Burns : journal of the International Society for Burn Injuries · 2026
Microcirculatory response to fluid resuscitation in severe burns.
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Dijkstra Annemieke, Ince Can, Gigengack Rolf, Guven Goksel, van Baar Margriet E, Trommel Nicole, Hofland Helma W C, van Dam Wijnie, van Leerdam Martin, van der Vlies Cornelis H
Аннотация
BACKGROUND: Major burn injury induces profound endothelial alterations and impaired tissue perfusion. Although early fluid resuscitation aims to restore organ perfusion using conventional systemic resuscitation endpoints, normalization of these parameters may not reflect restoration of tissue perfusion. This study investigated temporal changes in tissue perfusion (assessed by quantitative sublingual microcirculatory imaging), together with endothelial biomarkers, during the first 24 h after major burn injury.
METHODS: In this prospective observational study, 22 adults with burns involving ≥ 15% total body surface area admitted within 24 h after injury underwent serial quantitative sublingual microcirculatory imaging using incident dark field (IDF) imaging at baseline and 4, 8, 12 and 24 h. Plasma concentrations of syndecan-1, glypican-1, intercellular adhesion molecule (ICAM-1), and vascular endothelial cadherin (VE-cadherin) were measured concurrently. Fluid resuscitation was initiated at 3 mL/kg/%TBSA using lactated Ringer's solution and subsequently adjusted according to urine output and hemodynamic parameters. Mixed-effects models were used to evaluate temporal changes and the association between high fluid exposure (>5 mL/kg/%TBSA during the first 24 h) and tissue perfusion.
RESULTS: Twenty-two patients (mean TBSA 38 ± 21%; 95% male) were included. The actual fluid volume administered during the first 24 h was 4.0 ± 1.8 mL/kg/%TBSA. Total and functional capillary density decreased significantly over the 24-hour observation period, whereas the proportion of perfused vessels and red blood cell velocity increased over time (both p < 0.01). Mean arterial pressure remained stable, urine output was maintained (0.8 mL/kg/h), and lactate did not change, despite persistent impairment of tissue perfusion as demonstrated by quantitative microcirculatory assessment. Glypican-1 and VE-cadherin decreased over time (p < 0.05 and p < 0.001), whereas syndecan-1 remained stable, suggesting persistent endothelial alterations without unequivocal evidence of ongoing glycocalyx shedding. High fluid exposure occurred in 21.1% of patients and was not associated with improved tissue perfusion.
CONCLUSIONS: This study demonstrated persistent impairment of tissue perfusion during the early phase of burn resuscitation despite normalization of conventional systemic resuscitation endpoints. Endothelial biomarker profiles suggested persistent endothelial alterations without definitive evidence of ongoing glycocalyx degradation. Quantitative microcirculatory assessment and endothelial biomarkers may provide complementary physiological information beyond conventional systemic resuscitation parameters and warrant further investigation in burn resuscitation.
METHODS: In this prospective observational study, 22 adults with burns involving ≥ 15% total body surface area admitted within 24 h after injury underwent serial quantitative sublingual microcirculatory imaging using incident dark field (IDF) imaging at baseline and 4, 8, 12 and 24 h. Plasma concentrations of syndecan-1, glypican-1, intercellular adhesion molecule (ICAM-1), and vascular endothelial cadherin (VE-cadherin) were measured concurrently. Fluid resuscitation was initiated at 3 mL/kg/%TBSA using lactated Ringer's solution and subsequently adjusted according to urine output and hemodynamic parameters. Mixed-effects models were used to evaluate temporal changes and the association between high fluid exposure (>5 mL/kg/%TBSA during the first 24 h) and tissue perfusion.
RESULTS: Twenty-two patients (mean TBSA 38 ± 21%; 95% male) were included. The actual fluid volume administered during the first 24 h was 4.0 ± 1.8 mL/kg/%TBSA. Total and functional capillary density decreased significantly over the 24-hour observation period, whereas the proportion of perfused vessels and red blood cell velocity increased over time (both p < 0.01). Mean arterial pressure remained stable, urine output was maintained (0.8 mL/kg/h), and lactate did not change, despite persistent impairment of tissue perfusion as demonstrated by quantitative microcirculatory assessment. Glypican-1 and VE-cadherin decreased over time (p < 0.05 and p < 0.001), whereas syndecan-1 remained stable, suggesting persistent endothelial alterations without unequivocal evidence of ongoing glycocalyx shedding. High fluid exposure occurred in 21.1% of patients and was not associated with improved tissue perfusion.
CONCLUSIONS: This study demonstrated persistent impairment of tissue perfusion during the early phase of burn resuscitation despite normalization of conventional systemic resuscitation endpoints. Endothelial biomarker profiles suggested persistent endothelial alterations without definitive evidence of ongoing glycocalyx degradation. Quantitative microcirculatory assessment and endothelial biomarkers may provide complementary physiological information beyond conventional systemic resuscitation parameters and warrant further investigation in burn resuscitation.