see also Pediatric Severe traumatic Brain Injury.
56–60% of patients with GCS score ≤8 have 1 or more other organ system injured. 25% have “surgical” lesions.
Patients presenting with an early GCS score of 3-5 after blunt or penetrating skull-brain assaults are categorized as having sustained a very severe Traumatic Brain Injury (vs-TBI). This category is often overlooked in literature.
Neuroendocrine dysfunction occurs often in the acute phase of moderate-to-severe traumatic brain injury, more commonly in patients with severe traumatic brain injury, patients with pressure effects and low Glasgow Outcome Scale.
Autonomic impairment, as measured by heart rate variability and baroreflex sensitivity, is significantly associated with increased mortality after traumatic brain injury. These effects, though partially interlinked, seem to be independent of age, trauma severity, intracranial pressure, or autoregulatory status, and thus represent a discrete phenomenon in the pathophysiology of traumatic brain injury. Continuous measurements of heart rate variability and baroreflex sensitivity in the neuromonitoring setting of severe traumatic brain injury may carry novel pathophysiological and predictive information 4).
The timing of the second cCT scan is not standardized. Recommendations range from 6 to 48 hours after the first scan 5) 6) 7) 8). Over the years the time from accident to the first cCT immediately after admission has decreased continuously. Therefore initial cCT scans might be unremarkable despite intracranial trauma sequel 9) 10). . For that reason some trauma centres schedule the second scan 6 to 24 hours after the admission scan in order to detect early progression of brain injury 11) 12) 13) 14).
No Phase III trials have been clearly successful, in human neurotrauma, although several Phase II studies have shown apparent benefit. A review is an attempt to identify factors that could be responsible for some of these failures. Recommendations are made that attempt to avoid these pitfalls in the future. Five criteria for future conduct of clinical trials are proposed. The usefulness of animal models for traumatic brain injury and their ability are discussed. Clearly, it is now becoming accepted that mechanism-driven trials, in which individual pathophysiological mechanisms are targeted, may be preferable in this heterogeneous patient population. The degree of brain penetration, the safety and tolerability of the compound, and end points used for outcome assessment are major influences upon the success of these trials. New approaches in developing, conducting, and analyzing these clinical trials should be considered in the future, if the costly failures of the past are not to be repeated, with the advent of newer “neuroprotective agents” and techniques 15).