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Résumé: L’hypothermie thérapeutique (HT) est désormais un standard de soins dans la réanimation du post-arrêt cardiaque dans une stratégie de neuroprotection. En traumatologie crânienne grave, les principales études cliniques évaluant l’HT n’ont pas montré d’amélioration du devenir neurologique ou de la mortalité des patients traités par hypothermie. Le rationnel pour l’utilisation de cette thérapeutique reste pourtant élevé avec de nombreuses preuves expérimentales en sa faveur. Ainsi, l’absence de bénéfice de l’usage systématique précoce de l’HT chez les patients après un traumatisme crânien grave ne doit pas remettre en cause cette technique qui reste un traitement de deuxième intention pour l’hypertension intracrânienne (HTIC). Dans la majorité des études en effet, l’HT diminue la pression intracrânienne. Les modalités pratiques de mise en place de l’HT conditionnent son succès et font appel à une induction par refroidissement de surface ou intravasculaire jusqu’à la température cible de 35°C, au maintien de l’HT pour une durée supérieure à 48heures et à un réchauffement après la phase d’HTIC de l’ordre de 0,5 à 1°C/j. Au-delà du traitement de l’HTIC, la maîtrise des moyens de refroidissement des patients reste fondamentale en neuroréanimation pour limiter les épisodes délétères d’hyperthermie chez le patient cérébrolésé. L’objectif de cette mise au point est d’aborder la balance bénéfice/risque et les aspects pratiques de la réalisation de l’HT en traumatologie crânienne grave. [ABSTRACT FROM AUTHOR]

Abstract: Cerebral ischaemia plays a major role in the outcome of brain-injured patients. Because brain oxygenation can be assessed at bedside using intra-parenchymal devices, there has been a growing interest about whether therapeutic hyperoxia could be beneficial for severely head-injured patients. Normobaric hyperoxia increases brain oxygenation and may improve glucose-lactate metabolism in brain regions at risk for ischaemia. However, benefits of normobaric hyperoxia on neurological outcome are not established yet, that hinders the systematic use of therapeutic hyperoxia in head-injured patients. This therapeutic option might be proposed when brain ischemia persists despite the optimization of cerebral blood flow and arterial oxygen blood content. [Copyright &y& Elsevier]

Abstract: Objectives: The cessation of sedation in brain-injured patients may result in severe agitation and/or acute withdrawal syndrome related to the prolonged administration of large doses of benzodiazepines and/or opioids. The aim of the present study was to assess the clinical efficacy of a written protocol to withdraw sedation for these patients. Study design: Observational prospective study. Patients and methods: After approval by the Institutional Review Board, 40 severely brain-injured patients were included. They had received continuous administration of midazolam and sufentanil or fentanyl for median 15days. On cessation of midazolam infusion, patients were given clorazepate for 3days. On cessation of opioid infusion and clorazepate, clinical data were collected for 48hours: heart rate, systolic blood pressure, respiratory rate, agitation, and pupil diameter. If an opioid withdrawal syndrome occurred, patients received a 48-hour continuous infusion of buprenorphine. Results: Of 40 patients, there were 10 who did not require buprenorphine. An agitation occurred 5hours (1–21) after cessation of opioid, associated with tachycardia, arterial hypertension, and tachypnea. After 6hours buprenorphine treatment, these parameters were normalized. No patient needed the reintroduction of the initial sedation. Conclusion: The cessation of sedation in severely brain-injured patients can be successfully managed with the use of clorazepate, associated with buprenorphine in the presence of agitation. [Copyright &y& Elsevier]

Abstract: 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. [Copyright &y& Elsevier]

Abstract: Therapeutic hypothermia (less than 35°C) is a promising strategy to improve neuroprotection after severe brain injury. Except in patients resuscitated from cardiac arrest, its effectiveness has not yet been demonstrated. Therapeutic hypothermia results in various side effects, including cardiovascular, hydroelectrolytic and infectious disorders, which could explain, in part, the lack of conclusive clinical studies. These hazards are associated with practical difficulties to induce and maintain targeted hypothermia and with rewarming management. An improvement in the techniques for achieving targeted hypothermia, more knowledge about side effects and further randomized clinical trials are needed before recommending the use of therapeutic hypothermia for patients with severe traumatic brain injury. [Copyright &y& Elsevier]

