Quelle pression de perfusion cérébrale après traumatisme crânien chez l’enfant ?

The management of cerebral perfusion pressure (CPP) is the one of the main preoccupation for the care of paediatric traumatic brain injury (TBI). The physiology of cerebral autoregulation, CO₂ vasoreactivity, cerebral metabolism changes with age as well as the brain compliance. Low CPP leads to high morbidity and mortality in pediatric TBI. The recent guidelines for the management of CPP for the paediatric TBI indicate a CPP threshold 40–50 mmHg (infants for the lower and adolescent for the upper). But we must consider the importance of age-related differences in the arterial pressure and CPP. The best CPP is the one that allows to avoid cerebral ischaemia and oedema. In this way, the adaptation of optimal CPP must be individual. To assess this objective, interesting tools are available. Transcranial Doppler can be used to determine the best level of CPP. Other indicators can predict the impairment of autoregulation like pressure reactivity index (PRx) taking into consideration the respective changes in ICP and CPP. Measurement of brain tissue oxygen partial pressure is an other tool that can be used to determine the optimal CPP.     

Agressions cérébrales,immunité et infections

Infections are a major cause of death and morbidity after acute injury of the central nervous system (CNS). Acute lesions of the CNS alter immune homeostasis contributing to the development of immunosuppression (IS), and making the bed of the infection. IS results in a decreased phagocytic functions of neutrophils and macrophages as well as monocyte deactivation (decreased capacity of antigen presentation to lymphocytes). The immune abnormalities occur very quickly and may last for weeks. The neurovegetative system is closely connected to the secondary lymphoid organs where cells of innate immunity receive information from injured organs inducing the long lasting adaptive immune response (immune synapse). The sympathetic system is critically involved in the IS through production of anti-inflammatory mediators like interleukin-10. This may prove important as all types of acute injury of the CNS can lead to direct damage to sympathetic centers. Specialized units of care for ischemic stroke, taking into account the risk of infection related to the IS, have improved the prognosis until 18th month after the initial damage of the SNC. It is now well recognized that the improved long-term prognosis is related with the secondary prevention of recurrent ischaemia as well as aggressive management of pulmonary infections. A better understanding of the pathophysiology of IS can be considered in the near future, opening the door to immunomodulatory therapeutic trials.     

Intérêt du monitorage de l’index bispectral (BIS) pour la détection précoce des hypoperfusions cérébrales

Objectives

The goal of the study was to assess whether clinically significant cerebral hypoperfusion in awake patients would be associated with some alterations in the values of the bispectral index (BIS) monitoring.

Study design

Observational study.

Population and methods

We monitored the BIS during endovascular carotid artery occlusion testing in awake patients.

Results

Twenty-eight patients were included. Twenty-one adequately tolerated the procedure. Their BIS value remained stable throughout the procedure. Four patients had poor angiographic tolerance, but no clinical symptoms. Their BIS value slightly decreased during the test (minimal BIS: 83 [79–87]). Three patients had poor clinical and angiographic tolerance of the occlusion. They all experienced an immediate and dramatic decrease in their BIS value (minimal BIS: ipsilateral to clamping: 50 [45–60]; contralateral to clamping: 48 [45–52]). In all patients, the clinical symptoms and the BIS normalized after deflating the occlusion balloon.

Conclusion

In awake patients, the observed values of the BIS monitoring seem to be associated with clinically relevant cerebral hypoperfusion.     

Les dangers de l’hypothermie thérapeutique

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.     

EEG en réanimation : quelles indications,quel matériel ?

There is a growing development of continuous EEG monitoring (cEEG) in the intensive care unit (ICU) management of neurological patients. Its main objective is the detection of epileptic seizures or status epilepticus because the sensitivity of standard short-duration EEG recording in the ICU is poor. The aim of monitoring is to allow rapid recognition and treatment of epileptic complications in order to decrease secondary insults to the brain and improve outcome. Several studies have demonstrated that a large proportion of patients has epileptic crisis after subarachnoid haemorrhage, stroke or brain trauma, without any clinical manifestation. The EEG feature has also demonstrated a prognosis value but its value for clinical management needs further studies. Another application of EEG in the ICU is monitoring depth of anaesthesia or barbiturate treatment. Due to artifacts contamination, this is possible only in deeply sedated of paralyzed patients. The impact or cEEG monitoring on clinical management and its indications have to be further defined.     

