Background/Objectives: Sepsis is characterized by a dysregulated host response to infection, where immune-inflammatory and thrombo-inflammation drive organ dysfunction. Early recognition of high-risk patients is essential. In addition, the increasing prevalence of multidrug-resistant (MDR) pathogens complicates therapeutic strategies, as delays in appropriate antimicrobial therapy are strongly associated with poor outcomes. Methods: We conducted a retrospective, single-center cohort study including 120 critically ill patients fulfilling Sepsis-3 criteria. Demographic, clinical, and laboratory data were collected at intensive care unit (ICU) admission, 48 h, and 72 h. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were calculated from complete blood counts. At the same time, the Carmeli score was used as a surrogate for MDR infection risk. Prognostic accuracy was assessed using ROC curve analysis and multivariable logistic regression. Results: Persistently elevated NLR at 72 h and a delayed decline in platelet counts were associated with higher mortality. NLR at 72 h showed good predictive accuracy (AUC = 0.765; 95% CI 0.668–0.863), and the combination of APACHE II and NLR improved prognostic performance (AUC = 0.827). Importantly, the Carmeli score, reflecting MDR infection risk, was an independent predictor of outcome, linking antimicrobial resistance risk with sepsis prognosis. Conclusions: Dynamic immune-inflammatory biomarkers (NLR, platelets), when integrated with MDR risk assessment through the Carmeli score, provide a simple and cost-effective strategy for early prognostic stratification in sepsis. This combined approach may help facilitate early therapeutic decisions and patient care triage.

Background/Objectives: The clinical forms of coronavirus disease 2019 (COVID-19) vary widely in severity, ranging from asymptomatic or moderate cases to severe pneumonia that can lead to acute respiratory failure, acute respiratory distress syndrome, multiple organ dysfunction syndrome, and death. Our main objective was to determine the prevalence of bacterial and fungal secondary infections in an intensive care unit (ICU). Secondary objectives included analyzing the impact of these infections on mortality and medical resource utilization, as well as assessing antimicrobial resistance in this context. Methods: We conducted a retrospective cohort study that included critically ill severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) patients treated in an ICU and analyzed the prevalence of co-infections and superinfections. Results: A multivariate analysis of mortality found that the presence of superinfections increased the odds of death by more than 15-fold, while the Sequential Organ Failure Assessment (SOFA) score and C-reactive protein (adjusted for confounders) increased the odds of mortality by 51% and 13%, respectively. The antibiotic resistance profile of microorganisms indicated a high prevalence of resistant strains. Carbapenems, glycopeptides, and oxazolidinones were the most frequently used classes of antibiotics. Among patients, 27.9% received a single antibiotic, 47.5% received two from different classes, and 24.4% were treated with three or more. Conclusions: The incidence and spectrum of bacterial and fungal superinfections are higher in critically ill ICU patients, leading to worse outcomes in COVID-19 cases. Multidrug-resistant pathogens present significant challenges for ICU and public health settings. Early screening, accurate diagnosis, and minimal use of invasive devices are essential to reduce risks and improve patient outcomes.

Background: Acinetobacter spp., particularly A. baumannii, is a major intensive care unit (ICU) pathogen frequently associated with carbapenem non-susceptibility and delayed initiation of receipt of therapy. Methods: We conducted a single-center retrospective ICU cohort study in Romania (January 2019–December 2024) of adults with clinical cultures positive for Acinetobacter spp. (first isolate per patient). Susceptibility was interpreted per EUCAST. We assessed species distribution, carbapenem non-susceptibility, receipt of at least one in vitro active empiric agent, time to active therapy (TTAT, from index culture collection), early inflammatory biomarkers [neutrophile-to-lymphocyte ratio (NLR) and C-reactive protein (CRP)], and 30-day mortality. Predictors of mortality were evaluated using multivariable logistic regression and receiver operating characteristic (ROC) analysis. Results: A total of 234 episodes were included; A. baumannii accounted for 87.6% (205/234). Carbapenem non-susceptibility among Acinetobacter spp. isolates was 89.3% (209/234). Empiric antibiotics were initiated within 24 h in 95.7% of patients (224/234), yet only 49.6% (116/234) received at least one empiric agent later confirmed to be active. TTAT was 6 days (IQR 4–7), and active therapy within 72 h occurred in 8.5% (20/234). Thirty-day mortality was 73.1% (171/234) and did not differ between carbapenem non-susceptible (EUCAST I + R) and carbapenem-susceptible (EUCAST S) A. baumannii episodes (73.2% vs. 72.0%, p = 1.00). In multivariable analysis, age was independently associated with mortality (OR 1.36 per 10-year increase, 95% CI 1.04–1.90), with acceptable model discrimination (area under the curve = 0.74). Early NLR and CRP did not differ between carbapenem non-susceptible and carbapenem-susceptible A. baumannii episodes. Conclusions: In this ICU cohort, A. baumannii was the predominant species, and carbapenem non-susceptibility was highly prevalent. Despite early empiric therapy, receipt of at least one in vitro active agent was often delayed, and early inflammatory biomarkers had limited discriminatory value. These findings support locally tailored empiric strategies informed by local epidemiology and reinforce the need for improved diagnostics and stewardship interventions in high-burden ICU settings.

