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Purpose Contusion expansion is a key determinant of outcome after traumatic brain injury (TBI). Because many patients develop acute coagulopathy, it has been proposed that hemostatic changes may drive this expansion, but the link remains uncertain. Methods In this retrospective single-center cohort, we included adults with isolated moderate-to-severe TBI and no pre-injury antithrombotic therapy. The hemostatic markers activated partial thromboplastin time (APTT), prothrombin time (PT, reported as INR), platelet count (PLT), and fibrinogen were measured on admission and during the first 72 h. Contusion volumes were derived from serial CT scans. Associations between hemostatic markers and contusion volumes over time were analyzed using generalized additive mixed models (GAMMs), adjusting for confounders. Results Among 109 patients, median admission values were fibrinogen 2.4 g/L, PT-INR 1.0, APTT 29 s, and PLT 233 × 10 9 /L. After admission, fibrinogen and PLT declined, whereas PT-INR and APTT increased modestly. Contusion volume increased from a median of 0.7 ml at baseline to 4.6 ml on the third CT. In univariable models, higher APTT and PT-INR values and lower platelet counts were associated with larger contusion volumes, but these associations lost significance after adjustment for age and time from injury. Conclusion Hemostatic disturbances, as measured by standard coagulation assays, were common after TBI but not independently associated with contusion volume over time.

Background Cortical contusions are common in moderate-severe traumatic brain injury (TBI). Cortical contusions often expand, potentially causing neuro-worsening several hours to days post-trauma. While contusion expansion (CE) may affect outcome, potential clinical and radiological markers that can predict CE have been insufficiently explored. In the present single-center retrospective observational cohort study, we evaluated clinical outcome by the Glasgow Outcome Scale extended (GOSE) scale and evaluated risk factor for CE. Method Adult TBI patients > 18 years of age, and of all injury severities, were included. Main variables of interest were low platelet count, defined as < 150 × 10 9 /L, presence of bifrontal contusions and CE, defined as absolute contusion volume increase in cm 3 . Factors associated with CE and clinical outcome according to GOSE were analyzed. Results Between 2012–2022, 272 patients were included. Contusion size on admission correlated positively with CE, as did the Marshall and Rotterdam radiological classification scores. Bifrontal contusions were significantly larger at admission, experienced larger CE, and had a worse outcome than contusions in other locations. Patients with a platelet count < 150 × 10 9 /L experienced a greater volume CE and had a worse outcome when compared to patients with a normal platelet count. In a multivariate analysis, CE remained significantly associated with a poor outcome six months post- injury. Conclusion Contusion volume at admission, Marshall CT classification and Rotterdam CT score, positively correlated to CE. Bifrontal contusions and a platelet count < 150 × 10 9 /L were associated with CE, and a poor clinical outcome. Large CE volumes were associated with a worse clinical outcome, and CE was per se associated with outcome in a multivariate analysis. Management of these risk factors for CE in the acute post-injury setting may be needed to attenuate contusion expansion and to improve clinical outcome in TBI patients suffering from cortical contusion injuries.

Cerebral edema and contusion expansion are major determinants of morbidity and mortality after TBI. Current treatment options are reactive, suboptimal and associated with significant side effects. First discovered in models of focal cerebral ischemia, there is increasing evidence that the sulfonylurea receptor 1 (SUR1)—Transient receptor potential melastatin 4 (TRPM4) channel plays a key role in these critical secondary injury processes after TBI. Targeted SUR1-TRPM4 channel inhibition with glibenclamide has been shown to reduce edema and progression of hemorrhage, particularly in preclinical models of contusional TBI. Results from small clinical trials evaluating glibenclamide in TBI have been encouraging. A Phase-2 study evaluating the safety and efficacy of intravenous glibenclamide (BIIB093) in brain contusion is actively enrolling subjects. In this comprehensive narrative review, we summarize the molecular basis of SUR1-TRPM4 related pathology and discuss TBI-specific expression patterns, biomarker potential, genetic variation, preclinical experiments, and clinical studies evaluating the utility of treatment with glibenclamide in this disease.

