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severe_traumatic_brain_injury

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.

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.

Impact

The impact of a moderate to severe brain injury depends on the following:

Severity of initial injury

Rate/completeness of physiological recovery

Functions affected

Meaning of dysfunction to the individual

Resources available to aid recovery

Areas of function not affected by TBI

Epidemiology

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).

Acute subdural hematoma (ASD) is seen in 12% to 29% of severe traumatic brain injury (TBI)

Pathophysiology

Pathophysiological changes arising after primary brain injury lead to the secondary brain injury 2) 3) 4).

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).

Diagnosis

First cCT

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).

Guidelines

Complications

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).

Treatment

Outcome

Determining the prognostic significance of clinical factors for patients with severe head injury can lead to an improved understanding of the pathophysiology of head injury and to improvement in therapy. A technique known as the sequential Bayes method has been used previously for the purpose of prognosis. The application of this method assumes that prognostic factors are statistically independent. It is now known that they are not. Violation of the assumption of independence may produce errors in determining prognosis. As an alternative technique for predicting the outcome of patients with severe head injury, a logistic regression model is proposed. A preliminary evaluation of the method using data from 115 patients with head injury shows the feasibility of using early data to predict outcome accurately and of being able to rank input variables in order of their prognostc significance. 18).


A prospective and consecutive series of 225 patients with severe head injuries who were managed in a uniform way was analyzed to relate outcome to several clinical variables. Good recovery or moderate disability were achieved by 56% of the patients, 10% remained severely disabled or vegetative, and 34% died. Factors important in predicting a poor outcome included the presence of intracranial hematoma, increasing age, motor impairment, impaired or absent eye movements or pupillary light reflexes, early hypotension, hypoxemia or hypercarbia, and raised intracranial pressure over 20 mm Hg despite artificial ventilation. Most of these predictive factors were assessed on admission, but a subset of 158 patients was identified in whom coma was present on admission and was known to have persisted at least until the following day. Although the mortality in this subset (40%) was higher than in the total series, it was lower than in several comparable reported series of patients with severe head injury. Predictive correlations were equally strong in the entire series and in the subset of 158 patients with coma. A plea is made for inclusion in the definition of “severe head injury” of all patients who do not obey commands or utter recognizable words on admission to the hospital after early resuscitation 19).


Survival rate of isolated severe TBI patients who required an emergent neurosurgical intervention could be time dependent. These patients might benefit from expedited process (computed tomographic scan, neurosurgical consultation, etc.) to shorten the time to surgical intervention 20).

The impact of a moderate to severe brain injury can include:

Cognitive deficits including difficulties with:

Attention Concentration Distractibility Memory Speed of Processing Confusion Perseveration Impulsiveness Language Processing “Executive functions” Speech and Language

not understanding the spoken word (receptive aphasia) difficulty speaking and being understood (expressive aphasia) slurred speech speaking very fast or very slow problems reading problems writing Sensory

difficulties with interpretation of touch, temperature, movement, limb position and fine discrimination Perceptual

the integration or patterning of sensory impressions into psychologically meaningful data Vision

partial or total loss of vision weakness of eye muscles and double vision (diplopia) blurred vision problems judging distance involuntary eye movements (nystagmus) intolerance of light (photophobia) Hearing

decrease or loss of hearing ringing in the ears (tinnitus) increased sensitivity to sounds Smell

loss or diminished sense of smell (anosmia) Taste

loss or diminished sense of taste Seizures

the convulsions associated with epilepsy that can be several types and can involve disruption in consciousness, sensory perception, or motor movements Physical Changes

Physical paralysis/spasticity Chronic pain Control of bowel and bladder Sleep disorders Loss of stamina Appetite changes Regulation of body temperature Menstrual difficulties Social-Emotional

Dependent behaviors Emotional ability Lack of motivation Irritability Aggression Depression Disinhibition Denial/lack of awareness


Both single predictors from early clinical examination and multiple hospitalization variables/parameters can be used to determine the long-term prognosis of TBI. Predictive models like the IMPACT or CRASH prognosis calculator (based on large sample sizes) can predict mortality and unfavorable outcomes. Moreover, imaging techniques like MRI (Magnetic Resonance Imaging) can also predict consciousness recovery and mental recovery in severe TBI, while biomarkers associated with stress correlate with, and hence can be used to predict, severity and mortality. All predictors have limitations in clinical application. Further studies comparing different predictors and models are required to resolve limitations of current predictors 21).

Clinical trials

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 22).

1)
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2)
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.
3)
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.
4)
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5)
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.
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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.
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9)
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11)
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13)
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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.
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16)
Byrne JP, Mason SA, Gomez D, Hoeft C, Subacius H, Xiong W, Neal M, Pirouzmand F, Nathens AB. Timing of Pharmacologic Venous Thromboembolism Prophylaxis in Severe Traumatic Brain Injury: A Propensity-Matched Cohort Study. J Am Coll Surg. 2016 Jul 21. pii: S1072-7515(16)30651-2. doi: 10.1016/j.jamcollsurg.2016.06.382. [Epub ahead of print] PubMed PMID: 27453296.
17)
Nagata K, Kumasaka K, Browne KD, Li S, St-Pierre J, Cognetti J, Marks J, Johnson VE, Smith DH, Pascual JL. Unfractionated heparin after TBI reduces in vivo cerebrovascular inflammation, brain edema and accelerates cognitive recovery. J Trauma Acute Care Surg. 2016 Aug 16. [Epub ahead of print] PubMed PMID: 27533909.
18)
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19)
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20)
Matsushima K, Inaba K, Siboni S, Skiada D, Strumwasser AM, Magee GA, Sung GY, Benjaminm ER, Lam L, Demetriades D. Emergent operation for isolated severe traumatic brain injury: Does time matter? J Trauma Acute Care Surg. 2015 Aug 28. [Epub ahead of print] PubMed PMID: 26317818.
21)
Gao L, Wu X. Prediction of clinical outcome in severe traumatic brain injury. Front Biosci (Landmark Ed). 2015 Jan 1;20:763-771. PubMed PMID: 25553477.
22)
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.
severe_traumatic_brain_injury.txt · Last modified: 2017/11/12 11:55 by administrador