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Case Presentation A 53-year-old man presented to the ED at a time of low severe acute respiratory syndrome coronavirus 2, also known as coronavirus disease 2019 (COVID-19), prevalence and reported 2 weeks of progressive shortness of breath, dry cough, headache, myalgias, diarrhea, and recurrent low-grade fevers to 39°C for 1 week with several days of recorded peripheral capillary oxygen saturation of 80% to 90% (room air) on home pulse oximeter. Five days earlier, he had visited an urgent care center where a routine respiratory viral panel was reportedly negative. A COVID-19 reverse transcriptase polymerase chain reaction test result was pending at the time of ED visit. He reported a past medical history of gastroesophageal reflux disease that was treated with famotidine. Travel history included an out-of-state trip 3 weeks earlier, but no recent international travel.

Case Presentation A 70-year-old lifelong nonsmoking woman with a past medical history of hypertension was referred to the respiratory clinic for evaluation of chronic cough. She presented with a 5-month history of dry cough, night sweats, fatigue, and a 4.5-kg weight loss. Her cough tended to be worse while lying flat. She denied having shortness of breath, chest pain, wheeze, or hemoptysis. She was taking amlodipine for her blood pressure as well as omeprazole for indigestion. She denied having any reflux symptoms or heartburn. She worked as a receptionist for an optician. She did not have any pets at home and had no family history of asthma or allergic conditions. She had not been abroad recently.

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The diagnosis of COVID-19 has depended on the use of a Reverse transcriptase polymerase chase reaction test (RT-PCR) on respiratory samples. While this has directed the response and care of patients with suspected COVID-19, there have been false-negative results depending on when the test was administered in relation to time of exposure and symptom onset. CASE PRESENTATION: A 19-year-old male with no significant past medical history presented to the emergency department in July 2020 with a persistent fever of 100 -103F for 10 days. He returned from Texas 9 days prior with onset of fever one day before depature. He had a mild, non-productive cough, body aches, and poor oral intake. He also had diffuse abdominal pain with diarrhea and bilious, non-bloody vomiting - up to three times a day. He had elevated WBC, ESR, CRP and LDH with Lymphopenia. Blood cultures and HIV, Syphilis, EBV and Mycoplasma screening were negative as was a COVID-19 test. CT scan of his chest and abdomen revealed peripheral ground glass opacities suspicious of COVID 19. A repeat COVID test on hospital day 2 was again negative. He was treated with Azithromycin and Doxycycline and discharged home on Azithromycin on hospital day 4. He was readmitted 6 days later because of persistent fever to 103F, joint pains, malaise and weight loss of about 10 pounds. ESR, CRP, Ferritin and LDH were again elevated. A repeat CT scan showed resolution of previously seen ground glass opacities in the anterior lung fields and new confluent areas of ground glass attenuation and interlobular septal thickening posteriorly. A 3rd, 4th and 5th COVID-19 tests performed were negative. He was treated with Acetaminophen alternating with Ketorolac. A TTE showed a hyperlucency concerning for a right atrial thrombus or vegetation. Left ventricular ejection fraction was 50%. An MRI of the heart showed an inflammatory picture consistent with myocarditis. Further testing was done to reveal the etiology of his myocarditis to be Coxsackie A7,9, and 16. Clinically, there was significant improvement with resolution of fever and malaise and return of WBC count to normal. DISCUSSION: This patient's diagnosis of Coxsackie A myocarditis was clouded by the medical team's strong suspicion of COVID-19 pneumonia because of his clinical presentation and history of travel during the month of June to a part of the US with rising rates of COVID-19 cases. The unknown precise false-negative rate of the COVID-19 test, which can be anywhere from 2-27% depending on the time of testing from initial exposure meant that the diagnosis was never deemed impossible even with consecutive negative test results. CONCLUSIONS: While the attention COVID-19 is receiving is well deserved, anecdotal accumulation of evidence along with the scientific community's first wave of research has produced heuristics that need to be overcome to optimize patient care and outcomes. REFERENCE #1: Kucirka LM, Lauer SA, Laeyendecker O, Boon D, Lessler J. Variation in False-Negative Rate of Reverse Transcriptase Polymerase Chain Reaction–Based SARS-CoV-2 Tests by Time Since Exposure. Ann Intern Med [Internet]. 2020 May 13 REFERENCE #2: Arevalo-Rodriguez I, Arevalo-Rodriguez I, Buitrago-Garcia D, Simancas-Racines D, et al. False-negative results of initial RT-PCR assays for COVID-19: a systematic review. April 21, 2020 (preprint). REFERENCE #3: Steven Woloshin, M.D., Neeraj Patel, B.A., and Aaron S. Kesselheim, M.D., J.D., M.P.H. False Negative Tests for SARS-CoV-2 Infection — Challenges and Implications. DOI:10.1056/NEJMp2015897, June 5, 2020 DISCLOSURES: No relevant relationships by Christiana Atuaka, source=Web Response No relevant relationships by Carmina Aybar Rodriguez, source=Web Response No relevant relationships by Claudia De Araujo Duarte, source=Web Response No relevant relationships by Khurriyat Foziljonova, source=Web Response No relevant relationships by Varun tej Gonuguntla, source=Web Response No relevant relationships by Margaret Ku n-Basti, source=Web Response

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Coronavirus disease 2019 (COVID-19) most commonly presents with respiratory involvement. However, reports indicate that the central nervous system can also be affected. Neurological manifestations such as altered mental status, strokes, seizures, and even intracranial hemorrhage (ICH) have been noted in the literature. CASE PRESENTATION: A 28-year-old female with a past medical history of asthma presented to the emergency department (ED) with shortness of breath (SOB) that began 10 days prior. Four days earlier the patient went to urgent care for SOB and tested positive for COVID-19. She was provided an albuterol inhaler and prednisone 40 mg for five days. However, the patient's symptoms continued to worsen. In the ED, she was found to be saturating at 60% on room air. Therefore, she was placed on a non-rebreather mask and then high-flow nasal cannula at 55 liters/minutes. This improved her oxygen saturation to 90%;however, she was tachypneic with a respiratory rate of 30 bpm. Labs were significant for a pH 7.5, pCO2 28.6 mm Hg, white blood cell 16.94 x10

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: E-cigarette or vaping product use-associated lung injury (EVALI) encompass a host of pulmonary complications including diffuse alveolar hemorrhage, lipoid pneumonia, hypersensitivity pneumonitis, and rarely, acute eosinophilic pneumonia (AEP) [1]. AEP presents as an acute febrile illness with hypoxemia, diffuse pulmonary infiltrates, and eosinophilia on bronchoalveolar lavage (BAL) without evidence of prior infection or atopic illness [2]. Presented is a young adult patient with a history of continuous vaping and extended exposure to kitchen smoke who developed acute hypoxemic respiratory failure later diagnosed as AEP. CASE PRESENTATION: An 18-year-old male with no significant past medical history presented to the emergency department with acute onset malaise, fever, non-productive cough, and shortness of breath over 12 hours. Social history revealed 3-week workplace exposure to smoke as a barbeque cook and a 5-year history of daily vaping with reported cessation 3 weeks prior. Vitals were notable for hypoxemia which was corrected with administration of 8L of oxygen via nasal cannula. Quickly after admission, he had worsening respiratory status: tachypnea, increased oxygen requirement, use of accessory muscles, and bilaterally diminished breath sounds. He was transferred to the medical intensive care unit for emergent endotracheal intubation. Laboratory testing revealed a neutrophil predominant leukocytosis of 19.3x109/L. COVID-19, rapid influenza A and B, and urine antigens for streptococcus and legionella were negative as were autoimmune serologies. A computed tomography (CT) scan of the chest revealed diffuse bilateral consolidative opacities [Figure 1] with worsening over the next 24 hours [Figure 2]. Further investigation was undertaken with bronchoscopy. A BAL was obtained, and cell count and cultures were sent. BAL cell count was remarkable for 33% eosinophilia. The diagnosis of AEP was made, and the patient was started on systemic glucocorticoids, with significant improvement within 24 hours. DISCUSSION: The modified Philit criteria is used to make the diagnosis of AEP, which the patient satisfied [3]. Although a 5-year vaping history was present, no previous significant respiratory symptoms were reported. Prior studies have demonstrated a relationship between workplace smoke exposure and AEP [3]. Based on the modified Philit criteria, we suspect that the patient had acute respiratory failure from AEP as a result of chronic EVALI acutely exacerbated by workplace smoke exposure. The treatment of AEP treatment involves high-dose intravenous glucocorticoids followed by a prolonged oral steroid taper. CONCLUSIONS: Obtaining occupation history as well as smoke exposure is as important as obtaining vaping history in an otherwise healthy young patient who presents with acute hypoxemic respiratory failure with bilateral diffuse opacities on imaging. REFERENCE #1: Winnicka L, Shenoy MA. EVALI and the Pulmonary Toxicity of Electronic Cigarettes: A Review. J Gen Intern Med. 2020;35(7):2130-2135. doi:10.1007/s11606-020-05813-2 REFERENCE #2: Allen JN, Pacht ER, Gadek JE, Davis WB. Acute Eosinophilic Pneumonia as a Reversible Cause of Noninfectious Respiratory Failure. N Engl J Med. 1989;321(9):569-574. doi:10.1056/nejm198908313210903 REFERENCE #3: Philit F, Etienne-Mastroianni B, Parrot A, Guerin C, Robert D, Cordier JF. Idiopathic acute eosinophilic pneumonia: A study of 22 patients. Am J Respir Crit Care Med. 2002;166(9):1235-1239. doi:10.1164/rccm.2112056 DISCLOSURES: No relevant relationships by Nurjahan Khatun, source=Web Response No relevant relationships by Parth Patel, source=Web Response No relevant relationships by Naleen Patel, source=Web Response No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by SACHIN PATIL, source=Web Response No relevant relationships by Shyam Shankar, source=Web Response No relevant relationships by Rodger Wilhite, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Reports indicate a rare but serious complication of coronavirus disease 2019 (COVID-19) in children is a multisystem inflammatory syndrome in children (MIS-C). The cause of this is yet to be found. However, since the summer of 2020, some case reports have documented multisystem inflammatory syndrome in adults (MIS-A). CASE PRESENTATION: A 37-year-old male with a past medical history of diabetes and tobacco use presented to the emergency department (ED) for two days of fever, chest pain, and dyspnea. He had been diagnosed with COVID-19 and quarantined at home without symptom progression 17 days prior to his ED visit. In the ED, the patient was found to have a temperature of 39°C, heart rate of 145 bpm, and blood pressure of 95/41 mmHg. Lab values showed a creatinine of 4.74 mg/dL, lactic acid 4.7 mmol/L, C-reactive protein 640.4 mg/L, sedimentation rate 108 mm/hr, ferritin 2126 mcg/L, D-Dimer 2770 ng/mL and pro-B-type natriuretic peptide 629 ng/L. Chest computed tomography angiogram was negative for pulmonary embolism;however, it did show mediastinal lymphadenopathies (Figure 1). The patient was given intravenous fluids, piperacillin-tazobactam, vancomycin, and started on norepinephrine followed by admission to the medical intensive care unit (MICU). In the MICU, the patient required a second vasopressor (vasopressin) and hydrocortisone. Nephrology was consulted to start continuous renal replacement therapy. An echocardiogram revealed new-onset heart failure with an ejection fraction of 40%. Infectious, hematologic, and autoimmune investigations continued to be unremarkable;however, the patient's COVID-19 antibodies were reactive to spike and nucleocapsid antigens. After three days of treatment, the patient no longer required vasopressor support, and steroids were discontinued. Even so, the next morning he was again febrile and hypotension requiring vasopressors as well as new-onset atrial fibrillation with controlled rate. On exam, he developed a new non-blanching rash of his bilateral feet (Figure 2). Thereafter, infectious disease was consulted and diagnosed the patient with MIS-A. They started steroids along with intravenous immunoglobulin. This regimen saw a rapid resolution in fevers, despite holding antibiotics. DISCUSSION: Common symptoms of MIS-A are fever, chest pain, palpitations, and gastrointestinal distress. Elevated inflammatory markers include C-reactive protein, ferritin, and D-dimer [1]. Both children and adults have been reported to have cardiac dysfunction with MIS [1,2]. Recently the most common therapies provided to patients with MIS-C and -A are IVIG, vasoactive medications, and steroids [3]. CONCLUSIONS: Though MIS-C has been recognized in the pediatric population, MIS-A is beginning to present in adults after a COVID-19 infection. Increased awareness, as well as further study of this syndrome's pathophysiology, may lead to rapid treatment and improved outcomes. REFERENCE #1: Morris SB, Schwartz NG, Patel P, et al. 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 2020;69:1450–1456. DOI: http://dx.doi.org/10.15585/mmwr.mm6940e1 REFERENCE #2: Belhadjer, Z., Meot, M., Bajolle, F., Khraiche, D., Legendre, A., Abakka, S., Auriau, J., Grimaud, M., Oualha, M., Beghetti, M., Wacker, J., Ovaert, C., Hascoet, S., Selegny, M., Malekzadeh-Milani, S., Maltret, A., Bosser, G., Giroux, N., Bonnemains, L., Bordet, J., … Bonnet, D. (2020). Acute Heart Failure in Multisystem Inflammatory Syndrome in Children in the Context of Global SARS-CoV-2 Pandemic. Circulation, 142(5), 429–436. REFERENCE #3: Abrams, J. Y., Godfred-Cato, S. E., Oster, M. E., Chow, E. J., Koumans, E. H., Bryant, B., Leung, J. W., & Belay, E. D. (2020). Multisystem Inflammatory Syndrome in Children Associated with Severe Acute Respiratory Syndrome Coronavirus 2: A Systematic Review. The Journal of pediatrics, 226, 45–54 e1. Advance online publication. https://doi.org/10.1016/j.jpeds.2020.08.003 DISCLOSURES: No relevant relationships by Ojobumijo Agbaji, source=Web Response No relevant relationships by Abdelrahman Elfaham, source=Web Response No relevant relationships by Michael Hubbard, source=Web Response No relevant relationships by Tyler Kemnic, source=Web Response No relevant relationships by Micah Larsen, source=Web Response No relevant relationships by Amy Rechenberg, source=Web Response Site PI for VENT AVOID trial relationship with A-Lung Please note: $1-$1000 Added 12/03/2020 by Maximiliano Tamae Kakazu, source=Web Response, value=No direct payment to me

Case Presentation A 35-year-old woman without past medical history sought treatment for fatigue and dry cough of 3 weeks' duration. Basic laboratory tests revealed severe anemia. She had no history of bleeding, hemoptysis, dyspnea, or fever. The patient was admitted for RBC transfusion and more extensive diagnostics.

