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The COVID-19 pandemic could be considered as a career shock for employees in different industries around the world. The aim of this research was to gain insight into the dynamics of Serbian small business owners' career shocks caused by the COVID-19 pandemic by using personal construct psychology (PCP) as a theoretical framework. We conducted 18 semi-structured interviews with 9 small business owners on two separate occasions and analyzed their personal stories. The data were collected during the most restrictive lockdown in Serbia in April 2020 and again at the end of June 2020 when the number of the people infected was on a rapid rise. The reaction to the career shock caused by the pandemic can be understood by analyzing transitions (how people perceive career shocks), people's coping strategies and the way in which their dependencies were dispersed. This study contributes to understanding the career shock issue by viewing it through the lens of the personal construct theory. © 2021 Taylor & Francis Group, LLC.
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SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: TNFα plays a pivotal role in inflammation and maintenance of immune response against tuberculosis. The use of TNF inhibitors (TNFi) is associated with a significant increase in the incidence of tuberculosis (TB). TNFi may cause drug-induced lupus (ATIL) presenting as constitutional symptoms, rashes, pericardial and pleural effusions with positive autoantibodies. We present a case of pleural TB masquerading as drug-induced lupus. CASE PRESENTATION: A 68y/o woman with a history of ulcerative colitis (on infliximab, mesalamine), hypertension, T2DM, CAD, complained of low-grade fever, rashes, left-sided chest pain, dyspnea, and arthralgias for two weeks. Chest pain- worse with inspiration and cough. She emigrated from India to the USA 40 years ago. Six months before infliximab therapy, Quantiferon gold was negative. Exam: faint hyperpigmentation over shins, minimal swelling of MCPs and ankles, dullness to percussion over the left chest with decreased breath sounds. Labs: CRP 101 mg/dL, Hb 10.8 iron deficient, rheumatoid factor and anti-CCP negative, ANA 1:40, dsDNA 1:640, a reminder of ENA negative, anti-histone negative, C3/C4 normal, UA bland, protein/Cr 0.4 mg/gm, negative blood cultures, SPEP and LDH normal. CXR: opacification of the left lung up to midfield. CT chest: moderate left and small right pleural effusions, enlarged mediastinal lymph nodes. COVID and Quantiferon: negative. Thoracentesis: 850 ml of exudative fluid (2 out of 3 Light's criteria), lymphocytic predominance (76% of 4148 nucleated cells), adenosine deaminase (ADA) 42 U/L, gram stain, culture, acid-fast and MTB PCR negative, cytology negative. Thoracoscopy with biopsy of the parietal pleura: necrotizing granulomatous pleuritis with acid-fast bacilli. Sensitivity: pan-sensitive M. tuberculosis. Sputum: negative for TB. She was discharged on RIPE treatment for reactivation of TB. DISCUSSION: The incidence of infliximab-induced lupus is approximately 0.19% and confirming the diagnosis is challenging. The immunogenicity of infliximab is high, 66% of patients develop positive ANA. Anti-histone antibodies are less commonly associated with ATIL as opposed to classic drug-induced lupus and dsDNA is positive in up to 90% of cases of ATIL. Renal involvement is rare. The diagnostic usefulness of ADA (over 40 U/L) in lymphocytic pleural effusions for the diagnosis of tuberculosis in an immunosuppressed individual is demonstrated here. In countries with low TB burden, such as the USA, the positive predictive value of ADA in pleural fluid declines but the negative predictive value remains high. CONCLUSIONS: Tuberculous pleuritis is not always easily diagnosed since AFB smears and sputum may remain negative. When ADA level in lymphocytic pleural fluid is not low thorough search for TB with thoracoscopy and biopsy is justified. Reference #1: Shovman O, Tamar S, Amital H, Watad A, Shoenfeld Y. Diverse patterns of anti-TNF-α-induced lupus: case series and review of the literature. Clin Rheumatol. 2018 Feb;37(2):563-568. Reference #2: Benucci, M., Gobbi, F. L., Fossi, F., Manfredi, M. & Del Rosso, A. (2005). Drug-Induced Lupus After Treatment With Infliximab in Rheumatoid Arthritis. JCR: Journal of Clinical Rheumatology, 11 (1), 47-49. Reference #3: Valdés L, San José ME, Pose A, Gude F, González-Barcala FJ, Alvarez-Dobaño JM, Sahn SA. Diagnosing tuberculous pleural effusion using clinical data and pleural fluid analysis A study of patients less than 40 years-old in an area with a high incidence of tuberculosis. Respir Med. 2010 Aug;104(8):1211-7. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Zinobia Khan No relevant relationships by Milena Vukelic
