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Chest ; 162(4):A1365, 2022.
Article in English | EMBASE | ID: covidwho-2060810


SESSION TITLE: Bad bugs and Mediastinal Madness SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Non-traumatic bronchial injury (NTBI) incidence is not well described but traumatic Tracheobronchial injury (TBI) incidence is 3% with a 70 -100% mortality3. Causes identified for NTBI are associated with vascular supply compromise2. TBI presents with dyspnea, subcutaneous emphysema, pneumothorax, and/or pneumomediastinum4. It can be missed up to 68% of the cases. Bronchoscopy is the study of choice and management is based on studies from traumatic TBI2, 3. This report describes a unique case of NTBI in a patient with recent COVID-19 infection, uncontrolled diabetes, and invasive pseudomembranous Aspergillosis presenting with a left bronchial tear (LBT). CASE PRESENTATION: A 41-year-old with uncontrolled diabetes and prior admission for COVID-19 infection and diabetic ketoacidosis (DKA) managed with steroids and antibiotics. Presenting cough, fever, intermittent chest pain, and palpitations. He was afebrile, tachycardic, and hypoxemic requiring supplemental oxygen. Chest examination revealed crackles and decreased breath sounds at the lung bases. Laboratory studies showed leukocytosis, hyperglycemia, and anion gap metabolic acidosis. SARS-CoV-2 PCR was negative. CT chest revealed an anterior wall defect of the left bronchus with a pneumomediastinum. Bronchoscopy showed pseudomembranous necrotic debris of the tracheobronchial tree and left main bronchus tear with visible rhythm-beating pericardium surrounding the heart. Cytopathological findings of the bronchoalveolar fluid were consistent with Aspergillus species (AS). DISCUSSION: NTBI are rare with a high mortality3. NTBI due to AS has been described in post-lung transplant patients. AS produces endotoxins and proteases that damage the epithelium, leading to erosion of surrounding structures2,3. Since COVID-19, invasive fungal infections (IFI) have risen due to lung damage and immunologic deficits associated with the virus or immunomodulatory therapy6. Our patient risk factors for IFI included recent COVID-19 infection, steroid use, and uncontrolled diabetes. This unholy trinity has coexisted during COVID-19 self-potentiating the problem of immune dysregulation leading to IFI and tissue necrosis7. This may cause NTBI as in our case presenting with LBT. Despite antimicrobial therapy, he died due to massive hemoptysis from erosion of the pericardium or angio-invasion of surrounding vessels. CONCLUSIONS: Rarity of NTBI constitutes a challenge for early diagnosis and management. Identifying predisposing risk factors, a high clinical suspicion, and appropriate diagnostic workup is of vital importance. During the COVID-19 pandemic, IFI have an increased incidence associated with high mortality rates. Despite more cases being described there are still knowledge gaps related to prevention, diagnosis, and management. Reference #1: Jones D, Nelson A, Ma OJ. Pulmonary Trauma. In: Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8e. McGraw-Hill Education;2016. Reference #2: Aerni MR, Parambil JG, Allen MS, Utz JP. Nontraumatic Disruption of the Fibrocartilaginous Trachea: Causes and Clinical Outcomes. Chest. 2006;130(4):1143-1149. doi: Reference #3: AK AK, Anjum F. Tracheobronchial Tear. StatPearls Publishing;2022. Accessed March 13, 2022. DISCLOSURES: No relevant relationships by Jorge Alejandro Bernal No relevant relationships by Adriana Betancourth No relevant relationships by Reham Majzoub No relevant relationships by Juan Pablo Sarmiento Cano

Annals of the Rheumatic Diseases ; 80(SUPPL 1):610-611, 2021.
Article in English | EMBASE | ID: covidwho-1358706


Background: Factors associated with the development of chronic heart failure (CHF) in systemic lupus erythematosus (SLE) have received little attention. On the other hand, recent data from the use of hydroxychloroquine in the treatment of SARS-CoV-2 infection during the COVID19 pandemic have cast some doubts on its cardiological safety. Objectives: To identify factors associated to CHF in SLE. Methods: Retrospective cross-sectional study, including all patients with SLE (≥4 ACR-1997 criteria) recruited in RELESSER registry. The objectives and methodology of the registry have been described previously (1). CHF was defined according to the Charlson index item. Patients with CHF before diagnosis of SLE were excluded. Cumulative damage was measured with the SLICC/ ACR index, excluding cardiovascular (CV) items (mSDI). Multivariate analysis exploring factors associated with CHF was carried out. Results: 117 patients (3% of the entire cohort) with SLE and CHF and 3,506 controls with SLE without CHF were included. 90% were women. Disease duration: mean (SD), 120.2 (87.7) months. CHF appeared after a median (P25-P75) of 9.40 (4.2-18.3) years from SLE diagnosis. Patients with CHF were older (59.8 ± 18.2 vs. 46.2 ± 4.3). In the bivariate analysis, the association of CHF with greater severity [Katz severity index: median (IQR): 4 (3-5) vs. 2 (1-3)], damage [mSDI: 3 (2-4) vs 0 (0-1)], comorbidity [modified Charlson-excluding CV items: 4 (3-6) vs 1(1-3)] and both CV (37.5% vs 6.7%) and overall mortality (43.2% vs 4.7%) (p<0.0001 for all comparisons). Also, CHF patients were more refractory to SLE treatments (33.3% vs 24%, p=0.0377) and were more frequently hospitalised due SLE [median 3 (1-5) vs 1(0-2), p<0.0001]. The results of the multivariable model are depicted in table 1. Conclusion: -CHF is a rather late complication of SLE. -Patients with SLE and CHF have more severe SLE, with greater refractoriness to SLE treatments and higher overall mortality. -Treatment with antimalarials, as routinely used in SLE patients, is not only safe to heart, but even appears to have a cardioprotective effect. (Table Presented).