SESSION TITLE: Fellows Critical Care Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: It is known that viral infections increase the risk of a crisis in patients with known myasthenia gravis (1) While COVID-19 has been associated with an array of neurologic complications including encephalopathy, strokes, and seizures (2), there have been no published reports of new or exacerbated neuromuscular conditions as a result of said infection We present a case of myasthenia gravis crisis precipitated by COVID-19 infection CASE PRESENTATION: 79 year old female patient with a past medical history of myasthenia gravis, mixed connective tissue disease-associated ILD on home oxygen, heart failure with a reduced ejection fraction, and a history of VTE on Apixaban who presented with dry cough, nausea, and diarrhea She was found to have worsening of her chronic hypoxic respiratory failure on admission, requiring high flow nasal cannula She tested positive for COVID-19 Her admission ABG showed a Pa O2 77 mmHg without hypercapnia Inflammatory markers were elevated;CRP 65 mg/L, LDH 500 IU/L, and d-dimer 3 99 ug/mL Other admission labs were notable for lactate 5 2 mmol/L, BNP 258 pg/mL Patient initially improved, but then started exhibiting increasing weakness which similar to her prior myasthenic crises Her neurological exam became notable for decreased motor strength in neck flexion and extension, diffuse weakness of proximal muscles (3/5 strength in proximal upper extremities, 4+/5 in distal upper extremities, 2/5 in proximal lower extremities, 4/5 in distal lower extremities), with decreased but symmetrical DTRs Her respiratory status declined, requiring a combination of high flow nasal cannula and non-rebreather mask to maintain adequate oxygenation Negative inspiratory force measurements were found to be decreased (NIF 20 from normal on admission) She was diagnosed with a myasthenic crisis She received IVIG without significant improvement and was then transferred to the medical ICU for further management In the ICU, patient treated with plasmapheresis and initial supported with NIPPV therapy with Bi-level PAP She unfortunately continued to decline and required intubation for further management Patient's course was then complicated by an acute stroke and her family elected to pursue comfort care She passed thereafter DISCUSSION: While the primary signs and symptoms of COVID-19 are fever, cough, and dyspnea, several neurological manifestations of the disease that have been reported In our case, this SARS COV-2 virus was the precipitating cause of this patient’s myasthenic crisis We wonder if experimental therapy with Remdisivir, Convalescent plasma or other immunologic agents could have prevented or shortened the duration of the myasthenic crisis in this patient CONCLUSIONS: Myasthenia gravis crises can be associated with COVID-19 Prompt detection & diagnosis can help improve outcomes Reference #1: Gilhus NE, Romi F, Hong Y, Skeie GO Myasthenia gravis and infectious disease J Neurol 2018;265(6):1251-1258 doi:10 1007/s00415-018-8751-9 Reference #2: Haddad S, Tayyar R, Risch L, et al Encephalopathy and seizure activity in a COVID-19 well controlled HIV patient [published online ahead of print, 2020 May 16] IDCases 2020;21:e00814 doi:10 1016/j idcr 2020 e00814 DISCLOSURES: no disclosure on file for Christopher Damiano;No relevant relationships by Elie Fares, source=Web Response no disclosure on file for Catherine Kuntz;No relevant relationships by Kriti Pathak, source=Web Response No relevant relationships by Ralph Tayyar, source=Web Response

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Large-vessel strokes in patients younger than 50 years of age have been described as presenting symptoms for patients found to have COVID-19 Most patients with COVID-19 present with constitutional and respiratory symptoms, symptoms which range from asymptomatic disease to life-threatening disease including acute respiratory distress syndrome, acute kidney injury, multi-organ failure and death Here, we report a case of a patient presenting with both arterial and venous clots in the setting of COVID-19 that represents an extreme presentation of an entity now known as COVID-19 associated coagulopathy (CAC) CASE PRESENTATION: Our patient is a 74 year old female with past medical history of hypertension, hyperlipidemia and diabetes who presented after her daughter noticed that she was experiencing difficulty with balance She was taken to an outside hospital (OSH) where she was found to have left sided weakness and right sided gaze deviation History was notable for recent diagnosis of UTI as well as a new cough, dyspnea and dizziness that developed earlier in the day While at the OSH she suddenly became more unresponsive and was intubated for airway protection Her initial head CT showed a hyperdense right middle cerebral artery Intravenous tissue plasminogen activator was administered for her stroke and subsequently she was transferred to our hospital for further management A CTA head and neck was performed which showed a proximal right MCA occlusion (image 1) CT perfusion showed large infarct core as well as poor ASPECTS score (3-4) and she was therefore not a candidate for mechanical thrombectomy Incidentally, further chest imaging revealed a large pulmonary embolism (PE) in the right pulmonary artery, multiple segmental PE's and diffuse ground glass opacities (image 2) COVID-19 testing returned positive Bilateral lower extremity duplex was performed, this was significant for right soleal vein thrombus (image 3) The patient was started on a heparin infusion given her significant CAC despite the high risk of hemorrhagic transformation of her stroke Her condition improved and she was extubated on hospital day (HD) 4 and discharged to a skilled nursing facility on HD 20 Prior to discharge she was transitioned from heparin to rivaroxaban DISCUSSION: This case demonstrates the severity of CAC Our patients was found to have a large right MCA stroke, PE and right lower extremity DVT She was worked up extensively for other etiologies of her stroke but they were unrevealing The etiology of stroke was thought to be embolic of undetermined source and was most likely in the setting of COVID-19 CONCLUSIONS: CAC can be catastrophic for patients and can present with both arterial and venous thromboses Further studies are needed to elucidate the underlying pathophysiology of CAC and the optimal anticoagulation as well thrombolytic dosage regimens for thromboses secondary to CAC Reference #1: Avula A, Nalleballe K, Narula N, et al COVID-19 presenting as stroke [published online ahead of print, 2020 Apr 28] Brain Behav Immun 2020;S0889-1591(20)30685-1 doi:10 1016/j bbi 2020 04 077 Reference #2: Becker RC COVID-19 update: Covid-19-associated coagulopathy [published online ahead of print, 2020 May 15] J Thromb Thrombolysis 2020;1‐14 doi:10 1007/s11239-020-02134-3 DISCLOSURES: No relevant relationships by Daniel Condit, source=Web ResponseNo relevant relationships by Anand Muthu Krishnan, source=Web ResponseNo relevant relationships by Rudra Ramanathan, source=Web ResponseConsultant relationship with Boston Scientific Please note: $1001 - $5000 Added 06/01/2020 by Patrick Troy, source=Web Response, value=Consulting feeAdvisory Committee Member relationship with Boston Scientific Please note: $1001 - $5000 Added 06/01/2020 by Patrick Troy, source=Web Response, value=Consulting fee

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coronavirus disease 2019 (COVID-19) has caused a global pandemic in just a few months Worldwide, Health care officials are calling for social distancing and quarantine policies to limit the spread of COVID-19 This means most people will have to spend much, if not all, of their time at home Home environment offers abundant opportunities to be sedentary( sitting and reclining) The link between Immobility and increased risk of venous thromboembolism (VTE) has long been established We present a case of a young healthy patient who developed deep venous thrombosis (DVT) and bilateral acute pulmonary embolism following prolonged sitting during (COVID-19) outbreak quarantine CASE PRESENTATION: A 45-year-old male presented to our hospital with right leg pain and dyspnea of 1-week duration He denied fever, chest pain, cough, trauma, sick contact or recent travel He has no past medical history and never smoked Due to COVID-19 outbreak “stay home” orders, and, for four weeks prior to hospital presentation, he was spending about eight uninterrupted hours daily seated using his computer at home Initial vitals were Temp 98 3 F, heart rate 81 beat/min, respiratory rate 18 cycles/min, blood pressure 142/65 mmHg and oxygen saturation 100% on ambient air Physical exam was remarkable only for right calf swelling and tenderness BMI was 24 kg/m2 Laboratory data were notable for a D-dimer of 3035 (ref range;0-243 ng/ml DDU) and a creatinine of 1 5 ( ref range;0 7-1 2 mg/dl) Complete hemogram and coagulation profiles were normal Chest x ray was normal Ultrasound of the leg showed right popliteal vein DVT (Figure 1) CT angiogram of the chest confirmed multiple bilateral acute pulmonary emboli (Figures 2&3) Factor V Leiden mutation was negative and there was no protein C, S or antithrombin III deficiency Provoked VTE secondary to seated immobility was diagnosed The patient was started on enoxaparin and was thereafter transitioned to rivaroxaban on discharge DISCUSSION: Seated immobility thromboembolism (SIT) syndrome is the term used to describe VTE secondary to poor mobility due to prolonged seating Travel is a well-recognized risk factor for (SIT) syndrome A Less recognized forms of prolonged sitting are computer use, watching TV and video-gaming Many cases of VTE were described in these settings with most patients being young without other risk factors for VTE Having frequent breaks to walk and frequently moving legs is strongly advised during these activities to minimize the risk of VTE In our case, prolonged seating during computer use for more than eight hours a day is blamed for development of VTE Our patient had none of the other traditional risk factors CONCLUSIONS: People should be reminded that seated immobility, in its many and varied forms, is a risk factor for VTE During times of quarantine, maintaining active life style is good for physical as well as mental health Reference #1: 1 Beasley R, Heuser P, Raymond N SIT (seated immobility thromboembolism) syndrome: a 21st century lifestyle hazard N Z Med J 2005;118(1212):U1376 Reference #2: 2 Aldington, S , Pritchard, A , Perrin, K , James, K , Wijesinghe, M , & Beasley, R (2008) Prolonged seated immobility at work is a common risk factor for venous thromboembolism leading to hospital admission Internal Medicine Journal, 38(2), 133–135 Reference #3: 3 Healy B, Levin E, Perrin K, Weatherall M, Beasley R Prolonged work- and computer-related seated immobility and risk of venous thromboembolism J R Soc Med 2010;103(11):447-454 DISCLOSURES: No relevant relationships by Abdulla Ali, source=Web Response No relevant relationships by louisa Asare, source=Web Response No relevant relationships by Mohanad Gabani, source=Web Response No relevant relationships by Ibrahim Omore, source=Web Response No relevant relationships by Muhammad Riaz, source=Web Response

Case Presentation A 54-year-old man sought treatment at the ED for a productive cough with green phlegm of approximately 6 months’ duration that was accompanied by a 10-pound weight loss, night sweats, and occasional subjective fevers. He had made several prior visits to the ED for the cough and was hospitalized 4 months earlier for similar symptoms, at which time he underwent a bronchoscopy with BAL and was discharged with antibiotics for presumed pneumonia. He did not report any itching, rashes, sinus infections, joint swelling, joint pain, or GI symptoms. His long-term medications included omeprazole and amlodipine. The patient had a past medical history of grade III follicular lymphoma for which he completed six cycles of bendamustine 4 years before presentation and had been in remission since. He was a never smoker, had a recent travel history to the Dominican Republic 8 months before admission, and had no recent sick contacts.

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Coronavirus disease (COVID-19) is known to cause severe respiratory pathology such as acute respiratory distress syndrome. Although the pathophysiology of this lethal virus is still not fully understood, it has been suspected to attach to the ACE2 receptors leading to its deadly pathogenesis. Found to be the cause of venous thrombotic and embolic events, arterial thrombotic events such as ST-segment elevation myocardial infarction (STEMI) have been an unusual phenomenon. CASE PRESENTATION: A 37-year-old female with a past medical history of COVID-19 infection 12 days prior to admission presented to the emergency department (ED) complaining of shortness of breath for 2 to 3 days prior to admission. In the ED she was hypoxic with an oxygen saturation of 80% on room air for which she was placed on 90% FiO2 via OptiFlow and nonrebreather mask. Her D-Dimer on admission was noted to be 506 ng/mL (normal value 80.00 ng/mL (normal value

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The spectrum of autoimmune phenomena associated with Coronavirus disease 2019 (COVID-19) continues to expand. Guillain-Barre Syndrome (GBS) manifesting as a post-infectious sequela of COVID-19 has been increasingly reported [1]. Rare cases of autoimmune hemolytic anemia (AIHA) associated with COVID-19 are also emerging [2]. Our case describes a novel presentation of GBS and hemolysis in a patient with COVID-19. CASE PRESENTATION: A 62-year-old male with a past medical history of hypertension initially presented with 5 days of low-grade fever and cough. He denied dyspnea and was not hypoxic. Nasopharyngeal PCR confirmed COVID-19. He received bamlanivimab and etesevimab infusion and was discharged from the emergency room. He returned 6 days later with new-onset unsteady gait and weakness of the lower extremities. He had 1+ reflexes in the patellar and ankle bilaterally and 3+ in both triceps and biceps. This worsened into flaccid paralysis of bilateral lower extremities by admission day 2. Labs showed a drop in hemoglobin (Hgb) from 14.7 mg/dL to 10.9 mg/dL, haptoglobin 2) at time of discharge [1, 3]. AIHA has also been associated with COVID-19, with mixed warm and cold agglutin formation [2]. A negative CSF PCR panel with high protein suggests that novel antibodies may mediate myelin damage, which may also target other components such as fibrinogen in α/β chains. Immunoglobulin fragment alteration resulting in molecular mimicry may also occur following antigen-antibody complex formation directed against the virus [1]. CONCLUSIONS: GBS and AIHA are rare but important complications in patients with COVID-19. The spectrum of autoimmune phenomena associated with COVID-19 continues to expand. This case highlights the need for the differential to include autoimmune disease in patients with extrapulmonary manifestations of COVID-19. Further studies are needed to determine if causal relationships are present. REFERENCE #1: Sheikh AB, Chourasia PK, Javed N, et al. Association of Guillain-Barre syndrome with COVID-19 infection: An updated systematic review. 2021 Apr 18. J Neuroimmunol. 2021;355:577577. doi:10.1016/j.jneuroim.2021.577577 REFERENCE #2: Lazarian G, Quinquenel A, Bellal M, et al. Autoimmune haemolytic anaemia associated with COVID-19 infection. Br J Haematol. 2020;190(1):29-31. doi:10.1111/bjh.16794 REFERENCE #3: Hasan I, Saif-Ur-Rahman KM, Hayat S, et al. Guillain-Barre syndrome associated with SARS-CoV-2 infection: A systematic review and individual participant data meta-analysis. J Peripher Nerv Syst. 2020 Dec;25(4):335-343. doi: 10.1111/jns.12419. DISCLOSURES: No relevant relationships by Mateus Fernandes, source=Web Response No relevant relationships by Ifediba Nwachukwu, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Patients presenting in New York City, the epicenter for COVID in the United States, with severe hypoxic respiratory failure in the past year with acute respiratory distress syndrome (ARDS) signs were thought to exclusively have COVID-19 pneumonia. Even if initial tests were negative, physicians often anchored on the diagnosis of COVID as the disease was rapidly spreading and hospitals were at maximum capacity. We present a case of a young male who presented with severe hypoxic respiratory failure in the early stages of the pandemic who was found to be negative for COVID-19 and subsequently found to have pneumocystis jiroveci pneumonia (PJP). CASE PRESENTATION: This is a 42 year-old male with a past medical history of controlled diabetes mellitus type 2, hypertension, and a previous smoker who presented with worsening progressive shortness of breath for three days. On admission, the patient was found to be tachycardic, tachypneic and hypoxic. Chest x-ray showed bilateral diffuse infiltrates most consistent with ARDS. ABG revealed severe hypoxia with PO2 of 39 on room air. He was initially placed on bi-level with minimal improvement and was subsequently intubated. Initial oropharyngeal and nasopharyngeal COVID-19 swabs were negative. His influenza PCR also resulted as negative. Sputum cultures, endotracheal aspirate and blood cultures all returned back negative. On day three of his admission, the patient was tested for HIV and found to be positive with CD4 count

