).

The latest French Guidelines for the management in the first 24hours of patients with severe traumatic brain injury (TBI) were published in 1998. Due to recent changes (intracerebral monitoring, cerebral perfusion pressure management, treatment of raised intracranial pressure), an update was required. Our objective has been to specify the significant developments since 1998. These guidelines were conducted by a group of experts for the French Society of Anesthesia and Intensive Care Medicine (Société francaise d'anesthésie et de réanimation [SFAR]) in partnership with the Association de neuro-anesthésie-réanimation de langue française (ANARLF), The French Society of Emergency Medicine (Société française de médecine d'urgence (SFMU), the Société française de neurochirurgie (SFN), the Groupe francophone de réanimation et d'urgences pédiatriques (GFRUP) and the Association des anesthésistes-réanimateurs pédiatriques d'expression française (ADARPEF). The method used to elaborate these guidelines was the Grade® method. After two Delphi rounds, 32 recommendations were formally developed by the experts focusing on the evaluation the initial severity of traumatic brain injury, the modalities of prehospital management, imaging strategies, indications for neurosurgical interventions, sedation and analgesia, indications and modalities of cerebral monitoring, medical management of raised intracranial pressure, management of multiple trauma with severe traumatic brain injury, detection and prevention of post-traumatic epilepsia, biological homeostasis (osmolarity, glycaemia, adrenal axis) and paediatric specificities.

Cognitive Deficits and Inflammatory Response Resulting from Mild-to-Moderate Traumatic Brain Injury in Rats Are Exacerbated by Repeated Pre-Exposure to an Innate Stress Stimulus.

Traumatic brain injury (TBI) is common in both military and civilian populations, and often results in neurobehavioral sequelae that impair quality of life in both patients and their families. Although individuals who are chronically exposed to stress are more likely to experience TBI, it is still unknown whether pre-injury stress influences the outcome after TBI. The present study tested whether behavioral and cognitive long-term outcome after TBI in rats is affected by prior exposure to an innate stress stimulus. Young adult male Sprague-Dawley rats were exposed to the predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) or to water (WAT); exposure was repeated eight times at irregular intervals over a 2-week period. Rats were subsequently subjected to either mild-to-moderate bilateral brain injury (lateral fluid percussion [LFP]) or sham surgery (Sham). Four experimental groups were studied: Sham-WAT, Sham-TMT, LFP-WAT and LFP-TMT. Compared with Sham-WAT rats, LFP-WAT rats exhibited transient locomotor hyperactivity without signs of anxiety, minor spatial learning acquisition and hippocampal long-term potentiation deficits, and lower baseline activity of the hypothalamic-pituitary-adrenal axis with slightly stronger reactivity to restraint stress. Exposure to TMT had only negligible effects on Sham rats, whereas it exacerbated all deficits in LFP rats except for locomotor hyperactivity. Early brain inflammatory response (8 h post-trauma) was aggravated in rats pre-exposed to TMT, suggesting that increased brain inflammation may sustain functional deficits in these rats. Hence, these data suggest that pre-exposure to stressful conditions can aggravate long-term deficits induced by TBI, leading to severe stress response deficits, possibly due to dysregulated inflammatory response.

Altered hypermetabolic response to cortical spreading depolarizations after traumatic brain injury in rats.

Spreading depolarizations are waves of near-complete breakdown of neuronal transmembrane ion gradients, free energy starving, and mass depolarization. Spreading depolarizations in electrically inactive tissue are associated with poor outcome in patients with traumatic brain injury. Here, we studied changes in regional cerebral blood flow and brain oxygen (PbtO2), glucose ([Glc]b), and lactate ([Lac]b) concentrations in rats, using minimally invasive real-time sensors. Rats underwent either spreading depolarizations chemically triggered by KCl in naïve cortex in absence of traumatic brain injury or spontaneous spreading depolarizations in the traumatic penumbra after traumatic brain injury, or a cluster of spreading depolarizations triggered chemically by KCl in a remote window from which spreading depolarizations invaded penumbral tissue. Spreading depolarizations in noninjured cortex induced a hypermetabolic response characterized by a decline in [Glc]b and monophasic increases in regional cerebral blood flow, PbtO2, and [Lac]b, indicating transient hyperglycolysis. Following traumatic brain injury, spontaneous spreading depolarizations occurred, causing further decline in [Glc]b and reducing the increase in regional cerebral blood flow and biphasic responses of PbtO2 and [Lac]b, followed by prolonged decline. Recovery of PbtO2 and [Lac]b was significantly delayed in traumatized animals. Prespreading depolarization [Glc]b levels determined the metabolic response to clusters. The results suggest a compromised hypermetabolic response to spreading depolarizations and slower return to physiological conditions following traumatic brain injury-induced spreading depolarizations.

