STATE OF THE BLOOD COAGULATION SYSTEM IN CHILDREN WITH VASCULAR MALFORMATIONS AND INFLAMMATORY DISEASES OF THE MAXILLOFACIAL AREA

The article presents the results of a study of hemostasis in children with vascular malformations and inflammatory diseases of the maxillofacial region using standard and integrated methods for assessing hemostasis. Objective of the research: to assess the state of the hemostatic system in children with vascular malformations and inflammatory diseases of the maxillofacial region using standart and integrated methods. Materials and methods: on the basis of St. Vladimir's Children's Clinical Hospital in 2015–2019. А prospective open controlled comparative nonrandomized selective study of coagulological status was performed using standard coagulological tests and integral methods for assessing hemostasis (thromboelastography – TEG, thrombodynamics – TD) in 105 patients with lymphatic, lymphovenous, venous, arteriovenous vascular malformations of the head and neck (age 6 [5; 9] years), 47 children with infectious and inflammatory diseases of the maxillofacial area (age 10 [4; 17] years). The control group included 37 children (age 9 [5; 13] years). Results: according to the data, in most patients with vascular malformations, the coagulogram did not reveal pronounced shifts in hemostasis. TEG indices demonstrated hypercoagulability in vascular malformations: the onset time of clot R formation was 11,20 [8,72; 15,75] min (the norm is 9–27 min); clot K formation time was reduced to 3,90 [2,30; 6,02] min (the norm is 2–9 min). According to TD data, the process of fibrin clot growth in patients with vascular malformations accelerated: the clot V growth rate was 32,80 [28,70; 40,20] μm/min (norm 20–29 μm/min), an increase in the rate was observed mainly due to the acceleration of the clot growth initiation. The formation of spontaneous clots was noted in 32% of cases. In the group of infectious and inflammatory diseases of the maxillofacial area, the hypercoagulation was most pronounced: fibrinogen level significantly increased compared with the control group (3,21 [2,69; 4,72] g/l vs 2,69 [2,37; 3,17 ] g/l; p=0,0025). The soluble fibrin monomer complex (SFMC) indicator statistically significantly increased to 5,50 [0,00; 6,00] mg% (1,50 [0,00; 5,00] mg% in the control group, p=0,006). TEG showed a decrease in R (11,10 [8,82; 14,32] min vs 15,2 [11,8; 20,6] min; p=0,001) and K (3,65 [2,45; 5,10] min vs 6,70 [4,20; 8,25] min; p=0,0001), statistically significant compared to the control group. The alpha angle increased to 45,70 [36,20; 56,02] (30,8 [23,25; 41,15] in the control group, p=0,0001); maximum amplitude (MA) and clot density (G) increased in comparison with the control: 56,6±8,68 mm vs 48,10±6,20 mm; p=0,0001 and 6,50 [4,80; 8,00] Kd/sc vs 4,60 [3,60; 5,30] Kd/sc; p=0,0001. The TD indices in patients in this group also reflected a hypercoagulable state: the rate of V clot formation increased to 38,60 [33,00; 51,40] μm/min (30,45 [27,60; 33,30] μm/min in the control group, p