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: The novel coronavirus pandemic of 2019 (SARS COVID-19) has significant morbidity and mortality. The downstream complications resulting from this infection are not well characterized. There have been case reports of patients with COVID-19 infection presenting with Guillain-Barre Syndrome (GBS) Here, we present a case of one such patient, who failed initial management with intravenous immunoglobulin G (IVIG), requiring plasmapheresis as a treatment modality. CASE PRESENTATION: A 48-year-old male with a past medical history of hypertension and type 2 diabetes mellitus presented to the emergency department with a four day history of progressive paresthesias and weakness. This began in his bilateral lower extremities and ascended to the bilateral upper limb and face. Concurrent mild dysarthria and dysphagia were noted. On this encounter, he had a first time positive test for COVID-19 via nasopharyngeal polymerase chain reaction (PCR). On physical exam he had reduced dorsiflexion of the right ankle, with normal power throughout the rest of the body. He had graded sensory loss in the lower extremities, without a sensory level and diminished reflexes throughout. Lumbar puncture and MRI imaging were suggestive of demyelinating neuropathy. Due to the clinical history and albuminocytologic dissociation in the CSF, he was assessed with GBS and commenced on IVIG 0.4g/kg for 5 days. On day 4 of hospitalization, worsening dysarthria and dysphagia was noted and he was transferred to the intensive care unit (ICU). Subsequently, due to lack of adequate improvement in the patient's symptoms, plasmapheresis was initiated. The patient completed 7 additional sessions of plasmapheresis and had symptom resolution. DISCUSSION: There have been several case reports of GBS in the setting of COVID-19, which has been thought to be a para-infectious in origin. According to a systematic review, 96.6% of patients affected with COVID-19 GBS experienced typical COVID-19 symptoms prior to being diagnosed with GBS. This syndrome has been seen in other viral illnesses, such as West Nile virus and the Zika virus. Most of these cases have been treated successfully with IVIG, but in this report, the patient required plasmapheresis to achieve successful resolution of his symptoms. At this time, there have been approximately three published cases of GBS in the setting of COVID-19 in the USA which required plasmapheresis as a treatment modality. Additionally, all of these cases presented with typical clinical symptoms associated with COVID-19 infection. CONCLUSIONS: This patient's findings highlight one of the first cases of GBS in the setting of sub-clinical COVID-19 infection. This adds to the growing set of literature establishing a neurological component of the disease. It also demonstrates the use of plasmapheresis as an additional tool in the treatment of COVID-19 associated GBS. REFERENCE #1: Agosti, E., Giorgianni, A., D'Amore, F., Vinacci, G., Balbi, S., & Locatelli, D. (2021). Is Guillain-Barre syndrome triggered by SARS-CoV-2? Case report and literature review. Neurological Sciences, 42(2), 607-612. REFERENCE #2: Abrams, R. M., Kim, B. D., Markantone, D. M., Reilly, K., Paniz-Mondolfi, A. E., Gitman, M. R., … & Robinson-Papp, J. (2020). Severe rapidly progressive Guillain-Barre syndrome in the setting of acute COVID-19 disease. Journal of neurovirology, 26(5), 797-799. REFERENCE #3: Hasan, I., Saif-Ur-Rahman, K. M., Hayat, S., Papri, N., Jahan, I., Azam, R., … & Islam, Z. (2020). Guillain-Barre syndrome associated with SARS-CoV-2 infection: A systematic review and individual participant data meta-analysis. Journal of the Peripheral Nervous System, 25(4), 335-343. DISCLOSURES: No relevant relationships by Spencer Deleveaux, source=Web Response No relevant relationships by Sarah Usmani, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The first case of SARS-CoV-2 (COVID-19) virus was reported in December, 2019 and is well known to cause febrile illness, gastrointestinal symptoms, respiratory disease, and coagulopathy. One of the less common sequelae of this illness is myocarditis. Here we present an interesting case of delayed onset myocarditis which occurred following COVID-19 infection. CASE PRESENTATION: A 32-year-old female with a past medical history significant for obesity presented with complaints of dull, left sided chest pain. She had associated symptoms of diaphoresis, lightheadedness, and nausea. Patient denied prior history of angina. Patient had a strong family history of coronary artery disease.Chest pain was reproducible with palpation to the chest. EKG showed T wave inversions in anterolateral and inferior leads. Troponin was elevated to 1.12 ng/mL (

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: As the COVID-19 pandemic progresses, genetic variants have been identified globally, including the UK, South Africa, and Brazil strains. These variants exhibit genetic mutations in spike proteins and open reading frame regions. Rising cases of COVID-19 strains call to question the accuracy of current polymerase chain reaction (PCR) testing in detecting genetic variants. CASE PRESENTATION: A 76-year-old male nursing home resident was brought to the emergency department (ED) by ambulance due to progressively worsening dyspnea. His past medical history was remarkable for COPD and diabetes mellitus type II. On initial presentation, his respiratory rate was 30 breaths per minute, heart rate was 128 beats per minute, blood pressure was 135/64 mmHg, and oxygen saturation was 92% on supplemental oxygen via bilevel positive airway pressure (BIPAP). Physical exam was remarkable for bilateral rhonchi with accessory muscle use. Labs were remarkable for a white blood cell count of 16.5 109/L with lymphopenia, lactic acid of 2.2 mmol/L, and a d-dimer of 5250 ng/mL. Chest CT showed bilateral patchy ground glass infiltrates, fibrotic changes, and small bilateral pleural effusions (Image 1). He tested negative for influenza A and B, Mycoplasma pneumoniae, Streptococcus pneumonia, and Legionella. Sputum cultures showed no growth. The patient tested negative for COVID-19 twice by RT-PCR analysis (Abbott Laboratory, Chicago, IL). He was treated with intravenous steroids and broad-spectrum antibiotics. He was unable to be weaned from BIPAP to a lower level of supplemental oxygen. Eight days after hospital admission, the patient tested positive for COVID-19 IgM and IgG antibodies. After 12 days of treatment, the patient suffered a fatal cardiac arrest. DISCUSSION: We present an elderly man with a clinical symptoms and imaging findings highly suggestive of COVID-19, despite multiple negative RT-PCR tests. The patient did not improve despite treatment with broad spectrum antibiotic and intravenous corticosteroids. Patients had positive COVID-19 IgM antibodies, despite no known recent prior infection. Although the lab utilized for COVID-19 RT-PCR analysis asserts that testing is not impacted by genetic variants, these cases challenge the true sensitivity of this testing in detecting emerging strains. CONCLUSIONS: There are potentially many patients in the community hospitals presenting with COVID-19 variants that are not detected by existing RT-PCR testing. The genetic diversity of COVID-19 may diminish the sensitivity of RT-PCR testing, as labs across the country utilize different primers and probes with variable sensitivities in detecting variants. Clinicians should maintain a high suspicion for COVID-19, despite negative PCR testing. REFERENCE #1: Wang R, Hozumi Y, Yin C, Wei G-W. Mutations on COVID-19 diagnostic targets. Genomics. 2020;112(6):5204-5213. REFERENCE #2: Sapoval N, Mahmoud M, Jochum MD, et al. SARS-CoV-2 genomic diversity and the implications for qRT-PCR diagnostics and transmission. Genome Res. 2021;31(4):635-644. DISCLOSURES: No relevant relationships by Gustavo Avila, source=Web Response No relevant relationships by Jessica Baek, source=Web Response No relevant relationships by Renuka Reddy, source=Web Response No relevant relationships by Claudia Tejera Quesada, source=Web Response no disclosure on file for Adam Wellikoff

TOPIC: Disorders of the Mediastinum TYPE: Medical Student/Resident Case Reports INTRODUCTION: Lymphoma is the fourth most common malignancies in pregnancy, and a high portion is primary mediastinal (thymic) large B-cell lymphoma (PMBCL). It presents many challenges to diagnose lymphoma during pregnancy while avoiding fetal harm. CASE PRESENTATION: 41-year-old G2P1 female without significant past medical history experienced shortness of breath starting in her second trimester. She only had a telehealth appointment amid the COVID19 pandemic. The patient was offered a chest X-ray (CXR) but declined due to her concern of radiation. She was empirically managed as asthma triggered by acid reflux. At 39W of gestation, she presented to the hospital for labor and delivery. She was hypoxic and required three liters of oxygen. The physical exam was unremarkable. Lab were pertinent for mild leukocytosis and anemia. The patient still declined CXR. She was taken for C-section after failing trial of vacuum. The newborn was healthy. After delivering, she developed profound hypoxia in the OR requiring intubation. Tracheal compression was noted during intubation. CXR after intubation showed mediastinal widening. Following intubation, patient developed tachycardia, hypotension and ultimately cardiac arrest requiring CPR. Extracorporeal membrane oxygenation was activated. CT angiogram of the chest showed a 15 cm x 12 cm x 13 cm mass in the superior mediastinum that encases the aorta and great branches and was associated with direct extension into the sternum and invasion of the pericardium. The tumor also encased the trachea and left main bronchus. During her hospitalization, no neurological recovery was observed. The family decided to transition to comfort. The patient unfortunately passed away. The autopsy revealed neoplastic medium to large-size lymphoid cells in mediastinal mass, positive for CD45, CD20, BCL2, PAX-5, MUM-1, and MYC rearrangement negative for other markers. The final diagnosis was PMBCL. DISCUSSION: PMBCL is an aggressive B cell lymphoma arises from the thymus. Airway obstruction and superior vena cava syndrome are common due to local invasion. Dyspnea, B symptoms (fever, night sweats, weight loss) are possible symptoms. Labs may reveal elevated lactate dehydrogenase. Imaging studies typically illustrate an anterior mediastinal mass originating in the thymus. Final diagnosis can be made with biopsy and immunohistochemistry or flow cytometry analysis. Early recognition is important since these patients are at risk of cardiac and respiratory arrest during general anesthesia due to the mass location in the mediastinum. Pregnant patients should be informed that there is no evidence of fetal adverse outcome with imaging studies that expose the fetus to less than 50 mGy (CXR fetal dose: 0.0005 to 0.01 mGY). CONCLUSIONS: PMBCL should be identify early in pregnancy due to increased risk of cardiac and respiratory arrest. CXR is safe and harmless to the fetus. REFERENCE #1: Brenner B, Avivi I, Lishner M. Haematological cancers in pregnancy. Lancet. 2012;379(9815):580-587. REFERENCE #2: Dunleavy K, McLintock C. How I treat lymphoma in pregnancy. Blood. 2020 Nov 5;136(19):2118-2124. doi: 10.1182/blood.2019000961. PMID: 32797210. REFERENCE #3: Brent RL. The effect of embryonic and fetal exposure to x-ray, microwaves, and ultrasound: counseling the pregnant and nonpregnant patient about these risks. Semin Oncol. 1989 Oct;16(5):347-68. PMID: 2678486. DISCLOSURES: No relevant relationships by John Chronakas, source=Web Response No relevant relationships by Patrice Gillotti, source=Web Response No relevant relationships by Tien-Chan Hsieh, source=Web Response No relevant relationships by Oluwaseyi Olayinka, source=Web Response No relevant relationships by Nusrat Pathan, source=Web Response No relevant relationships by Akash Shah, source=Web Response No relevant relationships by Amanda Tissot, source=Web Response

TOPIC: Tobacco Cessation and Prevention TYPE: Medical Student/Resident Case Reports INTRODUCTION: Electronic cigarette or vaping product use associated lung injury (EVALI) has received increasing attention by the Centers for Disease Control and Prevention (CDC) within the last year due to a recent increase of cases of acute lung injury associated with vaping. The CDC has established criteria for EVALI: 1) the patient must have vaped within 90 days prior to symptom onset;2) there is evidence of pulmonary infiltrate on chest radiographs or chest CT;3) absence of pulmonary infection on initial work-up;4) no evidence alternative diagnoses.Spontaneous pneumothoraces (SPs) are often idiopathic in nature, classically in tall, thin males between the ages of 15-34 years old, as well as underlying lung or connective tissue diseases. There are few reported cases of SPs in association with vaping or e-cigarette use, with bilateral pneumothoraces being nearly unseen. CASE PRESENTATION: A 26-year-old Caucasian male with past medical history of polysubstance abuse presented to the emergency department with a one-day history of shortness of breath and chest pain. He was an active daily vaper. On arrival, he endorsed dyspnea, hemoptysis, presyncope, and pleuritic pain. Vitals showed hypotension, tachycardia, and tachypnea. Physical exam shows no trauma or tracheal deviation. Lung sounds were decreased at both apices. Chest X-ray showed bilateral apical pneumothoraces. Workup for respiratory virus panel and COVID were negative. CBC and CMP lab values were largely unremarkable, only with lactic acidosis to 4.4 mmol/L. Toxicology was positive for cocaine, THC, and opiates. A left sided thoracostomy was performed, resulting in resolution of the left sided pneumothorax. Shortly after placement, the patient traumatically removed his thoracostomy tube. 100% oxygen resulted in resolution of the right sided pneumothorax. The patient was downgraded from the ICU and discharged on hospital day three with resolution of symptoms. DISCUSSION: Spontaneous pneumothorax is a potentially life-threatening emergency condition. This patient's concerning presentation with spontaneous bilateral secondary pneumothoraces (SBSP) and multifocal opacities on the chest x-ray in the setting of vape use, without a prior or family history of lung disease, created a concerning clinical picture. EVALI is already a concerning condition. Per the CDC as of January 14, 2020, there were 2,668 cases of EVALI requiring hospitalization, with 68 cases resulting in mortality CONCLUSIONS: This case is highlighted in order to add to increasing evidence of the dangerous effects of vaping. Patients should be counseled on the wide variety of risks of vaping. Furthermore, cases of SBSP are quite rare, and this patient's history makes vaping and marijuana use the most likely contributing factors to his presentation. Patients with a history of spontaneous pneumothorax should be monitored over time for recurrences and counseled on vaping cessation. REFERENCE #1: Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products. https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html REFERENCE #2: Graf-Deuel E, Knoblauch A: Simultaneous bilateral spontaneous pneumothorax. Chest. 1994, 105:1142-1146. 10.1378/chest.105.4.1142 DISCLOSURES: No relevant relationships by Riley Ewen, source=Web Response No relevant relationships by Gilad Guez, source=Web Response no disclosure on file for Brijesh Patel;no disclosure on file for Farhan Shah

