The results of this retrospective, single center trial demonstrated that stress hyperglycemia develops in parallel to injury severity in patients with blunt spleen or kidney trauma. While consistent results were obtained for blood glucose levels in blunt liver injuries up to AAST IV, stress hyperglycemia was completely absent in the most severe cases (AAST V).
Over the last two decades, a vast number of publications have demonstrated the fundamental role of stress hyperglycemia in critical injury [1–4] and diverse critical conditions [21–24]. Up to date, there has been no consistency in defining blood glucose levels, wherefore this trial resigns from specifying any threshold values for stress hyperglycemia.
Pathophysiological source of stress hyperglycemia seems to be a rampant hepatic glycogenolysis  but also gluconeogenesis from lactate, free fatty acids, and alanine [7, 8, 25]. Decoupling of both processes from physiological feedback mechanisms controlling glucose homeostasis is thought to be caused by hepatic [11, 12, 26] and intensified by muscular insulin resistance . Hemorrhage is a potential multiplier of trauma associated stress hyperglycemia [5, 6], wherefore injuries of parenchymatous organs like the liver, spleen or kidney are capable of triggering stress hyperglycemia amongst others due to blood loss associated with increasing injury severity. With regards to the corresponding definitions of AAST classified injuries, active bleeding is included in AAST ≥ III injuries of the liver and kidney and AAST ≥ IV injuries of the spleen [15, 16]. AAST V injuries of the liver are furthermore defined as major juxtahepatic venous injury (vena cava, central major hepatic veins) or lacerations resulting in parenchymal disruption of more than 75% of one hepatic lobe [15, 16]. Assuming the liver is the primary origin of stress hyperglycemia, it seems clear that such destroying liver injuries, partially even resulting in devascularization (inflow or outflow) can impede hepatic glucose liberation provoked by trauma or hemorrhage, as demonstrated in this trial for the first time.
Surprisingly, besides one child, none of the surviving adults with AAST V hepatic injuries was in need of any additional glucose administration to maintain blood glucose levels within physiological range. In patients with initially low or very low (hypoglycemic) blood glucose levels, blood glucose levels recovered spontaneously to typically increased blood glucose levels following severe trauma. Apparently, the residual hepatic tissue was able to cover physiologic needs, but needed several hours to adopt. Nevertheless, the relatively low blood glucose levels were of high diagnostic importance.
In the literature, the kidneys are also seen as relevant source of blood glucose production (up to 40% of circulating blood glucose) following epinephrine stimulation [28, 29]. Although body’s own catecholamines should be relevantly increased during severe hemorrhage as detected in AAST V liver injuries in this study, blood glucose dropped in these patients and was not increased by renal glucose delivery. Possible attempts of explanation may include insufficient renal perfusion during hemorrhagic shock or mere lack of time or substances (glutamine, glycerol, lactate) for sufficient renal glucose production. In particular, circulating glutamine is mainly provided by the liver and therefore, in case of AAST V injury of the liver, probably lacking.
This study did not differ among adults, children or diabetics. We did not find significant differences between adults and children probably due to the low median age of analyzed patients. Besides observed outliers of high blood glucose levels, patients with diabetes mellitus had no relevant impact on our results. We did not exclude them from analysis as we felt they realistically represent the expectable extent of clinical settings.
Furthermore, we did not analyze lactatemia due to unreliability in initial laboratory results upon hospital admission . Lactatemia is influenced by circulation, production, metabolism and volume resuscitation as well as administration (Ringer’s lactate), if applicable. Therefore, initial laboratory results may vary fundamentally not always reflecting severity of injury and hemorrhage, respectively.
In contrast, blood glucose levels upon hospital admission seem to be independent from pre-hospital fluid and volume administration and a reliable, additional diagnostic tool for trauma patients  without collinearity to vital or laboratory parameters commonly used upon initial trauma assessment. However, if critically injured patients present with low blood glucose levels, questions should arise: besides most severe liver injuries, anti-diabetic drug overdose, alcohol abuse, severe hypothermia or any other reason for limited liver function could be causative [13, 30, 31].
Pancreatic injuries were rare in this population. Merely eight patients suffered from concomitant pancreatic injury: five pancreatic contusions treated conservatively and three pancreatic ruptures were in need of surgical intervention. One segment resection, one surgical closure of the rupture and one complete pancreas resection were performed. Severe pancreatic affection was mainly concomitant to liver injuries. Blood glucose differed widely and independent to extent of pancreatic injury from 5.05 to 24.81 mmol/L. Based on the limited number of those affected, the authors could not conclude that pancreatic injuries had relevant impact on initial blood glucose in this patient population.
Pre-hospital vital parameters were not sufficiently documented within the digitalized local hospital information system during the initial decade of the study phase. Therefore, pursued calculation of trauma scores was not possible. Further limitations of this study are the single center and retrospective design as well as the low patient number in certain subgroups.
Nevertheless, this large database of patients with blunt hepatic, splenic, and renal injuries sufficiently demonstrated significant results, especially regarding median blood glucose drop in most severe liver injuries (AAST V). Blood glucose levels should be part of diagnostic calculations, and also be considered in differentiation between severe liver injuries (AAST IV vs. V).