Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening cerebrovascular event associated with profound neurological and systemic disturbances. Among these, alterations in hypothalamic-pituitary function, water-electrolyte balance, and glucose metabolism are frequently observed but remain difficult to interpret, particularly in the setting of critical illness. Many endocrine abnormalities detected during the acute phase reflect adaptive neuroendocrine stress responses rather than true hormonal failure, whereas persistent deficiencies may emerge during recovery and contribute to long-term morbidity. This narrative review summarizes current evidence on endocrine disturbances after aSAH, emphasizing the distinction between acute neurocritical care physiology and chronic endocrine sequelae. We discuss the hypothalamic-pituitary-adrenal (HPA), thyroid, somatotropic, and gonadal axes, as well as dysnatremia and stress hyperglycemia, addressing their prevalence, pathophysiological background, diagnostic challenges, and therapeutic considerations in both intensive care unit (ICU) and post-acute settings. Available data remain heterogeneous and largely observational. Current evidence does not support routine hormonal intervention during the acute phase except in clearly defined endocrine emergencies. Careful interpretation of biochemical findings and structured endocrine follow-up after neurological stabilization appear essential for identifying clinically meaningful long-term dysfunction.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high early mortality and long-term disability. Prognostic assessment relies mainly on neurological grading scales, which may incompletely capture the systemic metabolic response to acute brain injury. Non-thyroidal illness syndrome (NTIS), particularly low triiodothyronine syndrome (LT3S), is common in critical illness, but its prognostic relevance in aSAH remains unclear. Objectives: To evaluate the prognostic impact of early thyroid hormone alterations on 30-day mortality and early clinical outcomes including delayed cerebral ischemia (DCI) in patients with aSAH, with particular emphasis on the magnitude of triiodothyronine (T3) deficiency. Methods: We conducted a retrospective single-center observational cohort study of 157 consecutive adult patients admitted with confirmed aSAH between 2014 and 2025. Serum free triiodothyronine (fT3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH) were measured within 72 h of admission. Hormone values were normalized to contemporaneous reference intervals to generate continuous reference-adjusted metrics (FT3_level, TSH_level). Associations with 30-day in-hospital mortality were analyzed using logistic regression and Cox proportional hazards models adjusted for admission variables including age, sex, APACHE II score, World Federation of Neurosurgical Societies grade, Fisher grade, and treatment modality. Results: Binary LT3S classification was frequent but not independently associated with 30-day mortality. In contrast, lower FT3_level values were significantly associated with increased mortality and shorter survival time. In logistic regression analyses, each 0.1 increase in FT3_level was associated with an 18% lower odds of death (adjusted OR 0.82, 95% CI 0.69-0.97). This association persisted after adjustment for established clinical severity measures and was concordant with time-to-event analyses. FT3_level was not correlated with TSH_level, consistent with NTIS. Endovascular coiling was associated with more pronounced peripheral fT3 deficiency (p < 0.05) but was not independently associated with mortality. FT3_level was not independently associated with early neurological status or functional outcome at hospital discharge. Conclusions: Lower FT3_level values were independently associated with higher 30-day mortality, indicating that early peripheral T3 reduction reflects clinically relevant metabolic vulnerability in aSAH.

