Prothrombin Time and Partial Thromboplastin Time Assay Considerations
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Prothrombin time
Thromboplastin
Coagulation testing
Activated clotting time
Clotting time
Poster: RANZCR ASM 2013 / R-0027 / Correlation between activated clotting time (ACT) and activated partial thromboplastin time (APTT) in interventional neuroradiology by: M. Saeidpour 1, A. Rao2, B. May2; 1Hervey Bay/AU, 2Brisbane/AU
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Neuroradiology
Clotting time
Thromboplastin
Prothrombin time
Interventional radiology
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Activated clotting time
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A modified method for determining the partial thromboplastin time (PTT) using vacuum tubes and a mechanical clot timer is described. Results for 70 normal subjects showed a coefficient of variation of 12%, compared with 30% for clotting times (CT). A linear relationship with a correlation coefficient of 0.62 (p < 0.001) was found between PTT and CT values in patients on heparin therapy. Therefore, the PTT appears both practical and preferable to the CT in regulating heparin therapy.
Activated clotting time
Clotting time
Thromboplastin
Prothrombin time
Coefficient of variation
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OBJECTIVE: To evaluate the clinical safety of heparin titration and the procedural cost of anticoagulation measurement using bedside low-range activated clotting time. DESIGN: Quasi-experimental study using data gathered through retrospective record review. SETTING: Coronary care, medical intensive care and telemetry units of a community hospital. SUBJECTS: Sample of 102 patients undergoing elective percutaneous transluminal coronary angioplasty. INTERVENTION: Intravenous heparin therapy was titrated using low-range activated clotting time in 51 percutaneous transluminal coronary angioplasty patients. Data from this group were compared to a matched sample of 51 angioplasty patients whose intravenous heparin therapy was titrated using activated partial thromboplastin time. RESULTS: No differences in procedural, early or late complications were found between the groups. The cost of managing heparin therapy with low-range activated clotting time was less than with activated partial thromboplastin time. CONCLUSION: These results suggest that titrating heparin therapy based on bedside low-range activated clotting time for the angioplasty patients in this sample was as safe as with activated partial thromboplastin time. Use of bedside low-range activated clotting time saved money for the hospital.
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To determine whether activated partial thromboplastin times are a better heparin management tool than activated clotting times in pediatric extracorporeal membrane oxygenation.A single-center retrospective analysis of perfusion and patient records.Academic pediatric tertiary care center.Pediatric patients (<21 yrs old) requiring extracorporeal membrane oxygenation support initiated at Children's Hospital of Pittsburgh.None.Point-of-care activated clotting time and activated partial thromboplastin time values, clinical laboratory activated partial thromboplastin time values, weight-normalized heparin administration (units/kg/hr), and reported outcomes were collected for pediatric patients treated for cardiac and/or respiratory failure with extracorporeal membrane oxygenation. Spearman's ranked correlations were performed for each coagulation test compared to heparin dosage. The Bland-Altman test was used to determine the validity of the point-of-care activated partial thromboplastin time. Hazard analysis was conducted for outcomes and complications for patients whose heparin management was based on the clinical laboratory activated partial thromboplastin time or the activated clotting time. Only the clinical laboratory activated partial thromboplastin time showed a correlation (ρ = 0.40 vs. ρ = -0.04 for activated clotting time) with the heparin administration (units/kg/hr). Point-of-care activated partial thromboplastin time and activated partial thromboplastin time values correlated well (ρ = 0.76), with <5% of samples showing a difference outside 2 SDs, but differences in their absolute values (Δactivated partial thromboplastin time = 100 secs) preclude them from being interchangeable measures. Furthermore, despite no effective change in the mean activated clotting time, cardiac patients showed a significantly improved correlation to heparin dose for all coagulation tests (e.g., point-of-care activated partial thromboplastin time ρ = 0.60). Management of patients with the clinical laboratory activated partial thromboplastin time did not significantly affect patient survival rates but did significantly reduce bleeding complications and significantly increased clotting in the extracorporeal membrane oxygenation circuit. A hazard analysis demonstrated that bleeding complications were associated with an increased risk of mortality, whereas clotting complications in the extracorporeal membrane oxygenation circuit were not.The activated clotting time is not an accurate monitoring tool for heparin management in pediatricextracorporeal membrane oxygenation. The point-of-care activated partial thromboplastin time correlates well with the clinical laboratory activated partial thromboplastin time but cannot be substituted for the clinical laboratory activated partial thromboplastin time values. Management of pediatric extracorporeal membrane oxygenation patients with the clinical laboratory activated partial thromboplastin time reduced bleeding complications which are associated with increases in mortality.
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The automated-activated coagulation time, manual-activated coagulation time and the activated partial thromboplastin time were compared to the whole blood clotting time in the measurement of hypocoagulation of heparinized blood. The normal ranges and degree of reproducibility were determined for each clotting assay. Each method was examined for its sensitivity to various concentrations of heparin. In addition, blood samples from patients treated with heparin were assayed by all four methods and their results were compared. The results indicated that the manual-activated clotting time correlated best with the whole blood clotting time, was sensitive to low concentrations of heparin, formed a discernible clot within a convenient time period in blood containing high concentrations of heparin, was reproducible and was easily performed.
