Secondary Logo

Journal Logo

Blood glucose concentrations in prehospital trauma patients with traumatic shock

A retrospective analysis

Kreutziger, Janett; Lederer, Wolfgang; Schmid, Stefan; Ulmer, Hanno; Wenzel, Volker; Nijsten, Maarten W.; Werner, Daniel; Schlechtriemen, Thomas

European Journal of Anaesthesiology (EJA): January 2018 - Volume 35 - Issue 1 - p 33–42
doi: 10.1097/EJA.0000000000000733
Trauma
Free

BACKGROUND Deranged glucose metabolism after moderate to severe trauma with either high or low concentrations of blood glucose is associated with poorer outcome. Data on prehospital blood glucose concentrations and trauma are scarce.

OBJECTIVES The primary aim was to describe the relationship between traumatic shock and prehospital blood glucose concentrations. The secondary aim was to determine the additional predictive value of prehospital blood glucose concentration for traumatic shock when compared with vital parameters alone.

DESIGN Retrospective analysis of the predefined, observational database of a nationwide Helicopter Emergency Medical Service (34 bases).

SETTING Emergency trauma patients treated by Helicopter Emergency Medical Service between 2005 and 2013 were investigated.

PATIENTS All adult trauma patients (≥18 years) with recorded blood glucose concentrations were enrolled.

OUTCOMES Primary outcome: upper and lower thresholds of blood glucose concentration more commonly associated with traumatic shock. Secondary outcome: additional predictive value of prehospital blood glucose concentrations when compared with vital parameters alone.

RESULTS Of 51 936 trauma patients, 20 177 were included. In total, 220 (1.1%) patients died on scene. Hypoglycaemia (blood glucose concentration 2.8 mmol l−1 or less) was observed in 132 (0.7%) patients, hyperglycaemia (blood glucose concentration exceeding 15 mmol l−1) was observed in 265 patients (1.3%). Blood glucose concentrations more than 10 mmol l−1 (n = 1308 (6.5%)) and 2.8 mmol l−1 or less were more common in patients with traumatic shock (P < 0.0001). The Youden index for traumatic shock ((sensitivity + specificity) − 1) was highest when blood glucose concentration was 3.35 mmol l−1 (P < 0.001) for patients with low blood glucose concentrations and 7.75 mmol l−1 (P < 0.001) for those with high blood glucose concentrations. In logistic regression analysis of patients with spontaneous circulation on scene, prehospital blood glucose concentrations (together with common vital parameters: Glasgow Coma Scale, heart rate, blood pressure, breathing frequency) significantly improved the prediction of traumatic shock in comparison with prediction by common vital parameters alone (P < 0.0001).

CONCLUSION In adult trauma patients, low and high blood glucose concentrations were more common in patients with traumatic shock. Prehospital blood glucose concentration measurements in addition to common vital parameters may help identify patients at risk of traumatic shock.

From the Department of Anaesthesia and Intensive Care Medicine (JK, WL), Department of General and Surgical Intensive Care Medicine (SS), Department of Medical Statistics, Informatics and Health Economics (HU), Medical University of Innsbruck, Innsbruck, Austria, Department of Anaesthesiology, Intensive Care Medicine, Emergency Medicine and Pain Therapy, Medizin Campus Bodensee, Friedrichshafen, Germany (VW), University Medical Centre Groningen, University of Groningen, Groningen, Netherlands (MWN), German Helicopter Emergency Medical Services (ADAC Luftrettung gGmbH) (DW), Emergency Medical Services of the Saarland, Bexbach; Formerly Quality Management of the German Helicopter Emergency Medical Services (ADAC Luftrettung gGmbH), Munich, Germany (TS)

Correspondence to Janett Kreutziger, MD, Department of Anaesthesia and Intensive Care Medicine, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria Tel: +43 512 504 80357; efax: +43 512 504 6780357; e-mail: janett.kreutziger@i-med.ac.at

Published online 11 November 2017

Back to Top | Article Outline

Introduction

Glucose derangements such as hypoglycaemia and hyperglycaemia have been proven to be predictive for outcome in severely ill and critically impaired patients.1–4 Trauma when associated with blood glucose derangements has a poor outcome.5–12 In a recent investigation, blood glucose on admission was found to be predictive for haemorrhagic shock in polytraumatised patients.13 Currently, data are scarce on blood glucose concentrations in prehospital trauma patients with traumatic shock. Blood glucose concentration measurement on-site could provide a useful, simple, rapid and inexpensive screening tool for patients at increased risk of traumatic shock.

