SESSION TITLE: Medical Student/Resident Critical Care Posters
SESSION TYPE: Med Student/Res Case Rep Postr
PRESENTED ON: October 18-21, 2020
INTRODUCTION: Approximately 6 million people have been diagnosed with severe acute respiratory syndrome coronavirus-2 (SARSCoV-2) and close to 400,000 people have died from this deadly disease worldwide (COVID-19, 2020). Almost all of the complications include pneumonia. The pulmonary symptoms associated with SARSCoV-2 vary from mild respiratory symptoms to severe respiratory failure. Of those infected with SARSCoV-2, 40% will progress to acute respiratory distress syndrome (ARDS) and of those, 20% will go on to develop pulmonary fibrosis (Spagnolo, 2020). We present a case of a middle-aged female with SARSCoV-2 with unusually rapid progressing pulmonary fibrosis.
CASE PRESENTATION: 53 year old female with history of hypertension and obesity, found to be SARSCoV-2 positive. The patient was treated with hydroxychloroquine, azithromycin, intravenous corticosteroids, tocilizumab, and convalescent plasma. She was successfully extubated after a prolonged course and discharged to rehabilitation facility after a length of stay of 15 days. Five days post-discharge the patient presented with sudden-onset shortness of breath secondary to large right-sided tension pneumothorax requiring pigtail and large bore chest tube insertion. Despite this, due to severe hypoxemia, the patient required immediate intubation. Repeat SARSCoV-2 testing was positive. Computed tomography (CT) of chest was significant for diffuse ground glass opacification with no fibrosis. Repeat CT chest just four days later showed severe diffuse bilateral fibrotic changes.
DISCUSSION: A large study of SARSCoV-2 patients based in Wuhan, China featured 138 hospitalized patients wherein 61% of patients developed ARDS. Pulmonary fibrosis is a known consequence of ARDS. It is characterized by epithelial cell damage and activation, fibroproliferation, and abnormal accumulation of extracellular matrix (ECM) in lung parenchyma. The pathogenesis of how this disease causes lung damage is still speculative. Diffuse alveolar damage occurs with cellular fibromyxoid exudates, desquamation of pneumocytes, and hyaline membrane formation typical of ARDS. This is similar to findings seen in pathology reports of post-mortem lung biopsies of SARS and Middle Eastern Respiratory Syndrome coronavirus’ and is likely similar to what is occurring in SARSCoV-2 patients (Spagnolo, 2020). CT findings of these cases showed areas of advanced fibrosis with bullae formation. Multiple factors that may contribute are virus-induced cytokine release syndrome, drug effects and increased airway pressure with hyperoxia-related lung injury secondary to mechanical ventilation.
CONCLUSIONS: Statistics reveal 2-3 million people recovered from SARSCoV-2 worldwide (COVID-19, 2020). This recovery is not always without consequences such as pulmonary fibrosis seen in this patient. Therefore, it is necessary to evaluate long-term ramifications and treatment options in surviving SARSCoV-2 patients.
Reference #1: COVID-19 dashboard by the center for systems science and engineering at Johns Hopkins University. Retrieved from https://www.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6
Reference #2: King TE Jr, Pardo A, Selman M. Idiopathic pulmonary fibrosis. Lancet. 2011;378(9807):1949-1961. doi:10.1016/S0140-6736(11)60052-4
Reference #3: Spagnolo et al., Pulmonary fibrosis secondary to COVID-19: a call to arms? Lancet Respiratory Medicine. 2020; doi: https://doi.org/10.1016/S2213-2600(20)30222-8
DISCLOSURES: No relevant relationships by Blessen George, source=Web Response
No relevant relationships by Michael Megally, source=Web Response
No relevant relationships by Visala Natarajan, source=Web Response
no disclosure on file for Benhoor Shamian;