L’oxymétrie cérébrale transcutanée en anesthésie pédiatrique

Cerebral oximetry allows continuous real-time and non-invasive monitoring of cerebral oxygen saturation (cSO₂), by measuring oxyhaemoglobin and deoxyhaemoglobin near infrared light absorption, similarly to pulse oximetry. cSO₂ measurement predominantly reflects brain venous compartment, and is correlated with jugular venous saturation. As jugular venous saturation, cSO₂ must therefore be interpreted as a measure of balance between transport and consumption of O₂ in the brain. Cerebral oximetry should be used as a trend monitoring, because its accuracy is insufficient to be considered as reliable measure of absolute value of ScO₂. In adult, correction of intraoperative cerebral desaturation reduces hospital stay, heavy morbidity and mortality, and serious postoperative neurocognitive impairment after cardiac and major abdominal surgery. In children, the occurrence of intra- and postoperative cerebral desaturations during congenital heart surgery is associated with increased neurological morbi-mortality. Cerebral oximetry could be a useful monitoring during anaesthesia of (ex) preterm neonates, due to the risk of impaired cerebral blood flow autoregulation in these patients.     

Pour ou contre les halogénés en neuroanesthésie pour chirurgie intracrânienne

Isoflurane, desflurane and sevoflurane all preserve cerebrovascular carbone dioxide (CO₂) reactivity. They are all concentration-dependant cerebral vasodilatators and decrease cerebral metabolism. Sevoflurane induces the smallest cerebral vasodilatation and preserve cerebral autoregulation up to 1.5 CAM, compared to isoflurane and desflurane which impair it upon 1 CAM. Propofol has been compared to inhaled agents. Propofol preserve cerebrovascular CO₂ reactivity, blood flow-metabolism coupling, cerebral autoregulation and has no vasodilatation effect. None of the three inhaled agents induce any clinical relevant increase of intracranial pressure (ICP), but studies were conducted in patients without any intracranial hypertension (ICHT). However, compared to propofol, ICP and brain swelling were higher with inhaled agents, more with isoflurane compared to sevoflurane. Finally, neuroprotective properties have been described in experimental model for all the inhaled agents but clinical proofs are still lacking. In conclusion, for intracranial surgery without any ICHT inhaled agents can be used as a maintenance anesthetic with a preference for sevoflurane. In case of ICHT or a risk of ICHT during the surgery, propofol is preferred for it slightest effect on ICP and cerebral hemodynamic.     

Peut-on prédire l’aggravation neurologique des patients traumatisés crâniens mineurs et modérés par le dosage sanguin de la protéine S-100β ?

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 12 hours 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 = 58 patients): 0.93 μg/l (0.14–4.85) vs 0.39 μg/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 > 0.5 μg/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 = 23 patients): 1.26 μg/l (0.14–6.40) vs 0.22 μg/l (0.04–6.20) in patients with ISS less than 16 (n = 44 patients).

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.     

Hyperthermia in the neurosurgical intensive care unit

OBJECTIVE: In patients with traumatic or ischemic brain injury, hyperthermia is thought to worsen the neurological injury. We studied fever in the neurosurgical intensive care unit (ICU) population using a definition common to surgical practice (rectal temperature >38.5 degrees C). We sought to determine fever incidence, fever duration, and peak temperature and to quantify the use of antipyretic therapy. We also attempted to determine the patient subgroups that are at highest risk for development of fever. METHODS: In a retrospective chart review of a 6-month period, all febrile episodes that occurred in a consecutive series of neurosurgical ICU patients in a university hospital setting were studied. A febrile episode was defined as a rectal temperature of at least 38.5 degrees C; an episode lasted until the temperature fell below this threshold. RESULTS: The 428 patients studied had 946 febrile episodes. Fever occurred in 47% of patients, with a mean of 4.7 febrile episodes in each febrile patient. Fevers occurred in more than 50% of patients who were admitted to the ICU for subarachnoid hemorrhage, a central nervous system infection, seizure control, or hemorrhagic stroke, but they occurred in only 27% of patients admitted for spinal disorders. Fevers occurred in 15% of the patients who stayed in the ICU less than 24 hours, but in 93% of those who remained longer than 14 days. Despite the use of antipyretic therapy for 86% of the febrile episodes, 57% lasted longer than 4 hours and 5% lasted longer than 12 hours. CONCLUSION: Fever is common in critically ill neurosurgical patients, especially those with a prolonged length of stay in the ICU or a cranial disease. If hyperthermia worsens the functional outcome after a primary ischemic or traumatic injury, as has been suggested by several studies of stroke patients, treatment of fever is a clinical issue that requires better management.     