The aim of this study was to analyse prehospital blood glucose concentrations in trauma patients and determine whether blood glucose concentrations correspond with severity of trauma and traumatic shock.

Back to Top | Article Outline

Methods

We retrospectively analysed data from prehospital missions conducted by the Helicopter Emergency Medical Service (HEMS) of Allgemeiner Deutscher Automobil Club (ADAC) in Germany. A nationwide, multicentre study including all 34 ADAC helicopter bases was conducted and involved all trauma patients treated by ADAC-HEMS between 1 January 2005 and 31 December 2013. The standardised definition of trauma used in all contributing centres was physical trauma caused by a sudden event. The study was approved by the Ethics Committee of the Medical Association of the Saarland (Ärztekammer des Saarlands, No. 69/14, 24 April 2014, chairman Professor Dr. med. Gerd Rettig-Stürmer) and by the Institutional Review Board. Inclusion criteria were adult trauma patients (≥18 years), in whom blood glucose concentration was measured on-site. Exclusion criteria were interhospital transfers and incomplete or incongruent data records regarding demographics, initial vital signs or important accident data such as injury pattern, trauma course and trauma causes.

The following parameters were recorded routinely according to the predefined emergency physician dataset (Minimaler Notarzt-Datensatz, MIND214) within the prospective, observational database of ADAC (Luftrettungs, Informations und Kommunikations System, LIKS®): demographic data, first vital parameters [heart rate (HR), breathing frequency, SBP] upon arrival of the professional rescuers, Glasgow Coma Scale (GCS), trauma mechanism, clinical evaluation of injury severity of the following body regions: head/brain, neck, face, chest, abdomen, thoracic and lumbar spine, pelvis, upper and lower extremities (1 = no injury, 2 = minor injury, 3 = moderate injury, 4 = severe injury, not life threatening, 5 = severe injury, life threatening, 6 = critical injury, life threatening, 7 = deadly injury), whole injury pattern (1 = single injury, 2 = multiple injuries, 3 = polytrauma defined as life-threatening multiple trauma), the National Advisory Committee for Aeronautics (NACA) index (0 = no injury, 1 = minor injury, no intervention by a physician necessary; 2 = minor to moderate injury, ambulatory evaluation, 3 = moderate to severe injury, not life threatening, in-patient care necessary, 4 = severe injury, potentially life threatening, emergency physician care necessary, 5 = acute life-threatening injury, 6 = apnoea and circulatory arrest/resuscitation, 7 = deceased; of note: we included only patients who were alive upon arrival of the HEMS emergency physician). In addition, the given volume, type of drug administered and rescue intervals were recorded.

Blood glucose concentration (in mmol l−1) was measured with point-of-care devices at the scene. In most cases, glucose was measured from blood drawn immediately after venous access. Glucose concentrations were categorised into three groups: 2.8 mmol l−1 or less, 2.81 to 10.0 mmol l−1, and more than 10.0 mmol l−1. The thresholds of 2.8 mmol l−1 and 10.0 mmol l−1 are commonly used in emergency medicine and intensive care.15,16

Traumatic shock was defined as SBP 90 mmHg or less or administration of catecholamines.