Background: Hyperglycemia after aneurysmal subarachnoid hemorrhage (aSAH) is associated with poor outcome, but admission glucose may not reflect dynamic metabolic stress during neurocritical care. Unlike previous studies focused primarily on admission measurements, we evaluated longitudinal glycemic trajectories and repeated glucose-potassium ratio (GPR) assessment across multiple observation windows in relation to clinical outcomes after aSAH. Methods: This retrospective single-center cohort study included 199 consecutive adults with aSAH treated between 2014 and 2025. Serial glucose and potassium measurements obtained during intensive care unit (ICU) stay were used to calculate admission values, longitudinal means across predefined observation windows, glycemic variability, hyperglycemia burden, and GPR. Primary outcomes were 30-day mortality and poor functional outcome at discharge (modified Rankin Scale ≥ 3). Secondary outcomes included delayed cerebral ischemia (DCI), delayed neurological deterioration (DND), transcranial Doppler (TCD) vasospasm, neurological deficit at ICU discharge, and length of stay. Results: Thirty-day mortality occurred in 35 patients (17.6%). Longitudinal metabolic markers demonstrated stronger associations with outcomes than admission values. Mean 30-day GPR was independently associated with mortality (OR 2.56, 95% CI 1.66-4.16; p < 0.001) and poor functional outcome (OR 2.90, 95% CI 1.80-5.03; p < 0.001). Hyperglycemia burden was associated with mortality (OR 1.10 per additional hyperglycemic day, 95% CI 1.02-1.20; p = 0.020) and poor functional outcome (OR 1.39, 95% CI 1.19-1.71; p < 0.001). Early GPR during the early brain injury period was associated with DCI (OR 1.40, 95% CI 1.01-1.93; p = 0.043), whereas 30-day GPR was associated with DND (OR 1.47, 95% CI 1.08-2.07; p = 0.019). ICU-specific GPR was associated with neurological deficit at ICU discharge (OR 2.06, 95% CI 1.29-3.50; p = 0.004), but not with TCD-defined vasospasm. Addition of GPR improved mortality prediction compared with the clinical model alone (AUC 0.86 vs. 0.77; p = 0.002). Conclusions: Longitudinal metabolic dysregulation after aSAH is strongly associated with mortality and neurological outcomes. Persistent hyperglycemia and repeated GPR assessment provide prognostic information beyond admission glucose, with early abnormalities associated with DCI and sustained disturbances linked to mortality and disability.

Background/Objectives: Healthcare-associated infections (HAIs) frequently complicate aneurysmal subarachnoid hemorrhage (aSAH) requiring neurocritical care. We assessed their incidence, timing, microbiology, associated factors, and outcomes. Methods: This retrospective, single-center cohort study included 106 consecutive adults with acute aSAH admitted to a neurocritical care unit during 2019–2024. Time to first HAI was analyzed using cause-specific Cox regression with competing risks; to limit immortal-time bias, HAI was modeled as a time-dependent exposure in outcome analyses. Results: HAIs occurred in 47 patients (44.3%; 95% CI 35.2–53.8); median onset was 10 days (IQR 8–12). Seventy-six episodes were recorded; site-specific figures denote affected patients, with no recurrent same-site episodes: ventilator-associated pneumonia, 30 (28.3%); catheter-associated urinary tract infection, 24 (22.6%); cerebrospinal fluid infections, 13 (12.3%); and central line-associated bloodstream infection, 9 (8.5%). Acinetobacter baumannii predominated, accounting for all extensively drug-resistant isolates. High World Federation of Neurosurgical Societies grade was associated with the first HAI (HR 4.168; 95% CI 2.072–8.384), as was higher modified Fisher grade in sensitivity analysis (HR 2.886; 95% CI 1.237–6.735). Time-dependent HAI was associated with a lower hazard of live discharge (HR 0.295; 95% CI 0.164–0.529) but not with in-hospital mortality (HR 1.178; 95% CI 0.478–2.902). Its association with the discharge Glasgow Outcome Scale (GOS) was threshold-dependent (GOS ≤ 1: OR 0.715, 95% CI 0.264–1.933; GOS ≤ 3: OR 7.939, 95% CI 2.580–24.436). Conclusions: HAIs affected nearly half of this cohort. Greater initial severity was associated with a higher hazard of first HAI; HAI, in turn, was associated with prolonged hospitalization and unfavorable functional outcome, but not with mortality. These associations are observational, not causal. Surveillance, timely diagnosis, and infection prevention remain integral to neurocritical care in aSAH.

