Matthias Manfred Deininger

Purpose: Stress-induced hyperglycemia is a frequent metabolic response to polytrauma. To date, studies primarily analyzed its association with mortality; however, its effect on functional outcomes remain unclear. This study investigated the association between sustained hyperglycemia across metabolic phases and functional outcomes in polytraumatized ICU patients. Methods: This retrospective single-center observational study included 176 adult ICU polytrauma patients admitted to a German level 1 university trauma center (2013–2023). Blood glucose was quantified using admission values, time-weighted averages, variability and time-unified hyperglycemic rate (TUHyperR; cutoffs 140/160/180 mg/dL) across the early “ebb” (≤ 48 h) and later “flow” (> 48 h) metabolic phases. Primary endpoint was functional outcome using Glasgow outcome scale (GOS; unfavorable GOS ≤ 3). Temporal trends were analyzed using mixed-effects models, and associations with outcomes were assessed using multivariable logistic regression. Results: Patients with unfavorable outcomes (39.2%) had higher cumulative hyperglycemic exposure throughout their ICU stay. Hyperglycemia was consistently higher during ebb than flow phase. Moderate hyperglycemia during the ebb phase was also in multivariable analysis most discriminative: TUHyperR>140 mg/dL (OR 1.015, 95%-CI [1.004–1.025], p = 0.008) and TUHyperR>160 mg/dL (OR 1.016, 95%-CI [1.003–1.030], p = 0.017) were independently associated with unfavorable outcomes, whereas TUHyperR>180 mg/dL, admission, mean glucose values as well as glycemic variability were not. Conclusion: Prolonged moderate hyperglycemia within the first 48 h after polytrauma was independently associated with poor functional outcome at hospital discharge. These exploratory findings support the value of cumulative glycemic exposure as a potential risk marker and highlight the need for prospective studies to determine whether time-based glucose metrics might improve risk stratification and guide metabolic management in polytrauma ICU patients.

Background: Traumatic brain injury (TBI) is a major cause of trauma-related deaths. Systemic glucose and lactate levels reflect secondary metabolic derangements over time; however, most prognostic models rely on admission values. This study compared static and longitudinal indices of glucose, lactate, and their ratio in relation to ICU mortality. Methods: This retrospective single-center study analyzed 479 non-diabetic adult patients with TBI admitted to a German university ICU (2013–2023). After 1:2 severity-balanced, outcome-stratified propensity score matching, 229 patients (150 survivors, 79 non-survivors) were included. Indices comprised admission values, means, clearance, time-weighted averages, variability, and dysglycemic burden. Outcome was ICU mortality, assessed using regression, mixed-effects modeling, and ROC analysis. Results: Longitudinal indices showed stronger associations. Time-weighted average lactate was the best independent predictor (OR 14.70, 95% CI [5.41–39.98], p < 0.001, AUC 0.73). Time-weighted average glucose–lactate ratio also independently predicted ICU mortality (OR 0.75, 95% CI [0.66–0.86], p < 0.001). Non-survivors exhibited persistently higher glucose, lactate and lower ratios, with lactate significantly elevated on all first ten ICU days (all p < 0.05). Admission values, clearance and variability were not predictive after adjustment. Conclusions: In critically ill non-diabetic patients with TBI, longitudinal time-weighted average lactate significantly outperformed admission values and glucose metrics for predicting ICU mortality in a severity-balanced cohort; the glucose–lactate ratio was associated but did not surpass lactate. These findings underscore the importance of longitudinal monitoring and support prioritizing lactate in multiparametric prognostic model to account for secondary injuries. Prospective validation is warranted to confirm external validity and assess therapeutic implications.

