LAUSR

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic infection to critical illness and death. Many patients report persistent dyspnea and fatigue for months following their acute illness. SARS-CoV-2 has an affinity for neural and muscular tissue which may lead to persistent dyspnea and fatigue among the survivors. Here, we discuss a case of diaphragmatic dysfunction due to COVID-19 infection contributing to persistent dyspnea. CASE PRESENTATION: A 49-year-old male smoker with medical history notable only for COVID-19 infection 5 months prior, was admitted for worsening shortness of breath associated with right sided chest discomfort and cough for several months. On evaluation, he was found to be tachypneic and tachycardic with mild hypoxia.Four weeks prior, he was hospitalized with similar complaints and was noted to have a newly found right middle and lower lobe atelectasis with elevation of right hemidiaphragm on chest x-ray (CXR) and CT. Bronchoscopy done during that admission revealed mucus plugs in the right middle and lower lobes which were evacuated. At that time, he was discharged with prednisone and ICS/LABA inhaler which did not improve his symptoms. At current presentation, CTA of the chest revealed persistent but improved atelectasis compared to CT imaging from previous admission, but the right hemidiaphragm elevation persisted. Subsequent sniff test was positive for paradoxical motion of the right hemidiaphragm with normal movement of the left hemidiaphragm suggestive of right diaphragmatic paralysiCardiologic evaluation, including echocardiogram and stress test were unremarkable. The patient failed conservative management and pulmonary rehabilitation. He then underwent surgical plication of the right hemidiaphragm. Post-operative CXR showed improved right lung atelectasis and improved position of the right hemi diaphragm, with subsequent amelioration of his symptoms. DISCUSSION: The mechanism of neuromuscular involvement in COVID-19 infection is not fully understood. The viral spike protein unique to SARS-CoV-2 has high affinity to ACE2 receptors on skeletal muscle fibers1. Direct neuromuscular involvement by SARS-CoV-2 virus has been postulated to cause diaphragmatic paralysis1. Viral replication activates an inflammatory response leading to myotoxic injury via a cytokine storm2. CONCLUSIONS: Diaphragm dysfunction can be one of the consequences of COVID-19 infection. Neuromuscular injury impairs contraction of the diaphragm, which inhibits lung movement and contributes to impaired clearance of secretion leading to persistent dyspnea. REFERENCE #1: Paliwal VK, Garg RK, Gupta A, Tejan N. Neuromuscular presentations in patients with COVID-19. Neurol Sci. 2020;41(11):3039-3056. doi:10.1007/s10072-020-04708-8 REFERENCE #2: Ramani SL, Samet J, Franz CK, et al. Musculoskeletal involvement of COVID-19: review of imaging. Skeletal Radiol. Published online 2021. doi:10.1007/s00256-021-03734-7 DISCLOSURES: No relevant relationships by Ammar Ahmed, source=Web Response No relevant relationships by Madeeha Banu, source=Web Response No relevant relationships by Clifford Hecht, source=Web Response No relevant relationships by Kenneth Joseph, source=Web Response No relevant relationships by Swetha Paduri, source=Web Response No relevant relationships by Azib Shahid, source=Web Response