No abstract

BACKGROUND Both hyperfibrinolysis and fibrinolysis shutdown can occur after severe trauma. The subgroup of trauma patients with fibrinolysis shutdown resistant to tissue plasminogen activator (t-PA)-mediated fibrinolysis have increased mortality. Fibrin polymerization and structure may influence fibrinolysis subgroups in trauma, but fibrin architecture has not been characterized in acutely injured subjects. We hypothesized that fibrin polymerization measured in situ will correlate with fibrinolysis subgroups. METHODS Blood samples were collected from trauma patients and noninjured controls. We selected samples across a range of fibrinolysis phenotypes (shutdown, physiologic, hyperfibrinolysis) and t-PA sensitivities (sensitive, physiologic, resistant) determined by thrombelastography. Plasma clots were created in situ with fluorescent fibrinogen and imaged using confocal microscopy for analysis of clot architecture in three dimensions. For each clot, we quantified the fiber resolvability, a metric of fiber distinctness or clarity, by mapping the variance of fluorescence intensity relative to background fluorescence. We also determined clot porosity by measuring the size and distribution of the gaps between fibrin fibers in three-dimensional space. We compared these measures across fibrinolysis subgroups. RESULTS Fiber resolvability was significantly lower in all trauma subgroups compared with controls (n = 35 and 5, respectively; p < 0.05). We observed markedly different patterns of fibrin architecture among trauma patients stratified by fibrinolysis subgroup. Subjects with t-PA–resistant fibrinolysis shutdown exhibited abnormal, densely packed fibrin clots nearly devoid of pores. Individuals with t-PA–hypersensitive fibrinolysis shutdown had highly irregular clots with pores as large as 2500 μm3 to 20,000 μm3, versus 78 μm3 to 1250 μm3 in noninjured controls. CONCLUSION Fiber resolvability was significantly lower in trauma patients than controls, and subgroups of fibrinolysis differ in the porosity of the fibrin clot structure. The dense fibrin network in the t-PA–resistant group may prevent access to plasmin, suggesting a mechanism for thrombotic morbidity after injury.

BACKGROUND: Pulse oximetry has become the standard of care in emergency medicine, operating rooms, and medical wards for the monitoring of oxygenation, but the use of pulse oximetry for assessment of hemoglobin (Hb) is controversial. The purpose of this study was to compare the accuracy and precision of 2 point-of-care Hb measurement devices, the Pronto-7 and the HemoCue 201؉, to laboratory testing. METHODS: We studied a convenience sample of patients in the emergency department who required a complete blood count. We excluded patients in critical condition or those with elevated methemoglobin, impaired perfusion, or finger deformities. Each subject provided 2 capillary samples for measurement with the HemoCue 201؉ and 2 consecutive readings with the Pronto-7. We used Bland-Altman analysis to compare the performance of the point-of-care devices to laboratory measurements. We also determined the diagnostic performance for the detection of anemia by sex (Hb < 11.6 g/dL for females, Hb < 13.8 g/dL for males). RESULTS: 201 of the 350 subjects enrolled (57%) were female. Mean (SD) age was 50.9 (19.0) y. Complete data were available for 297 (84.9%) of the Pronto-7 readings and 323 (92.3%) of the HemoCue 201؉ readings. Mean (SD) laboratory Hb was 13.1 g/dL (2.3). Mean bias (Bland-Altman limits of agreement) for the Pronto-7 was ؊0.52 g/dL (؊3.29 to 2.25), and for the HemoCue 201؉ the mean bias was ؊0.98 g/dL (؊3.57 to 1.61). Sensitivity and specificity for diagnosis of anemia were 81.6% (95% CI 72.5-88.7) and 75.4% (95% CI 68.8-81.1) for the Pronto-7 and 99.1% (95% CI 94.8-100.0) and 71.0% (95% CI 64.4-76.9) for HemoCue 201؉. CONCLUSION: Both devices provided clinically useful methods to screen for anemia.