AIMS:Landiolol is an ultrashort-acting, highly cardio-selective beta1-adrenergic receptor blocker used for short-term control of tachyarrhythmias. While its real-world use has been described in Japan, data from European clinical practice are lacking. This study aimed to collect real-world data on landiolol use, effectiveness, and safety across diverse clinical settings in Europe. METHODS AND RESULTS:This multicentre, observational study included adult patients with supraventricular arrhythmias treated with landiolol. Patient characteristics, drug utilization patterns, efficacy, and safety were assessed. In total, 450 patients were enrolled and 449 were analysed (median age: 72 years, IQR 63-78) from 17 sites across 8 European countries. Most patients (73.1%) received landiolol for atrial fibrillation. The median (IQR) duration of infusion was 8.9 (2.3-34.0) h, with starting, minimum, and maximum doses of 5.3 (2.5-10.0), 4.0 (1.7-10), and 10.0 (6.0-30.0) µg/kg/min, respectively. Heart rate (HR) control, defined as HR ≤110 b.p.m. or a reduction of >20% from baseline, was achieved in 74.2% of patients within 4 h after treatment discontinuation, with 36.9% of arrhythmia patients restoring sinus rhythm. Blood pressure (BP) remained stable throughout treatment. A total of 123 adverse events and 113 major adverse cardiac events were reported, none of which were related to landiolol. CONCLUSION:In European clinical practice, landiolol dosing adhered to product information recommendations. Landiolol was effective in controlling HR, with minimal impact on BP. The treatment was well tolerated, and no new safety signals were identified. These findings support the efficacy and safety of landiolol across diverse clinical settings in Europe.

S100 calcium-binding protein B (S100B) has been proposed as a biomarker of brain injury after aneurysmal subarachnoid hemorrhage (aSAH), although the clinical utility of serial measurements remains uncertain. This prospective observational study investigated whether longitudinal serum and cerebrospinal fluid (CSF) S100B concentrations are associated with delayed cerebral ischemia (DCI), inflammatory activation, and neurological outcome. Twenty-six consecutive patients with aSAH underwent serial serum and CSF S100B measurements throughout hospitalization. Associations between S100B concentrations, DCI, disease severity, inflammatory biomarkers, and 3-month neurological outcome were analyzed. Admission serum S100B concentrations were significantly higher in patients who subsequently developed DCI (152.6 vs. 21.0 ng/L, p = 0.012) and correlated with disease severity and inflammatory biomarkers. Admission serum S100B was associated with DCI and showed good discriminative ability for DCI (AUC 0.79) and unfavorable 3-month outcome (AUC 0.86). Longitudinal analyses showed persistently elevated serum S100B concentrations in patients who developed DCI, while serum and CSF S100B exhibited similar temporal profiles throughout the observation period Serial serum S100B measurements appear to reflect the temporal evolution of secondary brain injury after aSAH and may provide complementary biological information alongside established clinical assessment.

This study aimed to evaluate a molecular diagnostic system for the rapid identification of pathogens and determination of their antimicrobial susceptibility. By comparing its performance with standard microbiological methods, the study assessed whether the new system could shorten the time to optimal antimicrobial therapy and reliably complement, or potentially replace, conventional diagnostics. A retrospective study was conducted to evaluate the performance of the Accelerate Pheno system (ACC), a platform for rapid microorganism identification (ID) and antimicrobial susceptibility testing (AST), in comparison with standard-of-care (SOC) laboratory methods for positive blood cultures. The study included adult patients diagnosed with sepsis admitted to the Intensive Care Unit (ICU) who had a positive blood culture result. The total turnaround time (from ICU blood sample collection to the availability of both ID and AST results) was significantly reduced from approximately 3 days with SOC methods to 29 h with the ACC system (p < 0.001). In 67

