Fibrinogen has been shown to be responsible for most protein-mediated clot strength via thrombelastography. However, factor XIII (FXIII) activity also plays a prominent role in the development of clot strength. Thus, we hypothesized that changes in FXIII activity would significantly increase clot strength. FXIII (0%, 1%, 6.25%, 12.5%, 25%, 50%, and 100% normal activity) was placed in a fixed volume of citrated FXIII-deficient plasma with 1% tissue factor and calcium chloride and underwent thrombelastography for 10 min. We measured the variables reaction time (R; a measurement of clot initiation), alpha (a measure of the rate of clot formation), amplitude (A; a measure of clot strength), and shear elastic modulus (G; a measure of clot strength). FXIII activity significantly decreased R in a pattern of exponential decay (R2 = 0.77; P < 0.001). FXIII activity significantly increased alpha, following a sigmoidal pattern (R2 = 0.88; P < 0.001). Finally, increases in FXIII activity significantly increased A and G in a sigmoidal pattern (R = 0.89; P < 0.001). We concluded that FXHI significantly affects R, alpha, A, and G. Thus, transfusion decision making with protein-mediated thrombelastographic patterns must account for the contribution of both fibrinogen and FXIII.
This novel long-axis real-time ultrasound technique facilitates placement of femoral vein central venous line in critically ill neonates with cardiac disease at a higher rate of success with fewer attempts and lower occurrence of complications when compared with the landmark technique.
Hemodilution-associated hypercoagulability has been the focus of several investigations because significant morbidity and mortality have been associated with perioperative thrombophilia. Because most investigations implicate imbalances in procoagulant/anticoagulant activity as the etiology of hemodilution-associated hypercoagulability, we determined the effects of dilution on coagulation kinetics and clot strength with thrombelastography (TEG(R)). Control plasma (+/-celite activation) and antithrombin (AT)-deficient (<10% activity) plasma were diluted 0%, 10%, 20%, and 30% with saline. TEG(R) variables measured included time to clot initiation (reaction time, R), speed of clot propagation (angle, alpha), and clot strength (amplitude, A; or shear elastic modulus, G). Dilution of control plasma (10%-30%) resulted in a significant (P < 0.05) 16% decrease in R values, no change in alpha values, and decrease in A and G values. AT-deficient plasma had significantly smaller R values compared with control, and dilution did not change R values in AT-deficient plasma. Celite activation eliminated dilution-associated changes in R values in control plasma but resulted in linear decreases (R(2) = 0.88-0.96, P < 0.0001) in alpha, A, and G in response to dilution. Thus, our data indirectly support the concept that decreases in AT activity cause dilution-mediated hypercoagulability in plasma. Finally, celite activation permits quantification of dilution with TEG.
Lean and value stream mapping can be safely applied to the clinical algorithms of high-risk patient care. We demonstrate that elimination of non-value-added steps can safely decrease preincision time without increasing patient risk in patients who undergo pulmonary lobectomy. Selected centers may be able to adopt some of these lean-driven protocols.
We documented the hemostatic changes associated with placement of a EXCOR Berlin Heart left ventricular assist device in a 15-month-old child before heart transplantation. The development of hypercoagulability was rapid, manifested first by a plasmatic and subsequently platelet-mediated increase in coagulation kinetics and strength that persisted for weeks. The patient had no thrombotic complications for 6 wk before transplant but required extraordinary blood product administration to achieve hemostasis secondary to aggressive, multimodal anticoagulation. In summary, when proscribing anesthetic and surgical management of patients with a Berlin Heart, consideration of hypercoagulable features and anticoagulant therapy must be made to maximize patient safety.
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