Statistical analysis was conducted with International Buisness Machines; SPSS Statistics (Release 22.0, 2013, Armonk, New York, USA). The null hypothesis was that prehospital blood glucose concentration does not differ in patients with single injuries, multiple injuries or polytraumatised patients with and without traumatic shock. The Shapiro–Wilk test was used to test for normal distribution. Following descriptive analysis, the Mann–Whitney U test was used to compare group differences and the χ2 test was performed to detect frequency differences. Multivariable logistic regression analysis for prediction of traumatic shock necessitating fluid resuscitation and administration of catecholamines was performed using common vital parameters for model 1 common vital parameters (HR, respiratory frequency, SBP, GCS) and for model 2 common vital parameters and blood glucose on-site and blood glucose squared, respectively. Receiver operating characteristics (ROC) and comparison of ROC curves (area under the curve) to find the best fitting model were performed by MedCalc (Version 15.8, Ostend, Belgium) analysis. The Youden index17 was calculated to investigate blood glucose concentration thresholds. The Youden index is a single statistic ((sensitivity + specificity) − 1) that captures the performance of a dichotomous diagnostic test by the ROC. Its value ranges from −1 to 1, and has a zero value when a diagnostic test gives the same proportion of positive results for groups with and without the disease, that is, the test is useless. A value of 1 indicates that there are no false positives or false negatives, that is, the test is perfect. The index gives equal weight to false positive and false negative values, so all tests with the same value of the index give the same proportion of total misclassified results. The value correspond to a value of the influencing factor, which is then defined as the cut-off value for this test (in this case upper and lower blood glucose concentration thresholds more commonly associated with traumatic shock). Integrated discrimination improvement and net reclassification improvement were used to assess the improvement of outcome prediction comparing model 1 and model 2 (Statistics and Data, STATA/MP, release 13, College Station, Texas, USA). Confidence intervals in this study were 99%. A P value of 0.01 was deemed to be statistically significant.

Back to Top | Article Outline

Results

During the study period 51 936 trauma patients were registered in the ADAC-HEMS database. In 24 141 (46.5%) patients blood glucose concentration was measured and recorded. Ultimately, 20 177 patients were included resulting in an inclusion rate of eligible patients of 83.6% (Fig. 1). SBP 90 mmHg or less was found in 1638 patients, and traumatic shock was noted in 3039 (15.1%) patients (Table 1).

Fig. 1

Fig. 1

Table 1

Table 1

In total, 18 737 patients (92.9%) had initial blood glucose concentrations between 2.81 and 10.0 mmol l−1. Blood glucose concentration 2.80 mmol l−1 or less was detected in 132 (0.7%) patients, including 56 (0.3%) patients with severe hypoglycaemia, 2.20 mmol l−1 or less. This severe hypoglycaemia was more frequently seen in patients with polytrauma [20/2790 (0.7%)]. Hyperglycaemia exceeding 15 mmol l−1 was documented in 265 (1.3%) patients and most frequently detected in 57 single-injury patients with severe traumatic brain injury [57/3051 (1.9%)]. Of the 132 hypoglycaemic patients, 64 (48.5%) received glucose infusions on scene (Table 2).

Table 2

Table 2

Traumatic shock was noted in 377/1308 patients (28.8%) with hyperglycaemia (>10.0 mmol l−1), in 83/265 patients (31.3%) with excessive hyperglycaemia (≥15.01 mmol l−1) and in 44/132 patients (33.3%) with hypoglycaemia (≤2.80 mmol l−1).

In polytraumatised patients with traumatic shock, the blood glucose concentration profiles had significant U-shaped characteristics (P < 0.0001): in 47/66 patients (71.2%) with blood glucose concentrations 4.0 mmol l−1 or less and in 44/62 patients (71%) with blood glucose concentrations more than 14.0 mmol l−1 the frequency of traumatic shock was more than 60% (Fig. 2). This U-shaped pattern was less marked in patients with single injuries and was not observed in patients with multiple injuries (Fig. 2). In patients older than 65 years, traumatic shock was diagnosed even more frequently when blood glucose concentration was 4.0 mmol l−1 or less than in younger patients (Fig. 3).

Fig. 2

Fig. 2

Fig. 3

Fig. 3

The Youden index for traumatic shock was highest at 3.35 mmol l−1(P < 0.001) for patients with low blood glucose concentrations in the left segment of the curve and at 7.75 mmol l−1 (P < 0.001) for patients with high blood glucose concentrations in the right segment of the curve (Fig. 2).

Prehospital blood glucose concentrations significantly improved the prediction of traumatic shock necessitating fluid resuscitation and administration of catecholamines (Integrated Discrimination Improvement P < 0.0001) compared with prediction by GCS, HR, respiratory rate and blood pressure alone (Table 3).

Table 3

Table 3

Back to Top | Article Outline

Discussion

This retrospective, multicentre analysis demonstrates that prehospital deranged blood glucose concentration is common in trauma patients. Hypo- and hyperglycaemia were associated with traumatic shock in our study. Hyperglycaemia was especially common in young polytraumatised patients with traumatic shock. Hypoglycaemia was more frequently observed in older patients (>65 years) with traumatic shock (Fig. 2). In our study, blood glucose concentration showed predictive value for patients with traumatic shock in addition to common vital parameters concordant with a recent investigation.13 Thus, we recommend blood glucose concentration measurement in all trauma patients to get further information on the severity of trauma in the prehospital setting.

