After high-voltage electric injury, patients often show tissue necrosis and thrombosis of blood vessels even remote from entry and exit site of electrical current.
In this study, blood coagulation markers and fibrinolytic avtivity (plasma levels of thrombin-antithrombin (TAT), prothrombin fragment 1+2 (F1+2), tissue-type plasminogen activator (t-PA) and its inhibitor PAI-1 (type-1 plasminogen activator inhibitor)) were determined in vivo in three patients with high-voltage injury for 96 hours after trauma.
In order to examine a possible effect on haemostasis related to endothelial cell damage, protein S, tissue factor (TF), endothelin-1 (ET-1), prostacyclin (PGI2), nitric oxide (NO), t-PA, and PAI-1 were determined for 72 hours in vitro in cell culture supernatant of human umbilical vein endothelium cells (HUVECs) that had been exposed to 1, 10, 30, and 50 electric field periods of 50 Hz with field strength of 60 V/cm and duration of 20 ms. Furthermore, expression of thrombomodulin was determined.
Exposure duration: 20 ms periods interupted by 10 s intervals, 1, 10, 30 and 50 periods
|electric field strength||60 V/cm||unspecified||unspecified||-||-|
Blood clotting activation could be found in the patients by increased levels of F1+2 and TAT between 12 and 72 hours after injury, whereas fibrinolysis was disturbed due to high PAI-1. One patient presented thrombosis of vessels by day 3.
In vitro, PAI-1 increased significantly in medium of endothelium cells with an application of 30 and 50 periods between 2 and 48 hours after exposure. Between 4 and 72 hours, the concentration of t-PA was significantly lower in the medium of endothelium cells exposed to 10, 30, and 50 periods, whereas there was a significant increase in the concentration of TF in the cell groups with an application of 30 and 50 periods. 24, 48, and 72 hours after injury (exposure), there was just weak or no staining for thrombomodulin in the cells with an application of 30 and 50 periods.
The disturbed balance between blood clotting system and fibrinolysis observed in vitro after electric injury might explain the clinical observation of a progressive thrombosis of blood vessels after electric injury leading to tissue loss.