Abstract
Burn injuries kill thousands of people. The aim of this study was to investigate the dynamics of systemic inflammatory response parameters, endothelial dysfunction markers and hemostasis impairment in patients with thermal burn injuries. The study was conducted in 51 patients aged 16 to 80 years presenting with moderate to severe thermal burns. The systemic inflammatory response was assessed based on the levels of tumor necrosis factor α (TNFα), a number of interleukins (IL6, IL12), the С-reactive protein, and the monocyte chemoattractant protein 1 (MCP-1). Hemostatic impairments were inferred from the results of coagulation tests that measured the activated partial thromboplastin time (APTT), the prothrombin index (PI), the prothrombin time (PT) and the platelet count. Endothelial dysfunction was analyzed based on the levels of vascular endothelial growth factor (VEGF), total endothelin (TE) and circulating endothelial cells. The dynamics of the listed parameters were studied over 45 days following the injury. Endothelial dysfunction markers peaked on days 3–15 (VEGF 828.9 ± 993.2 pg/mL, TE 3.0 ± 1.7 fmol/mL, CEC 6.4 ± 6.0 • 104/l, IL6 264.4 ± 131.2 pg/mL, TNFα 41.4 ± 111.9 pg/ml, C-reactive protein 128.3 ± 52.4 nmol/mL). Coagulation was significantly impaired during the same period (APTT 41.4 ± 17.7 s, PI 83.6 ± 15.4%, PT 22.3 ± 10.0 s). By day 30–35, blood concentrations of proinflammatory cytokines and inflammation mediators had declined (TNFα 3.9 ± 9.6 pg/mL, IL6 49.0 ± 35.9 pg/mL, С-reactive protein 81.9 ± 341 nmol/ml); in that phase, the coagulation potential was continuing to decrease (APTT 51.8 ± 34.1 s, PI 82.9 ± 19.4%, PT 24.9 ± 21.4 s). The study demonstrates that damage to the endothelium results from both injured tissue breakdown and inflammation mediators. The risk of thromboembolic and hemorrhagic complications is the highest on days 7 through 15 following thermal injury. Further research is needed to study the mechanisms of endothelial damage in patients with thermal burns.
Highlights
Author contribution: Morrison VV — design of the experiment, data analysis, manuscript revision; Bozhedomov AYu — data collection and statistical analysis, manuscript draft
The primary cause of death in burned patients is multiple organ dysfunction syndrome (MODS) resulting from the inability of adaptation mechanisms to cope with severe trauma-induced stress, hypermetabolism and damage done by the toxic products of tissue destruction [2, 3]
This study aimed to investigate the dynamics of hemostasis, systemic inflammatory response and endothelial dysfunction markers in patients with thermal injury
Summary
Author contribution: Morrison VV — design of the experiment, data analysis, manuscript revision; Bozhedomov AYu — data collection and statistical analysis, manuscript draft. Наибольшую выраженность дисфункции эндотелия и воспалительной реакции выявили на 3–15-е сутки (VEGF 828,9 ± 993,2 пг/мл, общий эндотелин 3,0 ± 1,7 фмоль/мл, ЦЭК 6,4 ± 6,0 104/л, IL6 264,4 ± 131,2 пг/мл, ФНОα 41,4 ± 111,9 пг/мл, С-реактивный белок 128,3 ± 52,4 нмоль/мл). К 30–45-м суткам происходило уменьшение концентрации провоспалительных цитокинов и медиаторов воспаления в крови (ФНОα 3,9 ± 9,6 пг/мл, IL6 49,0 ± 35,9 пг/мл, С-реактивный белок 81,9 ± 34,1 нмоль/мл) и дальнейшее снижение коагуляционного потенциала крови (АЧТВ 51,8 ± 34,1 с, ПТИ 82,9 ± 19,4%, ПТВ 24,9 ± 21,4 с). The primary cause of death in burned patients is multiple organ dysfunction syndrome (MODS) resulting from the inability of adaptation mechanisms to cope with severe trauma-induced stress, hypermetabolism and damage done by the toxic products of tissue destruction [2, 3]. The pathophysiology of burn injury is relatively well studied, burns still kill thousands of people each year, posing a significant economic burden
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