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A Practical Concept for Pre-Operative Identification and Improved Management of Patients at Risk for Bleeding

  • Conference paper
36th Hemophilia Symposium Hamburg 2005

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Summary

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.

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Authors
  1. J. Koscielny
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  2. S. Ziemer
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  3. H. Radtke
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  4. P. Sinha
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  5. A. Salama
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  6. H. Kiesewetter
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Editor information

Editors and Affiliations

  1. III. Med. Clinic, University Hospital, Langenbeckstr. 1, D-55131, Mainz, Germany

    Inge Scharrer

  2. Dept. of Hemostaseology, University Hospital, Ziemssenstr. 1a, D-80336, München, Germany

    Wolfgang Schramm

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Koscielny, J., Ziemer, S., Radtke, H., Sinha, P., Salama, A., Kiesewetter, H. (2007). A Practical Concept for Pre-Operative Identification and Improved Management of Patients at Risk for Bleeding. In: Scharrer, I., Schramm, W. (eds) 36th Hemophilia Symposium Hamburg 2005. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-36715-4_14

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  • DOI: https://doi.org/10.1007/978-3-540-36715-4_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-36714-7

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