Placing intracerebral probes to optimise detection of delayed cerebral ischemia and allow for the prediction of patient outcome in aneurysmal subarachnoid haemorrhage.

Cerebral microdialysis could be useful to detect delayed cerebral ischemia in aneurysmal subarachnoid haemorrhage patients. The optimal location of the probes, however, remains controversial. Here, we determined the vascular territories with the highest infarct risk in relation to aneurysm location to define probe implantation guidelines. These guidelines were retrospectively validated by studying the likelihood of probe to fall in a secondary infarct area, and by analysing their influence to predict patient outcome. The vascular territories with highest risk of infarction were the anterior cerebral arteries for anterior communicating artery aneurysms and the ipsilateral middle cerebral artery for internal carotid artery, posterior communicating artery and middle cerebral artery aneurysms. When cerebral microdialysis probes had been implanted in these territories, 79% were located within an infarcted area versus 54% when they were implanted in other territories. Delayed cerebral ischemia was detected only when the probe was located within a brain area later affected by secondary infarction, which could justify the use of implantation guidelines. Moreover, individual patient outcomes could be predicted when probes were placed in the brain territories as suggested by this study. Thus, a precise probe placement algorithm can improve delayed cerebral ischemia detection sensitivity and allow for a better prediction concerning patient outcome.

The Decrease in Traumatic Brain Injury Epidemics Deriving from Road Traffic Collision Following Strengthened Legislative Measures in France.

BACKGROUND: Since 2002, France has been strengthening legislation on road traffic. This study is intended to evaluate the changes in Traumatic Brain Injury (TBI) incidence and mortality resulting from Road Traffic Collision (RTC) in the two 6-year periods before and after 2002. METHODS: We used a Registry of all RTC casualties in the Rhône Department of France. Each casualty was coded according to the Abbreviated Injury Scale (AIS). The study describes changes in demographic variables, TBI (AIS ≥ 2) incidence and mortality, other body lesions (AIS ≥ 3) associated with TBI, road user types, seatbelt and helmet wearing. FINDINGS: RTC casualty occurrences decreased by 21% (from 64,312 to 50,746) during the period after 2002. TBI occurrence accounted for 8.6% and 6.7% of all RTC in both periods. This corresponds to a reduction of TBI casualty incidence (-42%), which was much more pronounced than RTC casualty incidence (-25%) (p < 0.0001). Severe and critical TBI (AIS-4 and -5) incidences were reduced by half as much (-21%), compared to TBI incidence. TBI mortality rate (among population) and lethality (among TBI related to RTC casualties) decreased 56% and 23%, respectively. This reduction particularly affected car occupants and victims who deceased. TBI incidence decreased 43% in all 10-year age classes until 60 on average, this decrease declining with age in the period after 2002. After adjustment for age, sex, road user types, and severity of lesions at the head and other body regions, logistic regression analysis displayed a protective effect of the period following 2002, on the risk of death after RTC-related TBI. INTERPRETATION: The greater reductions in the incidence, severity and mortality of TBI when compared with the reduction of casualty incidence have mainly affected car users. These results should be attributable to the improvements in standards of care, primary safety of the car fleet and general road architecture safety. However, the increased reduction in the TBI epidemics in France, when compared to those observed in other developed countries for the same periods, suggests that the effects should be strongly attributable to changes in road user behaviour induced by law enforcement. The at-risk groups for TBI after RTC are now two-wheel users (motorized or not) and individuals over 60 years of age.

