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In the developed world, an increasing number of patients receive therapy with vitamin K antagonists (VKA). This group of patients poses an additional challenge in the perioperative management of emergency surgery and trauma. The present review offers a detailed description of some treatment options for reversal of VKA therapy. Optimal treatment of the anticoagulated patient requires a well-balanced intervention securing a reduced risk of haemorrhagic surgical complications as well as optimal anticoagulation post-operatively without exposing the patient to an increased risk of thromboembolic complications. The following factors must be considered in VKA-treated patients scheduled for emergency surgery: (1) the indication for VKA therapy, including the risk of thromboembolic events when the International normalized ratio (INR) is reduced, (2) type of surgery, including the risk of haemorrhagic complications and (3) the pharmacodynamic/-kinetic profile of the therapy used to revert the VKA therapy. Therapeutic options for acute reversal of VKA therapy include: vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrate (PCC) and perhaps activated recombinant factor VII. PCC is a relatively new drug in some European countries and clinical experience is limited compared with the use of FFP. Reversal of VKA anticoagulation with PCC is faster and more efficient compared with FFP, but there are currently no randomized studies demonstrating an improved clinical outcome.

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BackgroundCoagulation can be visualised using whole blood coagulation analyses such as thromboelastometry and platelet aggregation tests; however, the role of temperature in the analyses is ambiguous. The aim was to examine whether temperature influences the whole blood coagulation tests.MethodsWe included 40 patients treated with targeted temperature management (33 ± 1 °C) after out-of-hospital cardiac arrest. The blood samples were obtained on hypothermia and normothermia. Each blood sample was analysed simultaneously at 33 °C and 37 °C by thromboelastography (ROTEM®) employing the assays EXTEM®, INTEM®, FIBTEM® and HEPTEM®, and by Multiplate®Analyzer, using COLtest®, ADPtest®, ASPItest® and TRAPtest® as agonists. Data on antithrombotic drugs were collected systematically from medical records, and data were analysed using repeated measurement analysis of variance (ANOVA).ResultsThe ROTEM® analyses showed increased clotting time, lower maximum velocity and increased time to maximum velocity (all p values <0.02) when performed at 33 °C compared with 37 °C, irrespective of the patients being hypothermic (median 33.1 °C) or normothermic (median 37.5 °C). However, EXTEM® time to maximum velocity showed no difference between the analyses performed at 33 °C and 37 °C when the patients were hypothermic (p = 0.83). No differences were found in maximum clot firmness (all p values >0.09) analysed at 33 °C and 37 °C, independent of the body temperature.In the hypothermic blood sample, no difference was found when using the COLtest®, ASPItest® or TRAPtest® to compare platelet aggregation analysed at 33 °C and 37 °C (all p values >0.19), but platelet aggregation was significantly higher using the ADPtest® (p < 0.001) when analysed at 33 °C. In the normothermic blood sample, the TRAPtest® showed no difference (p = 0.73) when performed at 33 °C; however, significantly lower aggregation was found using the COLtest® and ASPItest® (all p values <0.001), while a higher aggregation at 33 °C was found using the ADPtest® (p = 0.003).ConclusionROTEM® analyses seemed not to be dependent on body temperature but showed a slower initiation of coagulation when analysed at 33 °C compared with 37 °C. The Multiplate®Analyzer results were dependent on the temperature used in the analyses and the body temperature. In whole blood coagulation tests, the temperature used in the analyses should be kept at 37 °C irrespective of the patient’s body temperature being 33 °C or 37 °C.

Recently, reports of severe thromboses, thrombocytopenia, and hemorrhage in persons vaccinated with the chimpanzee adenovirus-vectored vaccine (ChAdOx1 nCoV-19, AZD1222, Vaxzevria; Oxford/AstraZeneca) against severe acute respiratory syndrome coronavirus 2 have emerged. We describe an otherwise healthy 30-year-old woman who developed thrombocytopenia, ecchymosis, portal vein thrombosis, and cerebral venous sinus thrombosis the second week after she received the ChAdOx1 nCoV-19 vaccine. Extensive diagnostic workup for thrombosis predispositions showed heterozygosity for the prothrombin mutation, but no evidence of myeloproliferative neoplasia or infectious or autoimmune diseases. Her only temporary risk factor was long-term use of oral contraceptive pills (OCPs). Although both the prothrombin mutation and use of OCPs predispose to portal and cerebral vein thrombosis, the occurrence of multiple thromboses within a short time and the associated pattern of thrombocytopenia and consumption coagulopathy are highly unusual. A maximum 4T heparin-induced thrombocytopenia (HIT) score and a positive immunoassay for anti-platelet factor 4/heparin antibodies identified autoimmune HIT as a potential pathogenic mechanism. Although causality has not been established, our case emphasizes the importance of clinical awareness. Further studies of this potentially new clinical entity have suggested that it should be regarded as a vaccine-induced immune thrombotic thrombocytopenia.