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Prolonged or difficult weaning from mechanical ventilation is common, affecting approximately 20% of patients undergoing invasive mechanical ventilation.1 Delays in liberation from ventilation are associated with increased short-term and long-term morbidity and mortality2,3 and place a significant burden on health care systems, particularly notable during the peaks of the SARS-CoV-2 pandemic. Respiratory muscle insufficiency is a common reason for failure to wean from invasive ventilation and is known to be caused by a multitude of factors that may be disease related (eg, sepsis) and/or therapy related (eg, ventilator-induced diaphragm dysfunction).4
In this issue of Respiratory Care, Haaksma et al5 describe the changes in respiratory muscle mass using bedside ultrasound (US) measurements in subjects requiring mechanical ventilation for severe COVID-19 pneumonia. The study population represents a sick cohort of subjects with close to 50% mortality at 28 d, early in their ventilatory course. Daily measurements of resting thickness of both inspiratory (diaphragm) and expiratory (rectus abdominus and lateral abdominal wall) muscles were obtained for up to 7 d in 30 subjects requiring invasive ventilation for > 72 h. The study found that changes in inspiratory or expiratory muscle thickness over time were common. Between baseline (< 24 h of intubation) and extubation, death, or day 7 (whichever came first), approximately one third of subjects exhibited a ≥ 10% increase in diaphragm thickness (Tdi), and one third exhibited a ≥ 10% decrease in Tdi. These results correspond to previous observations6 suggesting that ventilatory myotrauma is likely a relevant concern in subjects with SARS-CoV-2. Of note, a previous study suggests specific diaphragm myocyte invasion by SARS-CoV-2 may lead to …
Correspondence: Ewan C Goligher MD PhD, Toronto General Hospital, 585 University Avenue, 9-MaRS-9024, Toronto, Canada, M5G 2N2. E-mail: ewan.goligher{at}uhn.ca
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