Delayed Intracranial Hemorrhage After Blunt Head Injury With Direct Oral Anticoagulants.

INTRODUCTION: Patients presenting to the Emergency Department (ED) following head injury are frequently evaluated with an initial computed tomography scan (CT) of the brain. Imaging is particularly important in patients who are receiving medications that alter normal blood hemostasis. As an imaging modality, CT has a high negative predictive value when used to rule out clinically significant acute intracranial hemorrhage. Patients receiving anticoagulant or antiplatelet therapy have both an increased risk of initial hemorrhage, as well as an increased risk of mortality above nonanticoagulated patients, should they suffer hemorrhage. Multiple studies of delayed intracranial hemorrhage have placed the risk among the patients taking warfarin at the time of head injury in the range of 0.6-6.0%. However, data regarding the risk of delayed intracranial hemorrhage in patients taking the class of agents referred to as Direct-Acting Oral Anticoagulants (DOACs) remains limited. This study aims to estimate this risk. METHODS: A retrospective chart review was performed to identify patients on DOACs who presented to our Level I trauma center following blunt head injury between January 2017 and August 2018. Patients with a negative initial head CT were selected. From this subset, data regarding demographics, injury characteristics, anticoagulant use, and antiplatelet use were collected. RESULTS: Overall, 314 patients were included; 129 patients taking rivaroxaban, 182 patients taking apixaban, and four patients taking dabigatran. In approximately 29% of the patients, the sole indication for admission was close monitoring following head injury while taking an anticoagulant agent. The mechanism of injury for the majority of the patients was fall. Of the 314 patients, three were found to have delayed intracranial hemorrhage on the repeated head CT (0.95%). Two of these three patients were on concomitant antiplatelet medication. None of the three individuals required neurosurgical intervention. CONCLUSIONS: at the time of submission, this is the largest study estimating the risk of delayed intracranial hemorrhage among patients on DOACs. Based on the results of this study, patients who sustain a blunt head injury while taking only DOACs; that is, without concurrent antiplatelet medication, admission, and repeat head CT may not be necessary after confirming a negative initial CT scan.

Role of macrophage chemoattractant protein-1 in acute inflammation after lung contusion.

Lung contusion (LC), commonly observed in patients with thoracic trauma is a leading risk factor for development of acute lung injury/acute respiratory distress syndrome. Previously, we have shown that CC chemokine ligand (CCL)-2, a monotactic chemokine abundant in the lungs, is significantly elevated in LC. This study investigated the nature of protection afforded by CCL-2 in acute lung injury/acute respiratory distress syndrome during LC, using rats and CC chemokine receptor (CCR) 2 knockout (CCR2(-/-)) mice. Rats injected with a polyclonal antibody to CCL-2 showed higher levels of albumin and IL-6 in the bronchoalveolar lavage and myeloperoxidase in the lung tissue after LC. Closed-chest bilateral LC demonstrated CCL-2 localization in alveolar macrophages (AMs) and epithelial cells. Subsequent experiments performed using a murine model of LC showed that the extent of injury, assessed by pulmonary compliance and albumin levels in the bronchoalveolar lavage, was higher in the CCR2(-/-) mice when compared with the wild-type (WT) mice. We also found increased release of IL-1ß, IL-6, macrophage inflammatory protein-1, and keratinocyte chemoattractant, lower recruitment of AMs, and higher neutrophil infiltration and phagocytic activity in CCR2(-/-) mice at 24 hours. However, impaired phagocytic activity was observed at 48 hours compared with the WT. Production of CCL-2 and macrophage chemoattractant protein-5 was increased in the absence of CCR2, thus suggesting a negative feedback mechanism of regulation. Isolated AMs in the CCR2(-/-) mice showed a predominant M1 phenotype compared with the predominant M2 phenotype in WT mice. Taken together, the above results show that CCL-2 is functionally important in the down-modulation of injury and inflammation in LC.