^* für die Arbeitsgruppe „Einarbeitung in der Intensivmedizin“ der Jungen DIVI Article published online: 14 January 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

Delayed cerebral ischemia (DCI) is a severe complication following aneurysmal subarachnoid hemorrhage (aSAH), linked to poor functional outcomes and prolonged intensive care unit (ICU) stays. Timely DCI diagnosis is crucial but remains challenging. Dysregulated blood glucose, commonly observed after aSAH, may impair the constant glucose supply that is vital for brain function, potentially contributing to DCI. This study aimed to assess whether glucose indices could help identify at-risk patients and improve DCI detection. This retrospective, single-center observational study examined 151 aSAH patients between 2016 and 2019. Additionally, 70 of these (46.4%) developed DCI and 81 did not (no-DCI). To determine the value of glycemic indices for DCI, they were analyzed separately in patients in the period before (pre-DCI) and after DCI (post-DCI). The time-weighted average glucose (TWAG, p = 0.024), mean blood glucose (p = 0.033), and novel time-unified dysglycemic rate (TUDR140, calculated as the ratio of dysglycemic to total periods within a glucose target range of 70–140 mg/dL, p = 0.042), showed significantly higher values in the pre-DCI period of the DCI group than in the no-DCI group. In the time-series analysis, significant increases in TWAG and TUDR140 were observed at the DCI onset. In conclusion, DCI patients showed elevated blood glucose levels before and a further increase at the DCI onset. Prospective studies are needed to confirm these findings, as this retrospective, single-center study cannot completely exclude confounders and limitations. In the future blood glucose indices might become valuable parameters in multiparametric models to identify patients at risk and detect DCI onset earlier.

About one in three critically ill patients requires mechanical ventilation (MV). Prolonged MV, however, results in diaphragmatic weakness, which itself is associated with delayed weaning and increased mortality. Inducing active diaphragmatic contraction via electrical phrenic nerve stimulation (PNS) not only provides the potential to reduce diaphragmatic muscular atrophy but also generates physiological-like ventilation and therefore offers a promising alternative to MV. Reasons why PNS is not yet used in critical care medicine are high procedural invasiveness, insufficient evidence, and lack of side-by-side comparison to MV. This study aims to establish a minimal-invasive percutaneous, bilateral electrode placement approach for sole PNS breathing and thereby enable, for the first time, a breath-by-breath comparison to MV. Six juvenile German Landrace pigs received general anesthesia and orotracheal intubation. Following the novel ultrasound-guided, landmark-based, 4-step approach, two echogenic needles per phrenic nerve were successfully placed. Stimulation effectiveness was evaluated measuring tidal volume, diaphragmatic thickening and tomographic electrical impedance in a breath-by-breath comparison to MV. Following sufficient bilateral phrenic nerve stimulation in all pigs, PNS breaths showed a 2.2-fold increase in diaphragmatic thickening. It induced tidal volumes in the lung-protective range by negative pressure inspiration and improved dorso-caudal regional ventilation in contrast to MV. Our study demonstrated the feasibility of a novel ultrasound-guided, percutaneous phrenic nerve stimulation approach, which generated sufficient tidal volumes and showed more resemblance to physiological breathing than MV in a breath-by-breath comparison.

Mechanical ventilation is essential in intensive care treatment but leads to diaphragmatic atrophy, which in turn contributes to prolonged weaning and increased mortality. One approach to prevent diaphragmatic atrophy while achieving pulmonary ventilation is electrical stimulation of the phrenic nerve. To automize phrenic nerve stimulation resulting in lung protective tidal volumes with lowest possible currents, mathematical models are required. Nerve stimulation models are often complex, so many parameters have to be identified prior to implementation. This paper presents a novel, simplified approach to model phrenic nerve excitation to obtain an individualized patient model using a few data points. The latter is based on the idea that nerve fibers are excited when the electric field exceeds a threshold. The effect of the geometry parameter on the model output was analyzed, and the model was validated with measurement data from a pig trial (RMSE in between 0.44 × 10⁻² and 1.64 × 10⁻² for parameterized models). The modeled phrenic nerve excitation behaved similarly to the measured tidal volumes, and thus could be used to develop automated phrenic nerve stimulation systems for lung protective ventilation.