BACKGROUND:Traumatic brain injury (TBI) remains a significant cause of morbidity and mortality worldwide. Given the pivotal role of proper triage and timely management in patients with TBI, physicians are seeking a readily informative, straightforward tool for evaluating patients in the emergency department. AIM:To evaluate the association between on-admission pulse pressure (PP) and clinical outcomes, including severity of injury, complications, and mortality, among patients hospitalized with TBI. METHODS:A retrospective observational study was conducted using data from adult patients with TBI admitted to the Hamad Trauma Center from 2011 to 2021. Patients were categorized into five PP groups at presentation in the emergency department: ≤ 30 mmHg, 31-40 mmHg, 41-50 mmHg, 51-60 mmHg, and > 60 mmHg. RESULTS:A total of 5029 patients with TBI (mean age 33.1 ± 12.6 years; 87% male) were included. Low PP (PP ≤ 30) was significantly associated with younger age; higher injury severity; worse physiological parameters; and increased rates of transfusion, intubation, and acute respiratory distress syndrome (P < 0.001). Mortality was higher in the low-PP group (24%) compared with mid- and high-PP groups (5%-7%, P < 0.001). Bivariate analysis revealed that PP was positively correlated with age (r = 0.21), mean arterial pressure (r = 0.35), and Glasgow Coma Scale score (r = 0.098), and negatively correlated with shock index (r = -0.47), Injury Severity Score (r = -0.115), and blood units transfused (r = -0.18). Multivariable regression identified age, head Abbreviated Injury Scale score, PP, transfused blood units, and acute respiratory distress syndrome as independent predictors of mortality (P < 0.001). CONCLUSION:Admission PP reflects both hemodynamic stability and injury severity in patients with TBI. Low PP (≤ 30 mmHg) independently predicts higher mortality, whereas moderate PP (41-60 mmHg) is associated with optimal outcomes, suggesting this range represents a potential hemodynamic target. PP is a simple, rapid bedside adjunct marker that may aid early risk stratification and guide timely intervention in the management of TBI.
Acute limb ischemia (ALI) is a serious complication of femoral artery cannulation during peripheral veno-arterial extracorporeal membrane oxygenation (VA-ECMO), with reported incidence rates approaching 17%. Although several contributing factors have been described, the fundamental problem is reduced arterial flow distal to the cannulation site, often worsened by systemic vasoconstriction. Distal perfusion catheters (DPC) are the most widely used strategy to prevent this, but the optimal device, technique, and timing remain uncertain due to limited evidence. Early detection with near-infrared spectroscopy, along with emerging approaches such as bidirectional cannulas and artificial intelligence-based prediction tools, may improve prevention and management. This narrative review brings together current evidence on ALI in peripheral VA-ECMO and places particular emphasis on contemporary techniques for DPC placement with practical monitoring.
BACKGROUND:Intramedullary spinal cord hemorrhage, also known as hematomyelia, is an uncommon but clinically significant condition. It accounts for approximately 0.82% of all spinal hematomas, making it one of the least frequently encountered etiologies of acute myelopathy. Hematomyelia may result from a variety of causes, including vascular malformations (such as cavernomas or arteriovenous fistulas), bleeding diatheses, spinal cord tumors, trauma, or complications related to anticoagulation therapy. CASE SUMMARY:Here, we describe a patient on acenocoumarol who developed incomplete Brown-Séquard syndrome secondary to spontaneous intramedullary hemorrhage. She presented to the emergency department with a one-week history of progressively worsening headache, neck pain, and left hemithoracic pain. Prompt magnetic resonance imaging allowed diagnosis, and conservative management led to neurological stabilization. Our case underscores the need for timely diagnostic imaging in patients taking anticoagulants who present with new neurological deficits. It also highlights the diagnostic challenges and therapeutic decisions associated with this rare complication. CONCLUSION:In some cases, the cause of hematomyelia remains idiopathic. Vitamin K antagonists are widely used for the long-term prevention of thromboembolic events; hence, prompt diagnosis of potential complications is important.