Hyperglycaemia may be a consequence of the hypothalamic–pituitary–adrenal stress response following trauma as levels of stress hormones correlate with injury severity and shock.19,20 In animal studies, severe haemorrhage and haemorrhagic shock are among the strongest stressors leading to the highest catecholamine concentrations.20–22 High catecholamine concentrations lead to massive release of pro-inflammatoric cytokines in the liver23,24 and trigger glycogenolysis and gluconeogenesis by degradation of muscle lactate and glucoplastic amino acids25 and lipolysis.26 In severe trauma and shock, renal gluconeogenesis produces up to 40% of blood glucose by renal degradation of lactate and glycerol.27,28 In parallel, tumor necrosis factor alpha mediates a peripheral insulin resistance mainly in muscles producing glucose from muscle glycogen.29–31 In addition, the stress response has impacts on immune defence and wound healing.32–34. Furthermore, hyperglycaemia facilitates glucose uptake because of a higher concentration gradient in tissue with disturbed microcirculation and increased need especially in the brain following injury,34–36 and improves cardiac function and resistance during stress.37–39

Hypoglycaemia in trauma patients may result from antihyperglycaemic drug overdose from insulin, antidiabetic drugs or glucagon. In some cases, hypoglycaemia may even be the cause of the accident and not a consequence. Other causes of hypoglycaemia may be from shivering because of hypothermia,40,41 chronic liver disease with limited functional reserves and organ failure of liver and kidney in patients with traumatic shock.13,42–44

Up to now, blood glucose concentration measurements are not advocated as routine investigation in Prehospital Trauma Care, Advanced Trauma Care and in German guidelines for the treatment of multiple-injured patients.45 In addition to standard vital parameters, blood glucose concentrations may provide advanced information on the volume state of patients, depending on age and injury pattern. (Table 1, Figs. 2 and 3) The large number of patients treated during a 9-year observation period in a nationwide study permits reliable interpretation of study results. However, there is no colinearity between blood glucose concentrations and arterial blood gas sample results.10,11,13 Furthermore, blood glucose concentrations seem to be independent of the volume administered on-site, but may be influenced by impaired circulation.13 The results of our study underline that there is a marked relation between blood glucose concentration and outcome in patients with trauma of varying severity.5–13

Although excessive hyperglycaemia and hypoglycaemia were predictive for traumatic shock in our study, we have no information on the impact that glucose infusion has on survival in trauma patients with proven hypoglycaemia.

Limitations of this study are because of its retrospective nature. No information on laboratory examination results after hospitalisation is available, including course of the disease, confirmed diagnoses, trauma scores and outcome at hospital discharge. No information on previous illnesses, especially diabetes mellitus, was obtainable. According to the German Diabetes Report,46 the prevalence of diabetes mellitus among adults averaged about 7 to 8% with increasing prevalence depending on age. Approximately, 1500 patients in that study population may have had diabetes mellitus in addition to the known increase in insulin resistance with age.47 This could in part explain why the age-dependent increase in initial blood glucose concentration did not depend on injury severity in our study (Fig. 4). No information on chronic medication, especially antidiabetic drugs and insulin, was obtainable. Blood glucose concentration may vary individually depending on the time of drug ingestion/administration, the extent of recent oral carbohydrate intake and the individual stress response after trauma. In addition, blood glucose concentrations in traumatised patients may increase during initial care with ongoing stress response and development of traumatic shock until hospital admission, especially in polytraumatised patients. The incidence of polytraumatised patients with blood glucose concentration exceeding 10.0 mmol l−1 increased from 376/2790 (13.5%) in the prehospital population to 195/834 (23.4%) on hospital admission (P < 0.0001).10,11,13

Fig. 4

Fig. 4

The number of patients in the included and excluded study population was similar and both populations were clinically comparable. (Table 4) However, those excluded because of missing documented blood glucose concentration contained nine-fold more patients who were declared dead or did not survive resuscitation on scene (NACA 7) [220/20 177 patients (1.1%) vs. 1970/20 479 patients (9.6%), P < 0.0001] compared with the study group. Consequently, this population differed in initial vital signs, state of consciousness and initial GCS, and included more severely injured patients. (Table 4) When excluding these NACA 7 patients, the study population and the sample lacking blood glucose concentration documentation were even more comparable. Nevertheless, a biased selection of patients in both groups cannot be excluded. In more severe cases, HEMS physicians focus on vital functions and cardiorespiratory support rather than on laboratory investigations. As blood glucose concentration can provide further information on severity and prognostic outcome, we recommend that on-site blood glucose concentration measurement should become a standard investigation in trauma patients.

