The clinical course of pneumomediastinum in patients with SARS-CoV-2 before invasive mechanical ventilation.

Pneumomediastinum and pneumothorax are recognised complications encountered in COVID-19 before or during invasive mechanical ventilation (IMV). The clinical course of patients developing pneumomediastinum before IMV is yet to be evaluated.Four-thousand, one-hundred and thirty-one patients hospitalised with COVID-19 over a 12-month period were retrospectively reviewed to evaluate for incidence, clinical characteristics and outcomes. A subgroup analysis was done to identify any clinical traits between survivors and non-survivors. The overall incidence of pneumomediastinum prior to IMV was 0.92% (n=38) and was seen at admission or during non-invasive respiratory support. Thirty-seven per cent had associated pneumothorax most commonly unilateral (right side). The median (interquartile range (IQR)) duration from admission to developing pneumomediastinum was 7 days (3-11) and complete resolution was seen in 53% of patients; median (IQR) duration to resolution was 8 days (4-17). The in-hospital mortality associated with pneumomediastinum in patients with SARS-CoV-2 (PneumoCoV) was 55%. Increasing age (68 ± 12 years vs 56 ± 14 years; p=0.01), higher body mass index (31 ± 5 kg/m2 vs 28 ± 5 kg/m2; p=0.04), lack of resolution of pneumomediastinum (67% vs 24%; p=0.01; odds ratio (OR) 6.5; 95% confidence interval (CI) 1.5-27.5), presence of concurrent pneumothorax (65% vs 14%; p=0.002; OR 11; 95% CI 2.2-53.1) and elevated procalcitonin levels (>0.5 ng/mL; 81% vs 41%; p=0.01; OR 6; 95% CI 1.4-26) were significant features in those who did not survive.The incidence of PneumoCoV, despite being low, is associated with increased mortality. It is a hallmark of moderate to severe disease with multifaceted contributory factors. Both demographic and clinical factors predict survival.

The Perils and Pitfalls of Esophageal Dysmotility in Idiopathic Pulmonary Fibrosis.

INTRODUCTION: Gastroesophageal reflux plays a significant role in idiopathic pulmonary fibrosis (IPF). Given the morbidity and mortality associated with IPF, understanding the mechanisms responsible for reflux is essential if patients are to receive optimal treatment and management, especially given the lack of clear benefit of antireflux therapies. Our aim was to understand the inter-relationships between esophageal motility, lung mechanics and reflux (particularly proximal reflux-a prerequisite of aspiration), and pulmonary function in patients with IPF. METHODS: We prospectively recruited 35 patients with IPF (aged 53-75 years; 27 men) who underwent high-resolution impedance manometry and 24-hour pH-impedance, together with pulmonary function assessment. RESULTS: Twenty-two patients (63%) exhibited dysmotility, 16 (73%) exhibited ineffective esophageal motility (IEM), and 6 (27%) exhibited esophagogastric junction outflow obstruction. Patients with IEM had more severe pulmonary disease (% forced vital capacity: P = 0.032) and more proximal reflux (P = 0.074) than patients with normal motility. In patients with IEM, intrathoracic pressure inversely correlated with the number of proximal events (r = -0.429; P = 0.098). Surprisingly, inspiratory lower esophageal sphincter pressure (LESP) positively correlated with the percentage of reflux events reaching the proximal esophagus (r = 0.583; P = 0.018), whereas in patients with normal motility, it inversely correlated with the bolus exposure time (r = -0.478; P = 0.098) and number of proximal events (r = -0.542; P = 0.056). % forced vital capacity in patients with IEM inversely correlated with the percentage of reflux events reaching the proximal esophagus (r = -0.520; P = 0.039) and inspiratory LESP (r = -0.477; P = 0.062) and positively correlated with intrathoracic pressure (r = 0.633; P = 0.008). DISCUSSION: We have shown that pulmonary function is worse in patients with IEM which is associated with more proximal reflux events, the latter correlating with lower intrathoracic pressures and higher LESPs.