Background Rebound bleeding as a result of loss of epinephrine effect is a common problem encountered during facelift surgery. Tranexamic acid (TXA) is an anti-fibrinolytic agent whose safety and efficacy in reducing bleeding are well documented. We have found that local infiltration of TXA combined with a lidocaine with epinephrine solution during facelift surgery has been effective in decreasing rebound bleeding and the time required to gain hemostasis. Objectives The authors sought to share their local infiltration protocol of TXA combined with epinephrine solution in facelift. Methods Patients who underwent facelift received subcutaneous injection of TXA-lidocaine 0.5% solution following the authors’ protocol. After completing both sides of the facelift and the submental platysmaplasty, the first and second sides were sequentially closed. The time to gain hemostasis on each side prior to closure was prospectively measured. Results Twenty-seven consecutive patients who underwent facelift surgery received local infiltration of TXA-lidocaine solution. In 23 of the 27 patients, the time required for hemostasis was prospectively recorded. The mean age was 62.1 years (±9.3) and all were females. The average time spent achieving hemostasis on the right, left, and both sides of the face was 6.5 (±2.7), 6.3 (±2.1), and 12.9 (±4.2) minutes, respectively. The total surgical time saving is approximately 25 to 60 minutes. Although primary facelift [13.6 (± 4.3)] exhibited a longer time of hemostasis compared with the secondary group [10.2 (± 2.8)], this was not statistically significant (P = 0.09). Conclusions Local infiltration of TXA with local anesthetic prior to a facelift appears to decrease bleeding, operative time, and postoperative facelift drainage output. Level of Evidence: 4
Specific immune responses are controlled by two counterbalancing mechanisms-co-stimulation and co-inhibition. Antigen receptors determine specificity, activate co-stimulation and/or co-inhibition, and interact with these co-stimulatory/co-inhibitory mechanisms to dictate the direction of the immune response, either positive or negative. Co-stimulatory or co-inhibitory ligands interact with their specific receptors and may indicate the context in which antigen is perceived by lymphocytes. Ligation of antigen receptors may activate only co-stimulatory or co-inhibitory mechanisms, and thus may influence secondarily the direction of the immune response. Furthermore, the activity of a given co-stimulator or co-inhibitory receptor is modified depending on signalling via the antigen receptor. If neither co-stimulators nor co-inhibitors are present, lymphocytes, activated in response to antigen receptor signalling, produce low levels of effector elements and then revert to inactivity. Co-inhibitors are defective in autoimmune disease.
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