Table 4

Table 4

In our study, blood glucose concentration was measured before intravenous treatment was started. In patients with haemodynamic shock it may be more difficult to obtain venous blood for glucose concentration measurement. In venous blood, measured blood glucose concentration may be lower than in capillary blood,48–50 but Ramachandran et al.51 did not find significant differences between venous and capillary blood glucose concentrations in children with shock. In contrast, Pulzi Júnior et al.52 found higher blood glucose concentrations in capillary blood from patients in shock who received noradrenaline (norepinephrine) or had diminished tissue perfusion. Furthermore, we do not know about the accuracy of glucose concentration measurements in different point-of-care devices53–55 used during the study phase. However, a study testing reflectometer analysis of venous blood from venous access in prehospital emergency patients found a very high congruence of the results with laboratory analysis.56 Nevertheless, especially when glucose concentrations are extremely low or high, repeated measurements are recommended.

Owing to rather short arrival intervals of the HEMS emergency physician, cases with delayed onset of shock may have been missed. Furthermore, the need for catecholamine administration during on-site treatment of critically injured patients is not always associated with bleeding and haemorrhagic shock. Patients with severe traumatic brain injury, for instance, may have received catecholamines to maintain cerebral perfusion pressure. However, in traumatic brain injury without clinical signs of hypovolaemia deranged blood glucose concentration is associated with poor outcome too.8,9

In conclusion, blood glucose concentration measurements in addition to common vital parameters (GCS, HR, blood pressure, breathing frequency) may help identify patients at risk of traumatic shock in adult trauma patients.

Back to Top | Article Outline

Acknowledgements relating to this article

Assistance with the study: the authors wish to thank all emergency physicians and emergency medical technicians of the German HEMS of ADAC for their devoted work and for collecting these important and valuable data over years. The authors also thank Ms Beatrice Möller for her demanding work in data editing and PD Martin Dünser, MD for critical reviewing of the manuscript.

Financial support and sponsorship: none.

Conflicts of interest: none.

Presentation: none.

