British Journal of Anaesthesia, Vol 76, Issue 6 822-828, Copyright © 1996 by The Board of Management and Trustees of the British Journal of Anaesthesia
T. T. Niemi, A. H. Kuitunen, E. M. Vahtera and P. H. Rosenberg
The various components of i.v. regional anaesthesia (IVRA), that is
ischaemia, tourniquet compression and the presence of high concentrations
of local anaesthetics in the blood vessels of the extremity, may affect
haemostatic mechanisms. We performed a cross-over study in 10 healthy male
volunteers to examine the role of lignocaine in IVRA on several haemostatic
variables, and those indicating fibrinolysis and platelet 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 pressure. The IVRA technique included
exsanguination by arm elevation and axillary artery compression, inflation
of the tourniquet cuff for 20 min and deflation of the cuff in one step
(after obtaining the venous sample). Each subject received, in random
order, either 0.5% lignocaine 3 mg kg-1 or the corresponding volume of
saline i.v. All fibrinolysis 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 indicated enhanced fibrinolysis by IVRA, but only t-PA antigen and PAI
showed greater changes in the lignocaine compared with the saline group in
the exposed arm at the time of cuff deflation. Platelet function tests
(ADP-induced platelet aggregation, beta-thromboglobulin and
thrombelastogram (TEG)) indicated no differences between the lignocaine and
saline groups. Although IVRA appeared to induce some platelet dysfunction,
there was a small increase in TEG amplitude indicative of improved
fibrin-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 micrograms ml-1 in cubital veins at the end of
the tourniquet time) potentiated ischaemia-induced fibrinolysis activation
during IVRA. Concomitant platelet dysfunction was not aggravated by
lignocaine.
CLINICAL INVESTIGATIONS
Haemostatic changes caused by i.v. regional anaesthesia with lignocaine
Department of Anaesthesiology, Helsinki University Central Hospital; Finnish Red Cross Blood Transfusion Service, Helsinki, Finland
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