HEMOSTATIC CHANGES CAUSED BY IV REGIONAL ANESTHESIA WITH LIGNOCAINE

The various components of i.v. regional anaesthesia (IVRA), that is is chaemia, tourniquet compression and the presence of high concentration s of local anaesthetics in the blood vessels of the extremity, may aff ect haemostatic mechanisms. We performed a cross-over study in 10 heal thy male volunteers to examine the role of lignocaine in IVRA on sever al haemostatic variables, and those indicating fibrinolysis and platel et function in particular. Venous blood samples were obtained from the test arm and the opposite arm before IVRA, at the time of tourniquet cuff deflation and 30 min thereafter. Metal needle punctures were used , and for the sample from the test arm at the time of cuff deflation, cuff pressure was reduced from 300 mm Hg to individual mean arterial p ressure. The IVRA technique included exsanguination by arm elevation a nd axillary artery compression, inflation of the tourniquet cuff for 2 0 min and deflation of the cuff in one step (after obtaining the venou s sample). Each subject received, in random order, either 0.5% lignoca ine 3 mg kg(-1) or the corresponding volume of saline i.v. All fibrino lysis markers, that is, D-dimer, tissue plasminogen activator antigen (t-PA antigen), tissue plasminogen activator activity (t-PA activity), plasminogen activator inhibitor activity (PAI) and protein C indicate d enhanced fibrinolysis by IVRA, but only t-PA antigen and PAI showed greater changes in the lignocaine compared with the saline group in th e exposed arm at the time of cuff deflation. Platelet function tests ( ADP-induced platelet aggregation, beta-thromboglobulin and thrombelast ogram (TEG)) indicated no differences between the lignocaine and salin e groups. Although IVRA appeared to induce some platelet dysfunction, there was a small increase in TEG amplitude indicative of improved fib rin-platelet interaction in the lignocaine-exposed arm at the time of cuff deflation. We conclude that the presence of high i.v. lignocaine concentrations (median 144.4 mu g ml(-1) in cubital veins at the end o f the tourniquet time) potentiated ischaemia-induced fibrinolysis acti vation during IVRA. Concomitant platelet dysfunction was not aggravate d by lignocaine.