Background Preventing intracranial hematoma expansion has been advertised as a possible treatment opportunity in traumatic brain injury (TBI). However, the time course of hematoma expansion, and whether the expansion affects outcome, remains poorly understood. In light of this, the aim of this study was to use 3D volume rendering to determine how traumatic intracranial hematomas expand over time and evaluate its impact on outcome. Methods Single-center, population-based, observational cohort study of adults with moderate-to-severe TBI. Hematoma expansion was defined as the change in hematoma volume from the baseline computed tomography scan until the lesion had stopped progressing. Volumes were calculated by using semiautomated volumetric segmentation. Functional outcome was measured by using the 12 month Glasgow outcome scale (GOS). Results In total, 643 patients were included. The mean baseline hematoma volume was 4.2 ml, and the subsequent mean hematoma expansion was 3.8 ml. Overall, 33% of hematomas had stopped progressing within 3 h, and 94% of hematomas had stopped progressing within 24 h of injury. Contusions expanded significantly more, and for a longer period of time, than extra-axial hematomas. There was a significant dose–response relationship between hematoma expansion and 12 month GOS, even after adjusting for known outcome predictors, with every 1-ml increase in hematoma volume associated with a 6% increased risk of 1-point GOS deduction. Conclusions Hematoma expansion is a driver of unfavorable outcome in TBI, with small changes in hematoma volume also impacting functional outcome. This study also proposes a wider window of opportunity to prevent lesion progression than what has previously been suggested.

Blood pressure variability (BPV) has been shown to correlate with intraparenchymal hematoma progression (HP) and worse outcomes in patients with spontaneous intracerebral hemorrhage (sICH). However, this association has not been elucidated in patients with traumatic intraparenchymal hemorrhage or contusion (tIPH). We hypothesized that 24 h-BPV from time of admission is associated with hemorrhagic progression of contusion or intraparenchymal hemorrhage (HPC), and worse outcomes in patients with tIPH. We performed a retrospective observational analysis of adult patients treated at an academic regional Level 1 trauma center between 01/2018–12/2019. We included patients who had tIPH and ≥ 2 computer tomography (CT) scans within 24 h of admission. HP, defined as ≥30% of admission hematoma volume, was calculated by the ABC/2 method. We performed stepwise multivariable logistic regressions for the association between clinical factors and outcomes. We analyzed 354 patients' charts. Mean age (Standard Deviation [SD]) was 56 (SD = 21) years, 260 (73%) were male. Mean admission hematoma volume was 7 (SD =19) cubic centimeters (cm3), 160 (45%) had HP. Coefficient of variation in systolic blood pressure (SBPCV) (OR 1.03, 95%CI 1.02–1.3, p = 0.026) was significantly associated with HPC among patients requiring external ventricular drain (EVD). Difference between highest and lowest systolic blood pressure (SBPmax-min) (OR 1.02, 95%CI 1.004–1.03, p = 0.007) was associated with hospital mortality. SBPCV was significantly associated with HP among patients who required EVD. Additionally, increased SBPmax-min was associated with an increase in mortality. Clinicians should be cautious with patients' blood pressure until further studies confirm these observations.

Hematoma expansion is an important consideration in patients with traumatic brain injury (TBI). No precise methods are available, however, for predicting the expansion of TBI-related hematoma. We aimed to establish a more sensitive predictor for contusional hematoma expansion based on the presence of leakage signs on computed tomography angiography (CTA). Thirty-three patients with pure contusion were included in the analysis (age: 64.1 ± 20.6 years; 24 men and 7 women). We compared Hounsfield unit (HU) values within set regions of interest (diameter, 10 mm) between serial CTA phase and delayed-phase CT images (5 min after CTA phase). Positive leakage signs were defined as >10% increases in HU value. Hematoma expansion was determined using plain CT at 24 h in patients who did not undergo emergent surgery. Glasgow Coma Scale (GCS) scores measured at admission and 24 h after admission were also compared. Leakage signs predicted hematoma expansion with high specificity (100%) and sensitivity (92.8%). Patients with positive leakage signs had significant decreases in GCS scores 24 h after the scan (GCS change: positive group, −0.92 ± 0.59; negative group, 1.14 ± 0.82). Positive leakage signs were clearly associated with surgical hematoma removal. Five patients without hematoma who had positive leakage signs at admission exhibited significant expansion of hematomas 24 h later. Our results indicate that leakage signs had high sensitivity in the prediction of contusional hematoma expansion and were significantly associated with delayed neurological deterioration and the necessity of surgical removal.

The active extravasation of contrast on CT angiography (CTA) in primary intracerebral hemorrhages (ICH) is recognized as a predictive factor for ICH expansion, unfavorable outcomes and mortality. However, few studies have been conducted on the setting of traumatic brain injury (TBI). To perform a literature systematic review and meta-analysis of the association of contrast extravasation on cerebral hemorrhagic contusion expansion, neurological outcomes and mortality. The PubMed, Cochrane Library, Medline, Scielo, VHL and IBECS databases up to September 21, 2019, were searched for eligible studies. The extravasation of contrast in the setting of TBI is a useful imaging sign to predict hematoma expansion, worse neurological outcomes and higher mortality.

Since the patient's condition was poor and the cardiac complications did not cause haemodynamic instability, it was decided not perform an aneurysmectomy.