MedElevator
Войти в исследования Enfermedades infecciosas y microbiologia clinica (English ed.) · 2026
Factors associated with high-flow therapy failure in COVID-19-related acute hypoxemic respiratory failure: A prospective single-centre cohort study.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Marín Toni, Galdeano Marina, Chirinos Roxana, Hernández Agnés, Roca Esther, Martín Adriana, Garcia Andrea, Mendiluce Leire, Fernández Carmen, Tebé Cristian, Garcia-Olivé Ignasi, Paredes Roger, Rosell Antoni, Aldás Irene
Аннотация
INTRODUCTION: The optimal selection of non-invasive respiratory support for patients with COVID-19-related acute hypoxemic respiratory failure remains uncertain. High-flow therapy (HFT) is frequently used as initial support, but early identification of patients at risk of escalation is clinically relevant. We evaluated clinical and laboratory variables associated with escalation from HFT to non-invasive positive-pressure ventilation (NPPV).
METHODS: We conducted a prospective single-centre cohort study including 139 consecutive patients initiated on HFT in a respiratory intermediate care unit. The primary outcome was HFT failure, defined as escalation from HFT to NPPV. Time to HFT failure was analysed from HFT initiation using cause-specific Cox regression; successful HFT withdrawal without escalation was treated as censoring. A parsimonious adjusted model included age, time from symptom onset to HFT initiation, baseline PaO2/FiO2 ratio, and lactate dehydrogenase (LDH). Logistic regression and a supplementary bicarbonate model were used as sensitivity analyses.
RESULTS: Seventy-two of 139 patients (51.8%) required escalation to NPPV. Seventeen escalations were recorded on day 0 and 44 of 72 failures (61.1%) occurred by day 1. In the adjusted Cox model, higher LDH levels were associated with an increased hazard of escalation (adjusted hazard ratio [aHR] per 100U/L, 1.33; 95% confidence interval [CI], 1.06-1.66; p=0.014), whereas higher baseline PaO2/FiO2 ratios were associated with a lower hazard (aHR per 25mmHg, 0.78; 95% CI, 0.67-0.90; p=0.001). A longer interval from symptom onset to HFT initiation was also associated with a lower hazard of escalation (aHR per day, 0.93; 95% CI, 0.86-0.99; p=0.033). In a supplementary sensitivity model, higher arterial bicarbonate levels were associated with a lower hazard of escalation (aHR per 3mmol/L, 0.81; 95% CI, 0.66-0.99; p=0.039).
CONCLUSION: In this prospective single-centre cohort, LDH and baseline PaO2/FiO2 were associated with escalation from HFT to NPPV after adjustment. Arterial bicarbonate showed a supportive exploratory signal in sensitivity analysis. These findings require external validation before incorporation into treatment-selection algorithms.
METHODS: We conducted a prospective single-centre cohort study including 139 consecutive patients initiated on HFT in a respiratory intermediate care unit. The primary outcome was HFT failure, defined as escalation from HFT to NPPV. Time to HFT failure was analysed from HFT initiation using cause-specific Cox regression; successful HFT withdrawal without escalation was treated as censoring. A parsimonious adjusted model included age, time from symptom onset to HFT initiation, baseline PaO2/FiO2 ratio, and lactate dehydrogenase (LDH). Logistic regression and a supplementary bicarbonate model were used as sensitivity analyses.
RESULTS: Seventy-two of 139 patients (51.8%) required escalation to NPPV. Seventeen escalations were recorded on day 0 and 44 of 72 failures (61.1%) occurred by day 1. In the adjusted Cox model, higher LDH levels were associated with an increased hazard of escalation (adjusted hazard ratio [aHR] per 100U/L, 1.33; 95% confidence interval [CI], 1.06-1.66; p=0.014), whereas higher baseline PaO2/FiO2 ratios were associated with a lower hazard (aHR per 25mmHg, 0.78; 95% CI, 0.67-0.90; p=0.001). A longer interval from symptom onset to HFT initiation was also associated with a lower hazard of escalation (aHR per day, 0.93; 95% CI, 0.86-0.99; p=0.033). In a supplementary sensitivity model, higher arterial bicarbonate levels were associated with a lower hazard of escalation (aHR per 3mmol/L, 0.81; 95% CI, 0.66-0.99; p=0.039).
CONCLUSION: In this prospective single-centre cohort, LDH and baseline PaO2/FiO2 were associated with escalation from HFT to NPPV after adjustment. Arterial bicarbonate showed a supportive exploratory signal in sensitivity analysis. These findings require external validation before incorporation into treatment-selection algorithms.