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The novel coronavirus disease (COVID-19) has been associated with diffuse lung injury. Corticosteroids have been shown to suppress inflammation-mediated lung injury and as a result, decrease progression to respiratory failure. Based on the RECOVERY trial, the use of dexamethasone in patients hospitalized with COVID-19 resulted in lower 28-day mortality among those who were receiving either invasive mechanical ventilation or supplemental oxygen at randomization [1]. Per IDSA treatment guidelines dexamethasone use in hospitalized patients is strongly recommended, thereby prompting most intuitions in the United States and worldwide to initiate its use. We present a unique case of Nocardia farcinica brain abscess in the setting of prolonged dexamethasone use in a patient with COVID-19 infection. CASE PRESENTATION: 80-year-old female from Pakistan with a past medical history of hypertension, who while in Pakistan was diagnosed with COVID-19 and treated with Xarelto and dexamethasone (dose and duration unknown). Her course was complicated by the development of left elbow and hand Zoster and over the 10 days prior to presentation, she was noted to develop increasing left-sided weakness and aphasia. Patient was transferred to the United States where a CT scan revealed a left frontal mass, prompting transfer to a tertiary care facility. MRI brain revealed a left frontal cystic rim-enhancing lesion that was concerning for a brain abscess. The patient subsequently underwent left frontal stereotactic brain biopsy with recovery of 3 mL of purulent fluid. Gram staining revealed beaded branching gram-positive rods. She was initially placed on vancomycin/cefepime/metronidazole/dexamethasone and was changed to IV Bactrim/ceftriaxone/doxycycline to cover for Nocardia and Actinomyces. Modified acid-fast stain returned positive with beaded, branching, filamentous rods, consistent with Nocardia. Cultures returned with Nocardia farcinica. DISCUSSION: Nocardia infection primarily occurs via inhalation or direct skin inoculation and subsequently disseminates hematogenously to end organs, which include the brain [2]. Nocardia typically presents as a respiratory or skin infection;brain abscesses are rare and primarily found in immunocompromised patients. As outlined in this case, an immunocompromised state was induced by high dose steroid use. Corticosteroids modulate inflammatory mediators and thereby cause immunosuppression. New symptoms should be monitored closely in patients undergoing steroid therapy, as seen in our patient who presented with new onset aphasia and left sided weakness. This is especially true during the COVID-19 pandemic that has prompted widespread use of dexamethasone in order to prevent respiratory failure and death. CONCLUSIONS: Physicians should be vigilant of superimposed infections in patients with COVID-19 receiving high dose steroids. REFERENCE #1: RECOVERY Collaborative Group. Dexamethasone in Hospitalized Patients with Covid-19. N Engl J Med. 2021;384(8):693-704. doi:10.1056/NEJMoa2021436. REFERENCE #2: Lin YJ, Yang KY, Ho JT, Lee TC, Wang HC, Su FW. Nocardial brain abscess. J Clin Neurosci. 2010;17(2):250-253. doi:10.1016/j.jocn.2009.01.032 DISCLOSURES: No relevant relationships by Waqas Bhatti, source=Web Response No relevant relationships by Tanisha Kaur, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Nocardia is an opportunistic aerobic actinomycete that most frequently affects the lungs, brain, and skin in 0.04% to 3.5%2 patients after solid organ transplant. Natural and synthetic glucocorticoids are at the forefront of anti-inflammatory and immunosuppressive therapies in transplant patients who often succumb to Nocardia infections. Out of the eight species, N. farcinica is potentially more lethal because of its tendency to disseminate and its resistance to antibiotics1. We present a unique patient who developed N. farcinica at the end of a 10-day course of dexamethasone for COVID-19. CASE PRESENTATION: A 61-year-old female with past medical history of non- insulin dependent type II diabetes (hgbA1c 6.3), hypertension, CHF on GDMT, and COVID-19 pneumonia presented with chest pain on the 10th and last day of per oral 4mg dexamethasone course. On admission patient's vitals were stable and labs were notable for leukocytosis, elevated glucose, BNP, and D-dimer prompting a CTA which showed subsegmental PE and a thrombus in SVC extending to the IVC. She was also found to have a right upper lobe 3.3 x 3.2 cm subpleural mass and a left upper lobe 1.9 x 1.5 cm nodule (figure 2). Percutaneous CT-guided coaxial core needle biopsy of right lung mass was done with pathology results notable for branching filamentous organisms consistent with Nocardia further refined by cultures growing Nocardia farcinica. The MRI brain did not show any abscess. She was started on IV Bactrim and meropenem. Eventually, the patient was discharged home on Bactrim and linezolid due to N. farcinica's high resistance rates to Bactrim alone. DISCUSSION: Nocardiosis usually occurs in immunosuppressed states, such as lymphomas, HIV, diabetics, transplant recipients or patients on long term immunosuppressants. Glucocorticoids are widely used as an effective treatment to control inflammatory and autoimmune diseases with more recent prevalent use for covid-19 infections to control immune-mediated damage of lung tissue. We are presenting the first case of N. farcinica infection in a COVID-19 patient after a brief steroid course. The case also highlights N. farcinica infection mimicking a lung mass and demonstrates that pulmonary Nocardia infections can easily be misdiagnosed, highlighting the importance of keeping a broad differential. CONCLUSIONS: steroid use in the management of COVID-19 infection can result in opportunistic infections, including N. farcinica. REFERENCE #1: Margalit I, Goldberg E, Ben Ari Y, Ben-Zvi H, Shostak Y, Krause I, Muhsen K. Clinical correlates of nocardiosis. Sci Rep. 2020 Aug 31;10(1):14272. doi: 10.1038/s41598-020-71214-4. PMID: 32868850;PMCID: PMC7459281 REFERENCE #2: Coussement J, Lebeaux D, van Delden C, Guillot H, Freund R, Marbus S, Melica G, Van Wijngaerden E, Douvry B, Van Laecke S, Vuotto F, Tricot L, Fernandez-Ruiz M, Dantal J, Hirzel C, Jais JP, Rodriguez-Nava V, Lortholary O, Jacobs F;European Study Group for Nocardia in Solid Organ Transplantation. Nocardia Infection in Solid Organ Transplant Recipients: A Multicenter European Case-control Study. Clin Infect Dis. 2016 Aug 1;63(3):338-45. doi: 10.1093/cid/ciw241. Epub 2016 Apr 18. PMID: 27090987. DISCLOSURES: No relevant relationships by Muhammad Arif, source=Web Response No relevant relationships by Ericka Charley, source=Web Response No relevant relationships by Jonathan Munoz, source=Web Response No relevant relationships by Hursh Sarma, source=Web Response No relevant relationships by Andrew Talon, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Severe thrombocytopenia has been shown to be associated with poor prognosis in COVID-19 disease (1). Thrombocytopenia seen in COVID-19 is most likely due to autoimmune destruction or thrombotic consumption and cytokine release (1). Limited literature is available on the management of COVID-induced thrombocytopenia (1). CASE PRESENTATION: A 40 year old male, smoker, with past medical history (PMH) significant for gastroesophageal disease (GERD) presented to the emergency department with a one day history of new onset petechial rash and epistaxis. His rash appeared distally on his legs and progressed proximally up to his torso and head. He had minor upper respiratory tract (URI) symptoms for three days prior to the onset of rash and epistaxis. He received Mucinex for his URI. He had no history of bleeding disorder. He had a family history of factor V Leiden deficiency in his maternal grandfather and aunt. He had no fever, chest pain, shortness of breath and cough. He was found to be COVID positive with a platelet count of 4000. His vital signs were stable. He had clear lungs on presentation and throughout his hospital stay. His hepatitis panel was negative. He had no findings of disseminated intravascular coagulation (DIC). His vitamin B12 and folate levels, ANA screen and rheumatoid screen were within normal limits. His CT Scan of Abdomen with IV contrast was negative for splenomegaly. His Chest X ray was normal. His flow cytometry analysis showed no evidence of lymphoproliferative disorder. He received one unit of platelets and a four day empiric treatment with steroids. His platelet count improved to 70,000 on the day of discharge (day 4). Nine days after discharge, he was found to have recurrent thrombocytopenia with a platelet count of 17,000. He received intravenous IV immune globulin (IVIG) along with a 35 day taper of prednisone started at a dose of 50mg once daily. His platelet count continued to remain near 35,000 suggestive of steroid-refractory thrombocytopenia. He was started on a weekly regimen of Rituxan. His platelet count continued to remain below 100,000. His treatment is monitored and ongoing. DISCUSSION: COVID-19 associated thrombocytopenia is proposed to have various mechanisms in different phases of disease in diverse patients (1). The causal relationship between COVID-19 and immune thrombocytopenia (ITP), although well studied, has not been established (2). The majority of patients with COVID-19 and ITP have responded to high dose IVIG (1). CONCLUSIONS: Our patient had severe ITP due to COVID-19 despite having mild disease. He had steroid and IVIG-refractory thrombocytopenia. Further research in areas such as the effect of anti-TPO antibodies and splenectomy on these patients is warranted. REFERENCE #1: Murt A, Eskazan AE, et.al. COVID-19 presenting with immune thrombocytopenia: a case report and review of the literature. J Med Virol. 2021;93(1):43-45. REFERENCE #2: Zong X, Gu Y, Yu H, Li Z, Wang Y. Thrombocytopenia Is Associated with COVID-19 Severity and Outcome: An Updated Meta-Analysis of 5637 Patients with Multiple Outcomes. Lab Med. 2021;52(1):10-15. DISCLOSURES: No relevant relationships by Sathyanarayana Machani, source=Web Response No relevant relationships by Edward Marks, source=Web Response No relevant relationships by Trishala Menon, source=Web Response No relevant relationships by Irvin Richard, source=Web Response No relevant relationships by Bradley Schmitt, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: IL-6 inhibitors have emerged as a treatment option for moderate to severe COVID-19 infections. A hyperinflammatory state has been theorized to be the driving factor for acute respiratory distress syndrome in COVID-19. We discuss the case of a patient who received sarilumab for severe Covid infection and later developed CMV pneumonitis. IL- 6 inhibitors have been associated with secondary bacterial infections;however, the data on secondary viral and atypical infections are limited. CASE PRESENTATION: A 55-year-old male with no known past medical history presented to the hospital with complaints of worsening cough and shortness of breath. The patient was found to be COVID positive 3 days prior to presentation. CT chest on admission showed extensive peripheral ground-glass and consolidative lung opacities. Treatment with Decadron and Remdesivir was initiated.On hospital day 9, the patient had worsening respiratory status requiring up to 40 liters of vapotherm at 100% FiO2. After ruling out superimposed bacterial infection, he was treated with Sarilumab 400mg for worsening acute hypoxemic respiratory failure felt to be due to a hyperimmune syndrome from COVID-19. 10 days following treatment with Sarilumab, the patient's CRP normalized and his oxygen requirement decreased, he eventually weaned down to 5L nasal cannula.On hospital day 27, the patient again developed acute respiratory distress requiring intubation. A repeat chest CT showed evolving ground-glass and consolidative opacities with new basilar predominant traction bronchiectasis and architectural distortion. Additional lab testing revealed, CMV IgG >10 ( 0.00-0.59 U/ml) CMV IgM of 37.2 (0.0-29.9 AU/ml), CMV PCR DNA of 325000 ( not detected), and negative fungitell. Samples from bronchoalveolar lavage showed a CMV PCR of 46500 IU/ml ( not detected). Treatment with ganciclovir 5mg/kg q12h was initiated. Following treatment, the patient had progressive improvement in respiratory status, was weaned from the ventilator, and eventually discharged from the hospital. DISCUSSION: Cytokine storm is thought to play a key role in the lung injury seen in COVID 19 and IL-6 is essential in the propagation of cytokine Storm. There is an ongoing concern for bacterial infections in the setting of IL-6 inhibitors but the data on viral infections in this setting is limited. Van Duin et al describes a case of CMV reactivation in the setting of treatment with tocilizumab for rheumatoid arthritis. The patient developed fever and shortness of breath following the 2nd infusion of tocilizumab. A CT scan of the chest showed pneumonitis. Labs were significant for viremia on CMV PCR and positive CMV IgG. The patient had improvement after treatment with ganciclovir, similar to our case. CONCLUSIONS: The adverse effects of IL-6 inhibitors are not fully understood. Based on our limited experience we recommend checking CMV IgG before initiation of IL-6 inhibitors. REFERENCE #1: Han, Q., Guo, M., Zheng, Y., Zhang, Y., De, Y., & Xu, C. et al. (2020). Current Evidence of Interleukin-6 Signaling Inhibitors in Patients With COVID-19: A Systematic Review and Meta-Analysis. Frontiers In Pharmacology, 11. doi: 10.3389/fphar.2020.615972 REFERENCE #2: Tleyjeh, I., Kashour, Z., Damlaj, M., Riaz, M., Tlayjeh, H., & Altannir, M. et al. (2021). Efficacy and safety of tocilizumab in COVID-19 patients: a living systematic review and meta-analysis. Clinical Microbiology And Infection, 27(2), 215-227. doi: 10.1016/j.cmi.2020.10.036 REFERENCE #3: van Duin D, Miranda C, Husni E. Cytomegalovirus viremia, pneumonitis, and tocilizumab therapy. Emerg Infect Dis. 2011;17(4):754-756. doi:10.3201/eid1706.101057 DISCLOSURES: No relevant relationships by Gretel D'Souza, source=Web Response No relevant relationships by Elizabeth Pandian, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: During the COVID-19 pandemic, superimposed infections with both bacterial and fungal organisms have been shown to complicate the viral process. Aspergillus and candida are the most common fungal organisms reported [2];but there have also been a few case reports with co-infection from Pneumocystis jirovecii pneumonia (PJP) [1,3]. We present a COVID patient with lymphopenia and diffuse ground glass opacities who was also diagnosed with PJP. CASE PRESENTATION: A 58-year-old male with past medical history of emphysema liver cirrhosis presented to the hospital with nausea, vomiting and abdominal distention. On examination he was afebrile, hypotensive with a blood pressure of 88/56, SpO2 was 96% on room air. His lungs were clear on auscultation and abdominal exam was notable for moderate ascites. There was 2+ pedal edema bilaterally. Laboratory work-up showed a WBC count of 12000/µL, only 7% of which were lymphocytes. Chest X-ray did not reveal any acute pathology and screening COVID-19 PCR was negative. He was admitted to the medical ward for management of alcohol withdrawal and decompensated liver cirrhosis. He developed hypoxic respiratory failure within 24 hours of presentation. CT chest (Figure 1) showed multifocal ground glass opacities along with bilateral pleural effusions and consolidative airspace disease at bases. A repeat COVID PCR resulted positive. His respiratory failure progressively worsened over the next two weeks despite being treated with remdesivir, dexamethasone and empiric broad spectrum antibiotics. He was intubated and placed on mechanical ventilation. Repeat imaging (Figure 2) showed worsening diffuse ground glass opacities now with more predominant cystic changes. Bronchoscopy with broncho-alveolar lavage (BAL) was performed, PCR testing of the BAL sample detected Pneumocystis jirovecii. He was then started on Bactrim in conjunction with steroids for the high A-a gradient. HIV antibody was negative, CD4 lymphocyte count was low at 304/µL and CD8 counts were normal at 311/µL. The patient slowly started to improve and was successfully extubated after three weeks. However, he later on developed septic shock from candidemia and was placed on hospice care by family due to his poor functional status. DISCUSSION: As with many viral infections, patient's with COVID-19 have demonstrated considerable risk for developing concomitant bacterial and fungal infections. We speculate that lymphopenia with low absolute CD4 count, combined with the use of corticosteroids may play a role in susceptibility to opportunistic infections in otherwise immunocompetent hosts. CONCLUSIONS: When critically ill COVID patient's fail to improve and have persistent lymphopenia, co-infections should be considered and appropriately worked up. REFERENCE #1: A case of COVID-19 and Pneumoncystis jirovecii Coinfection. A. Menon et al. Am J Respir Crit Care Med. 2020 Jul REFERENCE #2: Invasive Fungal Disease Complicating Coronavirus Disease 2019: When It Rains, It Spores. M.Hoenigl. Clinical infectious diseases. 2020 September REFERENCE #3: Pneumocystis and Severe Acute Respiratory Syndrome Coronavirus 2 Coinfection: A Case Report and Review of an Emerging Diagnostic Dilemma. C. Rubiano. Open Forum Infectious Diseases. January 2021. DISCLOSURES: No relevant relationships by Ahmed Mahgoub, source=Web Response No relevant relationships by Joseph Meharg, source=Web Response No relevant relationships by Leandro Ramirez, source=Web Response No relevant relationships by Ajit Thota, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The SARS-CoV-2 causing COVID-19 can have serious effects on the heart with recent data suggesting acute cardiac injury in almost one fifth of COVID-19 patients. Considering the recent role out of Covid-19 vaccine's to the general public there is a growing concern of COVID-19 related myocarditis being linked to the vaccine. Here we present a case of a young patient who presented with symptoms of COVID-19 after his second shot of COVID-19 vaccine, with subsequent development of myocarditis. CASE PRESENTATION: This patient is a 21 year old male with past medical history significant of mitral valve prolapse, and resting tachycardia, presented with a 2 day history of fevers, nausea, accompanied by shortness of breath, and chest pain. Patient had his 2nd shot of Pfizer-BioNTech Covid-19 vaccine 3 days prior to admission, symptom onset was after the administration of vaccine. Vitals on admissionm were within normal limits, EKG did not show any acute ischemic changes, no evidence pericarditis and or pulmonary embolism related changes. Troponins were trended, 460, 637, 832, significant for acute myocardial injury but with no evidence of MI based on character of chest pain and EKG changes. 2D echocardiogram showed Left Ventricular (LV) Ejection Fraction of 43%, with mildly reduced LV systolic function. CTA chest with IV contrast showed no aortic dissection., or pulmonary embolism. Cardiac MRI showed findings suggestive of acute myocarditis. Patient was treated symptomatically, troponins trended down, with resolution of chest pain. DISCUSSION: Myocarditis associated with the Pfizer-BioNTech Covid-19 vaccine, is a potential rare side effect. Even though a casual link has not been established. Considering the sequence of events for this patient, there is potentially a link between the two. Recently there have been 62 cases in Israel diagnosed after receiving the second dose of the Pfizer-BioNTech Covid-19 vaccine, incidentally most of these cases were in individuals under the age of 30, coinciding with our case. Investigations will be needed to determine what is making the younger population more prone to myocarditis after receiving the covid 19 vaccine. CONCLUSIONS: Myocarditis has been associated with COVID-19 infection. But the link with Pfizer-BioNTech Covid-19 vaccine is less established, with few cases providing a causal link. Recent studies have started to link the two, but further investigations are necessary to better understand the causal link, and what propogates the younger population to develop myocarditis after receiving the COVID-19 Vaccine. REFERENCE #1: https://www.forbes.com/sites/brucelee/2021/04/27/are-rare-cases-of-myocarditis-linked-to-pfizer-moderna-covid-19-vaccines/?sh=2b1641057442 DISCLOSURES: No relevant relationships by Tapan Buch, source=Web Response No relevant relationships by Pradeepto Ghosh, source=Web Response no disclosure on file for Amandeep Kaur;No relevant relationships by Kashyap Kela, source=Web Response No relevant relationships by jacob miller, source=Web Response no disclosure on file for Raza Naseer;no disclosure on file for Muhammad Siddique Pir;No relevant relationships by Princy Shah, source=Web Response No relevant relationships by Vijay Pratap Singh, source=Web Response

