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SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Corona Virus Disease (COVID-19) main presenting feature is hypoxia which coincidentally is a feature of Pulmonary Embolism (PE) that can be life-threatening if not diagnosed early. COVID-19 causes excessive inflammation that can induce expression tissue factors, which is a major coagulation activator1,2. Therefore, PE should also be a consideration for those presenting with COVID-19 with worsening hypoxia. CASE PRESENTATION: 79-year-old a man with non-ischemic cardiomyopathy with Ejection Fraction (EF) 45- 50% presented with worsening shortness of breath, dry cough, and bilateral lower limb edema for 2 weeks. On presentation, he was afebrile normotensive with tachypnea, tachycardia, and hypoxia. On physical examination, he was in respiratory distress with faint bilateral crackles and bilateral lower limb edema. Lab Investigations showed elevated Brain Natriuretic Peptide to 1830 pg/ml (normal range 0-100 PG/ml), troponin level to 6.89 ng/ml (normal range 0.00-0.03 ng/ml) and the D-dimer level was >20.00 UG/ml FEU (normal range 0.00-0.40 UG/ml FEU). Viral PCR confirmed COVID-19. No ischemic changes noted in EKG. Echocardiography (Echo) revealed EF (Ejection Fraction) at 10-15%, dilated right ventricle with reduced function, and left ventricular thrombus. In CT chest with contrast noted to have acute segmental right middle lobe pulmonary arterial embolus. He was therapeutically anti-coagulated with enoxaparin. He received antibiotics, systemic steroids, and diuresis On day 3 of admission, he had worsening hypoxia and dyspnea while on 100% oxygen therapy. The patient opted for no escalation in care with ventilation or resuscitation. As he had no clinical improvement, the family agreed on comfort care. He died on day 5 of admission. DISCUSSION: We described a case of COVID-19 complicated by PE, which is found among 13% of COVID-19 patients in a study done in Netherland1. Studies showed that elevated D-dimer levels can correlate with risk for pulmonary embolism. In this case, D-dimer found to be elevated which is consistent with prior cases 3. The patient found to have cardiomyopathy with ejection fraction at 15% during presentation despite prior Echo done about 6 months earlier revealed an EF 45%. Evidence of myocardial injury was found in previous articles from China as found in 19.7% of patients (total 416) with evidence of cardiac injury including elevated troponin and reduced ejection fraction. It was noted to be independently associated with a higher risk of mortality 4. CONCLUSIONS: Diagnosis of pulmonary embolism in COVID19 patients may represent a diagnostic challenge as hypoxia is arguably the feature of COVID19 that could be explained by a viral lung infection. Thus, it is necessary to have a lower index of suspicion and CT chest to be considered in patients with worsening hypoxia so as to evaluate for pulmonary embolism especially among patients with an elevated D- dimer level. Reference #1: Klok, F. A., Kruip, M. J. H. A., van der Meer, N. J. M., Arbous, M. S., Gommers, D. A. M. P. J., Kant, K. M., … Endeman, H. (2020). Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thrombosis Research. https://doi.org/10.1016/j.thromres.2020.04.013 Reference #2: Goeijenbier, M., van Wissen, M., van de Weg, C., Jong, E., Gerdes, V. E. A., Meijers, J. C. M., … van Gorp, E. C. M. (2012). Review: Viral infections and mechanisms of thrombosis and bleeding. Journal of Medical Virology, 84(10), 1680–1696. https://doi.org/10.1002/jmv.23354 Reference #3: J. Chen, X. Wang, S. Zhang, et al., Findings of acute pulmonary embolism in COVID-19 patients, The Lancet Infectious Diseases (3/1/2020), https://doi.org/10.2139/ ssrn.3548771 (preprint. Available at SSRN), https://ssrn.com/abstract=3548771. DISCLOSURES: No relevant relationships by Musaab Alfaki, source=Web Response No relevant relationships by Nia Flemming, source=Web Resp nse No relevant relationships by Janeen Grant, source=Web Response No relevant relationships by Fausto Lisung, source=Web Response No relevant relationships by Rani Sittol, source=Web Response
