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  • 1
    In: Journal of Trauma and Acute Care Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 6 ( 2016-06), p. 989-997
    Type of Medium: Online Resource
    ISSN: 2163-0755
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2651313-4
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  • 2
    In: Journal of Trauma and Acute Care Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 85, No. 1 ( 2018-7), p. 148-154
    Abstract: Posttraumatic acute respiratory distress syndrome (ARDS) is associated with prolonged mechanical ventilation and longer hospitalizations. The relationship between posttraumatic ARDS severity and financial burden has not been previously studied. We hypothesized that increasing ARDS severity is associated with incrementally higher health care costs. METHODS Adults arriving as the highest level of trauma activation were enrolled in an ongoing prospective cohort study. Patients who survived 6 hours or longer are included in the analysis. Blinded review of chest radiographs was performed by two independent physicians for any intubated patient with Pa o 2 :FIO 2 ratio of 300 mmHg or lower during the first 8 days of admission. The severity of ARDS was classified by the Berlin criteria. Hospital charge data were used to perform standard costing analysis. RESULTS Acute respiratory distress syndrome occurred in 13% (203 of 1,586). The distribution of disease severity was 33% mild, 42% moderate, and 25% severe. Patients with ARDS were older (41 years vs. 35 years, p 〈 0.01), had higher median Injury Severity Score (30 vs. 10, p 〈 0.01), more chest injury (Abbreviated Injury Scale score, ≥ 3: 51% vs. 21%, p 〈 0.01), and blunt mechanisms (85% vs. 53%, p 〈 0.01). By ARDS severity, there was no significant difference in age, mechanism, or rate of traumatic brain injury. Increasing ARDS severity was associated with higher Injury Severity Score and higher mortality rates. Standardized total hospital charges were fourfold higher for patients who developed ARDS compared with those who did not develop ARDS (US $434,000 vs. US $96,000; p 〈 0.01). Furthermore, the daily hospital charges significantly increased across categories of worsening ARDS severity (mild, US $20,451; moderate, US $23,994; severe, US $33,316; p 〈 0.01). CONCLUSION The development of posttraumatic ARDS is associated with higher health care costs. Among trauma patients who develop ARDS, total hospital charges per day increase with worsening severity of disease. Prevention, early recognition, and treatment of ARDS after trauma are potentially important objectives for efforts to control health care costs in this population. LEVEL OF EVIDENCE Economic and value-based evaluations, level IV.
    Type of Medium: Online Resource
    ISSN: 2163-0763 , 2163-0755
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2651313-4
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  • 3
    In: Journal of Trauma and Acute Care Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 85, No. 5 ( 2018-11), p. 873-880
    Abstract: Injury to the blood-brain barrier exposes endothelium rich in von Willebrand factor (vWF), which may play a role in altered platelet aggregation following traumatic brain injury (TBI). Ristocetin is an antimicrobial substance that induces vWF-mediated aggregation of platelets. We examined these mechanisms in injured patients by measuring the aggregation response of platelets to stimulating agonists (including ristocetin) via whole-blood multiple-electrode platelet aggregometry. We hypothesized that patients with TBI have an altered platelet aggregation response to ristocetin stimulation compared with patients without TBI. METHODS Blood was collected from 233 trauma patients without thrombocytopenia. Platelet aggregation was assessed using multiple-electrode platelet aggregometry (Multiplate). Platelet aggregation response to stimulating agonists collagen, thrombin receptor-activating peptide 6, adenosine diphosphate, arachidonic acid, and ristocetin was measured. Factor activity was measured. RESULTS Of the 233 patients, 23% had TBI. There were no differences in platelet aggregation responses to any agonists between TBI and non-TBI patients except ristocetin. Platelet aggregation response to ristocetin stimulation was significantly lower in TBI patients ( p = 0.03). Patients with TBI also had higher factor VIII activity (215% vs. 156%, p = 0.01). In multivariate analysis, there was a significant independent association of impaired platelet aggregation response to ristocetin stimulation with TBI (odds ratio, 3.05; p = 0.04). CONCLUSIONS Given the importance of platelets in hemostasis, understanding the mechanisms of impaired platelet aggregation following injury is critical. The impaired platelet aggregation response to ristocetin stimulation and corresponding increase in factor VIII activity in TBI patients may be secondary to a TBI-induced effect on vWF quantity (due to injury-driven consumption of vWF) or vWF function with resultant increase in circulating factor VIII activity (due to impaired carrying capacity of vWF). Given there are multiple known therapies for vWF deficits including desmopressin, purified and recombinant vWF, and estrogens, these lines of investigation are particularly compelling in patients with TBI and hemorrhage. LEVEL OF EVIDENCE Prognostic study, level II.
    Type of Medium: Online Resource
    ISSN: 2163-0763 , 2163-0755
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2651313-4
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of Trauma and Acute Care Surgery Vol. 84, No. 2 ( 2018-2), p. 365-371
    In: Journal of Trauma and Acute Care Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 84, No. 2 ( 2018-2), p. 365-371
    Abstract: The risk of the acute respiratory distress syndrome (ARDS) is increased in passive and active smokers after blunt trauma. However, the mechanisms responsible, including the role of platelet aggregation, for this association are unknown. METHODS We analyzed 215 patients with severe blunt trauma from a prospective observational cohort at a Level I trauma center between 2010 and 2015. Subjects underwent impedance-based platelet aggregometry in response to platelet agonists arachidonic acid, adenosine diphosphate, collagen, and thrombin receptor activating peptide-6. Acute respiratory distress syndrome within the first 8 days of admission was adjudicated using Berlin criteria. Plasma cotinine was measured to assess cigarette smoke exposure. Regression analyses were used to assess the relationship between (1) platelet aggregation and ARDS and (2) cigarette smoke exposure and platelet aggregation. RESULTS At both 0 hour and 24 hours, impaired platelet aggregation was associated with increased odds of developing ARDS. Cigarette smoke exposure was associated with increased platelet aggregation upon arrival to the emergency department. However, at 24 hours, cigarette smoke exposure was associated with increased impairment in platelet aggregation, reflecting a statistically significant decline in platelet aggregation over the initial 24 hours after trauma. The relationship between this decline in platelet aggregation and ARDS differed by cigarette smoke exposure status, suggesting that impaired platelet activation differentially affects the risk of ARDS in those with cigarette smoke exposure (arachidonic acid, p for interaction: 0.005, collagen p for interaction: 0.02, adenosine diphosphate, p for interaction: 0.05). CONCLUSION Impaired platelet aggregation at 0 hour and 24 hours is associated with an increased risk of developing ARDS after severe blunt trauma. Cigarette smoke–exposed patients are more likely to develop impaired platelet aggregation over the first 24 hours of admission, which may contribute to their increased risk of ARDS. Level of Evidence Prognostic/Epidemiological, level III.
    Type of Medium: Online Resource
    ISSN: 2163-0763 , 2163-0755
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2651313-4
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  • 5
    In: American Journal of Respiratory and Critical Care Medicine, American Thoracic Society, Vol. 197, No. 5 ( 2018-03-01), p. 621-631
    Type of Medium: Online Resource
    ISSN: 1073-449X , 1535-4970
    RVK:
    Language: English
    Publisher: American Thoracic Society
    Publication Date: 2018
    detail.hit.zdb_id: 1468352-0
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