Abstract: Introduction: Patients with moderate traumatic brain injury (TBI) (Glasgow Coma Scale, GCS, 9–13) or minor TBI (GCS 14–15) are at risk for subsequent neurological deterioration. Serum protein S-100 is believed to reflect brain damage following TBI. In patients with normal or minor CT scan abnormalities on admission, we tested whether the determination of serum protein S-100 beta could predict secondary neurological deterioration. Methods: Sixty-seven patients with moderate or minor TBI were prospectively studied. Serum samples were collected on admission within 12hours postinjury to measure serum protein S-100 levels. Neurological outcome was assessed up to seven days after trauma. Secondary neurological deterioration was defined as two points or more decrease from the initial GCS, or any treatment for neurological deterioration. Results: Nine patients had a secondary neurological deterioration after trauma. No differences in serum levels of protein S-100 were found between these patients and those without neurological aggravation (n =58patients): 0.93μg/l (0.14–4.85) vs 0.39μg/l (0.04–6.40), respectively. The proportion of patients with abnormal levels of serum protein S-100 at admission according to two admitted cut-off levels (>0.1 and >0.5μg/l) was comparable between the two groups of patients. Elevated serum levels of protein S-100 were found in patients with Injury Severity Score (ISS) of more than 16 (n =23patients): 1.26μg/l (0.14–6.40) vs 0.22μg/l (0.04–6.20) in patients with ISS less than 16 (n =44patients). Discussion: The dosage of serum protein S-100 on admission failed to predict patients at risk for neurological deterioration after minor or moderate TBI. Extracranial injuries can increase serum protein S-100 levels, then limiting the usefulness of this dosage in this clinical setting. [Copyright &y& Elsevier]

Abstract: Nuclear magnetic spectroscopy (MRS) is a useful method for noninvasively studying intracerebral metabolism. Proton MRS can identify markers of the neuronal viability (N-acetyl-aspartate, NAA), of the metabolism of cellular membranes (choline), of the cellular energy metabolism (creatine, lactate). In Phosphorus MRS, the peaks most readily identified are involved in the high-energy cellular metabolism (ATP, phosphocreatine, inorganic phosphate), and intracellular pH (pHi) can be determined using this method. MRS has been used in experimental models of traumatic brain injury (TBI), primarily to study the cellular metabolism and the relation between biochemical and histological changes after trauma. In trauma patients, significant changes in NAA, choline and pHi were found in both grey and white matter comparing with controls, and these alterations correlated with injury severity. Correlations have been reported between these biochimical changes (reduction in NAA, increase in choline) measured at 1 to 6 months after TBI and the clinical outcome of the patients. However, there are methodological issues which still impede to recommend MRS as a tool for predicting neurological outcome in the clinical setting. [Copyright &y& Elsevier]

Abstract: Near infrared spectroscopy (NIRS) can noninvasively measure cerebral saturation in oxygen, that permits to estimate brain oxygenation and metabolism. This technique could be incorporated into a multimodal monitoring for severely brain-injured patients. This review presents the principles of NIRS, its limits, the main results from clinical studies and its perspectives. More clinical studies are needed before recommending the routine use of NIRS in the ICU. [Copyright &y& Elsevier]

Abstract: Rehabilitation improves the functional prognosis of patients after a neurologic lesion, and tendency is to begin rehabilitation as soon as possible. This review focuses on the interest and the feasibility of very early rehabilitation, initiated from critical care units. It is necessary to precisely assess patients’ impairments and disabilities in order to define rehabilitation objectives. Valid and simple tools must support this evaluation. Rehabilitation will be directed to preventing decubitus complications and active rehabilitation. The sooner rehabilitation is started; the better functional prognosis seems to be. [Copyright &y& Elsevier]

Abstract: Pupil size reflects the balance between sympathetic and parasympathetic systems. Due to technological advances, accurate and repeated pupil size measurements are possible using infrared, video-recorded pupillometers. Two pupil size reflexes are assessed: the pupillary reflex dilation during noxious stimulation, and the pupil light reflex when the pupil is exposed to the light. The pupillary reflex dilation estimates the level of analgesia in response to a painful procedure or to a calibrated noxious stimulus, i.e., tetanic stimulus, in nonverbal patients. This might be of particular interest in optimizing the management of opioids in anaesthetized patients and in assessing pain levels in the intensive care unit. The pupil light reflex measurement is part of the routine monitoring for severely head-injured patients. The impact of pupillometry in this condition remains to be determined. [Copyright &y& Elsevier]