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The novel COVID-19 virus has been found to be associated in a wide variety of complications most commonly involving the lungs namely by pneumonia with resultant ARDS. We present a case of COVID19 related extensive pulmonary emboli. CASE PRESENTATION: A previously well 47-year-old male presented with an 8 day history of fever, cough & dyspnea. He tested positive for COVID-19 as an outpatient. Four days later, he developed left sided pleuritic chest pain & presented to hospital. On examination, blood pressure was 119/89mmHg, HR 124beats/min & RR 44breaths/min. Despite this, he was saturating 93% on room air. On examination, he had diminished breath sounds and faint crackles bilaterally. Significant laboratory investigations revealed, leucocytosis of 18 (4.00 -11.00 K/ul), troponin of 3.13 (0.00 - 0.03ng/ml), C-reactive protein was 236 (<10mg/l), D-dimer was >20 UG/ml FEU (0.00-0.04 ug/ml) and BNP of < 5 (0-100pg/ml). Electrocardiogram revealed sinus tachycardia with no ST segment changes. Plain chest radiograph had subsegmental airspace disease in the left lower lobe. CT pulmonary angiography revealed a saddle pulmonary embolus with filling defects throughout right upper middle and lower lobe and left upper and lower lobe pulmonary arteries, and evidence of right heart strain. There were airspace opacities in the left and right lungs. A transthoracic echocardiogram study confirmed right heart strain. He underwent emergent catheter directed thrombolysis and was placed on heparin infusion. Two days later, an IVC filter was placed. He was discharged on day 7 with a six month course apixaban. He received five days of hydroxychloroquine, thiamine, vitamin C and zinc. He was also given 5 days of ceftriaxone. At 2 month follow up, he continues to do well and no longer has any respiratory symptoms or further hypoxia DISCUSSION: COVID-19 causes excessive inflammation that can induce initiation and progression of both venous and arterial thromboembolism. The exact pathophysiology is unknown but it is hypothesized that the virus induces the expression of tissue factor which is a major coagulation activator. Therefore, pulmonary emboli (PE) should be a consideration in COVID-19 patients with acutely worsening respiratory symptoms. Interestingly, it has been highlighted that those with a d-dimer of greater than 1ug/ml have an odds ratio increased by 18 times for mortality. Despite this, our patient continues to do well on anticoagulation, presumably because of his age, health, as well as early intervention and anticoagulation. Data from China indicate that those who received heparin had a 20% survival rate. Apixaban maybe an acceptable long term therapy, but further study is needed. CONCLUSIONS: This case demonstrates that even though dyspnea and hypoxia are key presenting symptoms of COVID-19, one must be vigilant for acute worsening and consider other differentials such as pulmonary emboli. Reference #1: Gronagle Dennis, O’Donnell James S, Sharif Kassem, Emery Paul, Bridgewood Charles, Immune mechanism of pulmonary intravascular coagulopathy in COVID19 pneumonia, The Lancet Rheumatology, May 2020, https://doi.org/10.1016/ S2665-9913(20)30121-1 Reference #2: Ning Tang Huan Bai Xing Chen Jiale Gong Dengju Li, Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy, Journal of thrombosis and haemostasis, March 2020, https://doi.org/10.1111/jth.14817 Reference #3: Oudkerk Matthijs, Büller Harry R, Kuijpers Dirkjan, van Es Nick, Oudkerk Sytse F, McLoud Theresa C et al, RSNA Radiology, April 2020, ttps://doi.org/10.1148/radiol.2020201629 DISCLOSURES: No relevant relationships by Musaab Alfaki, source=Web Response No relevant relationships by Nia Flemming, source=Web Response No relevant relationships by Latoya Gayle, source=Web Response No relevant relationships by Janeen Grant, source=Web Response No relevant elationships by Fausto Lisung, source=Web Response No relevant relationships by Jason Lofters, source=Web Response No relevant relationships by Gene Otuonye, source=Web Response No relevant relationships by Ro-Kaye Simmonds, source=Web Response No relevant relationships by Rani Sittol, source=Web Response
