P1‐79: Diaphragm dysfunction developed after COVID‐19 infection without pneumonia

We reported a 50-year-old patient with no bad habits and no significant medical history except for obesity (BMI 32.7 kg/m) complained of progressive shortness of breath aggravated in a supine position. One month ago the patient suffered from mild COVID-19 with positive PCR test but no abnormalities on chest CT scan. At the moment of examination his oxygen saturation was decreased to 89% and 78% in standing and supine position correspondingly. Pulmonary embolism was excluded. Orthopnea and paradoxical abdominal wall movement during breathing in supine position were observed. Spirometry showed restrictive disorders (FVC 49%, FEV1 48%, FEV1/FVC ratio 0.78). In supine position FVC declined to 19%. Gas transfer for carbon monoxide (TLCO) was reduced to 4.81 mmol/min/kPa (49%) but KCO was normal. Patient was characterized by reduced lung volumes (TLC 74%), preserved RV (117%) and normal airway resistance (Reff < 30 кПа*s/l). Maximal inspiratory pressure was decreased (25 cmH20). Ultrasonography showed no diaphragm thickening with inspiration. CT scan of the chest revealed elevated diaphragmatic domes with significantly thinned diaphragmatic cruras and bibasilar atelectasis. Electromyography of the diaphragm was not performed as this method was unavailable neither in our clinic nor in the other regional medical institutions. Thus, the patient was diagnosed with bilateral diaphragm dysfunction that we believe may be a complication of COVID-19 infection. The underlying pathological mechanism of this disorder needs to be further elucidated.