Urine metanephrine measured on day 1 after SAH predicted ARF phenotype with high accuracy (AUROC 0.93), with cardiogenic ARF patients showing median urine metanephrine of 249 ng/mL vs 63.5 ng/mL in non-cardiogenic patients.
Prospective Observational (n=18)
No
Does urine metanephrine concentration accurately predict the etiology of acute respiratory failure in critically ill patients with subarachnoid hemorrhage?
Urine metanephrine concentration is a promising early biomarker for differentiating cardiogenic from non-cardiogenic acute respiratory failure in critically ill patients with subarachnoid hemorrhage.
Effect estimate: AUROC 0.93 (95% CI 95% CI 0.786–1.000)
Absolute Event Rate: 249% vs 63.5%
p-value: p=0.008
Background: Subarachnoid hemorrhage (SAH) can cause remote organ failure through complex systemic reactions. Acute respiratory failure (ARF) in the course of SAH may have a diverse etiology, including cardiogenic origin. The aim of the study was to evaluate the utility of urine metanephrine measurement in identifying the ARF phenotype in patients with SAH. Methods: A prospective single-center study was conducted between January 2022 and February 2023. The study included consecutive adult patients admitted to the Intensive Care Unit (ICU) within 24 h of SAH diagnosis and requiring mechanical ventilation due to ARF within the first 48 h of stay. Demographic and clinical data were collected. Metanephrine (MET) was determined in 24-h urine collection. The inflammatory profile was assessed by measuring serum levels of interleukin-6 (IL-6), CRP, and PCT. Cardiogenic ARF phenotype was diagnosed when concomitant elevation of hsTpI, CK-MB, and NT-proBNP was observed upon admission. Results: The study group consisted of 18 patients. The cardiogenic etiology group (n = 4) was characterized by higher MET concentrations (249 vs. 63.5 ng/mL; p = 0.007) and a lower oxygenation index (190 vs. 296 mmHg; p < 0.05) on admission. In the non-cardiogenic etiology group (n = 14), higher levels of IL-6 were found (34 vs. 8.3 pg/mL; p = 0.013). MET significantly correlated with the oxygenation index (R = −1.0; p < 0.001) on day 1 and with lactate levels on days 2 and 3 of stay (R = 1.0; p < 0.001). Baseline MET concentration accurately predicted the ARF phenotype (AUC 0.93; 95% CI 0.786–1.000, p = 0.008). Conclusions: Urine metanephrine levels show potential in differentiating the etiology of ARF and correlate with severity markers in critically ill SAH patients at an early stage. These preliminary results highlight the importance of a targeted approach to ARF diagnostics after SAH, which could support appropriate therapeutic decisions, although further validation in larger cohorts is required.
Zachura et al. (Mon,) conducted a prospective observational in Critically ill adult patients with subarachnoid hemorrhage admitted to ICU within 24 hours of diagnosis requiring mechanical ventilation due to acute respiratory failure within first 48 hours, excluding those with prior severe lung or heart disease and extracorporeal support (n=18). Measurement of urine metanephrine concentration vs. Non-cardiogenic ARF phenotype patients without elevated myocardial injury markers was evaluated on Differentiation of acute respiratory failure (ARF) phenotype (cardiogenic vs non-cardiogenic) based on urine metanephrine level at ICU admission (AUROC 0.93, 95% CI 95% CI 0.786–1.000, p=0.008). Urine metanephrine measured on day 1 after SAH predicted ARF phenotype with high accuracy (AUROC 0.93), with cardiogenic ARF patients showing median urine metanephrine of 249 ng/mL vs 63.5 ng/mL in non-cardiogenic patients.
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