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Electronic cigarette or vaping product use-associated lung injury (EVALI) is potentially life-threatening disease that has become increasingly recognized over the last years. However, the extra-pulmonary manifestations of this disease are not as well described. We present a patient who simultaneously developed acute EVALI and stress induced cardiomyopathy. CASE PRESENTATION: A 35-year-old female with a recent heavy vaping history presented to hospital via EMS due to disorganized behavior. Her past medical history was notable for polysubstance abuse and an extensive neuropsychiatric history. Her vital signs were notable for sinus tachycardia, hypotension and hypoxia with an oxyhemoglobin saturation 65%. Her physical exam was notable for cyanosis, rales to pulmonary auscultation and use of accessory muscles. She was intubated and started on empiric antibiotics for community acquired pneumonia, and vasopressors. A computer tomography pulmonary angiography (CTPE) was negative for acute pulmonary embolism but showed scattered bilateral airspace opacities with dependent consolidations (fig 1.). Relevant laboratory on admission included procalcitonin 28.17, WBC count 12.9 and troponin 1.58. SARs-COV-2, serum blood cultures, legionella antigen, streptococci pneumoniae antigen and HIV were negative. Urine toxicology was positive for cannabinoids. Bronchoalveolar lavage later demonstrated 50,000 TNC with neutrophil predominance. EKG showed sinus tachycardia and nonspecific ST depression. Echocardiogram revealed severe diffuse hypokinesis with left ventricular ejection fraction (LVEF) of 13%. During her ICU course she continued on mechanical ventilation with lung protective strategy, systemic glucocorticoids and antibiotics. Vasopressors were subsequently weaned off. Repeated echocardiogram on ICU day five demonstrated a recovered LVEF at 55%. Patient's hypoxemia improved, and she was successfully extubated on ICU day eight. DISCUSSION: Pulmonary injury is the most well described clinical manifestation of EVALI, however a large majority of these patients also present with gastrointestinal symptoms and malaise, suggesting a systemic disease process. Our patient had newly reduced LVEF suggestive of stress induced cardiomyopathy which consequently improved with standard and supportive care. CONCLUSIONS: It is important to maintain a high index of suspicion of secondary organ damage, as prompt diagnosis and treatment of EVALI associated cardiac dysfunction can have an impact in short- and long-term prognosis. REFERENCE #1: Kligerman S, Raptis C, Larsen B, Henry TS, Caporale A, Tazelaar H, Schiebler ML, Wehrli FW, Klein JS, Kanne J. Radiologic, Pathologic, Clinical, and Physiologic Findings of Electronic Cigarette or Vaping Product Use-associated Lung Injury (EVALI): Evolving Knowledge and Remaining Questions. Radiology. 2020 Mar;294(3):491-505. doi: 10.1148/radiol.2020192585. Epub 2020 Jan 28. PMID: 31990264. DISCLOSURES: No relevant relationships by David barounis, source=Web Response No relevant relationships by Xavier Fonseca, source=Web Response No relevant relationships by Dana Mueller, source=Web Response

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Emphysematous pyelonephritis (EPN) is an uncommon acute severe necrotizing infection of the renal parenchyma and its surrounding tissues that results in the presence of gas in the renal parenchyma, collecting system, or perinephric tissue. The clinical course of EPN can be life threatening if not managed astutely. The primary organisms responsible include Escherichia coli and Klebsiella Pneumoniae. We present a rare and uncommon case of severe EPN that was managed conservatively with good outcome. CASE PRESENTATION: A 63-year-old Hispanic female with a past medical history of uncontrolled diabetes and hypertension presented with a four-day history of abdominal pain, nausea, vomiting and diarrhea. Vital signs showed T 38.2°C, HR 99, BP 103/58 mmHg and saturating 100% on RA. Palpation and percussion of the left flank region elicited pain. Lab findings were significant for hyponatremia (132), hypochloremia (95), elevated BUN and Creatinine (43/2.4), hyperglycemia (264), elevated CRP 36.5. Initial lactic acid was found to be 2.8. Urinalysis showed findings suggestive of a UTI. Patient also was incidentally found to have COVID-19 Ag and PCR positive. Chest X-ray showed mild interstitial prominence. Emergent renal ultrasound reported scattered foci of air in the left renal upper pole calyces and proximal ureter. CT Abdomen Pelvis with contrast showed air in the bladder and left ureter and kidney. Despite adequate initial resuscitation with IV fluids and IV piperacillin-tazobactam, her lactic acid increased peaking at 8.5 and she was promptly moved to MICU for hemodynamic monitoring. With a working diagnosis of EPN and SARS-CoV-2 infection, she was switched to Meropenem, placed on IV fluids and her pain was managed supportively. Urology was consulted who recommended close monitoring and plan for emergent intervention if condition worsened. However, since patient started to recover, she did not undergo intervention. Antibiotics were de-escalated to Ceftriaxone after blood cultures grew sensitive Escherichia coli. Patient's condition improved and she was discharged with outpatient follow-up with urology. DISCUSSION: Based on CT findings, emphysematous UTI's are characterized into Class I to IV with increasing mortality associated as you move towards class IV. Our patient initially presented with Class I and as a result was promptly started on antibiotics. If EPN had progressed anymore, she would have needed a percutaneous drainage, or even nephrectomy in refractory cases, in addition to antibiotic therapy. However, due to prompt care and aggressive monitoring provided to her, she was able to improve without further interventions. The rarity of the condition and the decision-making involved while managing the disease makes this case unique. CONCLUSIONS: Emphysematous pyelonephritis is an uncommon severe infection of the renal parenchyma, which with early diagnosis can be managed conservatively. REFERENCE #1: Sharma PK, Sharma R, Vijay MK, Tiwari P, Goel A, Kundu AK. Emphysematous pyelonephritis: Our experience with conservative management in 14 cases. Urol Ann. 2013;5(3):157-162. doi:10.4103/0974-7796.115734 REFERENCE #2: Huang JJ, Tseng CC. Emphysematous pyelonephritis: clinicoradiological classification, management, prognosis, and pathogenesis. Arch Intern Med. 2000;160:797–805. DISCLOSURES: No relevant relationships by Rutwik Patel, source=Web Response No relevant relationships by Laxminarayan Prabhakar, source=Web Response No relevant relationships by Manogjna Prasad, source=Web Response

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: COVID-19 is thought to cause a prothrombotic state with a relatively high rate of associated thromboembolic disease. Priapism has previously been described in a single case report as a potential thrombotic complication of severe COVID-19.1 Priapism, the persistence of an erection not associated with sexual desire, mostly commonly results from ischemic (low-flow or veno-occlusive) causes. Medications and blood dyscrasias are among the most common etiologies of ischemic priapism. Here we report a case of priapism in a patient admitted to the medical ICU for ARDS caused by severe COVID-19. CASE PRESENTATION: A 68-year-old man with a past medical history of chronic kidney disease, benign prostatic hyperplasia, and diabetes mellitus presented to the emergency department for worsening dyspnea, nausea and fatigue. He had been diagnosed with COVID-19 eight days prior. On arrival, the patient was profoundly hypoxemic despite being placed on high-flow nasal cannula. He was then intubated and placed on mechanical ventilation. A chest x-ray showed bilateral patchy infiltrates consistent with COVID-19 pneumonia. The patient became hypotensive and was started on vasopressors. His platelet count was normal and he was maintained on heparin subcutaneously three times per day for DVT prophylaxis. On the morning of hospital day seven, it was noted that the patient had a persistent erection for > 4 hours. He had not received any alpha adrenergic antagonist, antipsychotic, or antidepressant medications.Urology was consulted who subsequently performed a corporal aspiration and irrigation. Approximately 75 cc of dark blood were evacuated, which led to flaccidity of the penis. A corporal blood gas was found to be consistent with ischemia with a pH

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hereditary Hemorrhagic Telangiectasia is a multisystem disease which results in AV Malformations and telangiectasia. It has autosomal dominant inheritance and prevalence of 1 in 5000 to 1 in 10,000. 1 Patients with Pulmonary AVMs can present with hypoxia, more post exercise and in sedentary position with improvement on standing. Patients presenting with hypoxia with history of HHT should undergo thorough evaluation including radiological imaging and echocardiography to rule out recurrence of AVMs and sequelae such as pulmonary hypertension or pulmonary arterial hypertension, respectively. CASE PRESENTATION: We present a case of 66 y/o male with Past medical history of HHT with AVM s/p repair presented with complaints of dyspnea with cough and sputum production. In ER patient was hypoxic with SPO2 88% on room air. Patient had coarse rhonchi, scattered wheeze and telangiectasia on the nose and hands. Routine labs were normal. Legionella antigen, SARS antigen, COVID PCR were negative. Chest x-ray revealed peri hilar and basilar reticular opacities. CT of chest with contrast revealed prior right lower lobe AVM repair with almost complete resolution and signs of severe COPD with emphysema. Transthoracic echocardiogram ruled out pulmonary artery hypertension. Patient was treated for COPD exacerbation with albuterol/ ipratropium nebulization, steroids, oxygen support and azithromycin. DISCUSSION: HHT is a familial genetic disease with autosomal dominant mutations of endoglin gene on chromosome 9q33-q34 or ALK-1 gene on chromosome 12q13.2 50% of all HHT patients develop pulmonary AV malformations. Clinical finding includes hypoxic respiratory failure. Pulmonary AVMs lead to right to left shunt formation impairing effective gas exchange leading to hypoxia, interestingly these patients can participate in high intensity physical activity despite of being severely hypoxic, this has been attributed to hemodynamic compensatory responses. 3 This shunt can lead to paradoxical emboli causing strokes and brain abscess. Management of Pulmonary AVMs includes trans catheter coil vaso-occlusion of the artery. Recanalization of treated pulmonary AVMs and development or growth of untreated pulmonary AVMs has been known, warranting long term follow up. Pulmonary AVMs itself is a life threating condition, its course can be further complicated by chronic lung disease like COPD. These patients can present with dyspnea not explained by right to left shunting, it is attributed more to underlying lung conditions, in our patient's case, COPD. CONCLUSIONS: While HHT is not known to cause COPD, it can lead to worsening of COPD by causing Pulmonary hypertension due to high output cardiac failure or pulmonary artery hypertension. Therefore, in patients with history of HHT presenting with hypoxia, it is crucial to have detailed evaluation for recurrence of AV malformations or new onset pulmonary hypertension. REFERENCE #1: Mary E. Meek, M.D., James C. Meek, D.O., Michael V. Beheshti, M.D. Management of Pulmonary AV Malformations [Google Scholar, PubMed] REFERENCE #2: C. Sabba, M. Gallitelli, G. Pasculli, P. Supressa, F. Resta and E. Tafaro. HHT: A rare disease with a broad spectrum of clinical aspects [PubMed] REFERENCE #3: Dupius-Girod S., Cottin V, Shovlin C. The lung in hereditary hemorrhagic telangiectasia [Google Scholar] DISCLOSURES: No relevant relationships by Khushdeep Chahal, source=Web Response No relevant relationships by priyanka kapoor, source=Web Response