BACKGROUND:Delirium is a frequent and serious complication following cardiac surgery, particularly in patients admitted to the intensive care unit (ICU), where it can negatively impact recovery and outcomes. AIM:To investigate the incidence, risk factors, and clinical consequences of delirium in post-cardiac surgery ICU patients. METHODS:A total of 202 consecutive patients admitted to the cardiac surgery ICU at the Onassis Cardiac Surgery Center were evaluated for delirium using the Confusion Assessment Method-ICU scale. RESULTS:Delirium was observed in 29.2% of the cohort and was independently associated with older age, longer total anesthesia/sedation duration, and higher EuroSCORE II. These variables showed poor-to-fair/modest discriminatory ability for delirium prediction. Patients who developed delirium experienced more frequent reintubation, higher rates of ICU-acquired weakness and hemodialysis, prolonged mechanical ventilation, and extended ICU stays. CONCLUSION:These findings underscore the multifactorial nature of postoperative delirium and suggest that older age, higher EuroSCORE II, and longer anesthesia exposure are associated with increased delirium risk. However, given the exploratory design and modest discriminatory performance of the identified variables, these findings should not be interpreted as a validated risk prediction tool and require confirmation in larger multicenter studies.
BACKGROUND:Non-compressible torso hemorrhage (NCTH) is a leading cause of preventable death in austere environments. Extended evacuation times prioritize far-forward hemorrhage control. Resuscitative endovascular balloon occlusion of the aorta (REBOA) preserves proximal perfusion, shifting from specialized centers to prehospital combat settings. AIM:To investigate the feasibility, safety, and clinical outcomes of REBOA for NCTH in combat and austere environments. METHODS:A PRISMA-ScR-guided scoping review searched five databases, with reference-list screening of included studies and key reviews, of humans receiving REBOA for NCTH in combat, prehospital, or austere environments. Two independent reviewers extracted patient characteristics, procedural parameters, and clinical outcomes. Quality was assessed via Joanna Briggs Institute tools and the Newcastle-Ottawa Scale. RESULTS:From 1138 records, 8 studies, met criteria: 35 individually reported cases and 15 eligible cases from one registry cohort, of 50. Because the registry reported aggregate data only, all denominators below refer to the 35 individually reported cases. Casualties were predominantly young men in severe hemorrhagic shock after penetrating or blast injury. Access was via the common femoral artery, percutaneous in 23 of 35 (65.7%), with the balloon in zone 1 in 31 of 35 (88.6%). Survival to transfer or discharge was 91.4% (32 of 35); crude mortality was 8.6% (3 of 35). Complications were access-site thrombosis or limb ischemia in 4 of 35 (11.4%), one balloon rupture, and one reperfusion-related acute kidney injury. CONCLUSION:REBOA has been utilized in select combat and austere casualties, demonstrating hemodynamic improvement. However, this uncontrolled evidence precludes conclusions regarding efficacy or superiority, thereby not supporting its routine clinical deployment.
Mechanical ventilation has evolved into a complex intervention that influences lung injuries, respiratory muscle function, and hemodynamic stability. Although lung-protective strategies improve outcomes in acute respiratory distress syndrome, bedside management remains limited by incomplete monitoring of key physiologic variables, including lung stress, inspiratory effort and regional ventilation. This constrains decision such as positive end-expiratory pressure titration and ventilatory assist targeting. Emerging technologies aim to address these gaps by improving physiological assessment and enabling more individualized care. Tools such as esophageal manometry, airway occlusion pressure (P0.1), diaphragm electrical activity, and electrical impedance tomography provide insight into lung mechanics, respiratory drive, and regional ventilation. Proportional modes of ventilation improve patient-synchrony, though their impact on patient-centered outcomes remains variables. Automation and artificial intelligence are increasingly applied to ventilator management, supporting wave analysis, detection of asynchrony, and prediction of weaning readiness. These tools may also assist clinical decision-making within predefined safety limit. We propose a pragmatic, clinical-directed framework integrating physiologic monitoring, proportional assist, and bounded decision support to optimize lung protection, diaphragm function, and hemodynamica stability.
Patients with advanced liver disease requiring intensive care were long considered to have limited benefit from aggressive treatment, given the high associated mortality. Over recent decades, outcomes have improved with advances in liver transplantation, critical care, and a better understanding of multiorgan failure. Acute liver failure and acute-on-chronic liver failure are now recognized as complex multisystem syndromes in which survival is determined not only by hepatic dysfunction but also by extrahepatic organ failure, systemic inflammation, and infection. Critical care hepatology has therefore evolved as a clinical discipline integrating hepatology, intensive care, and transplant medicine. Modern management requires adaptation of conventional intensive care strategies to the distinct pathophysiological features of liver failure syndromes, together with coordinated multidisciplinary care, often delivered within specialized liver intensive care units. Despite substantial progress, important challenges remain, including limitations of current prognostic models, ongoing debate surrounding transplant allocation policies, and complex decisions regarding transplant candidacy and futility. A structured approach to critical care hepatology may improve care integration and outcomes in critically ill patients with liver disease.
