Bertrand Fauvage

Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure.

Objective:To compare the effects of equimolar doses of 20% mannitol solution and of 7.45% hypertonic saline solution (HSS) in the treatment of patients with sustained elevated intracranial pressure (ICP). Design:Parallel, randomized, controlled trial. Setting:Two intensive care units in a university hospital. Patients:A total of 20 stable patients with a sustained ICP of >20 mm Hg secondary to traumatic brain injury (n = 17) or stroke (n = 3). Interventions:A single equimolar infusion (255 mOsm dose) of either 231 mL of 20% mannitol (mannitol group; n = 10 patients) or 100 mL of 7.45% hypertonic saline (HSS group; n = 10 patients) during 20 mins of administration. Measurements:ICP, arterial blood pressure, cerebral perfusion pressure, blood flow velocities of middle cerebral artery using continuous transcranial Doppler, brain tissue oxygen tension, serum sodium and osmolality, and urine output during a study period of 120 mins. Main Results:The two treatments equally and durably reduced ICP during the experiment. At 60 mins after the start of the infusion, ICP was reduced by 45% ± 19% of baseline values (mean ± sd) in the mannitol group vs. 35% ± 14% of baseline values in the HSS group. Cerebral perfusion pressure and diastolic and mean blood flow velocities were durably increased in the mannitol group, resulting in lower values of pulsatility index at the different times of the experiment (p < .01 vs. HSS). No major changes in brain tissue oxygen tension were found after each treatment. Mannitol caused a significantly greater increase in urine output (p < .05) than HSS, although there was no difference in the vascular filling requirement between the two treatments. HSS caused a significant elevation of serum sodium and chloride at 120 mins after the start of the infusion (p < .01). Conclusions:A single equimolar infusion of 20% mannitol is as effective as 7.45% HSS in decreasing ICP in patients with brain injury. Mannitol exerts additional effects on brain circulation through a possible improvement in blood rheology. Pretreatment factors, such as serum sodium, systemic hemodynamics, and brain hemodynamics, thus should be considered when choosing between mannitol and HSS for patients with increased ICP.

Do patients still require admission to an intensive care unit after elective craniotomy for brain surgery

BackgroundAfter elective craniotomy for brain surgery, patients are usually admitted to an intensive care unit (ICU). We sought to identify predictors of postoperative complications to define perioperative conditions that would safely allow ICU bypass. MethodsThis observational cohort study enrolled 358 patients admitted to neuro-ICU after elective intracranial procedures. Postoperative complications were defined as unexpected events occurring within 24 hours of surgery that required imaging or treatment for neurologic deterioration. ResultsFifty-two patients were transferred postoperatively to neuro-ICU with sedation and mechanical ventilation. Of the remaining 306 patients subjected to an attempt to awake and extubate in the operating room, 26 (8%) developed 1 postoperative complication, primarily a new motor deficit, unexpected awakening delay, or subsequent deterioration in consciousness. Four intracerebral hematomas required surgical evacuation and each of these was detected within 2 hours after surgery. Predictors of postoperative complications included failure to extubate the trachea in operating room [odds ratio 61.8; 95% confidence interval (CI) 12.2-312.5], and, to a lesser extent, a duration of surgery of more than 4 hours (odds ratio 3.3; 95% CI 1.4-7.8), and lateral positioning of the patient during the procedure (odds ratio 2.8, 95% CI 1.2-6.4). ConclusionsOur results encourage prospectively testing the hypothesis that patients with immediate, successful tracheal extubation after elective craniotomy for brain surgery, with a surgical duration of less than 4 hours in a nonlateral position could be monitored safely in the postanesthesia care unit before being discharged to a neurosurgical ward.

Perfusion CT to quantify the cerebral vasospasm following subarachnoid hemorrhage

BACKGROUND AND PURPOSE After subarachnoid hemorrhage (SAH), vasospasm is frequent and increases the risk of stroke and poor clinical outcome. The purpose of this study was to identify the best perfusion parameters in perfusion-CT (PCT) able to predict vasospasm diagnosed by angiography after SAH. METHODS Seventy-six patients with SAH were investigated by PCT and cerebral angiography. Using regions of interest (ROI) on parametric maps of mean transit time (MTT), time to peak (TTP), cerebral blood volume (CBV) and cerebral blood flow (CBF), PCT data were compared to an arteriographic score in two categories (severe vasospasm: ≥ 50% and non-severe vasospasm: <50%) for each artery. Best PCT predictors of the arteriographic score were tested using multiparametric logistic regression. RESULTS Among the 76 patients, PCT data were reliable in 65 patients. Twenty-seven patients had a severe vasospasm. Logistic regression showed that MTT was the best predictor of the arteriographic score. Using MTT, odds ratios having a vasospasm were superior to 3.1 and the occurrence of a vasospasm was accurately predicted in 78.5 to 100%, depending on the artery considered. However, no absolute value of the MTT could be identified to predict the occurrence of vasospasm. In fact, abnormal values of MTT ranged from 123 to 221% (m=146%) of the control values. DISCUSSION AND CONCLUSIONS PCT may accurately identify severe vasospasm and might be used as a convenient noninvasive imaging modality to monitor patients with SAH. When detected, severe vasospasm could be confirmed and managed using angiography and endovascular treatment, appropriately.