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TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Myopericarditis is inflammation of pericardium and myocardium caused by inflammatory and non-inflammatory etiologies. COVID-19 is known to cause multiple organ complications, including cardiovascular. Cases of myopericarditis have been reported, and believed to be one of the culprits of death in this disease. We present a case of myopericarditis in the setting of post-COVID-19 pneumonia CASE PRESENTATION: 56-year-old female with history of hypertension, hyperlipidemia, insulin-dependent type 2 diabetes and COVID-19 pneumonia (requiring hospitalization and nasal canula oxygenation one month prior, received 5 days of Remdesivir and 10 days of Dexamethasone);presented with four days of substernal pain, radiating to right neck and chest. On the day of admission, electrocardiogram (ECG) was sinus rhythm without ST changes and troponin was negative two times. During hospitalization, patient had episodes of fever with increased intensity of chest pain. Repeated ECG showed ST elevation in lead I, aVL, V3-V6 with ST depression in lead III;and significantly elevated troponin and pro-BNP. Echocardiogram showed mild diffuse hypokinesis with regional variations, slightly reduced left ventricular ejection fraction and normal right ventricle size and function. Patient was started on heparin drip, and underwent emergency left heart catheterization that demonstrated non-obstructive CAD. Cardiac MRI was inconclusive for late gadolinium enhancement due to respiratory motion artifact, but biventricular global hypokinesis and small pericardial effusion were evidenced. Patient persistently had high fever and elevated inflammatory markers (CRP was 406 mg/dL) despite on antibiotics, hence empiric methylprednisolone and IVIG were started. She was planned to get endomyocardial biopsy, however she improved symptomatically with concurrent decreased of inflammatory markers and troponin. Repeat echocardiogram showed normal biventricular function. Patient was discharged from the hospital after 6 days of hospitalization with cardiology and rheumatology follow up. DISCUSSION: Manifestations of myopericarditis are varied, from fatigue and shortness of breath, to severe chest pain and chest tightness. Some patients may develop right-sided heart failure, or even fulminant myocarditis with sepsis. Interestingly, manifestations may occur weeks after recovery from COVID-19. Elevations of both troponin and pro-brain natriuretic peptide (pro-BNP) are expected, but ECG may not show ST changes. Echocardiogram may show thickening of the wall, dilatation, and pericardial effusion. Gold standard for diagnosing myocarditis is endomyocardial biopsy (EMB), as recommended by AHA. However, practice is limited due to expertise requirement, risk of contagious spread, and false-negative rate. CONCLUSIONS: Differential diagnosis should always include myopericarditis in acute coronary syndrome, especially after viral infection. REFERENCE #1: Zeng J.-H., Liu Y.-X., Yuan J. First case of COVID-19 infection with fulminant myocarditis complication: case report and insights. Published online April 10. Infection. 2020. REFERENCE #2: Siripanthong B, Nazarian S, Muser D, Deo R, Santangeli P, Khanji MY, Cooper LT, Chahal AA. Recognizing COVID-19–related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. Heart Rhythm. 2020 Sep;17(9): 1463–1471. REFERENCE #3: Inciardi R.M., Lupi L., Zaccone G., Italia L., Raffo M., Tomasoni D. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19) JAMA Cardiol. 2020;5:819–824. DISCLOSURES: No relevant relationships by Chen Chao, source=Web Response No relevant relationships by Nahla Shihab, source=Web Response No relevant relationships by Milena Vukelic, source=Web Response