TOPIC: Chest Infections TYPE: Original Investigations PURPOSE: We retrospectively investigated COVID-19 patients on anticoagulation or antiplatelet medications as their home medication or used as inpatient treatment to evaluate if they exhibited lower levels of D-dimer and lower rates of embolic events and mortality. METHODS: This correlational retrospective study evaluated n=319 COVID-19 patients admitted to acute inpatient services across the Mercy Health Youngstown hospitals. A retrospective chart audit included home medications and admission medications, hospital and ICU length of stay, days on the ventilator, initial and follow-up labs (D-dimer), and thromboembolic events after diagnosis of COVID-19. We constructed a composite index for any embolic events occurring in inpatient: MI, DVT, PE, stroke, and cardiac arrest. The prevalence of these embolic events was 23.5% (n=75/319). For propensity modeling, comorbidities, initial D-dimer, demographics, days from a positive COVID-19 test result to admission, and a summative index of comorbidities were entered in a binary logistic regression model to predict embolic events. RESULTS: The rate of any embolic events among COVID inpatients was 23.5% (n=75/319). Initial D-dimer was 1648±1702 ng/mL among patients experiencing any embolic events and was lower among patients without embolic events, 1009±1205 ng/mL (t=3.638, p < 0.001). In iterative forward selection, logistic modeling retained in the model for embolic events were age, initial D-dimer, past medical history of ESRD, and ethnicity, which correctly classified 75% of embolic events in patients (AUC=0.702). The addition of home medications, antiplatelets and anticoagulants to the propensity model did not significantly improve AUC (0.704) which indicates that neither home use of anticoagulation nor antiplatelets was associated with inpatient embolic events in a propensity adjusted model. However, when inpatient anticoagulation therapy was initiated, statistically significant benefit in preventing embolic events was observed (AOR = 3.32 (95% CI 1.79-6.16);AUC 0.752 (p < 0.001)). Similarly, home use of antiplatelet and anticoagulation medications was not associated with mortality in COVID-19 patients, but in-hospital use of anticoagulation was statistically significant (p=0.036). CONCLUSIONS: Our study aimed to see if taking antiplatelet or anticoagulation medications as a home medication would have any effect on thromboembolic events and mortality in COVID-19 patients compared to when receiving antiplatelet or anticoagulation agents during hospitalization. We found that being on an antiplatelet or anticoagulation medication at home (before hospitalization) did not prevent COVID-19 patients from thromboembolic events or improve mortality. However, after adjusting for baseline risk of embolic events, in-hospital anticoagulation had a statistically significant benefit in preventing embolic events and mortality. CLINICAL IMPLICATIONS: It has been established that COVID-19 patients are at higher risk for embolic events that have been linked to increased mortality. In our current study using a composite index model to predict embolic events in COVID-19 patients, the use of anticoagulation agents during hospitalization revealed a significant reduction in embolic risks and mortality while patients on home antiplatelet or anticoagulation medications did not show benefits in reducing the same risks. DISCLOSURES: No relevant relationships by Omotooke Babalola, source=Web Response No relevant relationships by Timothy Barreiro, source=Web Response No relevant relationships by David Gemmel, source=Web Response No relevant relationships by Oyidiya Osoka, source=Web Response No relevant relationships by Jeannie Ur, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The complications of coronavirus disease 2019 (COVID-19) involve the nervous system, including acute stroke, which is currently linked to the hypercoagulable state associated with COVID-19 [1]. CASE PRESENTATION: Our patient is a 70-year-old man with past medical history of hypertension and diabetes mellitus who presented to the emergency department with shortness of breath and fatigue for five days duration. Vitaly was stable, except for saturating 88% on the room air. He was alert and oriented on physical exam, lung exam was remarkable for bibasilar rales. He had no focal neurological deficits. Lab Work showed elevated COVID-19 markers. Chest x-ray showed left-sided infiltrates. He was admitted to the respiratory care unit and was started on dexamethasone, remdesevir, ceftriaxone, azithromycin, and enoxaparin prophylactic dose. His oxygen requirement continued to increase, and on the ninth day, he was placed on a nasal high-flow oxygen device with 60 liters FiO2 of 90%. On the eleventh day, the patient developed right facial droop, aphasia and right-sided weakness. The National Institutes of Health Stroke Scale was 16. Code stroke was called, and a brain computed tomography scan without contrast revealed cortical infarct in the high left parietal cerebral hemisphere without hemorrhage. Computed tomography angiography (CTA) of the head and neck showed mild narrowing within the middle cerebral artery. Magnetic resonance imaging, later on, showed left medial frontoparietal infarct in ACA territory. Cardiology workup confirmed no cardiac pathology. The neurology team decided not to start the tissue plasminogen activator (tPA) because he was out of the tPA window, and as no large vessel occlusion was found, a thrombectomy was not performed. DISCUSSION: COVID-19 infection is considered a highly coagulable status, especially the severe form of the disease. The pathophysiology behind this is not well understood yet. However, Severe COVID-19 is associated with cytokine activation, which activates endothelial cells and mononuclear cells with expression of tissue factor leading to coagulation cascade activation [2]. It has also been observed that COVID-19 can induce Antiphospholipid antibodies, which might play a role in thrombosis in those patients [3]. Our case confirms that COVID-19 induced acute stroke can occur in multiple territories despite the patient being well anticoagulated. CONCLUSIONS: Acute stroke should be suspected in COVID-19 patients with acute neurological changes even if the patient is on prophylactic anticoagulation. Frequent screening neurological examination can lead to early detection and treatment of acute stroke. REFERENCE #1: Verstrepen, K., Baisier, L. & De Cauwer, H. Neurological manifestations of COVID-19, SARS and MERS. Acta Neurol Belg 120, 1051–1060 (2020). https://doi.org/10.1007/s13760-020-01412-4 REFERENCE #2: Beyrouti R, Adams ME, Benjamin L, et alCharacteristics of ischaemic stroke associated with COVID-19Journal of Neurology, Neurosurgery & Psychiatry 2020;91:889-891. REFERENCE #3: Zhang Y, Xiao M, Zhang S, Xia P, Cao W, Jiang W, Chen H, Ding X, Zhao H, Zhang H, Wang C, Zhao J, Sun X, Tian R, Wu W, Wu D, Ma J, Chen Y, Zhang D, Xie J, Yan X, Zhou X, Liu Z, Wang J, Du B, Qin Y, Gao P, Qin X, Xu Y, Zhang W, Li T, Zhang F, Zhao Y, Li Y, Zhang S. Coagulopathy and Antiphospholipid Antibodies in Patients with Covid-19. N Engl J Med. 2020 Apr 23;382(17):e38. doi: 10.1056/NEJMc2007575. Epub 2020 Apr 8. PMID: 32268022;PMCID: PMC7161262. DISCLOSURES: No relevant relationships by Abdul Rahman Al Armashi, source=Web Response No relevant relationships by Ameed Bawwab, source=Web Response No relevant relationships by Arthur Boyd, source=Web Response No relevant relationships by Kanchi Patell, source=Web Response No relevant relationships by Keyvan Ravakhah, source=Web Response No relevant relationships by Francisco Somoza-Cano, source=Web Response

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: MIS-C is described as a clinical syndrome developing secondary to Coronavirus disease 2019 (COVID-19) in children and adolescents. The presentation is similar to Kawasaki syndrome, hemophagocytic lymphohistiocytosis (HLH) and toxic shock syndrome. We present a case of MIS-C in a young adult two weeks after receiving vaccination for COVID-19. CASE PRESENTATION: 21 year old female with a past medical history of asthma who presented to the emergency department (ED) with fevers, chills and photophobia since receiving the JJ223:14–19.e2 REFERENCE #2: CDC COVID-19 Response Team. Coronavirus disease 2019 in children—United States, February 12–April 2, 2020. Morb. Mortal. Wkly. Rep. 2020, 69, 422–426. DISCLOSURES: No relevant relationships by Bilal Bangash, source=Web Response No relevant relationships by Issa Makki, source=Web Response No relevant relationships by Joseph Pitcher, source=Web Response

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Long COVID- 19 or post-acute COVID -19 syndrome is now recognized as a range of symptoms that can last weeks or months after first being infected with COVID-19 or SARS -CoV 2 virus. It can appear weeks after infection irrespective of the severity of the illness1. It can affect most, if not all, body systems including heart, lung, kidney, skin, and brain functions. Here we present a case with Covid-19 infection with hyporcortisolism presenting as dyspnea and fatigue as the dominant long Covid-19 symptom. CASE PRESENTATION: A 55-year-old female with a past medical history of hyperthyroidism on propranolol, was diagnosed with mild COVID -19 infection, advised to treat with self-isolation. She revisited ER 6 weeks later with persistent dyspnea, fatigue, and poor ability to focus and concentrate. She was given a trial of the direct oral anticoagulant for 4 weeks with no change in her symptoms. The subsequent workup done;head-computer tomography scan (CTS) was negative for subarachnoid hemorrhage and cerebral venous thrombosis. The Lungs CTS did not reveal any pulmonary fibrosis. The 6-minute walk test was impaired at 79%. The Pulmonary Function test did not show any significant obstruction or restriction. The Cardiopulmonary Exercise Test overall was suggestive of deconditioning. The laboratory work included creatine kinase, Aldolase, vitamin B12, Folic acid, C-reactive protein, Vitamin D, Antinuclear antibody Thyroid Function test all were unremarkable. The AM cortisol level came back as less than 2. The patient was started on oral prednisone for a diagnosis of relative adrenal insufficiency. All her symptoms improved within 2 weeks of treatment and resolved after 4 -6 weeks, she was tapered down and finally weaned off prednisone. DISCUSSION: The proposed mechanism of COVID-19 induced relative adrenal insufficiency is likely hypophysitis.2 The principal target for the virus entry is the angiotensin-converting Enzyme 2 (ACE-2) receptor which is found on pneumocytes, arterial and venous endothelial cells of many organs including adrenal glands and hypothalamic and pituitary tissues2. Furthermore, SARS- Cov2 virus has amino acid sequences which are similar to the host's ACTH, so antibodies made against the virus destroys the host ACTH and consequently may cause contribute to cortisol insufficiency.2,3 CONCLUSIONS: Post COVID-19 infection has a multifaceted manifestation. Hypocortisolism can persist in patients with post COVID-19 and should be sought for if the symptoms are suggestive. The treatment is simple and effective. REFERENCE #1: Naserghandi, S.F. Allameh and R. Saffarpour. All about COVID-19 in brief. New Microbes New Infect. 2020 May;35: 100678. Published online 2020 Apr 13. doi: 10.1016/j.nmni.2020.100678 PMID: 32292590. REFERENCE #2: Pal, R. COVID-19, hypothalamo-pituitary-adrenal axis and clinical implications. Endocrine 68, 251–252 (2020). https://doi.org/10.1007/s12020-020-02325-1. REFERENCE #3: R. Wheatland, Molecular mimicry of ACTH in SARS—implications for corticosteroid treatment and prophylaxis. Med. Hypoth. 63, 855–862 (2004) PMID: 15488660. DISCLOSURES: No relevant relationships by Parinaz Ayat, source=Web Response No relevant relationships by Aaliya Burza, source=Web Response No relevant relationships by Charlyn Habeeb, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Novel Coronavirus disease 2019 (COVID-19) pandemic represents the greatest global public health crisis since the influenza outbreak in 1918. It has been associated with hypercoagulability causing life-threatening cardiovascular and neurovascular complications. The pathogenesis of this predisposition is not well understood, and one of its consequences is an increased risk of stroke. Patients with patent foramen ovale (PFO), atrial fibrillation, previous history of stroke, and elderly patients with uncontrolled hypertension, may be at a higher risk of developing strokes with COVID-19. We present a rare case of acute multiple cerebral watershed infarctions in a COVID-19 patient. CASE PRESENTATION: 38 year-old obese male with past medical history of hypertension presented with confusion, left sided weakness, right lower extremity weakness, and right gaze preference. MRI brain demonstrated multiple patchy small areas of acute ischemic infarcts bilaterally consistent with watershed infarcts. An echocardiogram with bubble study was negative for PFO. Lower extremity venous Doppler ultrasound was negative for DVT. Telemetry didn't record any arrhythmias. Laboratory work-up ruled out autoimmune diseases, hypercoagulable states, and vasculitis including: antiphospholipid antibodies, lupus anticoagulants, anti-neutrophil cytoplasmic antibodies, anti-nuclear antibodies, anti-factor Xa, Anti-thrombin, Protein S and C, and rapid plasma regain. The patient was screened for COVID-19 due to increased reports of stroke in young patients nationwide, and surprisingly, the test was positive. Aspirin, clopidogrel, high-intensity statins, along with enoxaparin for DVT prophylaxis were initiated. DISCUSSION: Evidence increasingly shows that COVID-19 it is not always confined to the respiratory tract but can also induce neurologic diseases with increased risk of stroke in young patients. The reported incidence of stroke in COVID-19 positive patients is about 1-6%. The plausible proposed mechanisms include: viral neurotropism, coagulopathy from systemic inflammation and cytokine storm, and endothelial dysfunction leading to angiopathic thrombosis. There are handful of cases linking COVID-19 to large vessel macrothrombosis and antiphospholipid syndrome. We herein report an even more unusual case that presented with multiple focal neurologic symptoms and was found to have watershed infarctions secondary to COVID-19 with only mild respiratory symptoms, without typical vascular risk factors, PFO or arrhythmia, after excluding autoimmune diseases, hypercoagulability diseases, and vasculitis, shedding the light on the importance of suspecting this devastating disease in an otherwise healthy young patient who presents with focal neurological symptoms. CONCLUSIONS: In COVID-19 patients with mild respiratory symptoms, a low threshold for investigation for stroke should be adopted with any new neurological symptoms. REFERENCE #1: Tan YK, Goh C, Leow AST, et al. COVID-19 and ischemic stroke: a systematic review and meta-summary of the literature. J Thromb Thrombolysis. 2020;50(3):587-595. doi:10.1007/s11239-020-02228-y DISCLOSURES: No relevant relationships by Ramy Abdelmaseih, source=Web Response No relevant relationships by Randa Abdelmasih, source=Web Response

