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TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: COVID-19 infection is now well known to cause venous thrombotic complications. More recently, arterial thrombotic complications of COVID-19 have been reported. Incidence of Acute limb ischemia (ALI) ranges from 3 to 15%. CASE PRESENTATION: A 50-year-old male with a history of hypertension presented to the ED with left foot numbness, discoloration, and pain for 2 days. Two weeks before the presentation, he tested positive for SARS-CoV2 after an outpatient evaluation for acute cough. He did not have any other respiratory complaints and was quarantined at home. His cough persisted, but he denied any fever, shortness of breath, chest pain, or hemoptysis. On physical exam, he was afebrile, heart rate of 71 beats per minute, blood pressure 141/90 mm of Hg, respiratory rate of 19 breaths per minute, and oxygen saturation of 98% while breathing ambient air. His respiratory exam was unremarkable. There were no palpable femoral, popliteal, dorsalis pedis, and posterior tibial pulses on the left side. He had sensory loss in the left foot. Laboratory evaluation showed mild transaminitis. His CK was 767 U/L, and D-dimer was 4.92 mg/L. CTA abdominal aorta with iliofemoral runoff was performed, which showed partial occlusion of the distal abdominal aorta, near-complete occlusion of the left common iliac artery, and complete occlusion of the proximal popliteal artery at the level of the distal femur with no flow distal to this point.Anticoagulation with unfractionated heparin was initiated. The patient was emergently taken to the OR and underwent extensive embolectomy involving the aortoiliac, femoral, popliteal, and tibial artery of the left leg. Antiphospholipid antibodies were normal. He had no family or personal history of blood clots. His presentation was believed to be due to thrombotic complications of the COVID-19 infection. His postoperative course was unremarkable, and he was discharged home on postoperative day 5. DISCUSSION: ALI is a vascular emergency. The exact pathophysiology causing thrombosis is unknown, but endothelial dysfunction, cytokine production, acquired antiphospholipid syndrome, and hypoxia may contribute to thrombosis (1). The current prevalence of ALI is noted to be 4 to 21 per 100,000 COVID-19 hospitalizations. In one observational review and in most case series, the median age was over 60. Male sex, Hispanic ethnicity, history of myocardial infarction, CAD, and elevated D-dimer increase the risk of developing ALI (2). The patient usually presents with pain, pallor, numbness, and loss of pulses. CONCLUSIONS: We present a young patient with no significant risk factors and otherwise mild COVID-19 infection presenting with acute lower limb ischemia. A high index of suspicion and prompt recognition of ALI in patients with COVID-19 infection is critical. Surgical revascularization, either open or catheter-directed, and systemic anticoagulation is the mainstay of treatment. REFERENCE #1: Rahi MS, Jindal V, Reyes S-P, Gunasekaran K, Gupta R, Jaiyesimi I. Hematologic disorders associated with COVID-19: a review. Annals of Hematology. 2021. REFERENCE #2: Bilaloglu S, Aphinyanaphongs Y, Jones S, Iturrate E, Hochman J, Berger JS. Thrombosis in Hospitalized Patients With COVID-19 in a New York City Health System. Jama. 2020. DISCLOSURES: No relevant relationships by Kwesi Amoah, source=Web Response No relevant relationships by Kavitha Gopalratnam, source=Web Response No relevant relationships by Kulothungan Gunasekaran, source=Web Response No relevant relationships by Lakshmi Polisetty, source=Web Response No relevant relationships by Mandeep Singh Rahi, 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