Neuronal loss as evidenced by automated quantification of neuronal density following moderate and severe traumatic brain injury in rats.

Traumatic brain injury causes widespread neurological lesions that can be reproduced in animals with the lateral fluid percussion (LFP) model. The characterization of the pattern of neuronal death generated in this model remains unclear, involving both cortical and subcortical brain regions. Here, 7 days after moderate (3 atmospheres absolute [ATA]) or severe (3.8 ATA) LFP, we estimated neuronal loss by using immunohistochemistry together with a computer-assisted automated method for quantifying neuronal density in brain sections. Neuronal counts were performed ipsilateral to the impact, in the parietal cortex ventral to the site of percussion, in the temporal cortex, in the dorsal thalamus, and in the hippocampus. These results were compared with the counts observed at similar areas in sham animals. We found that neuronal density was severely decreased in the temporal cortex (-60%), in the dorsal thalamus (-63%), and in area CA3 of the hippocampus (-36%) of injured animals compared with controls but was not significantly modified in the cortices located immediately ventral to the impact. Total cellular density increased in brain structures displaying neuronal death, suggesting the presence of gliosis. The increase in the severity of LFP did not change the pattern of neuronal injury. This automated method simplified the study of neuronal loss following traumatic brain injury and allowed the identification of a pattern of neuronal loss that spreads from the dorsal thalamus to the temporal cortex, with the most severe lesions being in brain structures remote from the site of impact.

[Acute coronary syndrome following a 100 µg carbetocin injection during an emergency Cesarean delivery]. / Syndrome coronarien aigu après injection de carbétocine 100 µg au cours d'une césarienne en urgence.

PURPOSE: Postpartum hemorrhage affects 5% of parturients. Its prevention relies mainly on the administration of oxytocin derivatives. Carbetocin is a newly available analogue of oxytocin but has a considerable incidence of side effects. CLINICAL FEATURES: We report the case of a woman with no cardiovascular risk factors experiencing an acute coronary syndrome with significant electrocardiogram changes perioperatively after a single injection of carbetocin during an emergency Cesarean delivery. Postoperative cardiac enzyme levels and transthoracic echocardiogram results were normal. CONCLUSION: A 2012 retrospective analysis of the use of carbetocin in our institution revealed an incidence rate for coronary events of 1/245 (0.34%), a rate similar to the ones reported in previous studies. We discuss the management of patients with angina during a Cesarean delivery as well as the plans to care for these patients in the future.

Immobilization method to preserve enzyme specificity in biosensors: consequences for brain glutamate detection.

Microelectrode biosensors are a promising technique to probe the brain interstitial fluid and estimate the extracellular concentration of neurotransmitters like glutamate. Their selectivity is largely based on maintaining high substrate specificity for the enzymes immobilized on microelectrodes. However, the effect of enzyme immobilization on substrate specificity is poorly understood. Furthermore, the accuracy of biosensor measurements for brain biological extracts has not been reliably established in comparison with conventional analytical techniques. In this study, microelectrode biosensors were prepared using different enzyme immobilization methods, including glutaraldehyde, a conventional cross-linker, and poly(ethylene glycol) diglycidyl ether (PEGDE), a milder immobilization reagent. Glutaraldehyde, but not PEGDE, significantly decreased the apparent substrate specificity of glutamate and glucose oxidase. For glutaraldehyde prepared biosensors, detection of secondary substrates by glutamate oxidase increased, resulting in a significant overestimate of glutamate levels. This effect was not observed with PEGDE-based biosensors, and when brain microdialysates were analyzed, the levels of glutamate detected by biosensors were consistent with those detected by capillary electrophoresis. In addition, basal concentrations of glutamate detected in vivo were approximately 10-fold lower than the levels detected with glutaraldehyde-based biosensors (e.g., 1.2 µM vs 16 µM, respectively). Overall, enzyme immobilization can significantly impact substrate specificity, and PEGDE is well-suited for the preparation of stable and selective biosensors. This development questions some of the previous biosensor studies aimed at detecting glutamate in the brain and opens new possibilities for specific neurotransmitter detection.

Spinal cord injuries sustained in road crashes are not on the decrease in france: a study based on epidemiological trends.

