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Background. The COVID-19 pandemic has been associated with underreporting of pulmonary tuberculosis (PTB). Overlapping risk factors, clinical features, and chronicity of post COVID-19 sequelae can lead to attribution of respiratory disease solely to COVID-19 and result in delayed recognition of PTB. Methods. Identification of inpatients with both sputum (spu) culture (clt) positive TB and SARS-CoV-2 + PCR was achieved using data extraction tool Slicer Dicer Epic system during 3/2020-1/2022 followed by a retrospective review of electronic medical records. We defined COVID-PTB as a patient (pt) who had positive spu clt for TB <= 12 months (mos) following a COVID-19 diagnosis. Results. 8 pts had both PTB and COVID-19. Two had PTB > 5 mos prior to, and one had PTB > 12 mos after COVID-19. 3/8 were promptly suspected to have PTB [1 with right upper lobe (RUL) infiltrate;1 RUL cavitary infiltrate;1 with miliary nodules and cavities];in these 3, spu was tested for MTB <= 48 hours (h) (hrs) of presentation. 5/8 had COVID-PTB. All 5 had fever and/or respiratory symptoms and >= 1 risk factors for TB identified at the time of presentation with COVID-19. Spu was tested for MTB in 48 hs in 1 with RUL cavitary infiltrate, and 5 days after chest CT findings of apical densities and scattered nodules in another. In the remaining 3, spu testing was delayed a median of 36 days (range, 8-133) after initial TB consistent CT findings (LUL opacity and nodular densities in 1;RLL cavitary infiltrate in 1;and clustered RML nodules in 1) and despite immigration from high burden TB countries in all 3;known LTBI in 2;diabetes in 1, and immunosuppressive therapies in 2. Conclusion. We observed a delay in sputum collection after COVID-19 diagnosis in the presence of epidemiological risk factors for TB disease and clinical features consistent with PTB. Lack of familiarity with the range radiological TB features, a diagnostic bias towards more typical radiographic (e.g., cavities, miliary patterns) and COVID-19 anchoring bias may have contributed to delayed PTB diagnosis. PTB should be considered, when clinically appropriate, in the setting of COVID-19 or apparent post COVID-19 sequelae.
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SESSION TITLE: Dyspne Mysteries SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Anti-synthetase (AS) syndrome is characterized by interstitial lung disease (ILD), arthritis, myositis, fever, or Raynaud's phenomenon in the presence of an AS autoantibody (1). At least 70% of patients with AS syndrome develop ILD (2), and it represents the major cause of mortality in these patients with a 10 year survival rate of 73%. In a small cohort study, the anti-PL-12 antibody subtype was found to be strongly associated with ILD (3). CASE PRESENTATION: A 35 year old female with a history of tobacco use disorder presented to the hospital with three months of recurrent subjective fevers, non-productive cough, and dyspnea on exertion. She denied arthralgias, muscle weakness and hemoptysis. She initially presented to her primary care physician with these symptoms and was prescribed amoxicillin for streptococcal pharyngitis. The patient continued to be symptomatic and was treated empirically for COVID-19 pneumonia twice despite two negative COVID-19 tests and without any significant clinical improvement in her respiratory status. On admission, she was febrile, tachycardic, and had a new oxygen requirement with bilateral coarse breath sounds on exam. She had no leukocytosis and her COVID-19 test was negative. CT angiography of the chest showed extensive mixed reticular and airspace opacities with peribronchial predilection and peripheral sparing (figure 1). A bronchial alveolar lavage was notable only for neutrophilia (19%) and eosinophilia (4%). Rheumatological workup revealed elevated rheumatoid factor, positive antinuclear antibody (1:40), weakly positive anti–Sjögren's-syndrome-related antigen A antibody (50 AU/ml), undetectable anti-Jo-1 antibody and positive anti-PL-12 antibody. Pulmonary function testing revealed a TLC of 40% and DLCO of 28%, consistent with a restrictive pattern. Considering the patient's organizing pneumonia, positive antibodies, and findings of "mechanic's hands,” the patient was diagnosed with anti-synthetase syndrome with