NEW-ONSET SYSTEMIC LUPUS ERYTHEMATOSUS AND STEVEN JOHNSONS SYNDROME WITH SEVERE ARDS HERALDED BY POST-COVID-19 INFECTION MULTISYSTEM INFLAMMATORY SYNDROME IN AN ADULT (MIS-A)

SESSION TITLE: Autoimmune Diseases Gone Wild: Rare Cases of Pulmonary Manifestations SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Post-Covid-19 Multisystem Inflammatory Syndrome (MIS) is a severe hyperinflammatory syndrome associated with either the acute or recovery phase of covid-19 infection affecting multiple organ systems requiring hospitalization. This syndrome has been described in both children (MIS-C) and adults (MIS-A). Several case reports and systematic reviews have reported an association between post-covid-19 MIS-A and several autoimmune diseases. CASE PRESENTATION: We herein report a case of a 27-year-old female with no known chronic medical condition and a non-contributory family history who was diagnosed with post-covid-19 multisystem inflammatory syndrome in adults (MIS-A). She presented with generalized partial thickness erythematous skin ulcerations with tender blistering and painful erosion of her mucus membranes (oral and vaginal mucosa). This was diagnosed as Steven Johnsons syndrome. She was pulsed with intravenous methylprednisone. During this therapy, she progressed to severe acute respiratory distress syndrome (ARDS) requiring mechanical ventilation (fig 1). Bronchoscopy revealed mild pulmonary hemorrhage fig 2a&b). Serological testing heralded a new onset systemic lupus erythematosus in light of positive antinuclear antibodies, anti Ds DNA and anti Smith antibodies. Her course was complicated by significant proteinuria and an active renal cast suggestive of lupus nephritis. This necessitated further treatment for active lupus. She was successfully extubated and discharged home. DISCUSSION: We arrived at the diagnosis of post-covid-19 multisystem inflammatory syndrome in adults (MIS-A) in light of her presenting with fever, hypotension, persistent sinus tachycardia and new onset atrial fibrillation), acute pancreatitis, acute kidney injury, elevation in transaminases, new onset skin rash, elevated inflammatory markers and a recent history of positive SARS-CoV-2 infection. Covid-19 has been reported to induce wide spread vasculitis resulting in MIS-A or MIS-C by triggering type 3 hypersensitivity (1). Also, multiple case reports and systemic reviews have reported a direct association between MIS-A and several autoimmune diseases including SLE, SJS (2). The patient recovered with high dose corticosteroid and supportive therapy indicating her severe ARDS was most likely due associated to SJS, SLE and MIS-A. Clinicians should also keep in mind that SARS-CoV-2 PCR swab may be negative at the time patient presents with symptoms of MIS-A as the infection might have occurred about 4-5weeks prior just as in our patient(3) CONCLUSIONS: We cannot underscore enough the importance of clinicians having a high index of suspicion for this syndrome in patients with acute or recent covid-19 infection, with or without a positive PCR covid-19 test. Early involvement of a multidisciplinary approach and appropriate management is essential to mitigate morbidity and mortality in these patients. Reference #1: Roncati L, Ligabue G, Fabbiani L, Malagoli C, Gallo G, Lusenti B, et al. Type 3 hypersensitivity in COVID-19 vasculitis. Clin Immunol Orlando Fla. 2020 Aug;217:108487. Reference #2: Gracia-Ramos AE, Martin-Nares E, Hernández-Molina G. New Onset of Autoimmune Diseases Following COVID-19 Diagnosis. Cells [Internet]. 2021 Dec 20 [cited 2022 Mar 22];10(12):3592. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8700122/ Reference #3: Morris SB. Case Series of Multisystem Inflammatory Syndrome in Adults Associated with SARS-CoV-2 Infection — United Kingdom and United States, March–August 2020. MMWR Morb Mortal Wkly Rep [Internet]. 2020 [cited 2022 Mar 22];69. Available from: https://www.cdc.gov/mmwr/volumes/69/wr/mm6940e1.htm DISCLOSURES: No relevant relationships by Isaac Ikwu No relevant relationships by Anthony Lyonga Ngonge No relevant relationships by Alem Mehari No relevant relationships by Noordeep Panesar no disclosure on file for Vis al Poddar;No relevant relationships by Emnet Yibeltal