BACKGROUND:Acute intermittent porphyria (AIP) is the most common form of acute porphyria, a group of rare inherited disorders of heme biosynthesis. Severe attacks may be associated with life-threatening complications, including peripheral motor neuropathy, encephalopathy and seizures. Very rarely, an acute AIP attack can be complicated by rhabdomyolysis as illustrated in this case report. CASE SUMMARY:A 28-year-old female presented with severe abdominal pain and muscle weakness, which progressed to severe rhabdomyolysis and acute kidney injury requiring dialysis. The disease course was further complicated by an acute severe axonal peripheral motor neuropathy with quadriparesis and respiratory muscle weakness requiring prolonged invasive mechanical ventilation. An important clue for diagnosis was red urine without hematuria. The diagnosis was established by the finding of elevated δ-aminolevulinic acid and porphobilinogen in a random urine sample and later confirmed by genetic testing. The patient was initially treated with hemin and parenteral glucose. However, since she needed prolonged treatment, givosiran was commenced and continued after discharge. When the period between givosiran administrations was extended to two months, this led to a new (milder) attack. After 40 months of givosiran treatment and continued physical rehabilitation, the patient is ambulatory and without acute attacks. CONCLUSION:Our case illustrates that treatment with hemin and givosiran for longer than two years may be needed for neurological recovery after an AIP attack with severe motor polyneuropathy and multisystem involvement.
Sepsis remains a major cause of mortality worldwide despite advances in modern critical care. Elevated serum lactate is a key marker of metabolic dysfunction and is strongly associated with adverse outcomes of sepsis. Magnesium plays a crucial role in mitochondrial function, energy production, and cellular metabolism, and its deficiency is frequently observed in critically ill patients with reduced lactate clearance. The recent randomized controlled trial by Anbarasan et al published in World Journal of Critical Care Medicine provided an important evidence that magnesium supplementation enhance lactate clearance, reduced vasopressor requirements, and shortened both intensive care unit and hospital length of stay of septic patients. Their results are quite promising, but have several limitations. The absence of baseline magnesium measurements makes it difficult to determine whether the observed benefits are resulted from correction of hypomagnesemia or from other pharmacological effects of magnesium. Furthermore, the single-center design with relatively small sample size, and the lack of statistically significant mortality benefit limit the generalizationn of the findings. Overall, magnesium supplementation appears to be a promising, safe, and cost-effective adjunctive therapy for sepsis, large multicenter randomized trials and mechanistic studies are required before recommendation for routine clinical use.
Hemophagocytic lymphohistiocytosis (HLH) is a critical syndrome of immune dysregulation, marked by a hyperinflammatory cytokine storm and multiorgan failure. While primary forms are genetic, secondary HLH in adults is more prevalent and frequently precipitated by infections (notably viral), malignancies, or autoimmune diseases. Distinguishing secondary HLH from sepsis and multiorgan failure presents a significant clinical challenge due to overlapping clinical features, such as persistent fever and cytopenias. Diagnosis relies on clinical judgment and predictive frameworks like the HLH-2004 criteria or the HScore. Although elevated ferritin levels are a hallmark biomarker, isolated values lack sufficient specificity, necessitating a multifaceted diagnostic approach. Treatment strategies focus on controlling hyperinflammation while addressing the underlying trigger. Initial therapies often include corticosteroids, intravenous immunoglobulin, or the interleukin-1 receptor antagonist anakinra, with etoposide reserved for severe or refractory cases. Despite advances in management, mortality rates in the intensive care unit remain high, particularly when invasive organ support is required. Early recognition and multidisciplinary collaboration are essential to improve outcomes in this heterogeneous patient population. Further research is necessary to refine diagnostic cutoffs and identify personalized, phenotype-specific therapeutic interventions.
