von Willebrand factor and platelet count in ruptured abdominal aortic aneurysm repair

Objective: von Willebrand factor (vWF) is essential for the formation of platelet aggregates at sites of vascular endothelial cell (EC) injury. Peri-operative thrombocytopenia is associated with poor outcome in ruptured abdominal aortic aneurysm (AAA) repair. This prospective study examines the relationship between vWF and platelet count (PC) in ruptured AAA repair. Methods: plasma vWF antigen, PC and C-reactive protein (CRP) were measured pre-operatively, and immediately before and 5 min after aortic clamp release, and on post-operative days 1 and 2 in 20 patients (18 men and 2 women of median age 74, range 63-86, years) with ruptured AAA. Results: elevated vWF was present in 13 (65%) patients pre-operatively, and 14 of 16 (88%) survivors at 24 h post-operatively. All patients demonstrated an intra-operative fall in vWF. There was no significant difference in vWF levels between survivors and non-survivors. PC was below the normal range in 8 (40%) patients pre-operatively and all patients at 24 h. Eighteen (90%) patients demonstrated an intro-operative fall in PC. PC was significantly lower in non-survivors pre-operatively (p = 0.007), immediately before (p = 0.009) and 5 min (p = 0.009) and 24 h (p = 0.02) after clamp release. There was a significant positive correlation between vWF and PC pre-operatively (r = +0.48, p = 0.033), and immediately before (r = +0.47, p = 0.044) and 5 min after clamp release (r = +0.5, p = 0.043). There was a significant positive correlation between peak vWF level and the greatest fall in PC (r = +0.65, p = 0.006). There was a significant negative correlation between vWF and CRP and operative blood loss; and between PC and CRP, operative blood loss and aortic clamp time. Conclusions: these data demonstrate that EC activation, the acute phase protein response, operative blood loss and aortic clamp time all contribute to the peri-operative fall in PC in patients with ruptured AAA. The peri-operative fall in circulating levels of vWF and PC may represent consumption secondary to macro- and microvascular thrombus formation. The resultant procoagulant state may partly explain the association between low PC and poor outcome in ruptured AAA.