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Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema
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Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema
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Journal Article
Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema
2015
Overview
Key Points
Secondary injury following intracerebral haemorrhage (ICH) is caused by perihaemorrhagic inflammation, toxic products of blood breakdown, and perihaematomal oedema (PHO)
Secondary injury contributes to neurological deterioration over an extended period of hours to days and, therefore, offers a long therapeutic window
PHO forms in three stages in accordance with Starling's principle: stage 1 is characterized by ionic oedema, and stages 2 and 3 by progressive vasogenic oedema
PHO is a pathophysiological marker of secondary injury that could provide a useful surrogate end point for testing novel neuroprotective agents
PHO might also be clinically relevant, as it augments the mass effect of haemorrhage; further studies could identify subgroups of patients who would benefit from therapies that ameliorate PHO
Combination treatment regimens that target different stages of PHO formation might be most effective to reduce swelling
Perihaematomal oedema (PHO) is an important pathophysiological marker of secondary injury following intracerebral haemorrhage. In this Review, the authors consider PHO in a novel framework and highlight the clinical relevance of the condition, both as a therapeutic target and as a surrogate marker for novel interventions that target secondary injury.
Perihaematomal oedema (PHO) is an important pathophysiological marker of secondary injury in intracerebral haemorrhage (ICH). In this Review, we describe a novel method to conceptualize PHO formation within the framework of Starling's principle of movement of fluid across a capillary wall. We consider progression of PHO through three stages, characterized by ionic oedema (stage 1) and progressive vasogenic oedema (stages 2 and 3). In this context, possible modifiers of PHO volume and their value in identifying patients who would benefit from therapies that target secondary injury are discussed; the practicalities of using neuroimaging to measure PHO volume are also considered. We examine whether PHO can be used as a predictor of neurological outcome following ICH, and we provide an overview of emerging therapies. Our discussion emphasizes that PHO has clinical relevance both as a therapeutic target, owing to its augmentation of the mass effect of a haemorrhage, and as a surrogate marker for novel interventions that target secondary injury.
Publisher
Nature Publishing Group UK,Nature Publishing Group
