Discrepancies in the indicators of rotational thromboelastometry of umbilical cord blood in premature newborns after different types of tocolytic therapy

The unstable balance in the immature hemostatic system of the premature fetus and newborn can be easily disturbed under the influence of stressful factors associated with childbirth, including tocolytic therapy.The objective: to study in vivo the blood coagulation and fibrinolysis in newborns after tocolytic therapy.Materials and methods. The study was performed in two clinical groups of newborns (gestational term up to 34 weeks) from mothers who received tocolytic treatment with hexoprenaline (I group, 26 babies) or nifedipine (II group, 22 newborns) for a long time before birth. A group of preterm infants born without tocolysis (III group, 18 children) and a group of full-term infants (IV group, 18 children) were the comparison ones. The hemostatic profile of the newborn in vivo was determined using the ROTEM® delta device (Instrumentation Laboratory, Germany) in a portion of blood with a volume of 300–340 μl, which was obtained after the birth of the fetus from a fragment of the umbilical cord between two clamps. Clot formation and lysis were assessed by kinetic parameters of coagulation.The analysis of elastograms is performed by a program from the device interface. For coagulation analysis, the r ex-tem® and fib-tem® test systems (Tem Innovations GmbH, Germany) were used.Results. In the case of hexoprenaline tocolysis, the α angle was insignificantly different from the values ​​of the III and IV groups (70.8±9.47° vs. 76.7±4.84 and 79.9±4.62°; p>0.05), and after of tocolysis with nifedipine the angle α (54.8±10.16°; p<0.05) is probably smaller than the indicators of the III and IV groups, which indicates the slowing down of blood clot formation in the newborn.The characteristics of the process of clot formation – the amplitude at the 5th and 10th minutes (A5, A10) and the maximal clot firmness/maximal amplitude (MCF/MA) after hexoprenaline tocolysis (I group) exceeded those of newborns of the III group without tocolysis – 14.6±8.73; 19.3±6.20; 23.4±6.97 mm versus 13.2±3.34; 15.5±4.34; 15.2±11.37 mm with a significant difference according to A10 and MCF/MA (p<0.05) and term newborns of the IV group according to A10 and MCF/MA (16.0±7.39 and 17.4±7.04 ; p<0.05). The growth of clot amplitudes after tocolysis with hexoprenaline resembled the sequence of growth of the parameters of full-term newborns, differing quantitatively.In the case of nifedipine tocolysis, all parameters of the clot amplitude are significantly reduced – 8.2±3.34; 10.0±2.27; 11.4±3.03 mm compared to the III group – 13.2±3.34; 15.5±4.34; 15.2±11.37 mm (р<0.05), all the more, to the already the indicators of the IV group, as close as possible to the indicators of extremely premature newborns – 4.6±1.39, 8.0±3.01, 7.9±5.56 mm.Lysis index at 30 min (LI 30) lagged behind the indicators of the control groups (95.6±5.50 and 98.2±1.33% compared to 91.7±15.28 (p>0.05) and 85.4±22.81%; p<0.05). Maximum lysis (ML) had the lowest mean values among all premature infants (3.2±1.56; 4.4±4.25; 8.1±2.50%; p>0.05), lagging behind the index of full-term newborns (17.1±2.34%; p<0.05).Conclusions. 1. Tocolysis with the use of hexoprenaline sulfate is reflected in a premature newborn by the acceleration of the process of clot formation and the slowing down of fibrinolysis in umbilical cord blood. The reflection of this effect on the thromboelastogram is close to the kinetic processes of blood coagulation in full-term infants.2. After the use of nifedipine for tocolytic therapy, there are the signs of delayed clot formation and disordered fibrinolysis on the thromboelastogram, as indicated by a large variance in the maximal lysis index (4.4±4.25 mm).