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.     

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.     

Utilisation d’un ECMO (extracorporeal membrane oxygenation) dans un cas d’hypoxémie réfractaire associée à un traumatisme crânien grave

Traumatic brain injuries are fairly sensitive to hypoxia. For patient with associated lung and brain traumas, different means used to improve oxygen blood level are poorly described. We report the use of ECMO in a refractory hypoxemia occurred to a multitrauma young patient with neurological lesions.     

Hypothermie et protection cérébrale après traumatisme crânien. Influence des gaz du sang

The usefulness of therapeutic hypothermia is highly debated after traumatic brain injury. A neuroprotective effect has been demonstrated only in experimental studies: decrease in cerebral metabolism, restoration of ATP level, better control of cerebral edema and cellular effects. Despite negative multicenter clinical studies, therapeutic hypothermia is still used to a better control of intracranial pressure. However, important issues need to be clarified, particularly the level and duration of hypothermia, the depth and modalities of sedation. A clear understanding of blood gases variations induced by hypothermia is needed to understand the cerebral perfusion and oxygenation changes. It is essential to recognize and to use hypothermia-induced physiological hypocapnia and alkalosis under strict control of cerebral oxygen balance (jugular venous saturation or tissue PO₂) and also to take into account the increased affinity of hemoglobin for oxygen. Management of post-traumatic intracranial hypertension using hypothermia, directed by intracranial pressure level, and consequently for long duration, is potentially beneficial but needs further clarification.     

Le monitorage de la pression intracrânienne améliore-t-il le devenir des traumatisés crâniens graves ?

Raised intracranial pressure (ICP) is frequent and associated with poor outcome after severe traumatic brain injury (TBI). Information obtained by ICP monitoring allows early detection of high ICP and goal-directed therapy. There is a large body of clinical evidence showing that protocol driven neurocritical care improves outcomes after TBI. A monitoring method cannot be separated from therapeutic implications, which may have beneficial or deleterious consequences. ICP monitoring and guided therapy are not risk-free. A rational use of ICP as a guide to therapy must take into account of the absolute threshold for treatment, but also of the risk/benefit balance of the used intervention.     

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.     

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.     

Dissection coronaire traumatique compliquée d’infarctus du myocarde chez un patient traumatisé crânien

Acute myocardial infarction, following coronary artery dissection, is a rare, but potentially fatal, syndrome after blunt chest trauma. The treatment is more complicated when intracerebral lesions are present, because of the need of anticoagulation. We report the case of a 37-year-old male patient, suffering from a polytraumatism with intracranial petechial haemorrhages who have a left coronary artery dissection with acute myocardial infarction.     

Chirurgie périphérique chez le traumatisé crânien grave : précoce ou retardée ?

Head injuries are present in up to 65 % of multiple trauma patients with a frequent association with orthopaedic injuries. The concept of early surgical stabilization of long-bone fractures in patients with multiple injuries became firmly established in the 1980s. However, optimal timing of long bone fracture fixation in trauma patients with associated severe traumatic brain injury has been a lively topic. The available literature does not provide clear-cut guidance on the management of fractures in the presence of head injuries. The trend is toward a better outcome if the fractures are fixed early. In recent years, some studies reported a worse outcome, with secondary brain damage, resulting from hypotension, hypoxia and increased intraoperative fluid administration. This review summarises the current evidence available regarding the management of these patients in particular the recent concept of early temporary surgical stabilization in the era of “damage control orthopaedic surgery”.     

Oxygénothérapie hyperbare et gaz inertes dans l’ischémie cérébrale et le traumatisme crânien

Cerebral ischemia is a common thread of acute cerebral lesions, whether vascular or traumatic origin. Hyperbaric oxygen (HBO) improves tissue oxygenation and may prevent impairment of reversible lesions. In experimental models of cerebral ischemia or traumatic brain injury, HBO has neuroprotective effects which are related to various mechanisms such as modulation of oxidative stress, neuro-inflammation or cerebral and mitochondrial metabolism. However, results of clinical trials failed to prove any neuroprotective effects for cerebral ischemia and remained to be confirmed for traumatic brain injury despite preliminary encouraging results. The addition of inert gases to HBO sessions, especially argon or xenon which show neuroprotective experimental effects, may provide an additional improvement of cerebral lesions. Further multicentric studies with a strict methodology and a better targeted definition are required before drawing definitive conclusions about the efficiency of combined therapy with HBO and inert gases in acute cerebral lesions.     

