Abstract
Background: Stress hyperglycemia is common in trauma patients. Increasing injury severity and hemorrhage trigger hepatic gluconeogenesis, glycogenolysis, peripheral and hepatic insulin resistance. Consequently, we expect glucose levels to rise with injury severity in liver, kidney and spleen injuries. In contrast, we hypothesized that in the most severe form of blunt liver injury, stress hyperglycemia may be absent despite critical injury and hemorrhage. Methods: All patients with documented liver, kidney or spleen injuries, treated at a university hospital between 2000 and 2020 were charted. Demographic, laboratory, radiological, surgical and other data were analyzed. Results: A total of 772 patients were included. In liver (n = 456), spleen (n = 375) and kidney (n = 152) trauma, an increase in injury severity past moderate to severe (according to the American Association for the Surgery of Trauma, AAST III-IV) was associated with a concomitant rise in blood glucose levels independent of the affected organ. While stress-induced hyperglycemia was even more pronounced in the most severe forms (AAST V) of spleen (median 10.7 mmol/L, p < 0.0001) and kidney injuries (median 10.6 mmol/L, p = 0.004), it was absent in AAST V liver injuries, where median blood glucose level even fell (5.6 mmol/L, p < 0.0001). Conclusions: Absence of stress hyperglycemia on hospital admission could be a sign of most severe liver injury (AAST V). Blood glucose should be considered an additional diagnostic criterion for grading liver injury.
Highlights
Introduction published maps and institutional affilStress hyperglycemia is common in trauma patients, and critical illness on hospital admission and is often associated with poor outcome [1,2,3,4,5,6,7]
879 patients presenting at our Level 1 trauma center with suspected hepatic, splenic or renal injury were assessed for eligibility
The of thisthe single-center trial demonstrate that stress hyperglycemia developsproduction following epinephrine stimulation parallel to injury severity in patients with blunt spleen or kidney trauma
Summary
Stress hyperglycemia is common in trauma patients, and critical illness on hospital admission and is often associated with poor outcome [1,2,3,4,5,6,7]. This stress hyperglycemia is caused by neuroendocrine, inflammatory and metabolic responses to trauma-associated stressors. A traumatic brain injury may even lead to a sympathetic storm [8,9], further amplifying this neuroendocrine response Another very strong trigger for a stress response such as stress hyperglycemia is hemorrhage [10], which is mediated by baroreceptors and multifactorially released cytokines [11]. To distinguish between severe AAST IV and AAST V injuries of the liver—e.g., for scientific purposes—
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