There is a high degree of uncertainty regarding optimum care of patients with potential or known intake of oral anticoagulants and traumatic brain injury (TBI). Anticoagulation therapy aggravates the risk of intracerebral hemorrhage but, on the other hand, patients take anticoagulants because of an underlying prothrombotic risk, and this could be increased following trauma. Treatment decisions must be taken with due consideration of both these risks. An interdisciplinary group of Austrian experts was convened to develop recommendations for best clinical practice. The aim was to provide pragmatic, clear, and easy-to-follow clinical guidance for coagulation management in adult patients with TBI and potential or known intake of platelet inhibitors, vitamin K antagonists, or non-vitamin K antagonist oral anticoagulants. Diagnosis, coagulation testing, and reversal of anticoagulation were considered as key steps upon presentation. Post-trauma management (prophylaxis for thromboembolism and resumption of long-term anticoagulation therapy) was also explored. The lack of robust evidence on which to base treatment recommendations highlights the need for randomized controlled trials in this setting.

Background: Acute myeloid leukemia (AML) complicated by disseminated intravascular coagulation (DIC) poses major diagnostic and therapeutic challenges. While DIC is well documented in acute promyelocytic leukemia, its manifestations in non-APL AML remain underexplored, necessitating precise diagnostic strategies for effective management. Methods: AML patients with overt DIC were analyzed, including morphological, immunophenotypic, cytogenetic, and genetic evaluations. DIC was diagnosed using the ISTH scoring system, and AML subtypes were classified following WHO criteria. Results: Three diagnostic patterns were identified. (1) Acute promyelocytic leukemia: Leukemia characterized by PML::RARa rearrangements, FLT3 co-mutations, and frequent Auer rods and faggot bundles. Immunocytological analysis showed CD34 and HLA-DR negativity. (2) AML with FLT3 and/or NPM1 mutations: A high prevalence of cup-like blasts was found in 70% of cases. FLT3 mutations, often co-occurring with NPM1, dominated, while karyotypes were typically normal. Immunophenotyping revealed strong myeloid marker expression (MPO+, CD13+, and CD33+), with occasional CD34 negativity. (3) AML with monocytic differentiation: Leukemia defined by monoblastic/promonocytic morphology, DNMT3A mutations, and complex karyotypes or 11q23 rearrangements. Immunophenotyping demonstrated a dominance of monocytic markers (CD4+, CD14+, CD15+, and CD64+). Two patients presented unique profiles with no alignment to these patterns. Conclusions: This study highlights distinct hematopathological patterns of AML with overt DIC, providing a framework for early and precise diagnosis. Recognizing these patterns is critical for tailoring diagnostic and therapeutic approaches to improve outcomes in this high-risk population.

Nonacog beta pegol (N9-GP) is a glycoPEGylated FIX replacement product with extended half-life for treatment of haemophilia B patients. Monitoring of N9-GP with clotting-based one-stage FIX assays is complicated by high variations, mainly due to reagent-specific interference with polyethylene glycol. In 11 distinct specialized coagulation laboratories in Austria, N9-GP spiked samples were measured in replicates in two distinct surveys, 3 years apart, using five different one-stage assay reagents and one chromogenic FIX assay. Regression analysis was used to investigate if back-calculation of N9-GP levels is feasible. We could demonstrate a linear relationship between the spiked N9-GP concentration and measured FIX activity levels for all examined assays, suggesting that N9-GP activity may be back-calculated using reagent-/platform-specific conversion factors. Within-laboratory variation after 3 years was acceptable in most, but not all, laboratories. We demonstrate that back-calculation of N9-GP activity levels may be possible when using one-stage FIX assays. However, we recommend that every laboratory ascertain its own conversion factor. When measuring real patient samples, we encourage simultaneous measurement of N9-GP spiked control material with known concentrations to ensure the validity of the current back-calculation.

Background: The enzyme A Disintegrin and metalloprotease with thrombospondin type 1 motif, member 13 (ADAMTS13) regulates hemostasis by cleaving von Willebrand factor (VWF) multimers. ADAMTS13–VWF axis dysregulation leads to different thrombotic conditions. This study investigated changes in ADAMTS13 activity during major cardiac procedures and their relationship to VWF changes and clinical complications. Methods: A total of 628 ADAMTS13 activity and inhibitor measurements were carried out in 168 patients who underwent cardiac surgery. ADAMTS13 activity was measured after the initiation of anesthesia and daily for up to 6 days postoperatively via Technozym chromogenic ELISA. The von Willebrand factor antigen (VWF:Ag) and collagen binding (VWF:CB) were also measured. Clinical complications and correlations with liver function biomarkers were also assessed. Results: ADAMTS13 activity significantly decreased during surgery, with mean values markedly decreasing from preoperative to postoperative measurements (p = 0.01). A clear inverse relationship between ADAMTS13 activity and the VWF:CB/VWF:AG ratio was observed, indicating that increased high-molecular-weight VWF multimers are associated with decreased ADAMTS13 activity. Correlation analyses (CHE, Spearman’s rho = 0.39) indicated that the reduction in ADAMTS13 activity was not attributable to impaired liver synthesis but likely resulted from peripheral consumption, potentially influenced by surgical stress. Conclusions: Perioperative reductions in ADAMTS13 activity are associated with an accumulation of high-molecular-weight VWF multimers and a higher incidence of postoperative complications. These results demonstrate that ADAMTS13 could be a useful perioperative risk biomarker for cardiac surgery patients.