ILD. She was started on oral prednisone and mycophenolate mofetil. On follow-up, she was noted to have symptomatic improvement and stable hypoxia without clinical signs of disease progression. DISCUSSION: During the coronavirus pandemic, the resemblance of COVID-19 pneumonia to other diseases, in the absence of conscious suspicion for other etiologies, can lead to anchoring and availability bias thereby delaying diagnosis and appropriate treatment. Additionally, anti-synthetase syndrome should be considered in the differential diagnosis of ILD even in the absence of arthritis and myositis, as respiratory symptoms are often the first presenting signs. CONCLUSIONS: Increased responsibility is required of diagnosticians to exercise due diligence and active recognition of COVID availability and anchor bias to avoid missing crucial diagnoses. Reference #1: Cojocaru, Manole, Inimioara Mihaela Cojocaru, and Bogdan Chicos. "New insights into antisynthetase syndrome.” Maedica 11.2 (2016): 130. Reference #2: Marco, Joanna L., and Bridget F. Collins. "Clinical manifestations and treatment of antisynthetase syndrome.” Best Practice & Research Clinical Rheumatology 34.4 (2020): 101503. Reference #3: Kalluri, Meena, et al. "Clinical profile of anti-PL-12 autoantibody: cohort study and review of the literature.” Chest 135.6 (2009): 1550-1556. DISCLOSURES: No relevant relationships by Mario Flores No relevant relationships by David Jackson No relevant relationships by Lisa Saa No relevant relationships by Abu Baker Sheikh
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SESSION TITLE: Cases of Overdose, OTC, and Illegal Drug Critical Cases Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Anchoring bias is a cognitive bias where one relies too heavily on initial information early on in the decision making process, affecting subsequent decisions due to future arguments being discussed in relation to the "anchor. Overemphasis on COVID-19 due to the pandemic has impacted the timely diagnosis and treatment of other diseases. CASE PRESENTATION: A 39-year-old man with a past medical history of COVID 19 in 12/2020 presents to the ED with increasing weakness, chest pain, recurrent fevers, diarrhea, and cough. CXR revealed bilateral infiltrates suggestive of pneumonia/pulmonary edema. Patient was empirically started on ceftriaxone. CT chest was suspicious of COVID-19;however repeat testing was negative. Diarrhea did not improve. Patient later admitted to recent travel to Jamaica. Ova and parasite, C-difficile, and stool culture were negative. On hospital day 8, the patient was intubated and placed on mechanical ventilation for worsening hypoxic respiratory failure Infectious disease was consulted for recurrent fevers of unknown origin and diarrhea with recent travel. Testing for typhoid fever, hantavirus, malaria, HIV, zika virus, chikungunya, dengue, and yellow fever were performed. Consent was obtained for HIV testing. HIV antibody tests were positive, CD4 count of 7, and viral load greater than 900k. Since a new diagnosis of AIDS with a CD4 count of 7 was obtained, the patient was subsequently tested for opportunistic infections such as TB. TB sputum PCR testing was positive but AFB smear was negative for TB. Antiretroviral and tuberculosis treatments were initiated. DISCUSSION: Anchoring bias can delay critical diagnoses and impede patient care if it is not recognized. According to Watson et. al, one way physicians circumvent the thought of pretest probability when ordering tests based on patient history and the subsequent list of differential diagnoses is anchoring bias. Bypassing the pretest probability also alters the sensitivity and specificity of testing because results that do not confirm or rule out a top differential diagnosis are thought to be inaccurate and are then repeated attributing the initial result to a bad specimen or an improper collection of the specimen. CONCLUSIONS: The case presented exemplifies clearly the concept of anchoring bias. Upon initial presentation, the patient had nonspecific symptoms such as weakness, chest pain, recurrent fevers, diarrhea, and cough, all of which can be symptoms of COVID 19 in the setting of a global pandemic. It is clear that the initial diagnosis based on these symptoms was COVID 19. When initial testing was negative, anchoring bias still played a role