Janett Kreutziger

Zusammenfassung: Das ideale Anästhesieverfahren sollte den Spagat zwischen höchster Patient:innensicherheit, ökonomischer Effizienz und fehlender ökologischer Belastung meistern. Dabei stehen uns nach wie vor drei Grundverfahren, die Inhalationsanästhesie, die totale intravenöse Anästhesie (TIVA) und die Regionalanästhesie zur Verfügung. Deren ökologischen Stärken und Schwächen unter Berücksichtigung der ersten beiden Punkte werden in diesem Artikel beleuchtet.

Purpose of review: Stress hyperglycaemia occur often in critically injured patients. To gain new consideration about it, this review compile current as well as known immunological and biochemical findings about causes and emergence. Recent findings: Glucose is the preferred energy substrate for fending immune cells, reparative tissue and the cardiovascular system following trauma. To fulfil these energy needs, the liver is metabolically reprogrammed to rebuild glucose from lactate and glucogenic amino acids (hepatic insulin resistance) at the expenses of muscles mass and – to a less extent – fat tissue (proteolysis, lipolysis, peripheral insulin resistance). This inevitably leads to stress hyperglycaemia, which is evolutionary preserved and seems to be an essential and beneficial survival response. It is initiated by damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), intensified by immune cells itself and mainly ruled by tumour necrosis factor (TNF)α and catecholamines with lactate and hypoxia inducible factor (HIF)-1α as intracellular signals and lactate as an energy shuttle. Important biochemical mechanisms involved in this response are the Warburg effect as an efficient metabolic shortcut and the extended Cori cycle. Summary: Stress hyperglycaemia is beneficial in an acute life-threatening situation, but further research is necessary, to prevent trauma patients from the detrimental effects of persisting hyperglycaemia.

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.

Hyperphosphataemia can originate from tissue ischaemia and damage and may be associated with injury severity in polytrauma patients. In this retrospective, single-centre study, 166 polytrauma patients (injury severity score (ISS) ≥ 16) primarily requiring intensive care unit (ICU) treatment were analysed within a five-year timeframe. ICU-admission phosphate levels defined a hyperphosphataemic (>1.45 mmol/L; n = 56) opposed to a non-hyperphosphataemic group (n = 110). In the hyperphosphataemic group, injury severity was increased (ISS median and IQR: 38 (30–44) vs. 26 (22–34); p < 0.001), as were signs of shock (lactate, resuscitation requirements), tissue damage (ASAT, ALAT, creatinine) and lastly in-hospital mortality (35.7% vs. 5.5%; p < 0.001). Hyperphosphataemia at ICU admission was shown to be a risk factor for mortality (1.46–2.10 mmol/L: odds ratio (OR) 3.96 (95% confidence interval (CI) 1.03–15.16); p = 0.045; >2.10 mmol/L: OR 12.81 (CI 3.45–47.48); p < 0.001) and admission phosphate levels alone performed as good as injury severity score (ISS) in predicting in-hospital mortality (area under the ROC curve: 0.811 vs. 0.770; p = 0.389). Hyperphosphataemia at ICU admission is related to tissue damage and shock and indicates injury severity and subsequent mortality in polytrauma patients. Admission phosphate levels represent an easily feasible yet strong predictor for in-hospital mortality.

Background: Stress hyperglycemia is common in trauma patients. Increasing injury severity and hemorrhage is known to trigger hepatic gluconeogenesis and glycogenolysis and also 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 single, university hospital in Austria between 2000 and 2020 were charted in a register. Besides 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 increasing injury severity past moderate to severe (AAST III-IV) was associated with a concomitant rise in blood glucose levels independent of the affected organ. While this stress induced hyperglycemia was even more pronounced in the most severe forms (AAST V) of spleen (median 10.7 mmol/L, pConclusions: Absence of stress hyperglycemia is a sign of most severe liver injury (AAST V) and should prompt fundamental diagnostic and therapeutic procedures. Blood glucose should be considered as an additional diagnostic criterion in liver injury.