TOPIC: Allergy and Airway TYPE: Medical Student/Resident Case Reports INTRODUCTION: Magnetic resonance contrast agents are used to better characterize disease processes during Magnetic Resonance Imaging (MRI). Gadolinium based contrast agents (GBCA) are widely used due to their safety profile. The incidence of adverse events after receiving GBCAs is less than 2%, most being mild and transient [1,2]. Here, we see a patient who developed cardiopulmonary arrest after GBCA administration. CASE PRESENTATION: A 57 year old female with a past medical history of asthma, hypertension, diabetes, hyperlipidemia and mild COVID19 infection, presented to outpatient brain MRI for evaluation of new hearing loss. After receiving Gadobutrol, she developed shortness of breath, abdominal pain, and emesis. In the emergency department, the patient was hypothermic, tachypneic, and hypoxic;no urticaria or rash noted. She was placed on non-invasive ventilation and treated for presumed anaphylaxis, but remained hypoxic and in respiratory distress. Subsequent intubation (without angioedema visualized) was complicated by cardiac arrest, requiring six minutes of cardiopulmonary resuscitation. Initial imaging was significant for CT chest showing diffuse ground glass and consolidative opacities and normal CT head. Despite standard care treatment, the patient's neurological exam worsened, one week into her admission she was observed to have minimal brainstem reflexes, with head CT showing findings of anoxic brain injury, cerebral edema and possible uncal herniation. She worsened clinically and expired thirteen days after admission. Autopsy performed showed clinicopathological correlation attributing anoxic brain injury secondary to anaphylaxis. DISCUSSION: Gadobutrol is approved for multiple indications in most ages. It was introduced in 1998, its safety profile has been studied in patients worldwide. The incidence of adverse events of GBCA has been reported to be 0.32-3.8%, commonly nausea, vomiting, urticaria and dizziness. Risk factors include patients' history of respiratory allergic disease, asthma, COPD, or prior history of reactions to iodinated contrast media [1,2]. The incidence of serious adverse drug reactions (ADR) involving the cardiopulmonary system is reported to be

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Coronavirus Disease 2019 (COVID-19) continues to be a global pandemic with its management evolving as research continues to unveil innovative therapies. Dantrolene, approved in malignant hyperthermia, may have utility for hyperpyrexia in COVID-19 patients, given its cytoprotective effects (1). Here we present a COVID-19 case with persistent hyperpyrexia despite conventional antipyretic measures that abated after dantrolene administration. CASE PRESENTATION: A 57-year-old Hispanic male with no past medical history, presented with fever, palpitations, myalgias and worsening dyspnea. He denied other symptoms. His admission vitals were Temp 101.3F, BP 155/81, Pulse 106, Resp 22, SpO2 88% on RA and 98% on 50% Venturi Mask. Lung examination revealed decreased air entry throughout with scattered crackles. Laboratory investigations showed WBC of 5.61 with normal electrolytes. ABG showed pH 7.45, pCO2 36, pO2 59 with FiO2 0.35 which improved with increased oxygenation. CXR showed hallmark features for COVID-19 pneumonia. COVID-19 PCR was positive. Antibiotics and prophylactic anticoagulation were initiated. He was later admitted to the medical floor. His hospital course was unremarkable until day three when he developed acute hypoxic respiratory failure requiring high flow nasal cannula and intensive care transfer. Despite optimal oxygenation, PF ratio was 105F. Besides multiple positive COVID-19 tests, all other infectious investigations were negative. Antibiotics, antivirals and antifungals were started but pyrexia persisted. Intravenous dantrolene (2.5mg/kg then 1mg/kg) was given after which temperature abated. De-escalation of care ensued, with removal of antimicrobials, intubation and ECMO. Patient had an uneventful transfer from MICU and discharge from the hospital. DISCUSSION: Hyperpyrexia is an extreme elevation of core body temperature usually >106.7 °F due to an elevated hypothalamic thermo-regulatory threshold. It has been reported in COVID-19 patients and portends a poor outcome with up to 100% mortality. Proposed mechanisms include immune dysfunction, direct brain injury from SARS-CoV-2 and vascular thrombosis (2). Dantrolene has been shown to inhibit multiple cell damage induced by SARS-CoV-2 infection (1). In our index case, all conventional antipyretic measures failed, while dantrolene achieved normothermia. CONCLUSIONS: Our case had a favorable outcome juxtaposing those previously reported (1,2). The proposition that dantrolene can be repurposed in COVID-19 patients with hyperpyrexia is novel and hopefully will stimulate and unearth more research. REFERENCE #1: Jiang, B., Liang, S., Liang, G., & Wei, H. (2020). Could dantrolene be explored as a repurposed drug to treat COVID-19 patients by restoring intracellular calcium homeostasis?. European review for medical and pharmacological sciences, 24(19), 10228–10238. https://doi.org/10.26355/eurrev_202010_23247 REFERENCE #2: Suwanwongse, K., & Shabarek, N. (2020). Hyperpyrexia in patients with COVID-19. Journal of medical virology, 92(11), 2857–2862. https://doi.org/10.1002/jmv.26154 DISCLOSURES: No relevant relationships by Sneha Adidam, source=Web Response No relevant relationships by Sahai Donaldson, source=Web Response No relevant relationships by Lorenzo Leys, source=Web Response No relevant relationships by Alicia Thomas, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The ongoing coronavirus disease 2019 (COVID-19) pandemic has resulted in persistent pulmonary complications among survivors. As our understanding of post infectious pulmonary phenomena continues to evolve, it is clear there are multiple difference manifestations of pulmonary lung disease associated with severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Here we describe a case of bullous lung disease as a complication of COVID-19. CASE PRESENTATION: A 61-year-old gentleman without significant past medical history presented with worsening shortness of breath of two days duration. Three months prior to presentation he was hospitalized for acute hypoxemic respiratory failure due to COVID-19 requiring Bi-level Positive Airway Pressure which was complicated by pneumomediastinum and right-sided pneumothorax that required chemical pleurodesis. On this presentation, he was hypoxemic and CT scan of the chest showed extensive bullous lung disease (BLD) throughout the right lung with mediastinal shift, not noted on prior imaging. He denied family history of lung disease or connective tissue disease. Prior to COVID-19 infection he was an avid marathon-runner, worked as a civil engineer with no occupational exposures, and never smoked tobacco products, vaped electronic cigarettes, or used illicit drugs. Admission vitals were unremarkable and physical exam revealed decreased breath sounds on the right side. His laboratory data including repeat SARS CoV-2 nasal polymerase chain reaction, alpha-1 antitrypsin and angiotensin-converting enzyme levels were unrevealing. Cardiothoracic surgery was consulted and he successfully underwent Video-Assisted Thoracoscopic surgery with wedge resection of the right lower lobe and chemical pleurodesis. Pathology ruled out a loculated pneumothorax and confirmed the presence of bullae localized within the lung parenchyma. DISCUSSION: Bullous lung disease has been described secondary to cocaine, cigarette or marijuana smoking as well as Emphysema, Sarcoidosis, alpha1-antitrypsin deficiency, Marfan's syndrome, Ehlers-Danlos syndrome and inhaled fiberglass exposure. However, our patient did not have any family history of lung disease, occupational exposures or smoking history, and physical exam was not suggestive of either Marfan's or Ehlers-Danlos syndrome. Since there was no underlying lung disease prior to hospitalization, common etiologies of bullous lung disease were ruled out, and given temporal association with COVID-19 infection, we hypothesized that his lung disease was related to his infection. Although the relationship between bullous lung disease and COVID-19 has yet-to-be defined, case reports have described this emerging association. CONCLUSIONS: Further investigation in the development of chronic lung disease following COVID-19 infection is sorely needed given the growing population of COVID-19 survivors. REFERENCE #1: Berhane S, Tabor A, Sahu A, Singh A. Development of bullous lung disease in a patient with severe COVID-19 pneumonitis. BMJ Case Reports. 2020;13(10):e237455. REFERENCE #2: Sun R, Liu H, Wang X. Mediastinal Emphysema, Giant Bulla, and Pneumothorax Developed during the Course of COVID-19 Pneumonia. Korean J Radiol. 2020;21(5):541-544. REFERENCE #3: Goldberg C, Carey KE. Bullous lung disease. West J Emerg Med. 2013;14(5):450-451. doi:10.5811/westjem.2013.3.16276. DISCLOSURES: No relevant relationships by Kwesi Amoah, source=Web Response No relevant relationships by robert homer, source=Web Response No relevant relationships by Denyse Lutchmansingh, source=Web Response No relevant relationships by Prachi Pednekar, source=Web Response No relevant relationships by Changwan Ryu, source=Web Response

TOPIC: Signs and Symptoms of Chest Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Thoracic aortic aneurysm (TAA) is an uncommon clinical condition, commonly associated with atherosclerosis. It is mostly asymptomatic but aneurysm exceeding 6 cm are at risk of yearly rate of rupture or dissection of at least 6.9% and a death rate of 11.8%. We present to you a case of TAA with rupture presenting with cough, hemoptysis and pneumonitis. CASE PRESENTATION: Patient is a 68 years male who presented to the ED with cough, hemoptysis, chest discomfort for 2-3 days. He had intermittent episodes of fever. COVID test was negative 3 days ago. Past medical history was significant for HTN, Asthma, COPD, Diabetes mellitus, tobacco use disorder. Patient was afebrile with BP of 137/73, HR 72, RR 16, O2 saturation of 89% in room air. Physical examination including chest was unremarkable. Initial workup including CBC was remarkable for WBC of 12500, Hgb of 10.5, INR 0.8, PTT 24, Troponin 5 cm, smokers, COPD, advanced age, hypertension. Thoracic endovascular stent graft surgery, under epidural anesthesia, is the preferred surgical treatment especially in old TAA patients as in our case because of low morbidity, mortality and hospital stay. CONCLUSIONS: Rupture of TAAs is still very rare, but should remain on the differential for a patient with cough, hemoptysis with features of pneumonitis as it is associated with very high morbidity and mortality rates. REFERENCE #1: CL F, Esk, MK ari. Thoracic endovascular aneurysm Repair (TEVAR) for Ruptured THORACIC aortic aneurysms. Published May 2, 2017 REFERENCE #2: Inam, H., Zahid, I., Khan, S.D. et al. Hemoptysis secondary to rupture of infected aortic aneurysm– a case report. J Cardiothorac Surg 14, 144 (2019). https://doi.org/10.1186/s13019-019-0959-y REFERENCE #3: Sun D, Mehta S. Hemoptysis caused by erosion of thoracic aortic aneurysm. CMAJ. 2010;182(4):E186. doi:10.1503/cmaj.090447 DISCLOSURES: No relevant relationships by Luna Khanal, source=Web Response No relevant relationships by Adarsha Ojha, source=Web Response

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Acute airway obstruction is a life-threatening event requiring emergent identification and management. Limited reports of acute airway compromise in patients with recent novel coronavirus infection (COVID-19) suggest this may be a rare and late complication in COVID-19 patients. CASE PRESENTATION: A 19-year-old Guatemalan male with no known past medical history, unclear vaccination status, no smoking or alcohol history presented to the emergency department with complaints of worsening sore throat, muffled voice, difficulty swallowing, bloody vomitus, and subjective fever for two hours prior to arrival. He was diagnosed with mild COVID-19 3 weeks prior. History was limited by severe respiratory distress. On physical exam, the patient was afebrile. He had muffled voice, stridor, and a normal uvula. Labs were significant for leukocytosis, and respiratory panel positive for SARS-CoV-2. X-ray of chest and neck were unremarkable. Patient was given dexamethasone and antibiotics. Given concern for airway compromise and possible epiglottitis, the patient was urgently intubated. First attempt with video laryngoscopy was unsuccessful due to extensive edema and erythema of the hypopharyngeal tissues, then re-attempted successfully with a smaller endotracheal tube. The epiglottis could not be visualized. CT neck showed diffuse inflammation with enlargement of the adenoids and tonsils;epiglottis was obscured given presence of the endotracheal tube;no abscess seen. Differential included bacterial or viral epiglottitis, idiopathic angioedema reaction, and post-COVID reaction. The patient was admitted to the ICU for management of presumed epiglottitis and continued on dexamethasone for 40 hours and empiric antibiotics. He had rapid resolution of airway edema, was successfully extubated on day 4 of admission, and discharged home on day 6 with a 10-day course of cephalexin. DISCUSSION: Most mild, symptomatic cases of COVID-19 typically resolve within 2-3 weeks. This late presentation raises concern for epiglottitis as a rare but serious complication of COVID-19. The time course additionally suggests possible post-viral superinfection of the epiglottis and upper airway from other causes. Confirmation via direct visualization or imaging was not possible in this patient but he was treated presumptively for epiglottitis given his concerning physical exam findings. In cases of acute respiratory distress, airway management should supersede diagnostic evaluation due to the risk of rapid respiratory compromise. CONCLUSIONS: There are many known etiologies of acute airway obstruction, including epiglottitis, but it is important to consider COVID-19 as another possible etiology. While direct visualization is the gold standard for confirmation, diagnosis should not precede emergent intubation in cases of severe respiratory distress. REFERENCE #1: Caytemel B, Kilic H, Comoglu S. Approach to otolaryngology emergency in COVID-19 pandemic. Tr-ENT. 2020;30(50):24-36. DISCLOSURES: No relevant relationships by Gerardo Carino, source=Web Response No relevant relationships by Sugi Min, source=Web Response No relevant relationships by Claudia Sorin, source=Web Response

A 6-month-old infant with a past medical history of hypoxic ischemic encephalopathy was referred for evaluation of snoring. She was born at 41 weeks' gestational age to a 25-year-old gravida 1, para 1 mother via vacuum-assisted delivery due to cardiac decelerations. The infant's Apgar scores were 1, 4, and 6 with nuchal cord and meconium at delivery. She was started on positive-pressure ventilation but eventually required intubation at approximately 40 minutes of life. Brain MRI showed abnormal areas of restricted diffusion, involving the corpus callosum, bilateral posterior limb of the internal capsules, and possible scattered areas of frontal and occipital lobe cortices.

