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.
The impact of a moderate to severe brain injury depends on the following:
Severity of initial injury
Rate/completeness of physiological recovery
Meaning of dysfunction to the individual
Resources available to aid recovery
Areas of function not affected by TBI
In Spain there is a 13% reduction in the frequency of severe TBI from the first to the last time period. An increase in the mean age from 35 to 43 years, whereas the frequency of severe TBI according to sex remained approximately the same during the last decades of life. A distinct change was observed in the injury mechanism; traffic accidents decreased from 76% to 55%, particularly those involving 4-wheeled vehicles. However, falls increased significantly, especially in older women, and contusion and subdural haematoma were the most frequent structural injuries. Motor scores could not be reliably assessed for the last time period because of early intubation and sedative drug use 1).
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 5).
The timing of the second cCT scan is not standardized. Recommendations range from 6 to 48 hours after the first scan 6) 7) 8) 9). 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 10) 11). . 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 12) 13) 14) 15).
Traumatic brain injury (TBI) is independently associated with deep vein thrombosis (DVT) and pulmonary embolism (PE). However, early prevention with heparinoids is often withheld for its anticoagulant effect.
Evidence suggests low molecular weight heparin reduces cerebral edema and improves neurological recovery following stroke and TBI, through blunting of cerebral leukocyte (LEU) recruitment. It remains unknown if unfractionated heparin (UFH) similarly affects brain inflammation and neurological recovery post TBI.
Prophylaxis was associated with decreased risk of pulmonary embolism and deep vein thrombosis, but no increase in risk of late neurosurgical intervention or death. Early prophylaxis may be safe and should be the goal for each patient in the context of appropriate risk stratification 16).
Unfractionated heparin (UFH) after TBI reduces LEU recruitment, microvascular permeability and brain edema to injured brain. Lower UFH doses concurrently improve neurological recovery while higher UFH may worsen functional recovery. Further study is needed to determine if this is due to increased bleeding from injured brain with higher UFH doses 17).
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 18).