Back to Top | Article Outline

References

1. Bilotta F, Caramia R, Paoloni FP, et al. Safety and efficacy of intensive insulin therapy in critical neurosurgical patients. Anesthesiology 2009; 110:611–619.
2. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview. Lancet 2000; 355:773–778.
3. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycaemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke 2001; 32:2426–2432.
4. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006; 354:449–461.
5. Yendamuri S, Fulda GJ, Tinkoff GH. Admission hyperglycaemia as a prognostic indicator in trauma. J Trauma 2003; 55:33–38.
6. Bochicchio GV, Sung J, Joshi M, et al. Persistent hyperglycaemia is predictive of outcome in critically ill trauma patients. J Trauma 2005; 58:921–924.
7. Laird AM, Miller PR, Kilgo PD, et al. Relationship of early hyperglycaemia to mortality in trauma patients. J Trauma 2004; 56:1058–1062.
8. Jeremitsky E, Omert LA, Dunham CM, et al. The impact of hyperglycaemia on patients with severe brain injury. J Trauma 2005; 58:47–50.
9. Kinoshita K, Kraydieh S, Alonso O, et al. Effect of posttraumatic hyperglycaemia on contusion volume and neutrophil accumulation after moderate fluid-percussion brain injury in rats. J Neurotrauma 2002; 19:681–692.
10. Kreutziger J, Wenzel V, Kurz A, et al. Admission blood glucose is an independent predictive factor for hospital mortality in polytraumatized patients. Intensive Care Med 2009; 35:1234–1239.
11. Kreutziger J, Schlaepfer J, Wenzel V, et al. The role of admission blood glucose in outcome prediction of surviving patients with multiple injuries. J Trauma 2009; 67:704–708.
12. Vogelzang M, Nijboer JM, van der Horst IC, et al. Hyperglycaemia has a stronger relation with outcome in trauma patients than in other critically ill patients. J Trauma 2006; 60:873–877.
13. Kreutziger J, Rafetseder A, Mathis S, et al. Admission blood glucose predicts traumatic shock rather than in-hospital mortality in multiple injury patients. Injury 2015; 46:15–20.
14. Messelken M, Schlechtriemen Th. Der minimale notarztdatensatz MIND2. Notf Rettungsmed 2003; 6:189–192.
15. Hern HG, Kiefer M, Louie D, et al. D10 in the treatment of prehospital hypoglycemia: a 24 month observational cohort study. Prehosp Emerg Care 2017; 21:63–67.
16. Bilhimer MH, Treu CN, Acquisto NM. Current practice of hypoglycemia management in the ED. Am Emerg Med 2017; 35:87–91.
17. Youden WJ. Index for rating diagnostic tests. Cancer 1950; 3:32–35.
18. Brunauer A, Koköfer A, Bataar O, et al. The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients: a retrospective cohort study. Crit Care 2014; 18:719.
19. Marik PE, Bellomo R. Stress hyperglycemia: an essential survival response!. Critical Care 2013; 17:305.
20. Chernow B, Rainey TG, Lake CR. Endogenous and exogenous catecholamines in critical care medicine. Crit Care Med 1982; 10:409–416.
21. Hart BB, Stanford GG, Ziegler MG, et al. Catecholamines: study of interspecies variation. Crit Care Med 1989; 17:1203–1222.
22. Woolf PD. Endocrinology of shock. Ann Emerg Med 1986; 15:1401–1405.
23. Molina PE, Malek S, Lang CH, et al. Early organ-specific hemorrhage-induced increases in tissue cytokine content: associated neurohormonal and opioid alterations. Neuroimmunomodulation 1997; 4:28–36.
24. Shimizu T, Yu HP, Hsieh YC, et al. Flutamide attenuates pro-inflammatory cytokine production and hepatic injury following trauma-hemorrhage via estrogen receptor-related pathway. Ann Surg 2007; 245:297–304.
25. Blumberg D, Hochwald S, Burt M, et al. Tumor necrosis factor alpha stimulates gluconeogenesis from alanine in vivo. J Surg Oncol 1995; 59:220–224.
26. Verbruggen SC, Coss-Bu J, Wu M, et al. Current recommended parenteral protein intakes do not support protein synthesis in critically ill septic, insulin-resistant adolescents with tight glucose control. Crit Care Med 2011; 39:2518–2525.
27. Stumvoll M, Chintalapudi U, Perriello G, et al. Uptake and release of glucose by the human kidney. Postabsorptive rates and responses to epinephrine. J Clin Invest 1995; 96:2528–2533.
28. Meyer C, Stumvoll M, Welle S, et al. Relative importance of liver, kidney, and substrates in epinephrine-induced increased gluconeogenesis in humans. Am J Physiol Endocrinol Metab 2003; 285:E819–E826.
29. Dungan KM, Braithwaite SS, Preiser JC. Stress hyperglycaemia. Lancet 2009; 373:1798–1807.
30. Grimble RF. Inflammatory status and insulin resistance. Curr Opin Clin Nutr Metab Care 2002; 5:551–559.
31. Marette A. Mediators of cytokine-induced insulin resistance in obesity and other inflammatory settings. Curr Opin Clin Nutr Metab Care 2002; 5:377–383.
