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Extracranial injury is frequently present in patients with traumatic brain injury (TBI). However, no reliable biomarker exists nowadays to evaluate the magnitude and extension of extracranial injury as well as the identification of patients who are at risk of developing secondary injuries. The purpose of this study was to identify new possible peptide biomarkers by mass spectrometry analysis in patients with TBI and ascertain whether the novel biomarker discovered by peptide mass fingerprinting, serum amyloid A1 (SAA1), is capable of reflecting the condition of the patient and both intracranial and extracranial injury extension. Demographic characteristics, clinical data, and serum samples were prospectively collected from 120 patients with TBI (Glasgow Coma Scale [GCS] score 3-15) on admission. Biomarkers were quantified by enzyme-linked immunosorbent assay. Intracranial lesion volume was measured from the semiautomatic segmentation of hematoma on computed tomography (CT) using Analyze software. Functional outcome was evaluated using the Glasgow Outcome Scale (GOS) at hospital discharge and GOS extended scores at 6 months. The SAA1 levels were significantly associated with intracranial (GCS score at admission, lesion load measured with cranial CT, and pupil responsiveness) and extracranial clinical severity (all Abbreviated Injury Scale regions, Injury Severity Score, major extracranial injury, polytrauma, and orthopedic fractures presence), along with systemic secondary insults and functional outcome. SAA1 was is associated with the volume of traumatic intracranial lesions. The SAA1 levels were correlated with astroglial S100β and glial fibrillary acidic protein (GFAP), neuronal neuron-specific enolase (NSE), and axonal total tau (T-tau) and phosphorylated neurofilament heavy chain (pNF-H) injury markers. SAA1 predicts unfavorable outcome and mortality at hospital discharge (area under the curve [AUC] = 0.90, 0.82) and 6 months (AUC = 0.89). SAA1 can be established as a marker for the overall patient condition due to its involvement in the neuroendocrine axis of the systemic response to craniocerebral trauma.

OBJECTIVETraumatic intracerebral hemorrhage (TICH) represents approximately 13%–48% of the lesions after a traumatic brain injury (TBI), and hemorrhagic progression (HP) occurs in 38%–63% of cases. In previous studies, decompressive craniectomy (DC) has been characterized as a risk factor in the HP of TICH; however, few studies have focused exclusively on this relationship. The object of the present study was to analyze the relationship between DC and the growth of TICH and to reveal any correlation with the size of the craniectomy, degree of cerebral parenchymal herniation (CPH), or volumetric expansion of the TICH.METHODSThe authors retrospectively analyzed the records of 497 adult patients who had been consecutively admitted after suffering a severe or moderate closed TBI. An inclusion criterion was presentation with one or more TICHs on the initial or control CT. Demographic, clinical, radiological, and treatment variables were assessed for associations.RESULTSTwo hundred three patients presenting with 401 individual TICHs met the selection criteria. TICH growth was observed in 281 cases (70.1%). Eighty-two cases (20.4%) underwent craniectomy without TICH evacuation. In the craniectomy group, HP was observed in 71 cases (86.6%); in the noncraniectomy group (319 cases), HP occurred in 210 cases (65.8%). The difference in the incidence of HP between the two groups was statistically significant (OR 3.41, p < 0.01). The mean area of the craniectomy was 104.94 ± 27.5 cm2, and the mean CPH distance through the craniectomy was 17.85 ± 11.1 mm. The mean increase in the TICH volume was greater in the groups with a craniectomy area > 115 cm2 and CPH > 25 mm (16.12 and 14.47 cm3, respectively, p = 0.01 and 0.02). After calculating the propensity score (PS), the authors followed three statistical methods—matching, stratification, and inverse probability treatment weighting (IPTW)—thereby obtaining an adequate balance of the covariates. A statistically significant relationship was found between HP and craniectomy (OR 2.77, p = 0.004). This correlation was confirmed with the three methodologies based on the PS with odds greater than 2.CONCLUSIONSDC is a risk factor for the growth of TICH, and there is also an association between the size of the DC and the magnitude of the volume increase in the TICH.