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The objective of our study was to evaluate the performance characteristics of a new automated d-dimer, the Advanced D-Dimer (Dade Behring Inc., Deerfield, IL) for use in the diagnosis of venous thromboembolism (VTE). To do this we compared the Advanced D-Dimer to existing d-dimer methods using established target cut-off values in patients suspected of VTE who were to undergo definitive radiographic studies for VTE. We studied hospitalized patients and outpatients who were suspected of having VTE and who had whole blood d-dimer performed. The patients who underwent a diagnostic study for VTE had their D-dimer results used to determine sensitivity, specificity and negative predictive values. There was relatively poor correlation between the Advanced D-Dimer and D-Dimer Gold (r = 0.63; t-test: P < 0.005) and Asserachrome D-Di (r = 0.58; t-test: P < 0.005). The Advanced D-Dimer target cutoff values for excluding VTE in hospitalized and outpatients were < or = 1800 microg/L and < or = 1500 microg/l respectively. There were 139 patients suspected with pulmonary embolism (PE) and 328 evaluated for deep vein thrombosis (DVT). There were 24 patients with PE, and 43 with DVT. The Advanced D-Dimer had comparable sensitivity, specificity and negative predictive values (96, 43, 98% for PE and 96, 48, 99% for DVT respectively) to other d-dimer methods used for that purpose. We conclude that the Advanced D-Dimer correlates relatively poorly with enzyme-linked immunosorbent assay methods. This poor correlation is likely due to incorrect reporting units and concentration. When these factors are corrected correlations improved. Compared to existing d-dimer methods used for VTE exclusion, the high sensitivity and negative predictive value would suggest that this method can be used as part of a diagnostic algorithm for the exclusion of PE and DVT.

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BACKGROUND: Abnormal hemostasis is associated with many of the complications of trauma-associated morbidity and mortality. Platelets are integral in the maintenance of hemostasis. METHODS: Samples were obtained from 100 trauma patients on arrival at the emergency room (initial time) and at 24, 48, and 72 hours later. Samples were also obtained from 10 healthy controls at the same time intervals. Using flow cytometry, three parameters were used to measure platelet activation: platelet microparticles, expression of P-selectin (CD62P), and expression of the activated conformation of glycoprotein IIb-IIIa (PAC-1 binding). Platelet function was measured using a platelet function analyzer (PFA-100, Dade International Inc., Miami, FL). RESULTS: One hundred trauma patients were enrolled. The average age was 40 years, 75% were men, and 84% had blunt injuries. The mean Injury Severity Score was 22.3 +/- 10.9 (mean +/- SD) and the average Glasgow Coma Scale score was 11 +/- 4. All three platelet activation parameters were increased in trauma patients versus controls for all time periods (p < 0.001). Trauma patients had a trend toward a shorter initial collagen/epinephrine closure time versus controls (p = 0.096). Compared with the 24-, 48-, and 72-hour time intervals, initial collagen/epinephrine closure times were shortened (p < 0.001, p < 0.001, and p < 0.001). Platelet function returned to normal reference ranges within 24 hours but platelet activation parameters remained elevated at least 72 hours after initial trauma. In contrast, when trauma patients with and without brain injury were compared, brain injury patients had increased platelet activation but decreased platelet function (increased collagen/epinephrine closure times). In addition, there was a significant prolongation in collagen/epinephrine closure times for the 24-, 48-, and 72-hour time points in nonsurviving patients versus survivors. There was no association between platelet activation and function and other adverse outcomes including pulmonary embolism, deep venous thrombosis, and disseminated intravascular coagulation. CONCLUSION: Severe injury usually results in increased platelet activation and function. However, the combination of increased platelet activation with decreased function was associated with increased mortality.

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HYPOTHESIS: Cushing syndrome (CS) is associated with a hypercoagulable state that results in a 4-fold increase in the incidence of pulmonary embolism, deep venous thrombosis, and a 4-fold mortality rate compared with the general population. The incidence of CS in humans is approximately 2 to 5 per million per year, whereas in dogs it is much higher. The clinical complications of CS in humans are also manifested in dogs. We used a dog model of CS to better define the biochemical basis for the hypercoagulable state seen in the disease. DESIGN: A consecutive sample of dogs with CS and a cohort of healthy control dogs identified at a "well-dog check" were enrolled. All dogs underwent blood assays to identify the levels of procoagulant factors, natural antithrombotics, and the degree of ongoing activation of the coagulation cascade. SETTING: University veterinary medical teaching hospital. RESULTS: A total of 86 dogs were enrolled, 56 with CS and 30 control dogs. Levels of procoagulation factors II, V, VII, IX, X, XII, and fibrinogen were significantly increased in dogs with CS (P<.05). The natural antithrombotic antithrombin was significantly decreased in dogs with CS (P<.02). Thrombin-antithrombin complexes, a marker of subclinical thrombosis, were significantly increased in dogs with CS (P<.05). CONCLUSIONS: The hypercoagulable state of CS is demonstrated by an increase in thrombin-antithrombin complexes. This hypercoagulable state may be caused in part by (1) an elevation of procoagulant factors, and (2) a decrease in antithrombin. Because of the similar clinical and biochemical changes between dogs with CS and humans, this canine model may be a useful tool for the future study of the hypercoagulable state in CS.

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Hemothorax has been recognized as a clinical entity for centuries. However, the use of closed drainage has only recently been described in the last 50 years. Chest radiography remains the mainstay of diagnosis, however computed tomography and ultrasound are useful in some circumstances. The treatment of hemothorax is adequate drainage. Drainage allows for apposition of the visceral and parietal pleura, which aids hemostasis. Massive hemothorax and ongoing bleeding are indications for thoracotomy. Clotted hemothorax can be difficult to drain adequately with tube thoracostomy alone. Video assisted thoracic surgery (VATS) has proven most effective in obtaining adequate drainage if performed early in the patient's course.

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D-Dimer testing has been suggested as a non-invasive method for the exclusion of pulmonary embolism (PE) and deep vein thrombosis (DVT). In this study, we compared a new method, the Miniquant D-dimer (Biopool International, Ventura, California, USA) to other previously validated D-dimer methods used for the purpose. Patients who were undergoing a definitive diagnostic study for thromboembolism had a blood sample drawn at that time. A whole-blood D-dimer (SimpliRed; Agen Biomedical Ltd, Brisbane, Australia) test was performed, and residual plasma was frozen and later analyzed using two enzyme-linked immunosorbent assay (ELISA) methods (D-dimer Gold; Agen, and Asserachrome D-Di; Stago International, Parsippany, New Jersey, USA) and the Miniquant D-dimer. Once all samples were analyzed, the correlation and accuracy of the Miniquant was compared with the ELISA method using Spearman's regression and Dunn's multiple paired comparison. All D-dimer methods were compared with radiographic studies. The data was analyzed collectively and segregated into in-patient (n = 112) and out-patient (n = 143) populations. The Miniquant D-dimer sensitivity, specificity and negative predictive value (NPV) for all patients were 95, 21, and 94% for DVT, and 100, 26, and 100% for PE. This new D-dimer method demonstrates acceptable sensitivity in patients with PE and DVT and, based on the high NPV of this method, it can be used for the exclusion of thromboembolism.

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