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Coagulation testing
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To the Editor: In a recently published paper, Despotis et al. [1] confirmed that aprotinin prolonged whole blood activated partial thromboplastin time (APTT), a clotting test known to be triggered by the intrinsic clotting pathway. Furthermore, they demonstrated that whole blood prothrombin time (PT), a test triggered by the extrinsic clotting pathway, was not influenced by aprotinin. Based on these results, they suggested that, in patients receiving aprotinin during cardiopulmonary bypass (CPB), the value of postoperative whole blood activated partial thromboplastin time for controlling post-CPB microvascular bleeding must be interpreted with caution, and whole blood PT can be an alternative. We recently found similar results with another extrinsic pathway-associated test, activated clotting time (ACT), in the presence of aprotinin. In human whole blood containing a heparin concentration of 3 IU/mL and variable aprotinin concentrations of 0, 200, and 400 kallikrein inhibiting units (KIU)/mL, the conventional ACT, activated through the intrinsic pathway by celite, increased from 451 +/- 34 s at 0 KIU/mL aprotinin to 751 +/- 122 s at 400 KIU/mL aprotinin Table 1. In contrast, the extrinsic pathway-associated ACT, activated by thromboplastin in a final concentration of 4 mg/mL, was not influenced by aprotinin.Table 1: Effect of Aprotinin on Activated Clotting Time (Seconds)It thus seems that the extrinsic pathway-associated whole blood clotting test, whether it is based on a whole blood PT method to be used after CPB or on a Hemochron (Intl. Technidyne Co., Edison, NJ) ACT method to be used during CPB, has considerable value in monitoring heparin anticoagulation in the presence of aprotinin. Since aprotinin is being increasingly used during cardiac surgery, development of a reliable bedside test to exclude the artificial effect of aprotinin on anticoagulation monitoring is of great importance. Y. J. Gu, MD, PhD R. J. Huyzen, MD W. van Oeveren, PhD Departments of Cardiothoracic Surgery and Anesthesiology University Hospital Groningen, The Netherlands
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Objectives To assess the reliability of prothrombin time and activated partial thromboplastin time results generated from citrated whole blood samples following short‐term storage at room temperature. Methods Clotting times were measured in blood samples from 40 dogs that showed a variety of clinical signs. Before measurement of prothrombin time and activated partial thromboplastin time in citrated plasma, whole blood samples were split in three aliquots; one was processed within 30 minutes of collection (fresh) while the remaining two were stored unseparated at room temperature for 24 ( 24RT ) or 48 ( 48RT ) hours. Results The median prothrombin time for the 24RT (7 seconds) and 48RT (7·2 seconds) samples were not significantly different to those obtained from the fresh (7·1 seconds) samples but the median activated partial thromboplastin time for the 24RT (12·6 seconds) and 48RT (12 seconds) samples were significantly shorter than those obtained from the fresh samples (14·2 seconds). Clinical Significance Storage of citrated whole blood at room temperature for 24 or 48 hours did not significantly alter the measurement of prothrombin time but resulted in significantly shorter activated partial thromboplastin time results. Extrapolating from these findings, it is proposed that unseparated clinical samples that are submitted to an external diagnostic laboratory for the performance of clotting times, may generate reliable prothrombin time but unreliable activated partial thromboplastin time results.
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Activated clotting time
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In Brief BACKGROUND: When trauma patients arrive in the emergency department (ED), coagulopathy frequently is present. The time course, however, in which this coagulopathy develops is poorly understood. No study has fully evaluated the coagulation status, including thromboelastometry on-scene and at hospital arrival. We hypothesized that measured coagulation variables might change when measured at the scene of injury and upon arrival to the ED. METHODS: We performed a prospective, single-center, observational study investigating coagulation status in 50 trauma patients on-scene and at arrival in the ED. Measurements included arterial blood gases, ROTEM®, protein S100, protein C activity, protein S, Quick value, international normalized ratio, activated partial thromboplastin time, D-dimer, coagulation factor V (FV), coagulation factor XIII (FXIII), fibrinogen, hemoglobin, hematocrit, platelets, and volume and blood products being administered during the first 24 hours. RESULTS: Significant changes between on-scene and the ED were observed for the following values: partial venous oxygen pressure increased and sodium, glucose, and lactate decreased. For EXTEM, INTEM, and APTEM, clotting time and clot formation time increased significantly, whereas maximal clot firmness and angle α decreased significantly (all P ≤ 0.004). For FIBTEM, clotting time increased significantly and maximal clot firmness decreased significantly. In the laboratory, significant reductions in hemoglobin, hematocrit, platelets, activated partial thromboplastin time, fibrinogen, FV, FXIII, protein C activity, protein S, and protein S100 were observed (all P ≤ 0.001). CONCLUSIONS: Although most all laboratory and rotational thromboelastometry coagulation tests worsened over time when measured on-scene and in the ED, monitoring coagulation at the scene of trauma does not provide clinically important information in a majority of trauma patients. One hour after injury, significant activation and consumption of fibrinogen, FV, FXIII, protein C activity, and protein S were observed. Published ahead of print December 24, 2014.
Thromboelastometry
Coagulation testing
Clotting time
Prothrombin time
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