To the Editor:
The acute respiratory distress syndrome (ARDS) was originally described by Ashbaugh et al in 1967 as a syndrome of acute onset of tachypnea, hypoxemia, and loss of lung compliance.1 In 2015, the Pediatric Acute Lung Injury Consensus Conference introduced a definition of ARDS specific for pediatric patients (PARDS) that includes invasive and noninvasive mechanical ventilation and uses invasive and noninvasive markers of oxygenation to diagnose and classify the severity of PARDS.2
Dr Baird astutely observes that in pediatric patients with respiratory failure because of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease 2019 [COVID-19]), the incidence of PARDS is significantly higher than previously reported for patients with respiratory syncytial virus, human metapneumovirus, human rhinovirus/enterovirus infections, and pandemic 2009 H1N1 influenza A. Baird points out further that the incidence of severe PARDS because of SARS-CoV-2 infection appears similar to that reported for human metapneumovirus, pandemic 2009 H1N1 influenza A, and respiratory syncytial virus.
The increased incidence of PARDS correlates with an increased intubation rate in COVID-19 that we observed compared with other respiratory viruses. We pointed out that this may be due, at least in part, to an early recommendation to limit use of noninvasive ventilation because of the risk of aerosolization of the virus. Thus, limited use of noninvasive positive pressure ventilation may have led to higher rates of endotracheal intubation and invasive mechanical ventilation, thus, explaining, to some extent, the higher rate of PARDS seen with COVID-19 compared with that observed with other viral infections.
Whether or not pulmonary infection with SARS-CoV-2 results in a unique or different pathophysiologic state than other respiratory viruses is yet to be elucidated. Relatively well preserved pulmonary compliance in COVID-19 ARDS has been reported by others3 , 4 and observed by us. This high compliance type of ARDS may represent a very early stage or possible differences in the pathophysiology of ARDS in COVID-19 compared with that caused by other viral illnesses.
In addition, a substantial proportion of patients with PARDS in our study met criteria for severe sepsis and required vasoactive support, thus, indicating increased severity of illness. The presence of sepsis may be an additional risk factor for the development of PARDS and need for mechanical ventilation in this group, perhaps explaining the higher rate of PARDS in this cohort.
It is also worthy of note, though not explanatory, that the average age in our study cohort of patients who developed ARDS was 14 years, significantly higher than the average ages in the other virus studies noted by Baird, which were approximately 4-5 years.5
Although COVID-19 appears to confer a higher risk of PARDS in pediatric patients, mortality seems to be lower than that reported in the literature for PARDS of various etiologies; 28-day mortality in our cohort was 2.9%, whereas 90-day mortality in patients with PARDS has been reported at 17%.6 Further characterization of the pathophysiology of PARDS in COVID-19 may help explain this difference in mortality. Longer term follow-up and larger sample size will be paramount to determining the true mortality and morbidity associated with development of PARDS in children with COVID-19.
Footnotes
The authors declare no conflicts of interest.
References
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