Œdème cérébral par lésion de la barrière hématoencéphalique : mécanismes et diagnostic

Resume L’œdeme cerebral par lesion de la barriere hematoencephalique (BHE) ou œdeme vasogenique, est present dans la plupart des œdemes cerebraux. Selon la loi de Starling, le passage transmembranaire d’eau, d’ions et de proteines dans le secteur interstitiel peut s’effectuer en raison d’un gradient excessif de pression hydrostatique (origine mecanique) et/ou d’une augmentation de la permeabilite membranaire (origine chimique). Les deux mecanismes coexistent la plupart du temps. Le role d’une elevation du gradient de pression hydrostatique avec perte de l’autoregulation cerebrale a ete evoque dans la reperfusion d’une zone ischemique, le traumatisme crânien, le mal aigu des montagnes et l’eclampsie. La permeabilite de la BHE peut etre augmentee sous l’effet d’une reaction inflammatoire et/ou d’une atteinte de l’integrite membranaire. La reaction inflammatoire est mediee par de nombreux facteurs chimiques liberes par l’endothelium vasculaire (bradykinine) et par une reponse cellulaire secondaire (infiltrat leucocytaire et macrophagique). Ceci s’observe au cours du traumatisme crânien, de l’ischemie et des processus infectieux. Une atteinte de l’integrite physique de la BHE est aussi possible, soit de maniere transitoire (ouverture de la BHE), par exemple apres hyperosmolarite induite, soit de maniere permanente apres degradation enzymatique (metalloproteinases) ou par proliferation de neovaisseaux ayant une BHE absente ou partiellement rompue, sous l’influence du facteur de croissance endothelial (VEGF). C’est le cas des tumeurs et des lesions tissulaires postischemiques. La technique de choix pour le diagnostic d’œdeme vasogenique chez l’homme repose sur la mesure du coefficient de diffusion de l’eau par IRM, qui donne une information localisee et rapide sur la nature exacte de l’œdeme, vasogenique ou cellulaire.

Neurosédation en réanimation

The objectives for using sedation in neurointensive care unit (neuroICU) are somewhat different from those used for patients without severe brain injuries. One goal is to clinically reassess the neurological function following the initial brain insult in order to define subsequent strategies for diagnosis and treatment. Another goal is to prevent severely injured brain from additional aggravation of cerebral blood perfusion and intracranial pressure. Depending on these situations is the choice of sedatives and analgesics: short-term agents, e.g., remifentanil, if a timely neurological reassessment is required, long-term agents, e.g., midazolam and sufentanil, as part of the treatment for elevated intracranial pressure. In that situation, a multimodal monitoring is needed to overcome the lack of clinical monitoring, including repeated measurements of intracranial pressure, blood flow velocities (transcranial Doppler), cerebral oxygenation (brain tissue oxygen tension), and brain imaging. The ultimate stop of neurosedation can distinguish between no consciousness and an alteration of arousing in brain-injured patients. During this period, an elevation of intracranial pressure is usual, and should not always result in reintroducing the neurosedation.

Transcranial Doppler pulsatility index for initial management of brain-injured patients.

To the Editor: I read with interest the technical note by Krammer and Lumenta titled ‘‘The New Aneurysm Clip System for Particularly Complex Aneurysm Surgery: Technical Note’’ published in Neurosurgery in June 2010. I would like to inform them that a technical note on a conceptually same aneurysm clip had already been published in a past issue of this journal by my colleagues. I completely agree that the inverted opening mechanism of the aneurysm clip can offer better surgical vision during clip application, especially in complex aneurysm surgery.

Œdème cérébral: physiopathologie et diagnostic

L’œdeme cerebral (OC) est defini par l’accumulation nette d’eau et de solutes dans le secteur intracellulaire et/ou dans le secteur extracellulaire cerebral, a l’origine d’une augmentation de volume de la masse cerebrale. Il existe de nombreuses facons de classer l’OC: selon son type (cytotoxique, vasogenique, interstitiel, osmotique), sa localisation (intracellulaire ou extracellulaire), son atteinte tissulaire (substance grise ou blanche), la presence ou non d’une rupture de la barriere hemato-encephalique (BHE), le mecanisme en cause. A l’heure actuelle, la classification proposee en 1967 par Igor Klatzo reste la plus simple et la mieux admise par tous (1, 2). Cette classification est basee sur deux types d’OC: l’œdeme cytotoxique, qu’il est preferable d’appeler œdeme cellulaire, est lie a une atteinte de la permeabilite membranaire de la cellule, conduisant a l’accumulation intracellulaire d’eau et d’ions (Na+, Ca++); l’œdeme vasogenique, ou l’ouverture de la BHE provoque un passage d’eau, d’electrolytes et de proteines dans le secteur interstitiel. Certains auteurs distinguent aussi l’œdeme osmotique, lie a un gradient osmotique de part et d’autre de la BHE, combinant un œdeme cellulaire et un œdeme interstitiel pauvre en proteines (BHE intacte) (3).

Principes de traitement de l’hypertension intracrânienne

L’hypertension intracrânienne (HTIC) est la consequence de l’augmentation de volume de l’un ou de plusieurs des elements contenus dans la cavite rigide osteomeningee, aux capacites de compensation volumique reduite. Elle peut se developper a bas bruit ou au contraire prendre une forme rapidement menacante selon le mecanisme en cause et sa vitesse d’apparition, ce qui rend variables les signes cliniques et paracliniques d’HTIC. Lorsque les mecanismes intracerebraux de compensation face a l’augmentation du volume sont epuises, l’HTIC peut evoluer tres rapidement et devenir responsable d’une morbidite et d’une mortalite importante. Elle devient alors une urgence therapeutique pour prevenir deux complications majeures: l’ischemie cerebrale, diffuse ou focale, et le deplacement avec compression de structures parenchymateuses cerebrales.