Chinese Head Trauma Data Bank: effect of hyperthermia on the outcome of acute head trauma patients

Hyperthermia may accentuate the detrimental consequences of brain injury and worsen the outcome of patients with acute head trauma, especially severe traumatic brain injury (TBI). We explored the effect of different magnitudes and durations of hyperthermia in the first 3 days after injury on the outcome of 7145 patients with acute head trauma, including 1626 with severe TBI. The differences in mortality and unfavorable outcome between the normothermia group, mild fever group, moderate fever group, and high fever group were statistically significant (p<0.001). The mortality and unfavorable outcome of severe TBI patients in the groups also differed significantly (p<0.001). The mortality and unfavorable outcome of patients with 1 day, 2 days, and 3 days of high fever were significantly increased (p<0.01). Our data strongly indicate that both degree and duration of early post-trauma hyperthermia are closely correlated with the outcome of acute TBI patients, especially severely injured ones, which indicates that hyperthermia may play a detrimental role in the delayed mechanisms of damage after acute TBI. Prevention of early hyperthermia after acute head trauma is therefore essential to the management of TBI patients.     

Œdème cérébral : nouvelles pistes thérapeutiques

Cerebral oedema (CO) after brain injury can occur from different ways. The vasogenic and cytotoxic oedema are usually described but osmotic and hydrostatic CO, respectively secondary to plasmatic hypotonia or increase in blood pressure, can also be encountered. Addition of these several mechanisms can worsen injuries. Consequences are major, leading quickly to death secondary to intracerebral hypertension and later to neuropsychic sequelae. So therapeutic care to control this phenomenon is essential and osmotherapy is actually the only way. A better understanding of physiopathological disorders, particularly energetic ways (lactate), aquaporine function, inflammation lead to new therapeutic hopes. The promising experimental results need now to be confirmed by clinical data.     

Complications cardiovasculaires de l’agression cérébrale

The clinical importance of cardiovascular consequences resulting from cerebral injury has long been recognized. However, interactions between the brain and the cardiovascular system remain poorly defined and their importance for the management of patients suffering from acute brain injury is largely underestimated. This should have profound consequences on treatment strategies during anaesthesia and intensive cares of these patients, taking into account not only brain perfusion, but also cardiovascular optimisation. This report summarizes the main data available regarding the cardiovascular consequences of brain death, traumatic brain injury, stroke and epilepsy.     

Treatment of fever in neurosurgical patients

Even moderate temperature elevations soon acute cerebral damage may markedly worsen initial brain injury. These effects may justify aggressive antipyretic treatment in neurosurgical intensive care unit (NICU). On the basis of a literature survey, it is observed that fever is extraordinarily common in the neurosurgical intensive care unit during the acute phase of subarachnoid hemorrhage, stroke, and traumatic brain injury. Several clinical studies also suggest worsened neurologic outcome in patients who are febrile compared to those who are not. Pyrexia is more frequent in infected than noninfected patients. Infections (mainly in the respiratory tract) are usually diagnosed in the majority of febrile NICU patients. Laboratory investigations are quite clear regarding the adverse effects of fever in terms not only of functional outcomes, but also histological and neurochemical injury. Even though fever may cause diagnostic confusion (central fever vs infectious), the potentially devastating effects of pyrexia in patients with cerebral diseases may proceed to treat in any case. An attempt to correct fever appears warranted in all patients with acute cerebral damage in order to obtain a better functional recovery and to limit maximally any further insult to the brain. Some of the more common and innovative methods to control body temperature in order to mitigate the detrimental effects of pyrexia following acute neurological injury are explored. Maintenance of normothermia appears to be a desirable therapeutic goal in managing the patients with damaged or at-risk brain tissue. However, it has not been established conclusively that the benefits of antipyretic therapy outweigh its risks and that despite a sound physiologic argument for controlling fever in the brain-injured patient, there is no evidence that doing so will improve their outcome.     