Traumatic spinal cord injuries (SCI) are rare but extremely costly. In order to improve the modelling of inclusion criteria for studies of SCI it is necessary to determine what epidemiological trends affect SCI. Using the Rhone Registry, which contains all the casualties resulting from road crashes in the Rhône département of France and codes their injuries using the Abbreviated Injury Scale (AIS), we describe the epidemiological trends that affect spinal cord injury (SCI), major spinal trauma (MST) and severe injuries (AIS4+) to other body regions between two periods 1996-2001 and 2003-2008. Although there has been a marked decrease (35%) in the incidence of casualties after a road traffic crash, and reductions of 22% in the incidence of MST and 33% in that of severe injuries (AIS4+) (p<0.001), for SCI the incidence rate and number of casualties have remained surprisingly stable. In the second period, there was no change in the incidence of SCI resulting from road traffic crashes, nor in the associated fatality, mortality and survival rates. The incidence for car users was significantly lower in the second period. This contrasts with the incidences for motorcyclists and for the group including pedestrians and cyclists which were respectively 47% and 77% higher in the second period. The median age of the casualties, the age-adjusted incidence of SCI and the number of associated injuries were also higher in the second period. We have observed a marked reduction in the incidence of road trauma including the most severe injuries, but not SCI. The higher proportion of motorcyclists, the increase in the age of casualties and the greater presence of multiple injuries are new factors in the epidemiology of SCI after a road crash.

A 10-year population survey of spinal trauma and spinal cord injuries after road accidents in the Rhône area.

Fatalities or injuries following motorized and non-motorized vehicle accidents (MNMVA) are reported by police or health care systems. However, limited data exist for spinal injuries. Using an epidemiological database of road accidents occurring in a defined geographic area, we measured the incidence of major spinal trauma (MST, Abbreviated Injury Scale [AIS] score 2 or more), spinal cord injury (SCI, AIS score 4 or more), and associated lesions over a 10-year period (1997-2006). Among the 97,341 victims included, 21,623 (22.2%) suffered spinal trauma, but only 1523 (1.6%) and 144 (0.2%) sustained an MST or SCI, respectively, and among those 10% and 43% died, respectively, before reaching hospital facilities. Men were more likely to have SCI and die. Cervical injuries were more frequently observed for SCI (58%) than for MST (39%; p < 0.001). Motorcyclists were overrepresented in SCI (33%) compared to MST (21%; p < 0.001), and were at significant risk for fatality. Non-restrained car occupants were at risk of MST and SCI, whereas motorcyclists wearing helmets were not. The chest was the most frequently-injured body region. Nearly half of MNMVA victims suffering SCI die quickly after the crash. Young age, male gender, a motorcyclist, and non-restrained car occupant were risk factors for serious injury. These groups should be targeted in specific programs to decrease fatalities, spinal trauma, and SCI after MNMVA.

Characterization of the pharmacokinetics of human recombinant erythropoietin in blood and brain when administered immediately after lateral fluid percussion brain injury and its pharmacodynamic effects on IL-1beta and MIP-2 in rats.

This study sought to determine the bio-availability of recombinant human erythropoietin (EPO) in the brain and blood and its effects on the cerebral concentrations of the inflammatory mediators interleukin-1beta (IL-1beta) and macrophage-inflammation protein-2 (MIP-2) following lateral fluid percussion brain injury (FPI) in the rat. After induction of moderate FPI (1.6-1.8 atm), EPO was injected intraperitoneally (IP) or intravenously (IV) at doses of 1000-5000 U/kg in a randomized and blinded manner. Animals were then sacrificed at time points (4, 8, 12, 24 h) post-trauma, and the brain concentrations of EPO, IL-1beta, and MIP-2 were determined. EPO administration leads to a dose-dependent increase in the brain concentration of the drug; however, this could only be detected at doses of 3000 and 5000 U/kg. The cerebral concentration peaked in the first 4 h following trauma. EPO concentrations were significantly higher and decreased more slowly in the traumatized cortex compared to the contralateral side (p<0.0125). IV EPO (5000 U/kg) produced slightly higher concentrations of EPO than same doses injected IP; however, this was not significant. At a dose of 5000 U/kg, EPO significantly reduced the increase in IL-1beta at 8 and 12 h in both cortical sides. It also reduced the increase in MIP-2 but only after 8 h, on the contralateral side and after 12 h on the ipsilateral side. Our results suggest that EPO crosses the blood-brain barrier (BBB) by 4 h after trauma and is localized primarily in the traumatized cortex. Further, it has biological efficacy at 8 h on several inflammatory proteins, yet must be employed at high doses to cross the BBB.