SESSION TITLE: Medical Students/Residents' COVID-19 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coagulopathy in COVID-19 has been associated with increased mortality and can result in deep venous thrombosis/pulmonary embolism, ischemic stroke and disseminated intravascular coagulation (DIC) Herein we present a case of a patient with severe COVID-19 complicated by ischemic stroke despite therapeutic enoxaparin CASE PRESENTATION: Our patient was a 48 year-old-male with past medical history of morbid obesity, hypertension and hyperlipidemia who presented with one week history of progressive cough and dyspnea He was hypoxemic requiring non-rebreather oxygen at 15 liters/minute to maintain saturation's >92% Blood work was remarkable for an elevated c-reactive protein to 9 86 mg/dL and and high sensitivity d-dimer to 732 ng/dL Chest x-ray revealed extensive bilateral airspace opacities (Image 1) The patient was admitted to our intensive care unit and transitioned to high-flow nasal cannula oxygen Initial arterial blood gas revealed PaO2/FiO2 of 71 He was started on deep venous thrombosis prophylaxis with enoxaparin 40mg every 12 hours and continued on his home aspirin, 81mg daily On hospital day (HD) 1 patients COVID-19 PCR returned positive He received 400mg of intravenous tocilizumab and a unit of convalescent plasma Early HD 3 the patients d-dimer trended up to >1000 ng/mg and he was transitioned to therapeutic enoxaparin at a dose of 1mg/kg twice daily His platelet count remained stable and within normal limits Late HD 4 he was found to have paralysis of his left upper and lower extremity STAT imaging revealed large right middle cerebral artery infarction with mid-line shift (Image 2) He was not a candidate for systemic thrombolytic therapy or mechanical thrombectomy HD 6 patient required right hemicraniectomy for worsening cerebral vasogenic edema Brain biopsy revealed acute cerebritis characterized by marked perivascular and parenchymal neutrophilic infiltrates and associated acute hypoxic neurons, marked edema and small vessel thrombi (Image 3) Unfortunately the patient’s condition ultimately deteriorated and he expired on HD 13 DISCUSSION: The case presented is as striking as it is tragic Despite our patient’s home aspirin dose and therapeutic enoxaparin there was interval development of a devastating cerebral vascular event The initiation of prophylactic anti-coagulation in patients with COVID-19 is controversial and not currently recommended by the International Society of Thrombosis and Hemostasis One recent study demonstrated significantly increased inpatient median survival time without a significant change in inpatient mortality in patients with COVID-19 treated with prophylactic anti-coagulation CONCLUSIONS: Coagulopathy in COVID-19 predisposes patients to potentially devastating thrombotic events Further studies will need to be conducted to determine an ideal anti-coagulation strategy to minimize risk of these events Reference #1: Tang, Ning, Dengju Li, Xiong Wang, and Ziyong Sun 2020 “Abnormal Coagulation Parameters Are Associated with Poor Prognosis in Patients with Novel Coronavirus Pneumonia ” Journal of Thrombosis and Haemostasis: JTH 18 (4): 844–47 Reference #2: Thachil, Jecko, Ning Tang, Satoshi Gando, Anna Falanga, Marco Cattaneo, Marcel Levi, Cary Clark, and Toshiaki Iba 2020 “ISTH Interim Guidance on Recognition and Management of Coagulopathy in COVID-19 ” Journal of Thrombosis and Haemostasis: JTH 18 (5): 1023–26 3 Reference #3: Paranjpe, Ishan, Valentin Fuster, Anuradha Lala, Adam Russak, Benjamin S Glicksberg, Matthew A Levin, Alexander W Charney, et al 2020 “Association of Treatment Dose Anticoagulation with In-Hospital Survival Among Hospitalized Patients with COVID-19 ” Journal of the American College of Cardiology, May https://doi org/10 1016/j jacc 2020 05 001 DISCLOSURES: No relevant relationships by Daniel Condit, source=Web Response No relevant relationships by Rudra Ramanathan, sou ce=Web Response No relevant relationships by M Camila Trejo-Paredes, source=Web Response Consultant relationship with Boston Scientific Please note: $1001 - $5000 Added 06/01/2020 by Patrick Troy, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Boston Scientific Please note: $1001 - $5000 Added 06/01/2020 by Patrick Troy, source=Web Response, value=Consulting fee

SESSION TITLE: Medical Student/Resident Disorders of the Mediastinum Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: In March, 2020 the World Health Organization (“WHO”) declared SARS-CoV-2 as a global pandemic SARS-CoV-2 viral infection has been noted to present a variety of symptoms including anosmia (loss of sense of smell), dyspnea, cough, fever, diarrhea and acute respiratory failure Spontaneous pneumomediastinum is a rare complication with viral pneumonia We here present one of the two cases with this finding CASE PRESENTATION: 63-years-old male presented with fever, chills, and progressive shortness of breath over the past week Patient was previously diagnosed with corona virus disease with reverse transcriptase RNA PCR test Past medical history was significant for diabetes, hypertension and hyperlipidemia On presentation, patient was hypoxic (SaO2 84%) Physical examination revealed reduced breath sounds bilaterally and soft-tissue crepitus in bilateral clavicle area Laboratory test results showed elevated C-reactive protein concentration, leukocytosis, and lymphopenia Chest Computed Tomography (CT) showed diffuse lower neck/chest wall subcutaneous emphysema with associated diffuse pneumomediastinum and bilateral ground-glass airspace infiltrates (Figure 1,2,3) Patient was started on anti-infective therapy with vancomycin, piperacillin/tazobactam, and azithromycin, and placed on nasal cannula at 4 liter/minute On day four of admission, patient developed multi-organ failure requiring mechanical ventilation and vasopressor support Later on day twelve, patient expired due to cardiopulmonary arrest DISCUSSION: Pneumomediastinum is defined as the presence of free air in the mediastinum with an incidence of 1 in every 25,000 cases in ages between 5-34 years, predominantly found in males It may be spontaneous from a predisposing factor or due to secondary causes SARS-CoV-2 is a new addition to secondary pulmonary causes, being reported recently in literature The pathophysiology of spontaneous pneumomediastinum is explained due to pressure gradient difference between alveoli and lung interstitial tissue SARS-CoV-2 infects type I and II pneumocytes, disrupting alveolar membrane integrity leading to alveolar rupture and leakage of air into interstitial tissue, as well as severe hypoxemia increasing respiratory effort Associated clinical symptoms of pneumomediastinum are varying, including dyspnea, although a portion of patient are asymptomatic Pneumomediastinum is typically identified through chest x-ray with management being primary conservative CONCLUSIONS: Spontaneous pneumomediastinum in association with SARS-CoV-2 is a serious condition and merits early recognition Despite early diagnosis and optimal management, the mortality was 100% in our two patients of Covid-19 associated mediastinum Reference #1: Wang J, Su X, Zhang T, Zheng C Spontaneous Pneumomediastinum: A Probable Unusual Complication of Coronavirus Disease 2019 (COVID-19) Pneumonia Korean J Radiol 2020;21(5):627-628 doi:10 3348/kjr 2020 0281 Reference #2: Dionisio P, Martins L, Moreira S, et al Spontaneous pneumomediastinum: experience in 18 patients during the last 12 years J Bras Pneumol 2017;43(2):101-105 doi:10 1590/S1806-37562016000000052 Reference #3: Kolani S, Nawfal H, Haloua M, et al Spontaneous pneumomediastinum occurring in the SARS-COV-2 infection [published online ahead of print, 2020 May 11] IDCases 2020;21:e00806 doi:10 1016/j idcr 2020 e00806 DISCLOSURES: No relevant relationships by Darakhshan Ahmad, source=Web Response No relevant relationships by Marium Ghani, source=Web Response No relevant relationships by Parvez Mir, source=Web Response No relevant relationships by Judy Pham, source=Web Response No relevant relationships by Yariana Rodriguez-Ortiz, source=Web Response No relevant relationships by Phanthira Tamsukhin, source=Web Response

Case Presentation A 59-year-old man presented to the ED with a chief complaint of shortness of breath. His past medical history was significant for end-stage renal disease secondary to lithium toxicity, immunosuppression subsequent to cadaveric renal transplantation, bipolar disorder, and hypertension. His shortness of breath had begun 6 months previously and was initially intermittent; it then progressed to constant shortness of breath over the few weeks before presentation. He had no fever, hemoptysis, or chest pain. The patient was admitted to hospital for further evaluation.

A 34-year-old white woman who was 30 weeks' pregnant initially presented to her primary care physician with a cough for which she was given antibiotics, but she had persistent symptoms. These were followed by chest pain, as a result of which she was referred to our department. She had a past medical history of hypertension, and currently was in her sixth pregnancy, with no reported complications in the previous pregnancies. Review of systems was otherwise negative. She had a three-pack-year smoking history, but denied smoking during her current pregnancy.

A 56-year-old white woman was referred to the pulmonary clinic for evaluation of unexplained shortness of breath. She enjoyed good health until 3 months prior to this visit when she reported experiencing recurrent episodes of shortness of breath and oppressive retrosternal chest discomfort with radiation to the neck. Episodes lasting 5 to 10 min often occurred at rest and were inconsistently related to physical activity. These symptoms became progressively worse and were often associated with light-headedness and presyncope. Her past medical history was uneventful apart from a prior diagnosis of breast cysts and suspected prolactinoma. Her symptoms escalated to such a level that she was forced to seek urgent medical attention at our institutional ED on two separate occasions in the preceding weeks. These visits precipitated a number of investigations and, eventually, a referral to the pulmonary clinic.

An 80-year-old man presented because of superficial head trauma sustained after falling from bed. On review of systems, he reported worsening dyspnea on exertion, nonproductive cough, and weight loss over the preceding 2 to 3 months. There was no report of chest pain or leg swelling. He had a past medical history of hypertension, coronary artery disease, subclinical hypothyroidism, and renal cell carcinoma treated with partial right nephrectomy approximately 1 year before this presentation. Two months earlier he had been evaluated in the dermatology clinic for painful, dystrophic fingernails. At that time he was diagnosed with acropachy with onycholysis and suspected superinfection, and after failing to improve with vinegar soaks and topical antimicrobials, he underwent surgical nail removal on the second and fourth digits of the right hand. Histological examination of the operative specimens revealed dystrophic nails with negative fungal stains. His medications included levothyroxine, hydrochlorothiazide, and clopidogrel. He had never smoked and had done clerical work until retirement. He was originally from Colombia.

Background Asthma-COPD overlap syndrome (ACOS) has been recently described by international guidelines. A stepwise approach to diagnosis using usual features of both diseases is recommended although its clinical application is difficult. Methods To identify patients with ACOS, a cohort of well-characterized patients with COPD and up to 1 year of follow-up was analyzed. We evaluated the presence of specific characteristics associated with asthma in this COPD cohort, divided into major criteria (bronchodilator test > 400 mL and 15% and past medical history of asthma) and minor criteria (blood eosinophils > 5%, IgE > 100 IU/mL, or two separate bronchodilator tests > 200 mL and 12%). We defined ACOS by the presence of one major criterion or two minor criteria. Baseline characteristics, health status (COPD Assessment Test [CAT]), BMI, airflow obstruction, dyspnea, and exercise capacity (BODE) index, rate of exacerbations, and mortality up to 1 year of follow-up were compared between patients with and without criteria for ACOS. Results Of 831 patients with COPD included,125 (15%) fulfilled the criteria for ACOS, and 98.4% of them sustained these criteria after 1 year. Patients with ACOS were predominantly male (81.6%), with symptomatic mild to moderate disease (67%), who were receiving inhaled corticosteroids (63.2%). There were no significant differences in baseline characteristics, and only survival was worse in patients with non-ACOS COPD after 1 year of follow-up (P Conclusions The proposed ACOS criteria are present in 15% of a cohort of patients with COPD and these patients show better 1-year prognosis than clinically similar patients with COPD with no ACOS criteria. Trial Registry ClinicalTrials.gov; No.: NCT01122758; URL: www.clinicaltrials.gov

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Negative pressure pulmonary edema or post obstructive pulmonary edema occurs due to markedly increased negative intrathoracic pressure due to forced inspiration against a closed glottis1 In adults, it is most commonly caused by infections, tumors, or laryngospasm We present a case of negative pressure pulmonary edema secondary to upper airway obstruction due to radiotherapy-induced laryngeal edema in a young adult CASE PRESENTATION: Our patient is a 54-year-old Caucasian male who presented with complaint of having an acute onset of shortness of breath He had a past medical history of squamous cell carcinoma treated with chemoradiotherapy one year back He was admitted to the hospital two weeks back with complaint of having dysphagia to solids and facial swelling Laryngoscopy at that time reveal arytenoid edema with partially obstructed airway and patient was treated with intravenous steroids with complete resolution of symptoms During this admission, patient was reporting that for the past few days his facial edema and dysphagia have worsened In addition, patient was also having shortness of breath mostly on lying flat and he has recently started sleeping in a recliner Before coming to the hospital, patient had sudden onset shortness of breath and he could not pull air into his chest despite trying hard and heard a high pitched noise from his throat On presentation, patient was requiring oxygen otherwise hemodynamically stable Rapid flu and coronavirus disease 2019 (COVID-19) testing were unremarkable Contrast-enhanced computerized tomography (CT) scan of chest was remarkable for central upper lobe predominant ground-glass opacities Fiber optic flexible laryngoscopy revealed worsened arytenoid edema Patient was diagnosed with negative pressure pulmonary odema secondary to laryngeal narrowing in the supine position in the setting of radiotherapy-induced laryngeal edema Patient was treated with IV steroids with the resolution of symptoms and was transferred to tertiary care setting for tracheostomy DISCUSSION: Negative pressure pulmonary edema can cause acute respiratory failure and should be suspected in patients with laryngeal tumors or infections It is most commonly seen in children due to upper airway infections or in post-operative anesthesia care in the setting of laryngospasm In adults, it can occur due to a wide variety of conditions including angioedema, foreign body aspiration, goiter, and obstructive sleep apnea (OSA) There should be a low threshold of suspicion for this life-threatening emergency which must be treated urgently CONCLUSIONS: Considering the rarity of this condition in medical intensive care units with this being seen in a specific cohort of patients, increased awareness should be spread about this condition Further research is required to better understand the pathophysiology of this disease which will help in prevention Reference #1: Bhattacharya M, Kallet RH, Ware LB, Matthay MA Negative-Pressure Pulmonary Edema Chest 2016;150(4):927-933 doi:10 1016/j chest 2016 03 043 DISCLOSURES: No relevant relationships by Tariq Hassan, source=Web Response No relevant relationships by Haris Zia, source=Web Response

63-year-old man with an extensive smoking history presented with a complaint of persistent dry cough for 3 months. His past medical history was signifi cant for severe COPD with an FEV 1 at 40% predicted (stage III by GOLD [Global Initiative for Obstructive Lung Disease] criteria). The patient was retired and a current cigarette smoker, and he had no pets. There was no history of prior malignancy or recent travels. He had no fever, night sweats, or weight loss. He was not receiving any angiotensinconverting enzyme inhibitors. There were no symptoms suggestive of upper airway cough syndrome or gastroesophageal refl ux disease. Physical Examination Findings The patient was afebrile with stable vital signs. BP was 127/87 mm Hg, heart rate was 85 beats/min, and oxygen saturation was 94% on room air. A complete physical examination was remarkable for yellow nicotine stains on the fi ngernails without clubbing, wide subcostal angle, distant heart sounds, and prolonged expiratory phase bilaterally, with left-sided monophasic expiratory wheezing best heard over the left upper lobe. Diagnostic Studies CBC was normal, apart from a normocytic anemia, with hemoglobin level of 12 g/dL (normal, 14-18 g/dL). Complete metabolic panel results, includ ing electrolytes, renal, and liver function testing, were within normal limits. No acute abnormalities were detected on chest radiograph. Because of the presence of localized wheezing on physical examination, an endobronchial lesion was suspected, and a CT scan of the chest was obtained. The chest CT scan showed emphysematous changes with an upper lobe predom inance and an ovoid low-density endobronchial lesion in the distal left mainstem bronchus measuring 2.3 cm in maximum diameter ( Fig 1 ).