Critical care hemodynamics has long been centered on arterial pressure, cardiac output, and systemic vascular resistance. While these variables remain fundamental, organ perfusion is determined not only by arterial inflow but also by the pressure opposing venous outflow at the microcirculatory level. Emerging clinical and physiological evidence indicates that elevated venous pressure may contribute to organ dysfunction even when arterial pressure appears adequate. Effective organ perfusion reflects the balance between arterial driving pressure and venous outflow pressure, further modified by microcirculatory factors such as capillary density, flow heterogeneity, and cellular oxygen utilization, which are usually inferred at the bedside rather than directly measured. Consequently, abnormal tissue perfusion may arise from reduced arterial inflow, elevated venous pressure, microcirculatory dysfunction, or a combination of these mechanisms. In this narrative review, we present the arterial-venous perfusion gradient as a pragmatic clinical synthesis that reintegrates established venous physiology into bedside hemodynamic interpretation. The review examines the physiological determinants of venous return, the consequences of venous congestion for organ function, and the clinical conditions in which elevated venous pressure contributes to organ injury. Particular attention is given to the effects of venous congestion on renal, hepatic, splanchnic, cerebral, and right-heart function, alongside bedside tools for evaluating venous hemodynamics, including point-of-care ultrasound, venous Doppler assessment, and ultrasound-based congestion scoring. We also propose a phenotype-based bedside approach for integrating arterial pressure, forward flow, venous congestion, and tissue perfusion during shock assessment and management. Recognizing discordant hemodynamic states may help clinicians identify patients whose organ dysfunction stems from elevated venous back-pressure or persistent microcirculatory impairment, rather than from impaired arterial inflow alone.
Managing acute illness in older populations remains a major challenge because of the complex interplay between multimorbidity and reduced physiological reserve. While conventional acute severity scores (e.g., Sequential Organ Failure Assessment, Acute Physiology and Chronic Health Evaluation, and National Early Warning Score) track acute physiological derangements, they often fail to capture the biological heterogeneity seen in geriatric patients. Frailty provides a vital window into the baseline vulnerability of a patient, yet it remains underutilized in acute triage despite its established prognostic value. Current evidence demonstrates that integrating frailty measures, specifically the Clinical Frailty Scale (CFS), with existing severity scores significantly improves mortality prediction and risk stratification in emergency and critical care. This mini-review explores age-related physiological changes as well as the prognostic limitations of standard severity scores while evaluating their integration with validated frailty tools. To bridge current clinical gaps, we propose a practical 4-step clinical triage algorithm integrating a baseline "Two-Week Rule" CFS with acute severity scores via a synergistic 2 × 2 risk stratification matrix. By identifying distinct clinical phenotypes, this framework guides precise, person-centered triage, ensuring that treatment escalation and critical care interventions remain medically proportionate to an older adult's attainable functional recovery.
Healthcare systems are major contributors to global greenhouse gas emissions, with intensive care units (ICUs) among the most carbon-intensive environments due to continuous energy demand, extensive reliance on single-use medical devices, and high pharmaceutical consumption. This narrative review examines the environmental footprint of ICUs, synthesising contemporary life-cycle evidence and international case studies describing feasible and clinically safe sustainability interventions in critical care. We outline practical strategies for ICU decarbonisation, including energy-efficient infrastructure, sustainable procurement, waste reduction, digital optimisation, and re-evaluation of low-value clinical practices. Importantly, many of these interventions align with established quality-improvement principles and are associated with clinical co-benefits such as reduced iatrogenic harm, improved patient comfort, and enhanced staff wellbeing. Broader policy frameworks, including the Sustainable Development Goals and national net-zero healthcare commitments, are discussed as enabling levers for system-level adoption. Greening ICUs should therefore be viewed not as a competing priority, but as an opportunity to deliver safer, more resilient, and patient-centred critical care while advancing planetary health.
