Hormonal response following hemorrhage after severe trauma: an observational prospective study.

BACKGROUND

Following severe trauma, activation of the autonomic and neuroendocrine systems is key in the response to hemorrhage by triggering vasopressor secretion, sodium and water reabsorption to maintain blood pressure and organ perfusion. However, these adaptative mechanisms remain not yet well described in this setting. The main goal of this study was to explore hypothalamic-posterior-pituitary-vasopressin, hypothalamic–pituitary–adrenal and renin–angiotensin–aldosterone system responses to severe trauma.

METHODS

This is a single-centre prospective observational study among adult severe trauma patients (Injury Severity Score (ISS) ≥ 9) in a French level-1 trauma center.

RESULTS

Sixty-five patients were included with a mean age of 46 (± 20) years old and a median ISS of 25 (19–30). Twenty-eight (43%) patients presented with a hemorrhage (transfusion of at least one pack of red blood cells (pRBC) in the 6 first hours), and 15 (23%) of them had a severe hemorrhage (> 3 pRBC in the first 6 h). Evolution of copeptin level, reflecting vasopressin secretion, was significantly different over the 48 h between transfused and non-transfused patients (interaction; P < 0.001) and regarding hemorrhage severity (no transfusion, 1–3 pRBC, > 3 pRBC) (interaction; P < 0.001). Copeptin was maximum at admission and higher in transfused than in non-transfused patients (486 ± 433 pmol/L vs.208 ± 206 pmol/L; P < 0.001). It rapidly decreased without significant difference anymore between groups from 6 h after admission. Renin (time effect, P = 0.001; transfusion effect, P = 0.02; interaction, P = 0.04) and aldosterone (time effect, P < 0.001; transfusion effect, P = 0.7; interaction, P = 0.08) were significantly different over the first 48 h regarding hemorrhage severity. There was no difference between transfused and non-transfused patients regarding levels of cortisol (P = 0.06). Twenty-two patients presented a relative corticosteroid insufficiency and 44 presented mineralocorticoid deficiency (aldosterone/renin < 2) over the first 48 h.

CONCLUSIONS

The vasopressin and renin–angiotensin–aldosterone systems are key pathways in the response to hemorrhage following severe trauma, and their response is quickly exhausted with its severity. This study strengthens the pathophysiological rationale for exploring personalized vasopressor management, including the timely addition of vasopressin and/or angiotensin II in addition to norepinephrine during the resuscitation of traumatic hemorrhage.