• Anthony E Pusateri, Lauren T Moffatt, Dao H Ho, Leslie E Neidert, Clifford G Morgan, Shawn Tejiram, Sylvain Cardin, and Jeffrey W Shupp.
• Cellular and Immune-based Adjuncts for Casualty Care, Naval Medical Research Unit San Antonio, Joint Base San Antonio-Fort Sam Houston, Texas.
• Shock. 2025 Jan 1; 63 (1): 111811-18.

AbstractIn recent years, it has become apparent that fibrinolytic dysfunction and endotheliopathy develop in up to 40% of patients during the first hours following thermal injury and are associated with poor outcomes and increased resuscitation requirements. Rapidly following burn injury, the fibrinolytic system is activated, with activation generally greater with increased severity of injury. Very high plasma concentrations of plasmin-antiplasmin complex (marker of activation) have been associated with mortality. Patients display hyperfibrinolytic, physiologic/normal, or hypofibrinolytic/fibrinolytic shutdown phenotypes, as assessed by viscoelastic assay. Phenotypes change in over 50% of patients during the acute burn resuscitation period, with some patterns (maladaptive) associated with increased mortality risk and others (adaptive, trending toward the physiologic phenotype) associated with survival. Endotheliopathy, as reflected in elevated plasma concentrations of syndecan-1 has also been associated with increased mortality. Here we review the incidence and effects of these responses after burn injury and explore mechanisms and potential interactions with the early inflammatory response. Available data from burn and nonburn trauma suggest that the fibrinolytic, endothelial, and inflammatory systems interact extensively and that dysregulation in one may exacerbate dysregulation in the others. This raises the possibility that successful treatment of one may favorably impact the others.Copyright © 2024 by the Shock Society.

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