Efficacy of Antithrombotic Therapy and Risk of Hemorrhagic Complication in Blunt Cerebrovascular Injury Patients with Concomitant Injury: A Systematic Review.

BACKGROUND: The risk-benefit balance of antithrombotic therapy administration for blunt cerebrovascular injuries (BCVI) patients with concomitant injuries at high risk for bleeding is an ongoing therapeutic conundrum for trauma clinicians. We performed a systematic review to assess the reported efficacy and safety of treatment in this population with respect to prevention of ischemic stroke and risk of hemorrhagic complications. STUDY DESIGN: A systematic electronic literature search of MEDLINE, EMBASE, Cochrane Library, and Web of Science databases was performed from January 1, 1996 to December 31, 2021. Studies were included if they reported treatment-stratified clinical outcomes after antithrombotic therapy in BCVI patients with concomitant injuries at high risk of bleeding into a critical site. Data were extracted from selected studies by two independent reviewers, including the main outcomes of interest were BCVI-related ischemic stroke rates and rates of hemorrhagic complications. RESULTS: Of the 5,999 studies reviewed, 10 reported on the effects of treating BCVI patients with concurrent traumatic injuries and were included for review. In the pooled data, among patients with BCVI and concomitant injury who received any form of antithrombotic therapy, the BCVI-related stroke rate was 7.6%. The subgroup of patients who did not receive therapy had an overall BCVI-related stroke rate of 34%. The total rate of hemorrhagic complications in the treated population was 3.4%. CONCLUSIONS: In BCVI patients with concomitant injuries at high risk for bleeding, antithrombotic use reduces the risk of ischemic strokes with a low reported risk of serious hemorrhagic complications.

Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome.

BACKGROUND: The loss of alveolar epithelial and endothelial integrity is a central component in acute respiratory distress syndrome (ARDS); however, experimental models investigating the mechanisms of epithelial injury are lacking. The purpose of the present study was to design and develop an experimental porcine model of ARDS by inducing lung injury with intrapulmonary administration of sodium polyacrylate (SPA). METHODS: The present study was performed at the Centre for Comparative Medicine, University of British Columbia, Vancouver, British Columbia. Human alveolar epithelial cells were cultured with several different concentrations of SPA; a bioluminescence technique was used to assess cell death associated with each concentration. In the anesthetized pig model (female Yorkshire X pigs (n = 14)), lung injury was caused in 11 animals (SPA group) by injecting sequential aliquots (5 mL) of 1% SPA gel in aqueous solution into the distal airway via a rubber catheter through an endotracheal tube. The SPA was dispersed throughout the lungs by manual bag ventilation. Three control animals (CON group) underwent all experimental procedures and measurements with the exception of SPA administration. RESULTS: The mean (± SD) ATP concentration after incubation of human alveolar epithelial cells with 0.1% SPA (0.92 ± 0.27 µM/well) was approximately 15% of the value found for the background control (6.30 ± 0.37 µM/well; p < 0.001). Elastance of the respiratory system (E RS) and the lung (E L) increased in SPA-treated animals after injury (p = 0.003 and p < 0.001, respectively). Chest wall elastance (E CW) did not change in SPA-treated animals. There were no differences in E RS, E L, or E CW in the CON group when pre- and post-injury values were compared. Analysis of bronchoalveolar lavage fluid showed a significant shift toward neutrophil predominance from before to after injury in SPA-treated animals (p < 0.001) but not in the CON group (p = 0.38). Necropsy revealed marked consolidation and congestion of the dorsal lung lobes in SPA-treated animals, with light-microscopy evidence of bronchiolar and alveolar spaces filled with neutrophilic infiltrate, proteinaceous debris, and fibrin deposition. These findings were absent in animals in the CON group. Electron microscopy of lung tissue from SPA-treated animals revealed injury to the alveolar epithelium and basement membranes, including intra-alveolar neutrophils and fibrin on the alveolar surface and intravascular fibrin (microthrombosis). CONCLUSIONS: In this particular porcine model, the nonimmunogenic polymer SPA caused a rapid exudative lung injury. This model may be useful to study ARDS caused by epithelial injury and inflammation.

Hypernatremia in patients with severe traumatic brain injury: a systematic review.

BACKGROUND: Hypernatremia is common following traumatic brain injury (TBI) and occurs from a variety of mechanisms, including hyperosmotic fluids, limitation of free water, or diabetes insipidus. The purpose of this systematic review was to assess the relationship between hypernatremia and mortality in patients with TBI. METHODS: We searched the following databases up to November 2012: MEDLINE, EMBASE, and CENTRAL. Using a combination of MeSH and text terms, we developed search filters for the concepts of hypernatremia and TBI and included studies that met the following criteria: (1) compared hypernatremia to normonatremia, (2) adult patients with TBI, (3) presented adjusted outcomes for mortality or complications. RESULTS: Bibliographic and conference search yielded 1,152 citations and 11 abstracts, respectively. Sixty-five articles were selected for full-text review with 5 being included in our study. All were retrospective cohort studies totaling 5,594 (range 100-4,296) patients. There was marked between-study heterogeneity. The incidence of hypernatremia ranged between 16% and 40%. Use of hyperosmolar therapy was presented in three studies (range 14-85% of patients). Hypernatremia was associated with increased mortality across all four studies that presented this outcome. Only one study considered diabetes insipidus (DI) in their analysis where hypernatremia was associated with increased mortality in patients who did not receive DDAVP. CONCLUSIONS: Although hypernatremia was associated with increased mortality in the included studies, there was marked between-study heterogeneity. DI was a potential confounder in several studies. Considering these limitations, the clinical significance of hypernatremia in TBI is difficult to establish at this stage.