BACKGROUND:Perioperative beta blockade lowers heart rate and decreases the risk of myocardial infarction but increases the risk of hypotension, death, and stroke. Ivabradine, a selective heart rate-lowering agent, may prevent prognostically important myocardial injury after noncardiac surgery (MINS) without causing hemodynamic instability. METHODS:In this multicenter, double-blind, placebo-controlled trial, we assigned patients ≥45 years of age with, or at risk of, atherosclerotic disease undergoing noncardiac surgery to receive ivabradine (5 mg orally twice daily for up to 7 days, starting 1 hour before surgery) or placebo. The primary outcome was MINS within 30 days from randomization. RESULTS:All of the 2101 participants who underwent randomization were included in the intention-to-treat population. MINS occurred in 178 of 1050 patients (17.0%) in the ivabradine group and in 159 of 1051 patients (15.1%) in the placebo group (relative risk, 1.12 [95% CI, 0.92 to 1.37]; P=0.25). Enrollment was halted at the prespecified interim analysis because of a conditional power of 6%, below the futility boundary of 20%. The intraoperative mean heart rate was lower in the ivabradine group by 3.2 beats per minute than in the placebo group (95% CI, -4.07 to -2.36), with no difference in intraoperative mean arterial pressure. CONCLUSIONS:Among patients undergoing noncardiac surgery, ivabradine did not reduce the occurrence of MINS. REGISTRATION:URL: https://www.clinicaltrials.gov; Unique identifier: NCT05279651.

Despite advances in treatment, hemorrhage remains one of the leading causes of early death in trauma. Rapid, personalized treatment of coagulopathy in this population should therefore be a priority. The introduction of viscoelastic hemostatic assays may improve transfusion strategies. This prospective observational study aimed to compare the efficacy of a ROTEM-guided hemostatic treatment protocol for trauma patients with a historical control group who had received conventional coagulation testing. The study included adults with multiple trauma requiring transfusion (≥ 1 unit of RBC within 12 h). The aim was to compare transfusion requirements in the operating room, on the 1st and 2nd ICU days, the rate of massive transfusion, and the overall outcome. The data obtained were stored in a database and analyzed using Statistica™ 13.3 (Stat Soft Polska). A p-value < 0.05 was considered significant. Study was registered retrospectively at researchregistry.com (RR10995). A total of 78 patients were compared. The number of RBC units transfused in the OR and on the 1st ICU day decreased significantly after implementation of the ROTEM treatment protocol (p = 0.01, p = 0.04). Fewer patients in the study group required RBC transfusion on the 1st and 2nd ICU days (p = 0.01, p = 0.003), as well as the number of patients requiring FFP transfusion in all examined periods of time (p = 0.02, p = 0.006, p = 0.01). While FFP use per patient in the OR and on the 1st ICU day was lower, it was not statistically significant. Fibrinogen substitution in the OR remained similar, but more patients from the study group received it on the 1st ICU day (13 vs. 5, p = 0.04). The need for other blood products and coagulation factors remained unchanged. MT incidence decreased significantly in the first 24 h (p = 0.02), while 30-day mortality remained unchanged. The introduction of the ROTEM- guided hemostatic treatment protocol in trauma resulted in a changes in transfusion requirements and a reduction in the incidence of MT. ROTEM can be a useful clinical tool in the rapid and targeted management of bleeding trauma patients. Researchregistry.com (RR10995).

Myocardial injury is a major cause of death after noncardiac surgery and is associated with long-term cardiovascular outcomes. Perioperative tachycardia increases this risk. Although perioperative beta blockers prevent myocardial injury, they increase the risk of death and stroke, which analyses suggest is due to a significant increase in hypotension. Ivabradine, a selective heart rate-lowering drug, may offer a safer alternative. The primary objective of the PREVENT-MINS trial is to determine whether perioperative administration of ivabradine is superior to placebo for the prevention of myocardial injury after noncardiac surgery (MINS) in patients with or at risk of atherosclerotic disease having noncardiac surgery. The PREVENT-MINS trial is a multicentre, parallel-group, blinded, placebo-controlled trial conducted in 26 hospitals in Poland. It will enroll 2500 patients aged ≥ 45 years undergoing noncardiac surgery with at least one risk factor for myocardial injury. Participants will be randomized in a 1:1 ratio to receive ivabradine 5 mg orally twice daily for 7 days starting 1 h before surgery or placebo. The primary outcome is MINS within 30 days after randomization; independent experts will adjudicate this outcome. Secondary outcomes include vascular complications, mortality, haemodynamics, and quality of life at 30 days. Additional tertiary and 1-year outcomes will assess long-term cardiovascular and surgical complications. Analyses will follow an intention-to-treat approach. For the primary outcome, a chi-squared test will be conducted, with results presented as unadjusted relative risk (RR) accompanied by 95

