A prospective randomised controlled trial of postoperative autotransfusion with and without a heparin-bonded circuit

Abstract

Autotransfusion has been included in the routine protocol in some units as an effort towards blood conservation. In this study we aimed to measure the efficacy and limitations of autotransfusion and whether a heparin-bonded circuit had any advantage. One hundred five patients were randomised to one of three post-operative treatments. Group 1 (n = 34) was not autotransfused whereas groups 2 (n = 36) and 3 (n = 35) received autotransfusion with the circuit of group 3 coated with heparin. Homologous blood and blood products were given according to strict protocols identical for all groups. Transfused and circulating blood was analysed for haemostatic variables and the requirement for homologous blood was recorded. Autotransfused blood contained no intact platelets and very high levels of D-Dimers (a peptide fragment released when fibrin is lysed) which resulted in high levels of systemic D-Dimers in patients receiving autotransfusion. Flow cytometric analysis revealed that whilst platelet glycoprotein 1 b receptors were severely reduced immediately following surgery, there was no additional damage caused by autotransfusion. Furthermore, there was no difference in platelet aggregation, von Willebrand factor (vWF) multimetric analysis or clotting profiles between the groups. Median (interquartile range) blood loss was 898 ml (638-1195) in group 1, 853 ml (595-1348) in group 2 and 770 ml (615-1000) in group 3 (Kruskal-Wallis P = 0.46). Median transfusion requirements were 2 units in each group. Whilst auto-transfusion does not appear to compromise haemostasis, it does not reduce the requirement for homologous blood and heparin-bonding of the circuit has no impact.

Cardiac bypass haemostasis: putting blood through the mill

“…Many flow cytometric studies in CPB demonstrate reduction of surface GpIb (van Oeveren et al , 1990), whole‐platelet GpIb by radioassay being preserved (Orchard et al , 1993). Ristocetin‐induced platelet aggregation (RIPA; GpIb‐dependent) decreases during CPB (Lu et al , 1991); both RIPA and surface GpIb have been found to correlate with blood loss (Unsworth‐White et al , 1996). Aprotinin, which reduces post‐bypass bleeding (Laupacis et al , 1997; see below), seems to preserve surface GpIb when used during CPB (Van Oeveren et al , 1990), and permit the return of GpIb when used at the end (Kallis et al , 1994a).…”

“…van Oeveren et al , 1990) were due to using centrifuged and gel‐filtered platelets, compared to minimally disturbed whole blood, for flow cytometry. However, ~35% loss of surface GpIb has been found in subsequent studies using whole blood and FITC‐conjugated monoclonal antibodies (McAbs) (Kallis et al , 1994a; Mazer et al , 1995; Unsworth‐White et al , 1996; Maquelin et al , 1998). Differences in sampling, case‐mix, CPB techniques, or the use of biotinylated versus FITC‐conjugated McAbs may account for this; in CPB the scope for such variation between studies is vast (Royston, 1992).…”

“…If DDAVP improves haemostasis it suggests that circulating VWF is a determinant of post‐CPB bleeding. Reduced plasma VWF (Perrin et al , 1995) and platelet VWF (Kallis et al , 1994a) continue to be found in CPB; others have detected post‐CPB depletion of HMW‐VWF, if only in patients who bleed the most (Unsworth‐White et al , 1996). However, meta‐analysis indicates no significant blood‐sparing effect in the totality of trials of pre‐CPB DDAVP (Laupacis et al , 1997).…”

“…Mø‐TF expression by flow cytometry was found to be increased in CPB blood by Kappelmeyer et al (1993), but delayed for 20 h (Ernofsson et al , 1997) or undetectable (Parratt & Hunt, 1996) by others. Plasma VIIa, by clot‐based assay after heparin removal, is sub‐basal during CPB (Unsworth‐White et al , 1996; Cardigan et al , 1996), coinciding with a surge of UFH‐released TFPI (Cardigan et al , 1996), so if Mø TF/VIIa is responsible for thrombin generation in CPB it must be inaccessible to plasma assay and protected from TFPI. It must also evade the heparin/AT complex, which blocks TF/VIIa activity (Rao et al , 1995).…”

“…Protamine‐heparin mimics immune complexes, activating complement via the classic pathway, particularly in individuals with partial deficiency of C4A (Shastri et al , 1997). Rebound VIIa (Unsworth‐White et al , 1996) naturally appears after protamine reversal, but protamine has been defended against guilt‐by‐association for post‐CABG myocardial infarction (Horrow, 1994), and in any case rapid heparin reversal can hardly be avoided. Alternatives to protamine include heparinase I (Ammar & Fisher, 1997) and recombinant platelet factor 4 (D'Ambra, 1996); they reverse heparin rapidly and specifically, but these theoretical benefits do not yet justify the increase in cost.…”