Carpal tunnel syndrome (CTS) is the most common compressive mononeuropathy. In patients with type 2 diabetes mellitus (T2DM), chronic hyperglycemia, microangiopathy, and systemic inflammation increase the vulnerability of peripheral nerves to compression. This study aimed to assess the relationship between CTS severity and clinical, metabolic, inflammatory, and electrophysiological parameters in patients with T2DM. A cross-sectional study was conducted from June 2023 to June 2024, involving patients diagnosed with T2DM. Electrophysiological assessment of the upper and lower limbs was performed using a four-channel electromyography apparatus. Clinical and anthropometric data and laboratory parameters were obtained, as well as the results of nerve conduction studies (NCS). One hundred and twenty-three patients with T2DM were included in the study. The prevalence of moderate-to-severe forms of CTS was 43.9%, and bilateral involvement was present in 21.95% of patients. Patients with moderate-to-severe CTS had significantly higher hemoglobin A1c (HbA1c) (p = 0.004), glycemia (p < 0.001), and Triglyceride–Glucose Index (p = 0.018) compared with those without CTS/with mild forms. The number of monocytes was significantly higher in the group with moderate-to-severe forms (p = 0.012), suggesting a chronic inflammatory state. In the logistic regression analysis, hemoglobin HbA1c emerged as an independent predictor of CTS severity, with each 1% increase associated with approximately a 60% higher risk of moderate/severe CTS. NCS analysis showed significant correlations between median nerve parameters and those of the lower-limb peripheral nerves, particularly the tibial and sural nerves, suggesting an association with generalized diabetic peripheral neuropathy. Professional activity was significantly associated with moderate-to-severe CTS (OR = 3.5). CTS is a common complication in patients with T2DM and is associated with worse glycemic control, insulin resistance, systemic inflammation, and peripheral neuropathic damage.

Sarcopenia has a high prevalence among patients admitted to intensive care units, and it is associated with adverse outcomes and increased mortality. Its prevalence increases with advancing age; however, it is not a pathology specific to the geriatric population. The etiology is multifactorial, including metabolic, nutritional, inflammatory, endocrine and neuromuscular factors. In critically ill patients, the progression of sarcopenia is rapid. Diagnosis in the intensive care unit is most commonly based on objective assessment of muscle quantity and quality using computed tomography (CT), magnetic resonance imaging (MRI), dual-energy X-ray absorptiometry (DEXA), ultrasonography (US) and bioelectrical impedance analysis (BIA). The therapeutic management is multidisciplinary, individualized and multimodal, including nutritional support, physiotherapy, electrotherapy and pharmacological interventions. Early diagnosis and appropriate therapeutic management may significantly influence patient prognosis.

Vitamin D deficiency is extremely common in intensive care, and it is associated with poor prognosis. Beyond its classical role in calcium homeostasis, vitamin D influences the immune response, endothelial function and muscle integrity. Observational studies have shown consistent correlations between vitamin D deficiency and increased mortality, sepsis or prolonged duration of mechanical ventilation. However, randomized clinical trials (VITdAL-ICU, VIOLET) have not confirmed robust benefits on mortality, but only possible favorable effects in subgroups with severe deficiency. Recent meta-analyses remain heterogeneous, with evidence of low certainty and statistical fragility. In critical conditions, hepatic and renal dysfunction, systemic inflammation and hypoalbuminemia affect the conversion and transport of vitamin D, suggesting the limits of supplementation with classical vitamin D alone (D₂/‌D₃), without the use of active metabolites. Correction of vitamin D deficiency remains warranted as part of general care in the ICU, but supplementation cannot yet be recommended as standard therapy to reduce mortality. Future research needs to clarify the dose, the optimal form (cholecalciferol, calcifediol, or calcitriol), route of administration, and timing of administration.