A practical concept for pre-operative identification and improved management of patients at risk for bleeding

Abstract

Total of 5649 unselected adult patients were enrolled to identify impaired hemostasis prior to surgical interventions. Each patient was asked to answer a standardized questionnaire of bleeding history. Activated partial thromboplastin time (aPTT), prothrombin time (PT) and platelet counts (PC) including PFA-100 (platelet function analyzer): collagen-epinephrine (C/E) and collagen-ADP (C/ADP) were routinely done in all patients. Additional tests, bleeding time (BT) and von Willebrand factor (vWF: Ag) were performed only in patients with a positive bleeding history and/or evidence of impaired hemostasis, e.g. drug ingestion. The bleeding history was negative in 5021 patients (88.8%) but positive in the remaining 628 (11.2%). Impaired hemostasis could be verified only in 256 (40.8%) of these patients. The vast majority were identified by PFA-100: C/E (n = 250; 97.7%). The only abnormality found among patients with a negative bleeding history was a prolonged aPTT due to lupus anticoagulant in 9 patients (0.2%). The sensitivity of the PFA-100: collagen-epinephrine was the highest (90.8%) in comparison to the other screening tests (BT, aPTT, PT, vWF: Ag). The positive predictive value of the PFA-100: collagen-epinephrine was high (81.8%), but the negative predictive value was higher (93.4%).We identified 254 out of 5649 unselected patients scheduled for surgery at our hospital as having either acquired (n = 182) or inherited (n = 72) impaired primary hemostasis (platelet dysfunction including von Willebrand disease). All patients were initially pretreated with desmopressin (DDAVP) and further anti-bleeding drugs in case of DDAVP-non-response. Response to DDAVP or subsequent treatment(s) was defined as correction of any one of the abnormal PFA-100 platelet function tests. The non-responders were additionally treated with tranexamic acid or aprotinin; those with von Willebrand disease (vWD) received factor VIII concentrates with von Willebrand factor (vWF). Those still unresponsive to therapy received conjugated estrogens and, as a last attempt, a platelet transfusion. The administration of DDAVP led to a correction of platelet dysfunction in 229 of the 254 patients treated (90.2%). Tranexamic acid was effective in 12 of 16, aprotinin in 3 of 5 and factor VIII concentrates with vWF in all 4 patients with unresponsive to DDAVP. The remaining 6 patients were pretreated with conjugated estrogens, and 2 of these patients were additionally treated with platelet transfusion. The frequency of blood transfusion was lower, but not statistically significant (9.4% vs. 12.2%: p = 0.202) in preoperatively treated patients with impaired hemostasis than in patients without impaired hemostasis. In a retrospective group, the frequency of blood transfusion was statistically significant higher (89.3% vs. 11.3%: p < 0.001) in patients without preoperative correction of impaired than in patients without impaired hemostasis. Preoperative identification and correction of impaired primary hemostasis is possible in nearly all patients affected, and results in a reduction of homologous blood transfusions. © 2007 Springer Verlag Berlin Heidelberg.