Crack Lung: A Clinical Diagnosis

IntroductionCrack lung is a clinically diagnosed form of diffuse alveolar hemorrhage that occurs acutely within 48 hours of smoking crack cocaine. The diagnosis of crack lung is based on history, clinical presentation, laboratory, and radiographic findings. Unlike most other forms of alveolar hemorrhage, crack lung does not require extensive or invasive work up and is managed symptomatically. We hereby present a case of acute diffuse alveolar hemorrhage secondary to crack cocaine which was clinically diagnosed and managed symptomatically. Case reportPatient was a 46-year-old female with a past medical history of type II diabetes mellitus, chronic obstructive pulmonary disease and polysubstance abuse that was brought to the emergency room after she was found unresponsive. 4mg of Narcan was administered and she became alert. Following Narcan administration, patient remained altered and confused. At the emergency room patient endorsed shortness of breath at rest which she associated it with a prior COVID-19 pneumonia one month ago. Vital signs were significant for a Temperature:99.2 blood pressure: 130/66, heart rate: 125, respiratory rate:27, Oxygen saturation: 95% on non-rebreather at 15L/min. Laboratory investigations were significant elevated creatinine (1.38, baseline unknown);white blood cell count (30.25), arterial blood gas was reported as 7.26/45/69 on 100%. Serum troponin was elevated at 3.12. Electrocardiogram showed sinus tachycardia, chest x-ray showed diffuse bilateral patchy airspace disease, computed tomography of the chest showed bilateral diffuse lung consolidation with small ground glass opacities (figure 1). Computed tomography of the head showed no acute intracranial process and urine drug screen was positive for cocaine. Patient was started on 4 mg of Narcan, 125 mg of methylprednisolone and transferred to the medical intensive care unit (MICU). In the MICU, blood, sputum and urine culture were obtained. Pt was empirically managed on vancomycin and piperacillin-tozabactam. Because of diffuse alveolar hemorrhage was in the differential, patient was continued on 80 mg of IV methylprednisolone every 8 hours. Patient was observed in the unit for 2 days. During stay in the MICU, repeat chest x-ray showed improvement in lung opacities bilaterally. Vitals were within normal range. Patient was weaned down from non-rebreather to 2 Liters of oxygen and then transferred to the general floor. ConclusionPatients with crack lung often present with shortness of breath, fever, cough with or without hemoptysis and sometimes hypoxemia within 48 hours of insult. Early diagnosis based on history, physical examination, laboratory and radiographic findings can ensure prudent management.

SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 ISOLATION FROM PLEURAL FLUID WITH COVID-19 PNEUMONIA AND SUPERIMPOSED EMPYEMA

SESSION TITLE: Medical Students/Residents' COVID-19 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been detected in nasopharyngeal swabs (NPS), sputum, bronchoalveolar lavage, blood, feces and ocular fluid(1). To date, there are no reported cases of SARS-CoV-2 isolated in pleural fluid, that is associated with a life-threatening complication, empyema. CASE PRESENTATION: He is a 64-year-old male with a known history of type 2 diabetes mellitus and hypertension who presented with a three-day history of progressive shortness of breath and generalized weakness which was preceded by a dry cough for a few weeks. He otherwise had no complaints or ill-contacts. On presentation, he was noted to be hypoxemic (saturation 93% on 4 liters of oxygen), tachycardic and afebrile. Initial exam was significant for mild respiratory distress and bilateral crackles on lung auscultation. Labs showed an elevated white blood cell count (11.6 x 10 6 ), troponin, D-dimer, ferritin and C-reactive protein. Serum interleukin-6 was elevated at 17.26 pg/mL. However, creatine phosphokinase, lactate dehydrogenase, transaminases and quantiferon gold were within normal limits. A chest x-ray was done that showed bilateral patchy infiltrates and a follow-up computerized tomography (CT) of the chest showed diffuse ground glass opacity with a large thick-walled septated mass in the left lower thorax. He was subsequently admitted for hypoxic respiratory failure likely secondary to COVID-19 pneumonia with superimposed bacterial infection complicated by possible empyema. Nasopharyngeal swab for SARS-CoV-2 was positive. Thoracentesis with chest tube placement revealed purulent material with pH of 6.5, that then later also tested positive for SARS-CoV-2. Final pleural fluid cultures grew pan sensitive Streptococcus pneumoniae. Pleural adenosine deaminase was elevated, however acid-fast bacilli cultures were no growth. He was treated with empiric antibiotics and the chest tube was removed after adequate drainage of empyema. He was discharged on room air to complete a course of oral antibiotics, self-quarantine and to follow-up in the pulmonary clinic after two weeks. DISCUSSION: Empyema is defined by the presence of bacteria or pus in the pleural space and is a well-documented sequela of pneumonia with mortality of up to 20%(2). The isolation of SARS-CoV-2 within the pleural fluid with a superimposed bacterial infection highlights the increased risk of self-quarantine and delayed treatment pose to the management of high-risk patients. The MuLBSTA score, a 90-day mortality predictor for viral pneumonia, recognizes co-bacterial infection as an additional risk factor for mortality(3). CONCLUSIONS: The presence of SARS-CoV-2 in body fluids such as pleural fluid has not yet been reported, nor are the implications known in regard to shedding duration and prognostication. Reference #1: Wang W, Xu Y, Gao R, et al. Detection of SARS-CoV-2 in Different Types of Clinical Specimens. JAMA. 2020;323(18):1843-1844. doi:10.1001/jama.2020.3786 Reference #2: Morris DE, Cleary DW, Clarke SC. Secondary Bacterial Infections Associated with Influenza Pandemics. Front Microbiol. 2017;8:1041. doi:10.3389/fmicb.2017.01041 Reference #3: Guo L, Wei D, Zhang X, et al. Clinical Features Predicting Mortality Risk in Patients With Viral Pneumonia: The MuLBSTA Score. Front Microbiol. 2019;10. doi:10.3389/fmicb.2019.02752 DISCLOSURES: No relevant relationships by Sahai Donaldson, source=Web Response No relevant relationships by Lorenzo Leys, source=Web Response No relevant relationships by Vishal Poddar, source=Web Response No relevant relationships by Lamiaa Rougui, source=Web Response