Faculty Opinions recommendation of The role of secondary brain injury in determining outcome from severe head injury.

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Abstract
This manuscript led to the recognition that even brief episodes of hypotension or hypoxia are associated with a markedly worse outcome from severe traumatic brain injury (TBI). This was a landmark finding, and it helped to establish the notion of delayed injury to the central nervous system subsequent to the initial – or primary – injury. We now refer to insults that occur at the level of the organism as secondary insults (i.e., hypotension, hypoxia, fever). Preventing or minimizing secondary insults is now central to the critical care management of severe TBIs. In parallel, numerous cellular/biochemical mechanisms of delayed central nervous system injury have been delineated, which has been targeted – so far unsuccessfully – by experimental therapeutics. We now typically refer to these cellular/molecular processes (e.g., glutamatergic excitotoxicity, neuroinflammation, mitochondrial dysfunction, etc.) as secondary injuries to distinguish them from secondary insults. Prior to the publication of this article, it was not uncommon to under-resuscitate severe TBI patients out of fear that the administered fluid could contribute to the genesis of cerebral edema. This paper led to a durable change in the care of severe TBI patients. In recent years, care of TBI has increasingly recognized the importance of cerebral autoregulation. We now understand that hypotension and hypoxia can induce compensatory cerebral vasodilation, thus elevating intracranial pressure per the cerebral vasodilatory cascade previously described by Rosner. The avoidance of hypotension and hypoxia is now entrenched in severe TBI care, and this manuscript undoubtedly played an important role in the development and use of cerebral oxygenation monitors, which are showing promise in improving the clinical outcome of severe TBI patients (per the BOOST-II phase-II randomized controlled trial).

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