Background and Objectives: Coronavirus disease 2019 (COVID-19) triggers a dysregulated host response that may culminate in refractory hypoxaemic shock. Whether veno-venous ECMO modifies the inflammatory cascade more effectively in COVID-19 than in other septic states, and how it compares with conventional ventilatory support for COVID-19, remains uncertain. We compared three groups: COVID-19 patients supported with ECMO (COVID-ECMO, n = 25), non-COVID-19 septic shock patients on ECMO (SEPSIS-ECMO, n = 19) and critically ill COVID-19 patients managed without ECMO (COVID-CONV, n = 74). Methods: This retrospective study (January 2018–January 2025) extracted demographic, laboratory and clinical data at baseline, 48 h and 72 h. The primary end-point was the 72 h change in SOFA score (ΔSOFA). The secondary end-points included the evolution of interleukin-6 (IL-6), C-reactive protein (CRP), D-dimer and ferritin; haemodynamic variables; and 28 day mortality. A post hoc inverse-probability-of-treatment weighting (IPTW) sensitivity analysis adjusted for between-group severity imbalances. Results: Baseline APACHE II differed significantly (29.5 ± 5.8 COVID-ECMO, 27.4 ± 6.1 SEPSIS-ECMO, 18.2 ± 4.9 COVID-CONV; p < 0.001). At 48 h, IL-6 fell by 51.8% in COVID-ECMO (−1 116 ± 473 pg mL⁻¹) versus 32.4% in SEPSIS-ECMO and 18.7% in COVID-CONV (p < 0.001). The ΔSOFA values at 72 h were −4.6 ± 2.2, −3.1 ± 2.5 and −1.4 ± 1.9, respectively (p < 0.001). ECMO groups achieved larger mean arterial pressure rises (+16.8 and +14.2 mmHg) and greater norepinephrine reduction than COVID-CONV. The twenty-eight-day mortality was 36.0% (COVID-ECMO), 42.1% (SEPSIS-ECMO) and 39.2% (COVID-CONV) (p = 0.88). Across all patients, IL-6 clearance correlated with ΔSOFA (ρ = 0.48, p < 0.001) and with vasopressor-free days (ρ = 0.37, p = 0.002). Conclusions: ECMO, regardless of aetiology, accelerates inflammatory-marker decline and organ failure recovery compared with conventional COVID-19 management, but survival advantage remains elusive. COVID-19 appears to display a steeper cytokine-response curve to ECMO than bacterial sepsis, suggesting phenotype-specific benefits that merit confirmation in prospective trials.

Background and Objectives: The optimal effluent dose of continuous haemofiltration (CHF) when coupled to veno-venous extracorporeal membrane oxygenation (ECMO) for septic shock is unknown. We examined our 44-patient ECMO registry, contrasting a smaller high-dose subgroup (HDHF ≥ 45 mL kg⁻¹ h⁻¹; n = 13) with a larger standard-dose subgroup (SDHF 25–35 mL kg⁻¹ h⁻¹; n = 31). The primary endpoint was 72 h change in SOFA score (ΔSOFA). Materials and Methods: All adults cannulated for ECMO (January 2018–January 2025) and started on CHF within 2 h were eligible. Variables were abstracted at baseline, 24 h and 72 h. Continuous data were analysed by Student’s t or Mann–Whitney tests, categorical data by χ²/Fisher; and paired changes by Wilcoxon. Two-sided p < 0.05 signified significance. Results: Baseline characteristics were comparable (age 49.1 ± 15.2 vs. 50.4 ± 14.9 y; APACHE II 28.4 ± 5.3 vs. 27.5 ± 5.9). Median effluent reached 48.1 mL kg⁻¹ h⁻¹ (IQR 46.6–49.7) in HDHF and 29.7 mL kg⁻¹ h⁻¹ (27.5–31.9) in SDHF (p < 0.001). IL-6 fell by 1 061 ± 487 pg mL⁻¹ with HDHF versus 637 ± 425 pg mL⁻¹ with SDHF (p = 0.003). Mean arterial pressure rose 19.2 ± 8.1 vs. 12.7 ± 8.3 mmHg (p = 0.03), and norepinephrine declined 0.46 ± 0.22 vs. 0.30 ± 0.19 µg kg⁻¹ min⁻¹ (p = 0.04). ΔSOFA at 72 h was –4.4 ± 2.1 with HDHF and –2.6 ± 2.3 with SDHF (p = 0.01). Twenty-eight-day mortality was 38.5% (5/13) versus 45.2% (14/31), p = 0.64. Effluent dose correlated with ΔIL-6 (ρ = 0.53, p < 0.001) and ΔSOFA (ρ = 0.45, p = 0.003). Conclusions: In this ECMO cohort, high-dose haemofiltration, although applied in only 13 patients, appeared to achieve greater cytokine clearance, faster haemodynamic recovery and deeper early organ-failure improvement than standard dosing, without excess bleeding. Survival advantage was not demonstrable, underscoring the need for prospective randomised confirmation of the dose–response signal.