Hypernatremia severity and the risk of death after traumatic brain injury

Purpose

To investigate the relationship between severity of hypernatremia and the risk of death for patients with traumatic brain injury (TBI) who have been admitted to the neurosurgical intensive care unit (NICU).

Methods

A total of 1044 patients with TBI were admitted to our NICU from January 2005 to January 2010. Of these patients, 881 were included in this study. Based on blood serum sodium level in the NICU the 881 patients were divided into four groups: 614 had normal serum sodium (Na < 150 mmol/L), 34 had mild hypernatremia (Na 150–<155 mmol/L), 66 had moderate hypernatremia (Na 155–160 mmol/L) and 167 had severe hypernatremia (Na ≥ 160 mmol/L).

Results

The mortality rates for the mild, moderate, and severe hypernatremia groups were 20.6%, 42.4%, and 86.8%, respectively; the mortality rate for the normal group was 2.0%. In multivariable analysis, mild, moderate, and severe hypernatremia were independent risk factors for mortality; compared with the normal group the odds ratios of mild, moderate, and severe hypernatremia were 9.50, 4.34, and 29.35, respectively.

Conclusions

Severe hypernatremia is an independent risk factor with extremely high odds ratio for death in patients with TBI who are admitted to the NICU.     

Facteurs prédictifs de défaillance d’organes chez les patients admis en réanimation pour hémorragie digestive aiguë

Introduction

Gastrointestinal hemorrhage is an emergency requiring usually an admission in intensive care unit (ICU), which may prove abusive secondarily. The aim of this study was to identify predictive risk factors of organ failure in patients admitted for GH in our ICU.

Design

Retrospective and observational

Methods and measurements

Between January 2008 and December 2011, all patients admitted in our ICU for gastrointestinal hemorrhage were consecutively included. The primary endpoint was the occurrence of at least an organ failure. We realized an univariate analysis then a backward regression to identify independent risk factors associated with the occurrence of at least one organ failure during the ICU hospitalization.

Results

During this period study, 441 consecutive patients with a mean age of 67 ± 15 years were included. The median ICU length of stay was of 4 (3–7) days and 116 (26% [IC95%: 22–30]) patients presented at least one organ failure. The multivariate analysis identified predictive risk factors of organ failure: history of cirrhosis (OR = 3.5 [IC95%: 1.9–6.7], P < 0.001) and an increase in troponin at the admission above the 99th percentile (OR = 3.1 [IC95%: 1.8–5.5], P < 0.001).

Conclusion

Our results confirmed that a large proportion of patients admitted in ICU for the primary diagnosis of gastrointestinal hemorrhage developed any organ failure. The history of cirrhosis and the systemic consequences of the hemorrhagic syndrome as myocardial damage represents important risk factors of morbidity and mortality and thus should be considered during the management.     

Hypothermie thérapeutique en traumatologie crânienne grave

Therapeutic hypothermia (TH) is considered a standard of care in the post-resuscitation phase of cardiac arrest. In experimental models of traumatic brain injury (TBI), TH was found to have neuroprotective properties. However, TH failed to demonstrate beneficial effects on neurological outcome in patients with TBI. The absence of benefits of TH uniformly applied in TBI patients should not question the use of TH as a second-tier therapy to treat elevated intracranial pressure. The management of all the practical aspects of TH is a key factor to avoid side effects and to optimize the potential benefit of TH in the treatment of intracranial hypertension. Induction of TH can be achieved with external surface cooling or with intra-vascular devices. The therapeutic target should be set at a 35 °C using brain temperature as reference, and should be maintained at least during 48 hours and ideally over the entire period of elevated intracranial pressure. The control of the rewarming phase is crucial to avoid temperature overshooting and should not exceed 1 °C/day. Besides its use in the management of intracranial hypertension, therapeutic cooling is also essential to treat hyperthermia in brain-injured patients. In this review, we will discuss the benefit-risk balance and practical aspects of therapeutic temperature management in TBI patients.     

