Abstract
Intracranial hypertension after severe head injury may be caused by the swelling of brain tissues, the mass effect of expanding haematomas, or, rarely, the obstruction of cerebrospinal fluid outflow. Although the latter two causes usually require a neurosurgical intervention, tissue swelling is mostly managed medically. Tissue swelling results from intracellular fluid accumulation (cytotoxic oedema), fluid extravasation (vasogenic oedema), or hyperaemia with vascular engorgement. Accordingly, there are distinct strategies that can be applied to reduce intracranial pressure. These include (1) treatment aimed at reducing cerebral hyperperfusion by metabolic suppression and hyperventilation, (2) treatment aimed at reducing cerebral hypoperfusion and cytotoxic oedema by augmenting cerebral perfusion pressure and osmotherapy, and (3) treatment aimed at reducing fluid extravasation by decreasing cerebral perfusion pressure, and infusing colloids and vasoconstrictors. In this manuscript I discuss the rationale of each therapeutic strategy in relation to the status of cerebral flow-metabolism coupling, pressure autoregulation, blood-brain barrier permeability, and the temporal changes in cerebrovascular physiology observed after brain trauma.
Original language | English |
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Pages (from-to) | 13-18 |
Number of pages | 6 |
Journal | Netherlands Journal of Critical Care |
Volume | 11 |
Issue number | 1 |
Publication status | Published - 2007 |