Sugar Or Salt?: The Relative Roles Of The Glucocorticoid And Mineralocorticoid Axes In Traumatic Shock

Daniel Nelson, DO, George Black, MD, Mia Debarros, MD, Quinton Hatch, MD, Christopher Porta, MD, Derek McVay, DO, Matthew Eckert, MD, Matthew Martin, MD. Madigan Army Medical Center

OBJECTIVES:  Deficiency in glucocorticoids has been proposed as a key contributor to shock states and a target for therapy, but the presence and role of acute mineralocorticoid deficiency (MD) may be of equal or greater significance. We hypothesized that MD is present in post-hemorrhagic shock and results from ischemia/reperfusion (IR) injury.

METHODS:  57 swine underwent 35% volume-controlled hemorrhage followed by aortic cross clamping for 50 minutes to induce truncal I/R injury. Protocol-guided resuscitation and monitoring was performed for up to 24 hours. Laboratory analysis was performed including cortisol, aldosterone, and plasma renin activity (PRA). The aldosterone to renin ratio (ARR) was also calculated at each time point.

RESULTS:  Mean baseline cortisol levels for the entire cohort were 5.8 ug/dl. Following hemorrhage there was a significant increase in mean cortisol levels to 9.2 ug/dl (p<0.001). After 1 hour of reperfusion there was no change in mean cortisol levels at 9.8 ug/dl (p=0.12). Mean baseline aldosterone levels of this cohort were 13.3 pg/ml. Aldosterone levels prior to cross clamp removal increased significantly to 115.1 pg/ml (p<0.001) and then rapidly declined to 49.2 pg/ml (p<0.01) after one hour of reperfusion. Conversely, baseline plasma renin activity was 0.75 ng/ml/hr and increased significantly prior to cross clamp removal (1.8) and at 1 hour (8.9, both p<0.001). The ARR at baseline was 68.9 and increased to 132.3 (p=0.07) prior to cross clamp removal, but significantly declined following 1 hour of reperfusion to 8.7 (p<0.001). Overall, this represented a 93% reduction in mean ARR following reperfusion for the entire cohort. The degree of aldosterone deficiency correlated with degree of systemic shock as measured by arterial base deficit (r=0.47, p=0.04), while cortisol showed no correlation.

CONCLUSION:  Hemorrhagic shock with I/R injury resulted in only modest impact on the glucocorticoid axis but major dysfunction of the mineralocorticoid axis with resultant hyperreninemic hypoaldosteronism. The degree of aldosterone deficiency may provide prognostic information or offer a potential target for pharmacologic supplementation.

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