Ketamine Does Not Improve Severe TBI
Background: Ketamine is a phencyclidine congener synthetized in 1962. It produces a dissociative anesthesia by noncompetitive antagonism of the N-methyl- D -aspartate receptor calcium channel pore in the brain and spinal cord. Unlike most anesthetics, it has an indirect sympathomimetic effect supporting blood pressure, heart rate, and bronchodilation among anesthetized humans. Early studies suggested an increase in cerebral blood flow and metabolism with rises of the intracranial pressure (ICP) and intraocular pressure and, for that reason, was once thought to be contraindicated in brain-injured patients; however, more recent studies have suggested that these effects are not clinically significant. As ketamine is known to have pressure supporting, analgesic, and possible neuroprotective effects, it has been increasingly prescribed among brain-injured and neurosurgical patients. Objective: To study the effect of ketamine on 3-month neurologic outcomes and hemodynamic properties of ket
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