Viral and bacterial infections are the main cause of COPD exacerbations, accounting for 25% and 26% of cases respectively. To date no conclusive data are available on the risk of COPD exacerbations triggered by SARS-CoV-2. The present study was primarily aimed to identify the risk of acute respiratory failure (ARF) requiring non-invasive respiratory support up to Continuous Positive Airway Pressure (C-PAP) and Non-Invasive Ventilation (NIV) in patients affected by SARS-CoV-2 triggered COPD exacerbation compared to patients with COPD exacerbations without SARS-CoV-2 infection. Major secondary endpoints included the overall risk of ARF and its stratification according to severity and consequent respiratory support needed. Mortality in the SARS-CoV-2 cohort was also compared to the control group. 238 COPD patients admitted to hospital due to an acute exacerbation of COPD were consecutively enrolled: 120 patients (50.4%) tested positive for SARS-CoV-2 infection at nasopharyngeal swab, while 118 (49.6%) were negative. No significant difference could be demonstrated in the risk of ARF between SARS-CoV-2 and control groups (Relative Risk (RR) 0.89 (p = 0.303), 95% Confidence Interval (CI): 0.73 – 1.06). However, the risk of ARF with the need of ventilatory support up to C-PAP was significantly higher in the SARS-CoV-2 group (RR 4.42 (p = 0.009), 95% CI 1.37 – 14.35).nOn the contrary, the risk of ARF needing NIV was 39% lower in the SARS-CoV-2 group (RR 0.61 (p = 0.003), 95% CI 0.44 – 0.84). This result combined with blood gas analysis values reflected a predominant hypoxemic ARF among SARS-CoV-2, differently from hypercapnic ARF in the control group. A significantly higher mortality rate was detected among SARS-CoV-2 patients at Kaplan-Meier survival analysis (1 year mortality: 33.33% in SARS-CoV-2 group vs 3.06% in controls, p <0.0001). Hospitalization was longer in SARS-CoV-2 group than controls (12 days, IQR 7.5–24.5 vs 9 days, IQR 7–14.25, p < 0.01). In conclusion, our study demonstrated that SARS-CoV-2 infection can be considered a potent trigger of COPD exacerbation, able to induce severe hypoxic ARF, which significantly increased the risk of needing positive pressure respiratory support. SARS-CoV-2 profoundly impacted on the mortality, meanwhile prolonging the length of hospital stay. Screening for the presence of viral triggers, particularly of SARS-CoV-2, in case of acute exacerbation of COPD is key, to influence clinical outcomes treatment approach and long-term survival.

IMPACT OF SARS-COV-2 RESPIRATORY INFECTION ON CLINICAL OUTCOMES AND NEED FOR NON-INVASIVE VENTILATORY SUPPORT IN ACUTE EXACERBATIONS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A SINGLE-CENTER, PROSPECTIVE, OBSERVATIONAL STUDY

TIRELLI, CLAUDIO
2026

Abstract

Viral and bacterial infections are the main cause of COPD exacerbations, accounting for 25% and 26% of cases respectively. To date no conclusive data are available on the risk of COPD exacerbations triggered by SARS-CoV-2. The present study was primarily aimed to identify the risk of acute respiratory failure (ARF) requiring non-invasive respiratory support up to Continuous Positive Airway Pressure (C-PAP) and Non-Invasive Ventilation (NIV) in patients affected by SARS-CoV-2 triggered COPD exacerbation compared to patients with COPD exacerbations without SARS-CoV-2 infection. Major secondary endpoints included the overall risk of ARF and its stratification according to severity and consequent respiratory support needed. Mortality in the SARS-CoV-2 cohort was also compared to the control group. 238 COPD patients admitted to hospital due to an acute exacerbation of COPD were consecutively enrolled: 120 patients (50.4%) tested positive for SARS-CoV-2 infection at nasopharyngeal swab, while 118 (49.6%) were negative. No significant difference could be demonstrated in the risk of ARF between SARS-CoV-2 and control groups (Relative Risk (RR) 0.89 (p = 0.303), 95% Confidence Interval (CI): 0.73 – 1.06). However, the risk of ARF with the need of ventilatory support up to C-PAP was significantly higher in the SARS-CoV-2 group (RR 4.42 (p = 0.009), 95% CI 1.37 – 14.35).nOn the contrary, the risk of ARF needing NIV was 39% lower in the SARS-CoV-2 group (RR 0.61 (p = 0.003), 95% CI 0.44 – 0.84). This result combined with blood gas analysis values reflected a predominant hypoxemic ARF among SARS-CoV-2, differently from hypercapnic ARF in the control group. A significantly higher mortality rate was detected among SARS-CoV-2 patients at Kaplan-Meier survival analysis (1 year mortality: 33.33% in SARS-CoV-2 group vs 3.06% in controls, p <0.0001). Hospitalization was longer in SARS-CoV-2 group than controls (12 days, IQR 7.5–24.5 vs 9 days, IQR 7–14.25, p < 0.01). In conclusion, our study demonstrated that SARS-CoV-2 infection can be considered a potent trigger of COPD exacerbation, able to induce severe hypoxic ARF, which significantly increased the risk of needing positive pressure respiratory support. SARS-CoV-2 profoundly impacted on the mortality, meanwhile prolonging the length of hospital stay. Screening for the presence of viral triggers, particularly of SARS-CoV-2, in case of acute exacerbation of COPD is key, to influence clinical outcomes treatment approach and long-term survival.
20-mar-2026
Inglese
MONDONI, MICHELE
DEL FABBRO, MASSIMO
Università degli Studi di Milano
73
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14242/362025
Il codice NBN di questa tesi è URN:NBN:IT:UNIMI-362025