in the decision to test the patient once again, despite the first negative test. Repeat testing still did not support the diagnosis of COVID 19, which expanded the differential diagnosis and ultimately led to the correct diagnosis of AIDS with concomitant TB infection. Reference #1: Saposnik, et. Al. Cognitive Biases Associated with Medical Decisions: A Systematic Review. BMC Med Inform Decis Mak. 2016 Nov. 3. PMID: 27809908 Reference #2: Harada, et. al. COVID Blindness: Delayed Diagnosis of Aseptic Meningitis in the COVID-19 Era. Eur J Case Rep Intern Med. 2020 Oct 23. PMID: 33194872. Reference #3: Singh, et. al. The Global Burden of Diagnostic Errors in Primary Care. BMJ Qual Saf. 2016 Aug 16. PMID: 27530239. DISCLOSURES: No relevant relationships by Sagar Bhula
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SESSION TITLE: Pulmonary Involvement in Critical Care Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Hemophagocytic Lymphohistiocytosis (HLH) is a condition in which the body's natural ability to end an immune or inflammatory response is defective1. COVID-19 also presents with severe inflammation, and like HLH, leads to significantly elevated ferritin2. We present a case that was initially thought to be COVID-19, but the patient was diagnosed with HLH in the setting of S. aureus endocarditis. CASE PRESENTATION: A 62-year-old male with a history of atrial fibrillation, mechanical mitral valve on warfarin, type II diabetes, chronic obstructive pulmonary disease, and recently diagnosed COVID-19 presented to the hospital with progressive dyspnea. In the emergency department, he was found to be hypoxemic and in atrial fibrillation with rapid ventricular response. He had a fever of 39.3°C and his initial laboratory workup revealed hemoglobin of 11.9 g/dL, leukocytes of 5,700, platelets of 83,000, AST 35 U/L, ALT 34 U/L, CRP of 31.89 mg/dL, and ferritin of 1994 ug/L. The patient was admitted and started on dexamethasone 6 mg daily. The following day, the patient's blood work revealed a significant worsening of AST and ALT to 7280 U/L and 3319 U/L, respectively. D-dimer increased to 11861 ng/mL (DDU) and ferritin to 36,470 ug/L. On the third day of admission, his clinical status declined acutely as he became significantly bradycardic, progressing to a cardiac arrest after which he required cardiopulmonary resuscitation, intubation, and was transferred to the intensive care unit. A CT scan obtained revealed hepatomegaly of 22 cm and blood cultures were positive for S. aureus requiring vancomycin treatment. The patient was kept on dexamethasone due to concerns for HLH. Ferritin continued to worsen, reaching 50,749 ug/L. His sCD25 came back positive. Unfortunately, the patient expired on his fifth day of hospitalization after discussing with his family their goals for his care and switching his care to comfort only. DISCUSSION: HLH is a challenging condition since diagnosis is difficult and mortality is high. There are a few methods used to diagnose HLH. Usually, 5 of 8 criteria must be met, which was achieved with this patient. However, often the patient only fulfills 4 of 8 since many criteria are difficult to obtain such as bone marrow biopsy, sCD25, and CXCL9. A useful tool is the H-calculator3. Our patient scored a 180 indicating a 50-75% likelihood of HLH. Assessing the likelihood of disease is important since sCD25 and CXCL9 take time and if the patient is clinically deteriorating treatment should not be delayed. CONCLUSIONS: HLH is catastrophic and rare. Physicians should always have it as a differential diagnosis in patients with severe inflammatory states and elevated ferritins to avoid anchoring bias. If suspicion is high based on clinical evaluation and scores, treatment should not be delayed. Reference #1: Filipovich A, McClain K, Grom A. Histiocytic disorders: recent insights into pathophysiology and practical guidelines. Biol Blood Marrow Transplant. 2010;16(1 Suppl):S82-S89. doi:10.1016/j.bbmt.2009.11.014 Reference #2: Cheng L, Li H, Li L, et al. Ferritin in the coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis. J Clin Lab Anal. 2020;34(10):e23618. doi:10.1002/jcla.23618 Reference #3: Fardet L, Galicier L, Lambotte O, et al. Development and validation of the HScore, a score for the diagnosis of reactive hemophagocytic syndrome. Arthritis Rheumatol. 2014;66(9):2613-2620. doi:10.1002/art.38690 DISCLOSURES: No relevant relationships by Areeka Memon No relevant relationships by Carissa Monterroso No relevant relationships by Carson Oprysko No relevant relationships by Eduardo Padrao No relevant relationships by Mouna Penmetsa
