Published online Feb 4, 2012. doi: 10.5492/wjccm.v1.i1.15
Revised: October 27, 2011
Accepted: December 21, 2011
Published online: February 4, 2012
Evolving brain damage following traumatic brain injury (TBI) is strongly influenced by complex pathophysiologic cascades including local as well as systemic influences. To successfully prevent secondary progression of the primary damage we must actively search and identify secondary insults e.g. hypoxia, hypotension, uncontrolled hyperventilation, anemia, and hypoglycemia, which are known to aggravate existing brain damage. For this, we must rely on specific cerebral monitoring. Only then can we unmask changes which otherwise would remain hidden, and prevent adequate intensive care treatment. Apart from intracranial pressure (ICP) and calculated cerebral perfusion pressure (CPP), extended neuromonitoring (SjvO2, ptiO2, microdialysis, transcranial Doppler sonography, electrocorticography) also allows us to define individual pathologic ICP and CPP levels. This, in turn, will support our therapeutic decision-making and also allow a more individualized and flexible treatment concept for each patient. For this, however, we need to learn to integrate several dimensions with their own possible treatment options into a complete picture. The present review summarizes the current understanding of extended neuromonitoring to guide therapeutic interventions with the aim of improving intensive care treatment following severe TBI, which is the basis for ameliorated outcome.