Prehospital Resuscitation of Traumatic Hemorrhagic Shock with Hypertonic Solutions Worsens Hypocoagulation and Hyperfibrinolysis

Abstract

Impaired hemostasis frequently occurs after traumatic shock and resuscitation. The prehospital fluid administered can exacerbate subsequent bleeding and coagulopathy. Hypertonic solutions are recommended as first-line treatment of traumatic shock; however, their effects on coagulation are unclear. This study explores the impact of resuscitation with various hypertonic solutions on early coagulopathy after trauma. We conducted a prospective observational subgroup analysis of large clinical trial on out-of-hospital single-bolus (250 mL) hypertonic fluid resuscitation of hemorrhagic shock trauma patients (systolic blood pressure, ≤70 mmHg). Patients received 7.5% NaCl (HS), 7.5% NaCl/6% Dextran 70 (HSD), or 0.9% NaCl (normal saline [NS]) in the prehospital setting. Thirty-four patients were included: 9 HS, 8 HSD, 17 NS. Treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. The HSD-resuscitated patients had higher admission international normalized ratio values and more hypocoagulable patients, 62% (vs. 55% HS, 47% NS; P < 0.05). Prothrombotic tissue factor was elevated in shock treated with NS but depressed in both HS and HSD groups. Fibrinolytic tissue plasminogen activator and anti-fibrinolytic plasminogen activator inhibitor type 1 were increased by shock but not thrombin-activatable fibrinolysis inhibitor. The HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in more hypocoagulability and hyperfibrinolysis. We concluded that resuscitation with hypertonic solutions, particularly HSD, worsens hypocoagulability and hyperfibrinolysis after hemorrhagic shock in trauma through imbalances in both procoagulants and anticoagulants and both profibrinolytic and antifibrinolytic activities.

Figures

Fig. 1. Plasma concentrations of TF (A), TFPI (B), TM (C), TAFI (D) were determined on emergency department (ED) admission (≤3 h) and at 12 and 24 h after resuscitation in trauma patients treated prehospital with HS (n = 9), HSD (n = 8), or NS (n = 17) and in healthy controls (n = 20)

Data are shown as mean ± SEM; aP < 0.05 vs. age-matched controls; bP < 0.05 vs. time-matched NS-treated patients; cP < 0.05 vs. time-matched HS-treated patients, by ANOVA.

Fig. 2. Plasma d-dimer levels determined on emergency department (ED) admission (≤3 h) and at 12 and 24 h after resuscitation in trauma patients treated prehospital with HS (n = 9), HSD (n = 8), or NS (n = 17) and in healthy controls (n = 20)

Data are shown as mean ± SEM; aP < 0.05 vs. age-matched controls; bP < 0.05 vs. time-matched NS-treated patients; cP < 0.05 vs. time-matched HS-treated patients, by ANOVA.