Severe traumatic brain injury

see also Pediatric Severe Traumatic Brain Injury.

Severe traumatic brain injury is defined as a brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8.

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.

Severe Traumatic Brain Injury Epidemiology.

Pathophysiological changes arising after primary brain injury lead to the secondary brain injury 1) 2) 3).

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).

First cCT

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).

see Severe traumatic brain injury guidelines.

see also Pediatric traumatic brain injury guidelines.

Severe traumatic brain injury complications.

see Severe traumatic brain injury treatment.

see Severe traumatic brain injury outcome.

see Severe traumatic brain injury cost.

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).

see Severe traumatic brain injury case series

R. S. Cooke, B. P. McNicholl, and D. P. Byrnes, “Early management of severe head injury in Northern Ireland,” Injury, vol. 26, no. 6, pp. 395–397, 1995.
R. M. Chesnut, L. F. Marshall, M. R. Klauber et al., “The role of secondary brain injury in determining outcome from severe head injury,” Journal of Trauma, vol. 34, no. 2, pp. 216–222, 1993.
P. A. Jones, P. J. D. Andrews, S. Midgley et al., “Measuring the burden of secondary insults in head-injured patients during intensive care,” Journal of Neurosurgical Anesthesiology, vol. 6, no. 1, pp. 4–14, 1994.
Sykora M, Czosnyka M, Liu X, Donnelly J, Nasr N, Diedler J, Okoroafor F, Hutchinson P, Menon D, Smielewski P. Autonomic Impairment in Severe Traumatic Brain Injury: A Multimodal Neuromonitoring Study. Crit Care Med. 2016 Mar 10. [Epub ahead of print] PubMed PMID: 26968025.
Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. The New England Journal of Medicine. 2012;367:2471–2481.
Cope DN, Date ES, Mar EY. Serial computerized tomographic evaluations in traumatic head injury. Archives of Physical Medicine and Rehabilitation. 1988;69(7):483–486.
7) , 9) , 11)
Servadei F, Nanni A, Nasi MT, et al. Evolving brain lesions in the first 12 hours after head injury: analysis of 37 comatose patients. Neurosurgery. 1995;37(5):899–907.
Stein SC, Spettell CM. Delayed and progressive brain injury in children and adolescents with head trauma. Pediatric Neurosurgery. 1995;23(6):299–304.
Maas AIR, Dearden M, Servadei F, Stocchetti N, Unterberg A. Current recommendations for neurotrauma. Current Opinion in Critical Care. 2000;6(4):281–292.
Muakkassa FF, Marley RA, Paranjape C, Horattas E, Salvator A, Muakkassa K. Predictors of new findings on repeat head CT scan in blunt trauma patients with an initially negative head CT scan. Journal of the American College of Surgeons. 2012;214:965–972.
Lee TT, Aldana PR, Kirton OC, Green BA. Follow-up Computerized Tomography (CT) scans in moderate and severe head injuries: correlation with Glasgow Coma Scores (GCS), and complication rate. Acta Neurochirurgica. 1997;139(11):1042–1048.
Stein SC, Spettell C, Young G, Ross SE, Kaufman HH, Marshall LF. Delayed and progressive brain injury in closed-head trauma: radiological demonstration. Neurosurgery. 1993;32(1):25–31.
Doppenberg EM, Bullock R. Clinical neuro-protection trials in severe traumatic brain injury: lessons from previous studies. J Neurotrauma. 1997 Feb;14(2):71-80. Review. PubMed PMID: 9069438.
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