Antibacterial therapy in sepsis complicated by disseminated intravascular coagulation: analytical review

Vollständiger Abstract

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Sepsis remains one of the leading causes of mortality in intensive care units, and its course is frequently complicated by sepsis-induced coagulopathy and disseminated intravascular coagulation, which substantially worsen the prognosis. The aim of this review was to systematize current concepts regarding the role of antibacterial therapy in the comprehensive management of patients with sepsis complicated by coagulopathy. Antibacterial therapy is regarded as an essential component of treatment directed at eliminating the infectious trigger of thromboinflammation. The most strongly supported requirement that remains is early infection control when there is a high probability of bacterial sepsis or septic shock, including adequate empiric therapy and source control. At the same time, the extent to which antibiotics specifically influence the dynamics of coagulopathy remains less well studied, as most studies do not stratify patients by coagulation status or source of infection. The review discusses the diagnostic role of biomarkers — namely, procalcitonin, presepsin, C-reactive protein, extracellular free DNA, complement markers, antithrombin activity, and fibrinogen. Evidence indicates that these may assist in assessing infectious burden, the risk of disseminated intravascular coagulation, and prognosis; however, none should be used as an autonomous criterion for initiating or discontinuing antibiotics and anticoagulants. The organ-specific nature of sepsis-associated disseminated intravascular coagulation further demonstrates that the source of infection influences prognosis, the feasibility of source control, baseline antithrombin activity, and the potential applicability of anticoagulant interventions. A clinical framework is proposed, founded on early adequate antibacterial therapy, concurrent assessment of coagulation status, active source control, individualized antibiotic dosing in the presence of organ dysfunction and extracorporeal support, and the consideration of anticoagulant therapy only after evaluation of the coagulation phenotype, source of infection, and bleeding risk. The need for prospective studies stratified by coagulation status and source of infection is emphasized in order to refine optimal therapeutic strategies.