Annales françaises d'anesthèsie et de rèanimation
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Ann Fr Anesth Reanim · Apr 2003
Review[Blood-brain barrier pathophysiology and ischaemic brain oedema].
Cerebral oedema is a potentially lethal complication of brain infarction. Ischemia, by altering membrane ionic pump function, induces cell swelling and cytotoxic oedema. It also initiates early oxidative and inflammatory cascades leading to blood-brain barrier disruption, vasogenic oedema and haemorrhagic transformation. ⋯ This treatment also increases vasogenic oedema and the risk of symptomatic haemorrhagic transformation, reducing the benefit of reperfusion. Experimental studies suggest that the inhibition of blood-brain barrier proteolysis reduces vasogenic oedema and the risk of haemorrhage. This recent progress in the understanding of blood-brain barrier disruption during ischaemia brings forward new therapeutic strategies using agents capable of interfering with the ischaemic cascade in order to increase the therapeutic window between the onset of ischaemia and thrombolytic reperfusion.
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Progress in brain imaging, monitoring and physiopathology allows the identification of brain oedema from brain swelling, determination of its interstitial or intracellular nature, as well as blood-brain barrier permeability and the evaluation of the impact on cerebral haemodynamic. Common treatment of all types of cerebral oedema is based on prevention of self-sustained disorders due to increased intracranial pressure resulting in ischemic cerebral oedema. The specific treatment of each type of cerebral oedema is reviewed. Optimization of conventional anti-oedematous strategies is based on the precise determination of the nature of the cerebral oedema and of the blood-brain barrier status.
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Acute mountain sickness and high altitude cerebral edema are specific pathologies of high altitude exposure. The usual symptoms of acute mountain sickness are headache, nausea, vomiting, insomnia, lassitude, dizziness and ataxia. ⋯ Molecular and cellular mechanisms underlying acute mountain sickness and high altitude cerebral oedema are still poorly understood. The regulation of cerebral blood flow by nitric oxide seems to play a major role.
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Brain oedema leading to intracranial hypertension occurs in a significant proportion of patients with acute liver failure in whom it is a leading cause of death. Although precise pathogenic mechanisms associated to this severe complication remain incompletely understood, increasing evidence points to gut-derived neurotoxins including ammonia as key mediators in cerebral osmotic and perfusion disturbances. The management of brain oedema and intracranial hypertension requires a multidisciplinar approach in a center where liver transplantation is available, as this option is the only treatment modality that provides improvement in outcome. This article reviews the most common causes of acute liver failure and the standard of supportive care management, and describes future potential therapeutic aspects of brain oedema and intracranial hypertension.
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Ann Fr Anesth Reanim · Apr 2003
Review[Cerebral oedema in children compared to cerebral oedema in adults].
About 50% of deaths, in the pediatric population between 1-15 years of age, are due to trauma. This high mortality rate, associated with the frequent sequelae, leading sometimes to severe handicaps, constitutes a major problem for public health in the developed countries. ⋯ The anaesthesiologist must have a complete understanding of the pathophysiology involved in this clinical presentation if one wishes to develop a practical knowledge of initial management of such patients. Traumatic brain injury may have intracranial and systemic effects that combine to give global cerebral ischaemia.