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 infection has varied presentations and complications inclusive of pneumonia(PNA),gastroenteritis(GE) and Acute kidney injury(AKI).Prompt identification with aggressive therapy is needed to reduce morbidity and mortality.We present a case of COVID-19 infection with septic shock and severe AKI,successfully treated CASE PRESENTATION: A 65-year-old female presented with 7-days of vomiting,diarrhea,fever,dry cough,fatigue & confusion.Multiple household members had recently tested positive for SARS CoV-19.She had a history of localized breast cancer on tamoxifen,HTN and CKD3a.Baseline creatinine(Cr) 3 months prior was 1.2.On exam,BP was 86/48mm/hg, T 95F,RR 27 breaths/min.She had dry mucous membranes, coarse breath sounds & rales bilaterally on auscultation,confusion & flapping wrist tremor.Significant labs were a Cr of 21.5,BUN 162, CO2 9,D-dimer >20,CRP 55 & random urine protein on 19 (<12mg/dl).ABG on 3L nasal cannula showed PH 7.21, PO2 104, PCO2 30.CXR noted right upper lobe infiltrate.CT head and EEG were unremarkable.SARS-CoV-2 PCR was positive.She was transferred to ICU for management of septic shock from COVID-19 PNA & GE with severe AKI.Despite aggressive IV fluids,she remained hypotensive requiring phenylephrine for pressor support.She received IV D5 ½ NS with bicarbonate, doxycycline,ceftriaxone & vancomycin.Dialysis was considered but her renal function rapidly improved: within 24 hours she was weaned off phenylephrine & Cr decreased to 12.She was started on full dose Enoxaparin in light of elevated D-dimer, worsening bilateral infiltrates on CXR and PO2 falling to 68 on 6L NC with monitoring of anti-factor XA levels in light of AKI.Within 5 days she had complete return of baseline mentation, improved ventilation & resolution of asterixis.On discharge at day 10 her Cr was 1.0, with BUN 17,D-dimer 8.5 & CRP 24.She was discharged on Apixaban 5mg bid. DISCUSSION: The Covid-19 global pandemic has resulted in numerous deaths and disability.Prompt identification and aggressive treatment of the critically ill is paramount in the attempt to prevent multi-organ failure and death.AKI occurs in as much as 23% of Covid 19 patients and confers increased mortality especially when associated with septic shock. In our patient,with severe AKI,uremia with encephalopathy she had marked improvement and resolution with supportive therapy.Her renal recovery with this degree of impairment is unusual as the majority of patients with similar characteristics have poor outcomes.This recovery may be attributed to aggressive fluid resuscitation,correction of metabolic acidosis and possible early initiation of anticoagulation. CONCLUSIONS: It is well known that AKI in critically ill Covid-19 patients is associated with high mortality.This case reminds us that renal and overall clinical recovery is still possible in these patients. More research is needed to identify predictors of prompt recovery. Reference #1: Batlle, D., Soler, M., Sparks, M., Hiremath, S., South, A., Welling, P.,… Kidney Working Group. (2020, May 04). Acute Kidney Injury in COVID-19: Emerging Evidence of a Distinct Pathophysiology. Retrieved June 01, 2020, from https://jasn.asnjournals.org/content/early/2020/05/04/ASN.2020040419 Reference #2: Cheng, Y., Luo, R., Wang, K., Zhang, M., Wang, Z., Dong, L., Li, J., Yao, Y., Ge, S., & Xu, G. (2020). Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney international, 97(5), 829–838. https://doi.org/10.1016/j.kint.2020.03.005 DISCLOSURES: No relevant relationships by Deborah Fein, source=Web Response No relevant relationships by Latoya Gayle, source=Web Response No relevant relationships by Maha Imran, source=Web Response No relevant relationships by Gene Otuonye, source=Web Response No relevant relationships by Rani Sittol, source=Web Response No relevant relationships by Karlene Williams, source=Web Response