32. Lang CH, Dobrescu C. Gram-negative infection increases noninsulin-mediated glucose disposal. Endocrinology 1991; 128:645–653.
33. Meszaros K, Lang CH, Bagby GJ, et al. In vivo glucose utilization by individual tissues during nonlethal hypermetabolic sepsis. FASEB J 1988; 2:3083–3086.
34. Hamlin GP, Cernak I, Wixey JA, et al. Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats. J Neurotrauma 2001; 18:1011–1018.
35. Losser MR, Damoisel C, Payen D. Bench-to-bedside review: glucose and stress conditions in the intensive care unit. Crit Care 2010; 14:231.
36. Van Cromphaut SJ. Hyperglycaemia as part of the stress response: the underlying mechanisms. Best Pract Res Clin Anaesthesiol 2009; 23:375–386.
37. Ma G, Al-Shabrawey M, Johnson JA, et al. Protection against myocardial ischemia/reperfusion injury by short-term diabetes: enhancement of VEGF formation, capillary density, and activation of cell survival signaling. Naunyn Schmiedebergs Arch Pharmacol 2006; 373:415–427.
38. Malfitano C, Alba Loureiro TC, Rodrigues B, et al. Hyperglycaemia protects the heart after myocardial infarction: aspects of programmed cell survival and cell death. Eur J Heart Fail 2010; 12:659–667.
39. Malfitano C, de Souza Junior AL, Irigoyen MC. Impact of conditioning hyperglycemic on myocardial infarction rats: Cardiac cell survival factors. World J Cardiol 2014; 6:449–454.
40. Alfonsi P, Nourredine K, Adam F, et al. The effect of postoperative skin-surface warming on oxygen consumption and the shivering threshold. Anaesthesia 2003; 58:1228–1234.
41. Frank SM, Fleisher LA, Olson KF, et al. Multivariate determinants of early postoperative oxygen consumption in elderly patients. Effects of shivering, body temperature, and gender. Anesthesiology 1995; 83:241–249.
42. Chen JH, Michiue T, Inamori-Kawamoto O, et al. Comprehensive investigation of postmortem glucose levels in blood and body fluids with regard to the cause of death in forensic autopsy cases. Leg Med (Tokyo) 2015; 17:475–482.
43. Strapazzon G, Nardin M, Zanon P, et al. Respiratory failure and spontaneous hypoglycemia during noninvasive rewarming from 24.7°C (76.5°F) core body temperature after prolonged avalanche burial. Ann Emerg Med 2012; 60:193–196.
44. Wouters M, Posma RA, van der Weerd L, et al. Incidence, causes and consequences of early hypoglycaemia in severe trauma patients. Abstract presented at the ESICM Paris 2013
45. Deutsche Gesellschaft für Unfallchirurgie. Leitlinie Polytrauma /Schwerverletzten Behandlung. 2016. http://www.awmf.org/uploads/tx_szleitlinien/012-019l_S3_Polytrauma_Schwerverletzten-Behandlung_2016-10.pdf. [Accessed 22 February 2017]
46. Deutsche Diabetes Hilfe. Deutscher Gesundheitsbericht Diabetes 2016. http://www.diabetesde.org/system/files/documents/fileadmin/users/Patientenseite/PDFs_und_TEXTE/Infomaterial/Gesundheitsbericht_2016.pdf. [Accessed 13 November 2016]
47. Fink RI, Kolterman OG, Griffin J, et al. Mechanisms of insulin resistance in aging. J Clin Invest 1983; 71:1523–1535.
48. Holtkamp HC, Verhoef NJ, Leijnse B. The difference between the glucose concentrations in plasma and whole blood. Clin Chim Acta 1975; 59:41–49.
49. Morrison B, Fleck A. Plasma or whole blood glucose? Clin Chim Acta 1973; 45:293–297.
50. Pereira AJ, Corrêa TD, de Almeida FP, et al. Inaccuracy of venous point-of-care glucose measurements in critically ill patients: a cross-sectional study. PLoS One 2015; 10:e0129568.
51. Ramachandran B, Sethuraman R, Ravikumar KG, et al. Comparison of bedside and laboratory blood glucose estimations in critically ill children with shock. Ped Crit Care Med 2011; 12:e297–e301.
52. Pulzi Júnior SA, Assunção MS, Mazza BF, et al. Accuracy of different methods for blood glucose measurement in critically ill patients. Sao Paulo Med J 2009; 127:259–265.
53. Stiftung-Warentest. Bestechend genau. Blutzuckermessgeräte. Test 2012; 7:86–91.
54. Aslan B, Stemp J, Yip P, et al. Method precision and frequent causes of errors observed in point-of-care glucose testing: a proficiency testing program perspective. Am J Clin Pathol 2014; 142:857–863.
55. Gijzen K, Moolenaar DL, Weusten JJ, et al. Is there a suitable point-of-care glucose meter for tight glycemic control? Evaluation of one home-use and four hospital-use meters in an intensive care unit. Clin Chem Lab Med 2012; 50:1985–1992.
56. Holstein A, Kühne D, Elsing HG, et al. Practicality and accuracy of prehospital rapid venous blood glucose determination. Am J Emerg Med 2000; 18:690–694.
© 2018 European Society of Anaesthesiology