Acute limb ischemia is a limb-threatening condition that is associated with a high degree of mortality and morbidity, with the latter related to acute kidney injury and rhabdomyolysis that can rapidly lead to multiple organ failure. The aim of this study was to assess the efficacy and safety of catheter-directed arterial thrombolysis in acute lower limb ischemia in the Department of Vascular Surgery, Timișoara, Romania. A total of 158 patients (114 males—72.15% and 44 females—27.85%) with symptoms of acute lower limb ischemia were admitted and treated with catheter-directed arterial thrombolysis following our protocol. The amputation-free survival rate at 1 month after the thrombolysis was 82.3%, and at 6 months it was 77.85%. The performance of additional procedures to obtain distal perfusion was predictive of an improved outcome at 30 days. The estimated survival rate at 6 months was 84.81% (SE 0.02). The mean survival time was 158.74 days. We recommend the usage of a thrombolytic regimen in patients with a life expectancy of more than 6 months, even in Rutherford stage IIb patients, if there is no major impairment in the sensorial and mobility function of the ischemic leg.

Background and Objectives: Severe COVID-19 frequently fulfills Sepsis-3 criteria and is characterized by thrombo-inflammation and endothelial injury. We evaluated whether a bedside endothelial activation index (EAI = D-dimer/fibrinogen) identifies biologically distinct phenotypes and relates to interleukin-6 (IL-6) response after therapeutic plasma exchange (TPE), and whether baseline IL-6 predicts a ≥50% IL-6 reduction. Methods: Retrospective single-center ICU cohort of adults with SARS-CoV-2 infection, sepsis-related organ dysfunction, and ≥1 TPE session (n = 51). Patients were stratified by median EAI (low vs. high). Outcomes included peri-procedural biomarker/physiology changes (post–baseline), IL-6 responder status (≥50% reduction), correlations with IL-6 reduction (%), and multivariable predictors of response. Results: Compared with low EAI (n = 25), high EAI (n = 26) had higher baseline D-dimer (6.2 vs. 2.2 µg/mL) and lower fibrinogen (2.9 vs. 7.1 g/L) (both p < 0.001). Low EAI showed larger CRP decreases (ΔCRP −84.0 vs. −2.3 mg/L; p = 0.001) and larger fibrinogen falls (Δ −3.1 vs. −0.4 g/L; p < 0.001), while high EAI had larger D-dimer decreases (Δ −2.5 vs. −0.6 µg/mL; p = 0.004) and a modest SOFA improvement (Δ −0.3 vs. +0.1; p = 0.026). IL-6 responders (n = 20) had higher baseline IL-6 than non-responders (365.2 vs. 47.1 pg/mL; p < 0.001). Baseline IL-6 independently predicted response (per doubling: OR 1.94, 95% CI 1.27–2.95; p = 0.002), while age reduced odds (OR 0.91/year, 95% CI 0.84–0.99; p = 0.032). IL-6 reduction correlated with ΔCRP (ρ = −0.41; p = 0.003) and ΔPaO₂/FiO₂ (ρ = 0.37; p = 0.01). Conclusions: EAI stratifies distinct thrombo-inflammatory patterns around TPE, while baseline IL-6 is the dominant predictor of achieving large IL-6 reductions. To emphasize the novelty and clarify the study objective, this exploratory analysis used a phenotype-stratified framework to test whether a simple bedside endothelial activation index could enrich biological response assessment to adjunctive TPE. The prespecified primary outcome was achievement of a ≥50% IL-6 reduction after completion of the TPE course; secondary outcomes included peri-procedural biomarker, oxygenation, SOFA, and ICU endpoints.

