FEATURES OF THE HEMOSTASIS SYSTEM IN INFANTS WITH ACUTE PNEUMONIA ON THE BACKGROUND OF PERINATAL CENTRAL NERVOUS SYSTEM INJURY

Abstract

Introduction. Acute pneumonia remains one of the leading causes of morbidity and mortality in early childhood. According to WHO data, approximately 15–18% of deaths among children under five years of age are due to lower respiratory tract infections. The course of pneumonia in infants with perinatal central nervous system (CNS) injury—resulting from hypoxia, ischemia, or perinatal asphyxia—is often severe and prolonged. These patients exhibit impaired immune responses, endothelial dysfunction, and disturbances in microcirculation, predisposing them to coagulation abnormalities. Therefore, assessment of the hemostatic system in this population is of critical clinical and prognostic importance. Objective. To evaluate the changes in hemostatic parameters among infants with acute pneumonia associated with perinatal CNS injury and to determine their relationship with disease severity and inflammatory activity. Materials and Methods. A comprehensive review and meta-analysis of 40 national and international studies published between 2015 and 2024 were conducted. Key parameters assessed included fibrinogen, D-dimer, APTT, PT, antithrombin III, protein C, and protein S levels. The concentrations of inflammatory cytokines (IL-6, TNF-α) were also evaluated. Statistical correlation and regression analyses were applied with a significance level of p < 0.05. Results. Infants with perinatal CNS injury demonstrated significant hemostatic imbalance characterized by hypercoagulation and impaired anticoagulant activity. Fibrinogen and D-dimer levels were increased by 1.5–2 times, while APTT and PT were shortened. Antithrombin III activity decreased by 25–30%. Elevated IL-6 and TNF-α levels showed strong positive correlations with D-dimer concentration (r = 0.62; p < 0.01), confirming the existence of a “coagulation–inflammation” feedback loop. Prophylactic anticoagulant therapy (microdose heparin, dipyridamole, pentoxifylline) significantly reduced thromboembolic complications (by 3–4 times) and accelerated clinical recovery and radiological resolution of pulmonary infiltrates. Discussion. These findings support that hemostatic disturbances constitute a fundamental pathophysiological mechanism in pneumonia associated with perinatal CNS injury. Hypercoagulability, endothelial injury, and suppressed fibrinolysis contribute to microcirculatory failure, tissue hypoxia, and prolonged inflammation. Conclusion. Regular monitoring of hemostatic markers (fibrinogen, D-dimer, antithrombin III) and inflammatory cytokines (IL-6, TNF-α) is essential for early detection of complications. Implementing timely anticoagulant therapy may improve outcomes, shorten recovery time, and reduce morbidity in infants with perinatal CNS injury.