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The coronavirus disease 2019 (COVID-19) is characterized by flu-like symptoms or complications related to pneumonia and acute respiratory distress syndrome. Later in the disease course, clinically significant thrombotic events, both venous and arterial, are being recognized. Our case describes ST elevation myocardial infarction (STEMI) as a complication of COVID-19. CASE PRESENTATION: A 38-year-old male with no medical history and non-smoker presented with 10 days of fever, cough, malaise, myalgia, and exertional dyspnea. He denied chest pain. He had completed a five-day course of azithromycin and steroids. No personal or family history of clotting disorders or heart disease. Exam revealed oxygen saturation of 89% on room air with bilateral crepitations. Chest x-ray showed bilateral patchy parenchymal airspace disease. Electrocardiogram (EKG) showed sinus tachycardia without ischemic changes. Labs showed C-reactive protein 179 mg/L and D-dimer 0.64 ug/mL. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by polymerase chain reaction assay was positive. He was started on ceftriaxone, doxycycline, hydroxychloroquine, enoxaparin, and methylprednisolone. After 5 days, he was discharged on prophylactic apixaban. He returned 1 day later with substernal chest pain. EKG showed ST elevation in the inferior leads. Troponin T was 3.74 ng/mL, D-dimer 0.75 ug/mL, and coagulation profile was normal. Emergent coronary angiography revealed 100% occlusion of mid-right coronary artery and right posterolateral branch requiring extensive thrombectomy and placement of drug eluting stents. He was started on aspirin, ticagrelor, eptifibatide, high intensity statin, and metoprolol. Echocardiography revealed severe basal to mid- inferior and posterior wall hypokinesis with left ventricular ejection fraction of 40%. He was discharged on ticagrelor, apixaban, atorvastatin and metoprolol. Anti-phospholipid antibody panel testing results returned normal. DISCUSSION: It is becoming increasingly evident that SARS-CoV-2 predisposes to venous thromboembolism, but arterial thromboembolism, especially manifest as acute STEMI, is rare. A recent Dutch study of 184 ICU patients with COVID-19 demonstrated confirmed arterial thrombotic events in 3.7%.(1) The pro-coagulant pattern is characterized by increased clot strength, elevated platelet and fibrinogen contribution to clot strength, elevated D-dimer levels, and hyperfibrinogenemia.(2) In a recent case series, 67% of patients with COVID-19 undergoing coronary angiography for STEMI had obstructive coronary artery disease (CAD) with 83% requiring PTCA (3). Interestingly, none of these patients had a known prior history of CAD. CONCLUSIONS: Further discussion regarding prophylactic anti-platelet and anti-coagulation strategies in patients with COVID-19 and studies to identify risk factors for thrombotic disease is warranted. Reference #1: Kloka, F A, Kruipb M J H A, van der Meerc N J M, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thrombosis Research. 2020. doi:10.1016/j.thromres.2020.04.013 Reference #2: Ranucci, M, Ballotta, A, Di Dedda, U, et al. The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome. Journal of Thrombosis and Haemostasis. April 2020. doi:10.1111/jth.14854 Reference #3: Bangalore, S, Sharma, A, Slotwiner, A, et al. ST-Segment Elevation in Patients with Covid-19 — A Case Series. NEJM. April 17, 2020. doi: 10.1056/NEJMc2009020 DISCLOSURES: No relevant relationships by Juliann Allen, source=Web Response No relevant relationships by Aalap Chokshi, source=Web Response No relevant relationships by Kyle Foster, source=Web Response No relevant relationships by Rani Sittol, source=Web Response No relevant relationships by Matthew Tavares, source=Web Response
