COVID-associated coagulopathy is currently widely discussed in the medical press. There are no unambiguous ideas about its mechanisms and significance at the present time. One of the manifestations is hyperfibrinogenemia. The study of specific changes in this laboratory indicator is of interest from the point of view of evaluating the prognosis of the course of coronavirus infection and selecting therapy. Objectives. Analysis of plasma fibrinogen dynamics in patients with COVID-19, assessment of clinical and prognostic significance of the indicator. Materials and methods. The retrospective study included 350 patients undergoing inpatient treatment for SARS-CoV-2 infection. At the time of analysis, 49 patients (14 %) died, and the rest were discharged from the hospital. The dynamics of fibrinogen content was evaluated, compared with the outcomes of the disease, clinical complications of a thrombotic or hemorrhagic nature, and other laboratory indicators. Results and conclusion. A characteristic feature of COVID-associated coagulopathy is hyperfibrinogenemia (the maximum value of fibrinogen is 6.2 ± 1.7 g/l) as a manifestation of systemic inflammation with a transition in 14 % of patients to hypofibrinogenemia (the minimum value is 1.57 ± 0.29) due to hepatic dysfunction and consumption coagulopathy. In the context of pharmacological antithrombotic prevention, hyperfibrinogenemia did not show clinical significance as a risk factor for thrombosis, while a decrease in fibrinogen less than 2.0 g/l was associated with a 9-fold increase in the risk of hemorrhagic complications in patients with coronavirus infection (OR 9.913 CI 95 % [1.613-60.931]). A decrease in fibrinogen below normal values and an excess of 9.0 g/l are equally predictors of an adverse outcome in patients with COVID-19. The relative risk of death was 3.263 CI 95 % (1.970-5.407) and 2.574 CI 95 % (1.265-5.237), respectively.
INTRODUCTION: Thrombocytopenia is common in critically ill patients. Its development is associated with a high risk of bleeding and other complications, including adverse outcomes. ОBJECTIVE: To analyze the incidence, severity, predictive significance of thrombocytopenia in critically ill patients before and during coronavirus infection. MATERIALS AND METHODS: The observational study included patients from intensive care units of a multidisciplinary hospital at different periods: before the COVID-19 and during the period when the hospital was operating as a COVID hospital. Patients from all intensive care units, excluding the hematology unit, were analyzed. RESULTS: Non-infectious period. Among 314 patients, 91 cases of thrombocytopenia were identified, representing 29 %. Severe thrombocytopenia among them was noted in 35 % (n = 32). The main etiological causes: performing extracorporeal procedures, liver disease, ischemic stroke, acute coronary syndrome. The infectious period. Thrombocytopenia occurred more frequently than in non-COVID patients (in 209 of 396 patients - 52.8 %) and was more uniform in severity. The most frequent cause of thrombocytopenia was a combination of sepsis, acute liver injury, performance of extracorporeal procedures and specific drug therapy of COVID-19 infection. CONCLUSIONS: According to our data, thrombocytopenia in the intensive care units of a multidisciplinary hospital (non-infectious period) occurred in one-third of critically ill patients. COVID 19 infection demonstrated an i ncreased incidence of thrombocytopenia in critical patients (in the presented study up to half of the patients). Severe thrombocytopenia is more common in patients of non-infectious period (35 % vs 20 %). In patients with coronavirus infection, thrombocytopenia was more frequently associated with a bleeding clinic (6.2 % vs 2.2 %), with less prognostic value as a criterion for adverse outcome: the presence of thrombocytopenia increased the risk of death by 5.5 times (95 % CI 2.97910.031) in noninfectious and by 1.54 times (95 % CI 1.3-1.82) in COVID-19 infection.
We summarize the possible benefits and risks of using various anticoagulants during hemoperfusion. Clotting in the extracorporeal circuit can lead to a decrease in the effectiveness of therapy, additional workload, risk to the patient and economic losses. At the same time, relatively excessive anticoagulation against the background of existing hemostasis disorders can lead to severe hemorrhagic complications, which in turn worsen the prognosis of patients. The article describes the causes of heparin resistance, the main techniques for overcoming it, and provides practical guidelines for anticoagulant therapy during hemoperfusion. It is well known that routine methods of monitoring hemostasis (such as platelet count, activated partial thromboplastin time) are unable to assess the balance of pro/anticoagulants. The authors have proposed a reasonable personalized approach to anticoagulant therapy of extracorporeal blood purification depending on the pathology in patient and thromboelastography (TEG) data, and antithrombin III levels.
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