Traumatic brain injury (TBI) is the damage to the brain tissue as sequelae of an external mechanical force, such as rapid acceleration or deceleration, penetration by an object, or direct blow. Brain functions are temporarily or permanently impaired and structural damage may or may not be detectable with current investigation techniques [2, 12].
Disturbed conscious level and post-traumatic amnesia are neurobehavioral trademarks of TBI. According to the classic definition of moderate TBI, there should be loss of consciousness more than 30 min and more than at least 24 h of post-traumatic amnesia. Patients may also suffer from agitations and disturbed sleep-wake cycles. Usually, this acute confusional state resolves within several days in uncomplicated cases. However, 65% of moderate and severe TBI patients have long-term cognitive function impairment interfering with their normal activities and work. Nearly 25% of moderate and severe TBI patients fail to return to their work in the year following their injury [13].
The primary mechanical injury in TBI triggers a dynamic neuropathologic process ending to a cascade of metabolic, vascular, cellular, and molecular consequences that lead to neurologic deterioration and secondary brain injury. This cascade of events has several serum biomarkers including D-dimer. In this study, we are trying to find a correlation between elevated levels of serum D-dimer and impairment of cognitive functions following moderate traumatic brain injury [14].
This study included 87 cases presenting with moderate TBI. 72.4% of cases were male and 27.6% were females. The median age was 28 years, ranging from 18 and 63 years. 55.2% of cases experienced road traffic accidents, 24.1% had isolated traumas to the head, 13.8% had fall from height, and 6.9% of cases had an old trivial head trauma. These numbers are similar to most of the previously published series of head trauma patients. Middle age males are always predominant in head trauma studies, as these males are more socially active and aggressive than females and older ages [12]. In the study published by Iskhakov et al., falling from height was the most common cause of head injury in 45.2% of cases and the study published by Subedi et al. in 46.6% of cases [1]. This difference in the incidence of the mode of trauma can be explained by the driving attitudes and the conditions of the roads in Egypt.
Nearly 60% of our patients represented within 12 h of ictus and the rest 40% presented only after 12 h. In the study published by Subedi et al. [1], 32% of our patients represented within 12 h of ictus and the rest 68% presented only after 12 h.
In our study, 27.6% of cases suffered from motor weakness, 24.1% had raccoon eye, and 17.2% experienced CSF rhinorrhea and otorrhea whereas 3.4% experienced bleeding per ear. Hemorrhagic brain contusion came first in incidence among our cases, followed by extradural hemorrhages, compound depressed fractures, skull base fractures, and then chronic subdural hemorrhages. Similar results were published in the study Subedi et al. and by Naseri et al. [1, 15].
Our study showed D-dimer elevations above the normal range in 86.2% of cases. The highest percentage of cases (41.4%) had twofold increases in their serum D-dimers level, followed by a threefold increase in 17.2% of cases. 13.8% of cases had normal serum D-dimer levels. These numbers were higher than the incidence found by Subedi et al. in their published study. They stated an increase in the serum D-dimer levels in only 31.1% of their cases [1]. However, our results were consistent with other studies published by Gomez PA et al. and Harhangi et al., who had increased D- dimer levels in 95.2% and 84.6% of cases respectively [16, 17].
The mean MoCA-B score among our cases was 24, the highest score was 27, and the lowest score was 13. 55% of cases had normal MoCA-B score, denoting normal cognitive functions. Thirty-one percent of cases had borderline MoCA-B score denoting slight affection of their cognitive functions. The remaining 14% had low MoCA-B scores denoting severe impairment of cognitive functions. We did not detect any statistically significant correlation between D-dimer and MoCA-B scores, or between the D-dimer levels and other variables. This was inconsistent with the results published by Subedi et al., who found a correlation between D-dimer levels and the duration of hospital stay, ICU stay, as well as the Glasgow outcome score [1]. This can be explained by the fact that they were lacking the quantitative assay of D-dimer in their study. Therefore, the role played by D-dimer in the pathophysiology of cognitive deficits and structural abnormalities in moderate TBI is not proved. It takes more thorough and extensive multi-centric studies to be devoted to that purpose. Our study limitations were the lack of a larger number of cases, multicentricity should be taken into consideration, and also a more specific biomarker to TBI should be investigated.
Limitations of the study
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The number of cases included shall be larger covering all age groups with stratification.
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Multi-centricity shall be taken into consideration for more concrete evidence and results.
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D-dimer is not a specific biomarker or prognostic indicator for traumatic brain injury. Much more specific biomarkers shall be taken into consideration, and this shall raise the idea of much more sophisticated laboratory and imaging investigations to be done and hence the need for more budget to cover.
