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1.
Journal of Investigative Medicine ; 70(2):562-563, 2022.
Article in English | EMBASE | ID: covidwho-1701061

ABSTRACT

Introduction Coronavirus 19 (COVID-19) is a viral illness that is caused by SARS-CoV-2. It has a surface spike protein that binds to human angiotensin-converting enzyme 2 receptors expressed in the kidneys, lung, and vascular endothelium. Here we present a case of a 73-year-old critically ill male with COVID pneumonia and acute respiratory distress syndrome (ARDS), who developed compartment syndrome and rhabdomyolysis as a consequence of extensive right lower extremity arterial thrombosis related to a COVID induced hypercoagulable state. Case A 73-year-old COVID positive male with past medical history of coronary artery disease status-post triple coronary artery bypass 10 years ago and type 2 diabetes mellitus presented to the emergency department with progressively worsening dyspnea for one week. His initial oxygen saturation on room air measured 85%, so he was placed on 3 liters per minute supplementation via nasal cannula. CXR showed bilateral diffuse alveolar infiltrates and he was admitted for observation. He developed worsening respiratory failure five days into hospitalization, placed on maximum supplementation via high flow nasal cannula (HFNC), and transferred to the medical ICU. Ultimately, he was intubated and mechanically ventilated for the remainder of his hospitalization due to severe ARDS. After three days in the ICU, his right lower extremity was cold, without palpable nor detectable pulses via bedside Doppler from the femoral to pedal landmarks. Formal ultrasound Doppler that morning confirmed arterial clot extending from the right external iliac to posterior tibial arteries. The patient received embolectomy, stenting, and therapeutic heparin. Within 24 hours, though his creatinine kinase was normal, he developed significantly elevated myoglobin, lactate and worsening acidosis. The patient had a fasciotomy to the right lower extremity at bedside. The next day, he was anuric, with severe acidosis, hyperkalemia, and hypotension, requiring continuous renal replacement therapy (CRRT) and vasopressor support. Discussion Compartment syndrome is characterized by increased pressure within fascial compartments, leading to circulatory compromise, cellular necrosis, and rhabdomyolysis. In this case, the COVID-19 viral effect on coagulation led to extensive arterial thrombosis, complicated by compartment syndrome and renal failure necessitating CRRT. While the exact pathophysiology of the hypercoagulable state in COVID-19 illness is debated, we have observed its manifestations ranging from deep venous thrombosis (DVT), pulmonary embolism (PE), to stroke. Conclusion COVID-19 is known to be a virulent, multifactorial, intelligent virus with myriad end-organ and vascular consequences. When attending to the most critically ill patients with COVID-19, it is wise to consider all forms of vascular thromboembolism.

2.
Chest ; 158(4):A2565, 2020.
Article in English | EMBASE | ID: covidwho-871912

ABSTRACT

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Sever coronavirus disease 2019 (COVID-19) represents viral pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leading to acute respiratory distress syndrome (ARDS). COVID-19 is a novel disease initially recognized in Wuhan, Hubei Province, China in December 2019 further declared as a global pandemic in January 2020. Along with other serious coronavirus infections, severe acute respiratory syndrome (SARS) and middle east respiratory syndrome, that also cause ARDS, COVID-19 represents an ongoing global threat as this viral family has potential to mutate and infect nonimmune patients. Here we present a case of severe COVID-19 pneumonia leading to rapid ARDS requiring long hospital stay. CASE PRESENTATION: 47 years old male newly diagnosed with type 2 diabetes mellitus presented to the hospital in late March with five-day history of fever, chills, body aches, and dyspnea;only known exposure was working at a gas station. On admission he was febrile, tachycardic, and hypoxic requiring 4 liters via nasal canula, labs showed lymphopenia, elevated D-Dimer, LDH, CRP, ESR, and ferritin. Chest x-ray with bilateral multifocal airspace opacities (Figure 1). Admitted to the medical intensive care unit (MICU) for respiratory management, seven hours after admission he acutely decompensated requiring intubation, repeat chest x-ray showed worsening of bilateral opacities consistent with ARDS (figure 2). COVID-19 testing was positive the following day. Prone ventilation was initiated for 16 hours per day for a total of five days, with high PEEP, high FiO2, and tidal volumes 6ml/kg. Hospitalization complicated by acute kidney injury requiring continuous renal replacement therapy/intermittent hemodialysis and atrial fibrillation requiring amiodarone drip. He had prolonged mechanical ventilation and tracheotomy was delayed to high PEEP and hemodynamic lability but he had tracheotomy placement. Within one week of tracheostomy, he was weaned and placed on trach collar, discharged to nursing home to work with physical therapy and work towards getting back home to his family. DISCUSSION: COVID-19 pneumonia due to SARS-CoV-2 in general is an acute resolved disease with a mortality rate of 2%. However, severe disease might result in death due to massive alveolar hemorrhage such as in ARDS, progressive respiratory failure, and multiorgan failure. COVID-19 illness can be diagnosed by a consistent clinical history and positive SARS-CoV-2 testing. COVID-19 ARDS is diagnosed when COVID-19 positive patient meets the Berlin 2012 for ARDS. COVID-19 ARDS has worse outcomes compared to ARDS due to other causes, mortality can range from 65.7%-94% who received mechanical ventilation. There is ongoing research for treatment of COVID-19 ARDS. CONCLUSIONS: COVID-19 ARDS has worse outcomes when compared to ARDS due to other causes, there is on going research for treatment of COVID-19 related ARDS. Reference #1: Singhal T. (2020). A Review of Coronavirus Disease-2019 (COVID-19). Indian journal of pediatrics, 87(4), 281–286. Reference #2: Xu, Z., Shi, L., Wang, Y., Zhang, J., Huang, L., Zhang, C., Liu, S., Zhao, P., Liu, H., Zhu, L., Tai, Y., Bai, C., Gao, T., Song, J., Xia, P., Dong, J., Zhao, J., & Wang, F. S. (2020). Pathological findings of COVID-19 associated with acute respiratory distress syndrome. The Lancet. Respiratory medicine, 8(4), 420–422. Reference #3: Gibson, P., Qin, L., Puah, S. (2020). COVID-19 ARDS: clinical features and differences to "usual” pre-COVID ARDS. The Medical Journal of Australia. DISCLOSURES: No relevant relationships by Hazim Bukamur, source=Web Response No relevant relationships by Kendall Creed, source=Web Response No relevant relationships by Jasmine Sekhon, source=Web Response No relevant relationships by Divya Vangipuram, source=Web Response

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