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: As worldwide incidence of COVID-19 increases, so too does the heterogeneity of patients affected. This includes those with underlying neuromuscular disorders. Myasthenia gravis (MG) & myasthenic crises (MC) in the presence of SARS-CoV-2 is a relatively unknown entity. Herein we present such a case. CASE PRESENTATION: A previously well 35-year-old female health care worker presented with 5-days of fever, malaise & dyspnea. She had been in contact with COVID-19 positive patients. Her BP was 117/65mmhg, HR 104 beats/min, RR 22 breath/min, T 98.2°F & O2 sat 87% on 5L nasal cannula. At that time examination was solely significant for dullness to percussion & decreased air entry on the right lung zones. Only significant labs were WBC 18.47 & Hb 10.5. CT chest showed right lower lobe consolidation, air bronchograms, bilateral alveolar infiltrates & a 7.6x4 x10.7cm right anterior mediastinal mass concerning for thymoma or lymphoma. There were no pulmonary emboli. Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) PCR was positive. Within 24 hours her tachycardia, tachypnea & O2 sat worsened. Repeat examination revealed bilateral ptosis, no neck control & grade 2 power in all limbs. ABG showed pH 7.39, pCO2 35.4, pO2 52.9, HCO3 21.3. She was emergently intubated. A significant amount of blood was noted in the endotracheal tube which resolved with nebulized tranexamic acid. There was consideration of a new diagnosis of MG as well as diffuse alveolar hemorrhage. She received IV methylprednisolone, hydroxychloroquine, thiamine, vitamin C & zinc in addition to inhaled epoprostenol and intermittent proning. Antibodies for acetylcholine receptors were positive & IVIG was started. Her oxygenation subsequently improved & she was extubated on day 16 of admission. She was discharged on pyridostigmine, prednisone & apixaban with planned outpatient thymectomy. DISCUSSION: Over 5 million cases of COVID-19 have been reported. The infection stimulates a robust inflammatory cascade & may result in respiratory failure. The presence of concurrent comorbidities worsens prognosis. It is well known that MC may be triggered by infectious processes. In this case, a new diagnosis of MG was uncovered during SARS-CoV-2 infection. MC is the initial presentation for 20% of patients with MG with only 1/3 surviving. IVIG is recognized treatment for severe MG. Although there is no consensus on definitive COVID-19 therapy, there are reports of patients with severe ARDS due to COVID-19 improving with IVIG. We opine that this patient’s condition may have improved due to a combination of corticosteroid use and IVIG. At minimum, it did not worsen her outcome. The mechanism behind this is unclear and further study is needed to determine an association with improved outcome. CONCLUSIONS: IVIG may be a valid treatment modality for COVID-19, especially with concurrent autoimmune disease. Further study is required. Reference #1: Barth D, Nabavi Nouri M, Ng E, Nwe P, Bril V. Comparison of IVIg and PLEX in patients with myasthenia gravis. Neurology 2011;76:2017-2023 Reference #2: Moeinzadeh F, Dezfouli M, Naimi A, Shahidi S, Moradi H1. Newly Diagnosed Glomerulonephritis During COVID-19 Infection Undergoing Immunosuppression Therapy, a Case Report. Iran J Kidney Dis. 2020 May;14(3):239-242. Reference #3: Shi H1, Zhou C2, He P2, Huang S3, Duan Y3, Wang X3, Lin K3, Zhou C3, Zhang X4, Zha Y5.Successful treatment of plasma exchange followed by intravenous immunogloblin in a critically ill patient with 2019 novel coronavirus infection. Int J Antimicrob Agents. 2020 Apr 13:105974. doi: 10.1016/j.ijantimicag.2020.105974. [Epub ahead of print] DISCLOSURES: No relevant relationships by Musaab Alfaki, source=Web Response No relevant relationships by Samarth Beri, source=Web Response No relevant relationships by Latoya Gayle, source=Web Response No relevant relationships by Janeen Grant, source=Web Response No re evant relationships by Fausto Lisung, source=Web Response No relevant relationships by Gene Otuonye, source=Web Response No relevant relationships by Rani Sittol, source=Web Response