Background: Hemolysis during sepsis may be driven by patient-specific factors, including the intensity of the inflammatory response and the etiology of infection, as well as treatment-related factors, such as the use of extracorporeal life-support devices. Methods: We evaluated the incidence of hemolysis—reflected by decreased plasma levels of haptoglobin and hemopexin—in a cohort of septic patients with acute respiratory failure (n = 50) admitted to the intensive care unit (ICU). Results: Hemolysis was observed in 60% of patients. Its incidence was significantly higher among those with septic shock (86%) and those receiving extracorporeal membrane oxygenation (ECMO) therapy (81%). While continuous renal replacement therapy (CRRT) alone did not increase the incidence of hemolysis, its combination with ECMO was associated with hemolysis in 100% of those treated. Logistic regression analysis identified low haptoglobin levels (odds ratio [OR] 27.1), advanced age (OR 1.2), and stage 3 acute kidney injury (OR 22.2) as significant predictors of mortality. Conclusions: These findings highlight the clinical relevance of monitoring hemolysis in septic patients. Given the routine availability of haptoglobin and hemopexin assays in most hospital laboratories, these biomarkers offer practical and accessible tools for the detection and monitoring of hemolysis in critically ill patients.

BACKGROUND:Cardiogenic shock (CS) remains a complex syndrome with alarmingly high mortality despite treatment advances. AIMS:This study aimed to describe the experience of the management of patients with CS according to a standardized multidisciplinary team-based protocols. MATERIAL AND METHODS:This is a retrospective analysis of patients with a diagnosis of CS admitted to a large academic tertiary hospital between 2021 and 2023. Patients were managed according to the CS protocols developed at our institution by a dedicated multidisciplinary shock team. We report patients' clinical characteristics, mechanical circulatory support (MCS) utilization, and in-hospital outcomes. RESULTS:Over the three-year period, we identified 257 patients (median age: 69 years, 69% males). In this cohort, acute coronary syndrome was the most common cause of CS (55% of patients), 17% presented with out-of-hospital cardiac arrest, 18% experienced in-hospital cardiac arrest, and 20% of patients were transferred from remote centers. An MCS system was used in 39% of all patients. In-hospital mortality was 62% with significant improvement in consecutive 1-year periods: 75% in 2021 vs. 69% in 2022 vs. 44% in 2023, respectively, P = 0.004 for trend. This improvement was particularly evident in the group supported with MCS: all-cause mortality: 75% in 2021, 50% in 2022, and 29% in 2023 (P = 0.005). The use of MCS was a significant independent predictor of improved survival in 2022 and 2023 (odds ratio, 0.38; confidence interval, 0.149-0.996; P = 0.04). CONCLUSIONS:Our results suggest that a standardized multidisciplinary approach incorporating the availability of MCS therapies and heart transplantation may be associated with improved outcomes in patients with CS.

Background: This study compares organ dysfunction, treatment strategies, and unfavorable outcome rates between pregnant and nonpregnant women admitted to the ICU with severe COVID-19, highlighting the increased susceptibility of pregnant women to respiratory infections due to physiological changes. Methods: A retrospective, age-matched study was conducted at a referral center specializing in critical care for pregnant women. Data from 14 pregnant/postpartum and 11 nonpregnant women were analyzed at ICU admission and on days 3, 5, and 7. Results: Acute respiratory distress syndrome was diagnosed in 100% of the pregnant/postpartum group and 64% of the nonpregnant group (p = 0.026). Inflammatory parameters were similar between groups, except for lower ferritin levels in the pregnant/postpartum group compared to the nonpregnant (120 vs. 568 µg/L at admission and 90 vs. 616 µg/L on day 3). Creatinine, lactate, and lactate dehydrogenase levels were significantly lower in the pregnant/postpartum group. A reduction in the SOFA score was observed over time in the pregnant/postpartum group (from 7.0 to 4.0 points, p = 0.009), while no change was noticed in the nonpregnant group (from 3.0 to 2.5 points, p = 0.181). Unfavorable outcome rates were similar, with two patients from each group succumbing to the disease (p = 0.604). Conclusions: The findings suggest that pregnancy does not increase the risk of unfavorable outcomes among women with severe COVID-19 receiving ICU treatment. However, additional studies with larger sample sizes are needed to validate these observations.