BACKGROUND:Mechanical power (MP) integrates tidal volume, airway pressures, flow, and respiratory rate into a single estimate of ventilatory energy delivery and serves as an integrative physiologic marker of ventilator-induced lung injury. Lung ultrasound score (LUS) is a bedside tool that quantifies lung aeration loss, reflecting the structural expression of lung injury in acute respiratory distress syndrome (ARDS). However, data correlating MP with LUS and clinically relevant outcomes in ARDS remain limited. AIM:To explore whether MP is associated with lung ultrasound-derived aeration loss and clinical outcomes in moderate-to-severe ARDS. METHODS:This prospective observational study enrolled adult patients with moderate-to-severe ARDS requiring invasive mechanical ventilation for more than 48 hours. MP and LUS were assessed at 0, 24, 48, and 72 hours. Their association was evaluated using Pearson correlation analysis. Associations between MP and 28-day mortality and weaning outcomes were analyzed using logistic regression and receiver operating characteristic curve analysis. Mean MP was defined as the arithmetic mean across the four time points. RESULTS:Forty-four patients were included. MP was strongly correlated with LUS at baseline (r = 0.84, 95%CI: 0.72-0.91), 24 hours (r = 0.83, 95%CI: 0.71-0.91), 48 hours (r = 0.91, 95%CI: 0.85-0.95), and 72 hours (r = 0.93, 95%CI: 0.87-0.96) (all P < 0.001). In exploratory analyses, higher mean MP was associated with increased mortality [odds ratio (OR) = 2.11 per J/minute increase, 95%CI: 1.31-3.39] and demonstrated numerically higher area under the receiver operating characteristic curve than driving pressure (0.98, 95%CI: 0.94-1.00 vs 0.91, 95%CI: 0.82-0.98). Higher mean MP was also associated with difficult (OR = 2.20, 95%CI: 1.11-4.36) and prolonged weaning (OR = 1.61, 95%CI: 1.04-2.50). CONCLUSION:MP parallels lung ultrasound-derived aeration loss in ARDS and demonstrates associations with mortality and adverse weaning, supporting its potential role as an integrative physiologic marker in individualized ventilatory management.
Sepsis remains a major cause of global mortality, yet its underlying pathogenesis is still incompletely understood. The current Sepsis-3 definition describes sepsis as a "life-threatening organ dysfunction caused by a dysregulated host response to infection", but offers no mechanistic explanation for how infection or inflammation lead to metabolic collapse and organ failure. This work proposes a unifying biochemical model in which sepsis originates as an intramitochondrial disturbance of redox homeostasis triggered by an early hypermetabolic surge in mitochondrial hydrogen peroxide. According to this framework, excess hydrogen peroxide overwhelms mitochondrial reductive buffering systems, leading to aconitase (Krebs cycle) inhibition, impaired NADH and FADH2 generation, dissipation of the proton motive force, and subsequent failure of oxidative phosphorylation. This sequence provides a coherent explanation for hallmark features of sepsis, including hyperlactatemia, metabolic acidosis, hypothermia, ATP depletion, bioenergetic failure and increased mortality. The model also accounts for interindividual variability in sepsis susceptibility through differences in mitochondrial reductive capacity and offers insight into why animal models fail to translate to humans. Additionally, toxic systemic hydrogen peroxide elevation may contribute independently to sepsis heterogeneity by oxidatively inhibiting multiple enzyme systems and inducing lymphocyte apoptosis, providing a mechanistic basis for immunosuppression and post-sepsis syndrome. Confirming a role for hydrogen peroxide in initiating and perpetuating these events positions impaired mitochondrial redox homeostasis as a central driver of sepsis pathogenesis and generates testable predictions regarding specific therapy and future research.
The molecular adsorbent recirculating system (MARS) is an extracorporeal liver support therapy used in acute liver failure, including cases related to trauma; however, evidence supporting its use in trauma-induced liver dysfunction remains limited. This scoping review aimed to systematically map the available literature on the use of MARS therapy in trauma patients and to identify knowledge gaps to guide future research. The review was conducted according to Joanna Briggs Institute methodology and reported in accordance with Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews guidelines, with a protocol prospectively registered in the Open Science Framework. Six electronic databases and two clinical trial registries were searched through December 2025, with additional backward citation tracking. Four observational studies met inclusion criteria, comprising 247 patients treated with MARS therapy, of whom only 11 had confirmed trauma-related acute liver failure. No randomized controlled trials were identified. Trauma-specific outcomes were inconsistently reported, and adverse events were not uniformly documented. Survival and liver function recovery varied across studies, and methodological heterogeneity precluded reliable assessment of clinical effectiveness or safety. Current evidence remains sparse and insufficient to support routine clinical use in trauma populations.