Hypothermie et hypertension intracrânienne

There is a large body of experimental evidence showing benefits of deliberate mild hypothermia (33–35 °C) on the injured brain as well as an improvement of neurological outcome after cardiac arrest in humans. However, the clinical evidence of any benefit of hypothermia following stroke, brain trauma and neonatal asphyxia is still lacking. Controversial results have been published in patients with brain trauma or neonatal asphyxia. Hypothermia can reduce the elevation of intracranial pressure, through mechanisms not completely understood. Hypothermia-induced hypocapnia should have a role on the reduction of intracranial pressure. The temperature target is unknown but no additional benefit was found below 34 °C. The duration of deliberate hypothermia for the treatment of elevated intracranial pressure might be at least 48 hours, and the subsequent rewarming period must be very slow to prevent adverse effects.     

Chirurgie éveillée des gliomes cérébraux : plaidoyer pour un investissement accru des anesthésistes

The recent development of awake surgery in neuro-oncology allowed a conceptual change, i.e. the realization of resection for invasive brain tumors according to functional and not anatomic boundaries. This paradigmatic shift enabled a significant improvement of results in surgery for gliomas, by opening the door to resections within eloquent areas classically considered as “inoperable”, while preserving and even improving the quality of life of patients. In addition, the extent of resections has been maximized, leading to an increase of median survival – especially in low-grade gliomas. Strong relationships between the different teams (surgeons, neuropsychologists, anaesthesiologists) are crucial for the development and improvement of awake surgery. Thus, it seems important that anesthesiologists can benefit from a clear and accurate knowledge of the real contribution of this procedure, in order to better evaluate the balance between the theoretical risks of surgery under local anesthesia versus the actual risk of not performing resection with a maximum of safety and efficiency for the patients. The purpose of this plea is to advocate the spread of awake surgery in routine practice, due to its major impact on both functional and survival outcomes, by nonetheless keeping in mind that a multidisciplinary staff is mandatory for selection of patients as well as into the operating room. In this state of mind, anaesthesiologists have to play a central role, through an increased involvement in this field.     

Impact de la mise en place d’un réseau de soins en traumatologie sur la mortalité des patients traumatisés graves du bassin

Aim

To evaluate the impact of a regional trauma network on intra-hospital mortality rates of patients admitted with severe pelvic trauma.

Study

Retrospective observational study.

Patients

Sixty-five trauma patients with serious pelvic fracture (pelvic abbreviated injury scale [AIS] score of 3 or more).

Methods

Demographic, physiologic and biological parameters were recorded. Observed mortality rates were compared to predicted mortality according to the Trauma Revised Injury Severity Score methodology adjusted by a case mix variation model.

Results

Twenty-nine patients were admitted in a level I trauma centre (reference centre) and 36 in level II trauma centres (centres with interventional radiology facility and/or neurosurgery). Patients from the level I trauma centre were more severely injured than those who were admitted at the level II trauma centres (Injury Severity Score [ISS]: 30 [13–75] vs 22 [9–59]; P < 0.01). Time from trauma to hospital admission was also longer in level I trauma centre (115 [50–290] min vs 90 [28–240] min, P < 0.01). Observed mortality rates (14%; 95% confidence interval, 95% CI, [1–26%]) were lower than the predicted mortality (29%; 95% CI [13–44%]) in the level I trauma centre. No difference in mortality rates was found in the level II trauma centres.

Conclusion

The regional trauma network could screen the most severely injured patients with pelvic trauma to admit them at a level I trauma centre. The observed mortality of these patients was lower than the predicted mortality despite increased time from trauma to admission.     

Hyperoxie normobarique chez le patient traumatisé crânien

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.