Abstract Funding Acknowledgements None. Background The mortality in cardiogenic shock (CS) remains high but the report mostly concerns CS in the course of acute myocardial syndrome (ACS). There is limited data about non- ischaemic CS. Purpose The aim of this study was to analyse the clinical characteristics, treatments and outcomes in patients with non-ACS CS in comparison to ischemic aetiology CS. Methods 80 patients with an average age of 62 ± 13 years (81 % male) with CS admitted in 2021 and 2022 to tertiary hospital were divided into 2 subgroups: non-acute myocardial infarction cardiogenic shock (non-ACS-CS) consisted of 16 individuals (20%) and CS in the course of ACS (ACS-CS) consisted of 64 (80%) individuals. The main cause of CS in non-ACS group was worsening of previously diagnosed heart failure 11 (14%). Results Patients from non-ACS group were younger 52±16 vs. 65±11 years old, p=0.005. There were no differences in baseline heart rate 90 [72;100] vs. 95 [80;107] beats per minute and mean artery pressure 89 [73;97] vs. 80 [70;97] mmHg for non-ACS-CS vs. ACS-CS, respectively all p&gt;0.05. Patients from non-ACS-CS group had lower baseline troponin level 0.29 [0.04;0.96] vs. 7.05 [0.69;57.4] ng/mL, p=0.003, white blood cell count 11 [9;13] vs. 15 [10;19] × 109/L; p=0.035, procalcitonin 0.06 [0.05;0.28] vs. 0.69 [0.10;2,48] ng/mL, p=0.001 and higher pH 7.4 [7.3;7.5] vs. 7.2 [7.0;7.4], p=0.012 in blood gas analysis when compared with ACS-CS. There were no significant differences in the severity of the shock according to Society for Cardiovascular Angiography and Interventions (SCAI) SHOCK classification among the groups: from C: 1 (6%) vs. 6 (10%), D: 11 (69%) vs. 27 (42%), E: 4 (25%) vs. 31 (48%), respectively for non-ACS vs. ACS-shock. The non-ACS-CS was more often treated with V-A ECMO 10 (63%) vs. 20 (32%) in ACS-CS, p=0.024. The overall number of in-hospital deaths was 57 (71%). The non-ACS-CS group had significantly lower in-hospital mortality 8 (50%) compared to the ACS-CS patients 49 (77%), p=0.034. Conclusion Patients experiencing non-ACS-CS were younger, have lower levels of inflammatory markers and a higher pH in blood gas analysis at admission. Despite more favourable biomarker profile non-ACS-CS group was treated more aggressively and had significantly lower in-hospital mortality rates when compared with patients facing ACS-CS, which indicates the need to look at CS differently depending on its aetiology.

Coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB) is associated with the transient activation of a systemic inflammatory response. Fibronectin (FN), an endogenous inflammatory mediator, is a key component of the extracellular matrix. This study aimed to detect changes in cellular and plasma FN levels, as well as its potential fragmentation or FN-fibrin complex formation, in 40 patients undergoing CABG with CPB. Our results indicate that CPB was associated with changes in the levels of cellular and plasma FN and with intensified FN fragmentation. Moreover, FN-fibrin complexes were detected in all patients, indicating activation of the coagulation process during CPB. In a multivariate regression analysis, a history of arterial hypertension and CPB duration influenced plasma FN levels at 6 h (beta = -0.458, p = 0.001; -0.375, p = 0.008, respectively) and 12 h (beta = -0.293, p = 0.026; -0.554, p = 0.000) after surgery. Alterations in FN concentration, intensified FN degradation, and the presence of FN-fibrin complexes after surgery may suggest that these changes are related to the remodelling of the extracellular matrix resulting from cardiac surgery and the associated repair processes. The results indicate that FN has clinical potential as a marker of repair processes.