Troubles de la coagulation lors du traumatisme cranio-encéphalique : physiopathologie et conséquences thérapeutiques

Early activation of coagulation is common after traumatic brain injury. Its origin is probably mainly intracerebral, due to tissue factor release from the injured brain. Abnormalities in blood coagulation tests are associated with poor neurological prognosis. Coagulation activation may induce disseminated intravascular coagulation and fibrinolysis. Disseminated intravascular coagulation is linked to brain ischemia caused by intravascular microthrombosis. This review will focus on pathophysiology of coagulation disorders after traumatic brain injury, and on their implications for therapeutic approaches.     

Association hélium-sévoflurane : une thérapeutique de sauvetage dans l’asthme aigu grave

We report the case of a severe acute asthma, which required, after optimal medical therapy, helium and sevoflurane CO-administration after tracheal intubation. The Anesthetic Conserving Device^® allowed sevoflurane use with intensive care unit's ventilator. The helium-sevoflurane association was maintained during 9 days to decrease the bronchospasm, waiting for the efficiency of an aetiologic treatment. We discuss the suitability of this association to treat severe acute asthma, and its administration modalities.     

Syndrome post-arrêt cardiaque : aspects physiopathologiques,cliniques et thérapeutiques

Objective

This review aims at providing an update on post-cardiac arrest syndrome, from pathophysiology to treatment.

Data sources

Medline database.

Data extraction

All data on pathophysiology, clinical manifestations and therapeutic management, with focus on the publications of the 5 last years.

Data synthesis

Care of the patients after cardiac arrest is a medical challenge, in face of “post-cardiac arrest syndrome”, which culminates into multi-organ failure. This syndrome mimics sepsis-related dysfunctions, with all clinical and biological manifestations related to the phenomenon of global ischemia-reperfusion. Acute cardiocirculatory dysfunction is usually controlled through pharmacological and mechanical support. Meanwhile, as a majority of cardiac arrest is related to myocardial infarction, early angiographic exploration should then be discussed when there is no obvious extracardiac cause, percutaneous coronary revascularization being associated with improved short and long-term prognosis. Therapeutic hypothermia is the cornerstone of neuroprotective armamentarium, beyond hemodynamic stabilization and metabolic maintenance.

Conclusion

If ongoing evaluations should shed light on potential efficiency of new therapeutic drugs, a multidisciplinary approach of the post-cardiac arrest syndrome in expertise centre is essential.     

Rôle délétère de l’hyperthermie en neuroréanimation

Fever is a secondary brain injury and may worsen neurological prognosis of neurological intensive care unit (NICU) patients. In response to an immunological threat, fever associates various physiological reactions, including hyperthermia. Its definition may vary but the most commonly used threshold is 37.5 °C. In animal studies, hyperthermia applied before, during or after cerebral ischemia may increase the volume of ischemic lesions. The mechanism of this effect may include increase in blood brain barrier permeability, increase in excitatory amino acid release and increase in free radical production. In NICU patients, fever is frequent, occurring in up to 20–30% of patients. Moreover, after haemorrhagic stroke, fever has been reported in 40–50% of patients. In half of the patients, fever may be related to an infectious cause but in more than 25% of patients, hyperthermia may be of central origin. After ischemic stroke, hyperthermia during the first 72 hours is associated with an increase in infarct size and increase in morbidity and mortality. This holds true also after subarachnoid haemorrhage. After traumatic brain injury, fever is not related to mortality but may increase morbidity. Whereas no causal link has been established between fever and unfavourable outcome, it seems reasonable to treat hyperthermia in patients suffering from brain injuries. In such patients, antipyretics have a moderate efficacy. In case of failure, they should be replaced by physical cooling techniques.     

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.     

Mesure de la pression intracrânienne sans capteur : comment et pour qui ?

The invasive monitoring of intracranial pressure is useful in circumstances associated with high-risk of raised intracranial pressure. However the placement of intracranial probe is not always possible and non-invasive assessment of intracranial pressure may be useful, particularly in case of emergencies. Transcranial Doppler measurements allow the estimation of perfusion pressure with the pulsatility index. Recently, new ultrasonographic methods of cerebral monitoring have been developed: the diameter of the optic nerve sheath diameter, a surrogate marker of raised intracranial pressure and the estimation of median shift line deviation.