Introduction: Therapeutic plasma exchange (TPE) is increasingly used as an adjunctive intervention in severe, hyperinflammatory critical illness, including COVID-19, yet clinical guidance remains syndromic and evidence is heterogeneous. We present an integrated, interpretable machine-learning framework designed to support protocolizable TPE decision-making by identifying biochemical phenotypes associated with short-horizon laboratory response to TPE. Our dataset consists of real-world intensive care unit cases and captures the treatment heterogeneity and operational constraints that a workable institutional protocol must accommodate, being well-suited as a “protocol seed” for iterative validation. Methods: We jointly analyze a COVID-19 cohort and a non-COVID comparator cohort receiving TPE. Three decision trees were constructed to represent: (1) global biochemical improvement, (2) strict improvement dependent on key inflammatory/coagulation markers, and (3) early interleukin-6 (IL-6) response. The models revealed distinct favorable phenotypes—particularly patients with IL-6 > 86 pg/mL, lactate dehydrogenase (LDH) >346 U/L, lymphopenia, and fibrinogen ≤ 8.3 g/L. Apriori analysis further identified high-confidence patterns linking high values of IL-6 and LDH with TPE responsiveness. We constructed a unified four-tier clinical algorithm for candidate stratification. Results: The resulting logic aligns with how TPE has been applied in practice in published severe COVID-19 series and trials, where candidate selection typically targets cytokine release syndrome-like phenotypes, organ dysfunction, and hyperinflammatory biomarker profiles. We further contextualize these findings against American Society for Apheresis guidance and COVID-era operational considerations, demonstrating convergence while adding quantitative biomarker thresholds. Conclusion: These findings support two complementary perspectives of benefit: (i) an algorithmic framework that provides transparent, protocol-ready guidelines, and (ii) a phenotype-based clinical approach consistent with observed post-TPE marker changes in severe COVID-19 cases. Larger multicenter validation is warranted; however, the present work provides a practical foundation for protocol construction and auditable decision support in settings already performing TPE.

Background/Objectives: This exploratory study described interleukin-6 (IL-6) and vasopressor-dependency trajectories during continuous renal replacement therapy (CRRT) with oXiris, CytoSorb, or standard haemofilters in sepsis-associated acute kidney injury, and their lagged and prognostic associations. Methods: This retrospective single-centre cohort included 48 adults receiving standard CRRT (n = 22), oXiris (n = 21), or CytoSorb (n = 5; analysed descriptively), assessed at baseline and 12, 24, and 48 h; devices were clinician-selected, implying confounding by indication. The vasopressor dependency index (VDI) was vasoactive-inotropic score/mean arterial pressure. Results: Twenty-eight-day survival was 13.6%, 33.3%, and 40.0%, respectively (p = 0.240). The unadjusted 24 h VDI decline was largest with CytoSorb (p = 0.018), but this group had much higher baseline IL-6 and VDI, and the contrast was attenuated and non-significant after baseline adjustment. No lagged association was detectable between IL-6 and subsequent VDI (β = 0.04, 95% confidence interval (CI) −0.04 to 0.13) or VDI and subsequent IL-6 (β = −0.05, 95% CI −0.20 to 0.09). In a 24 h landmark analysis, favourable haemodynamic status was associated with survival (odds ratio 7.57, 95% CI 1.75–32.69) without improving optimism-corrected discrimination beyond baseline severity and age (area under the curve 0.882). Conclusions: These hypothesis-generating findings do not establish a benefit of any device; early haemodynamic response criteria warrant prospective evaluation.