BACKGROUND:Early mobility in the pediatric intensive care unit (PICU) is safe and associated with improved cognitive and functional outcomes while reducing complications and hospital length of stay. Protocolized early mobility programs guide activity based on physiologic criteria and increase mobilization rates. However, critically ill children remain under-mobilized. Nurses, key agents of mobility implementation, continue to report barriers even when protocols are in place, yet the extent to which these barriers contribute to deviations from early mobility protocols remains unknown. AIM:To evaluate discrepancies between nurse-reported mobility, electronic health record documentation, and early mobility protocol expectations in the PICU. METHODS:We conducted an observational study evaluating nursing-led mobility in 101 patients admitted ≥ 3 days to a large, academic PICU. Key variables included physiologic mobility level (1 = most restrictive to 3 = most liberal), the highest level of mobility (HLM) achieved, and the number of mobilizations. Data were obtained from the electronic health record, end-of-shift nurse interview [registered nurse report (RN-report)], and compared with protocol-expected mobility using Cohen's Kappa. Firth penalized logistic regression assessed age, pediatric risk of mortality score, and pediatric cerebral performance category as predictors of discordance. RESULTS:Agreement between protocol-expected and RN-reported mobility level was moderate (53.5%; κ = 0.32) and agreement between protocol-expected and RN-reported HLM was poor (40.6%; κ = 0.20). In univariate analysis, mechanical ventilation [odds ratio (OR) = 0.34, 95% confidence interval (CI): 0.19-0.97, P = 0.016], vascular access lines (OR = 0.43, 95%CI: 0.13-0.69, P = 0.043), and sedation > 30 minutes (OR = 0.30, 95%CI: 0.13-0.69, P = 0.005) were associated with reduced odds of HLM discordance. Conversely, severe disability at baseline was associated with higher odds of having a discordant mobility level (OR = 8.33, 95%CI: 2.50-27.76, P = 0.001), and a discordant HLM (OR = 3.71, 95%CI: 1.15-12.01, P = 0.029), even after adjusting for age and illness severity. CONCLUSION:In a longstanding PICU mobility program, discordance exists between protocol-expected and RN-reported mobility. Severe baseline disability increases this discordance, highlighting the need to evaluate the fidelity of early mobility programs.
BACKGROUND:Timely administration of adrenaline during in-hospital cardiac arrest (IHCA) with non-shockable rhythms is recommended, yet delays are common when drug administration depends on physician authorisation. AIM:To evaluate whether empowering nurses to administer the first dose of adrenaline could reduce delays and improve outcomes. METHODS:In this study of prospectively collected registry data, the primary outcome of time to first dose of adrenaline in IHCA events with non-shockable rhythms (asystole/pulseless electrical activity) was compared between the pre-intervention phase (September 1, 2018 to November 26, 2019), when adrenaline administration was physician-led, and the post-intervention phase (November 27, 2019 to December 31, 2021), when nurse-led administration of adrenaline without physician order was implemented. Secondary outcomes included return of spontaneous circulation (ROSC), time to ROSC, 24-hour survival, and survival to discharge. Logistic regression analysis was performed to assess for factors associated with ROSC and whether timely adrenaline administration (defined as within 2-minutes) was independently associated with ROSC. RESULTS:Among 450 IHCA events, 162 occurred in the pre-intervention and 288 in the post- intervention period. The mean (standard deviation) age was 52.5 (16.1) years; 63.1% were male. Timely adrenaline administration improved from 46% in the pre-intervention period to 74.3% (P < 0.001) in the post-intervention period, reducing the median (interquartile range) time to first dose from 4 (1-6) minutes to 2 (0-3) minutes (P < 0.001). Although this did not improve ROSC rates, pre-post intervention (56.8% vs 58.3%, P = 0.74), ROSC was achieved faster (P < 0.001) in the post-intervention period when compared with the pre-intervention period. Combining pre- and post-intervention data, timely adrenaline administration when compared with delayed administration was associated with shorter time to ROSC (P = 0.006) but did not improve survival. On multivariate logistic regression analysis, shorter time to Cardiac Arrest and Resuscitation Team arrival and identification of a reversible cause were independently associated with ROSC, whereas the time to first dose of adrenaline was not. CONCLUSION:Nurse-led early adrenaline administration during IHCA significantly reduced treatment delays and enhanced resuscitation efficiency, though it did not translate to reduced hospital mortality. This model is feasible in low- and middle-income settings and underscores the value of system-level empowerment to improve IHCA care.
