# Urine Metanephrine Concentration Can Early and Accurately Predict Etiology of Acute Respiratory Failure in Critically Ill Patients with Subarachnoid Hemorrhage: A Prospective Single-Center Pilot Study

## TL;DR

Urine metanephrine levels can help determine the cause of breathing failure in patients with brain hemorrhage, guiding better treatment decisions.

## Contribution

Urine metanephrine is proposed as an early diagnostic marker for cardiogenic vs non-cardiogenic acute respiratory failure in subarachnoid hemorrhage patients.

## Key findings

- Higher urine metanephrine levels were associated with cardiogenic acute respiratory failure in SAH patients.
- Urine metanephrine correlated strongly with oxygenation index and lactate levels in early ICU stages.
- Baseline metanephrine concentration accurately predicted ARF phenotype with high AUC.

## Abstract

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.