Long-term follow-up of meningiomas of the cavernous sinus after surgical treatment alone.

OBJECT: The authors report on the long-term outcome in 100 consecutive patients with meningiomas arising from the cavernous sinus (CS) with compressive extension outside the CS. The treatment in all cases was surgery alone without adjuvant radiosurgery or radiotherapy. The aim of this study was to evaluate the percentage of patients in whom surgery alone was able to produce long-term tumor control. METHODS: All 100 patients harbored meningiomas with supra- and/or laterocavernous extension, and 27 had petroclival extension. Surgery was performed via frontopterionotemporal craniotomy associated with orbital and/or zygomatic osteotomy in 97 patients. Proximal control of the internal carotid artery at the foramen lacerum was undertaken in 65 patients; the paraclinoid carotid segment was exposed extradurally at the space made by the anterior clinoidectomy in 81 patients. For the petroclival tumor extension, a second-stage surgery was performed via a presigmoid-retrolabyrinthine or retrosigmoid approach in 13 and 14 patients, respectively. RESULTS: The mortality rate was 5% and two patients had severe hemiplegic or aphasic sequelae. The creation or aggravation of disorders in vision, ocular motility, or trigeminal function occurred in 19, 29, and 24% of patients respectively, with a significantly higher rate of complications when resection was performed inside the CS (p < 0.05). Gross-total removal of both the extra- and intracavernous portions was achieved in 12 patients (Group 1), removal of the extracavernous portions with only a partial resection of the intracavernous portion in 28 patients (Group 2), and removal only of the extracavernous portions was performed in 60 patients (Group 3). The follow-up period ranged from 3 to 20 years (mean 8.3 years). There was no tumor recurrence in Group 1. In the 83 surviving patients in Groups 2 and 3 combined, the tumor remnant did not regrow in 72 patients (86.7%); regrowth was noted in 11 (13.3%). CONCLUSIONS: The results suggest that there is no significant oncological benefit in performing surgery within the CS. Because entering the CS entails a significantly higher risk of complications, radiosurgical treatment should be reserved for remnants with secondary growth and clinical manifestations.

Muscle relaxation and increasing doses of propofol improve intubating conditions.

PURPOSE: Muscle relaxants and anesthetics are usually associated during intubation. However, their relative role to facilitate the process is not clearly defined. This study was designed to determine, during intubation: i). the relative role of anesthetics and atracurium-induced neuromuscular block and; ii). the effect of different doses of propofol in the presence of complete muscle block. METHODS: Patients were randomized to four groups and received fentanyl and a standardized anesthetic procedure. Patients from groups high (H; n = 45), medium (M; n = 48) and low (L; n = 47) received 2.5 mg x kg(-1), 2.0 mg x kg(-1), and 1.5 mg x kg(-1) of propofol respectively. Atracurium (0.5 mg x kg(-1)) was then injected and tracheal intubation performed once complete block was achieved at the orbicularis oculi. Patients from group without atracurium (WA; n = 20) received propofol as in group H. Intubation was performed at the expected onset time of action of atracurium. RESULTS: Using the same dose of propofol, the incidence of good or excellent intubating conditions was 35% without atracurium and 95% with atracurium (P < 0.0001). In patients receiving atracurium, clinically acceptable intubating conditions were more frequently achieved in groups receiving the highest propofol doses (group H or M vs group L; P < 0.03). CONCLUSION: Our study confirms the interaction between anesthesia and muscle relaxation to produce adequate intubating conditions. In the conditions described, intubating conditions were more dependent on atracurium-induced neuromuscular blockade than on anesthetics, but both atracurium and propofol improved intubating conditions.