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SESSION TITLE: Pathology Identifying Chest Infections Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Pulmonary histoplasmosis typically affects immunocompromised individuals. Symptomatic infection in immunocompetent patients is rare, however, important risk factors include living in an endemic region and the size of inoculation. We present a case of subacute pulmonary histoplasmosis in a healthy young male and discuss how availability bias during the COVID-19 pandemic may pose challenges in the diagnosis. CASE PRESENTATION: A healthy 30-year-old male presented to our hospital complaining of left flank and bilateral chest pain for one week. The patient returned from Veracruz, Mexico three weeks prior after spending two months there studying to become a chef. While in Mexico, the patient experienced low-grade fevers, night sweats, and pleuritic chest pain for which he was treated with steroids and antibiotics for presumed COVID-19 infection despite negative testing. Treatment provided the patient temporary relief, however, some of his symptoms returned prompting him to present to the emergency department. Upon presentation, the patient was afebrile and had a normal resting pulse oximetry. CT angiogram of the chest demonstrated three lung nodules and prominent mediastinal lymphadenopathy. A complete infectious and rheumatologic workup was performed. BAL, transbronchial biopsies and EBUS-TBNA were performed. Lung biopsy showed reactive pneumocytes, focal intra-alveolar fibrinous material, congestion, and hemorrhage. Lymph node cytology revealed an aggregate of necrotizing and nonnecrotizing granulomas and GMS stain was positive for yeast. Fungitell and Histoplasma antibodies returned positive. The patient was discharged on Itraconazole and followed up with infectious disease specialists two months later in stable condition. DISCUSSION: Patients with subacute pulmonary histoplasmosis and viral pneumonia may present with similar clinical and radiological findings making the diagnosis arduous. In addition, the prevalence of COVID-19 pneumonia makes clinicians susceptible to using availability bias and further obscuring diagnosis. Some clues that help differentiate subacute pulmonary histoplasmosis include a longer duration of symptoms, pulmonary nodules, and mediastinal and hilar adenopathy. CONCLUSIONS: While pulmonary histoplasmosis is an uncommon finding in immunocompetent patients, suspicion should be raised in patients from endemic regions. Despite the COVID-19 pandemic, clinicians should avoid anchoring biases and keep differential diagnoses in mind. Reference #1: Azar MM, Hage CA. Clinical Perspectives in the Diagnosis and Management of Histoplasmosis. Clin Chest Med. 2017;38(3):403-415. doi:10.1016/j.ccm.2017.04.004 Reference #2: Staffolani S, Buonfrate D, Angheben A, et al. Acute histoplasmosis in immunocompetent travelers: a systematic review of literature. BMC Infect Dis. 2018;18(1):673. Published 2018 Dec 18. doi:10.1186/s12879-018-3476-z DISCLOSURES: No relevant relationships by Steven Douedi No relevant relationships by Justin Ilagan No relevant relationships by TAIMOOR KHAN No relevant relationships by Romany Nightingale No relevant relationships by Mihir Odak No relevant relationships by Noor Salam No relevant relationships by Kameron Tavakolian
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SESSION TITLE: Severe and Unusual Blastomycosis Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Severe pulmonary blastomycosis (PB) usually affects immunocompromised patients, with very high mortality rate of up to 40%. PB can mimic pneumonia caused by other organisms (1), which can delay diagnosis and treatment initiation. We present a case of severe PB that was initially thought to be COVID-19 pneumonia, to our knowledge this is 2nd case of concomitant PB and COVID-19 infection in literature. (2) CASE PRESENTATION: Patient is 52 year old female with past medical history of atrial fibrillation, asthma, bariatric surgery, that presents with shortness of breath for 2 weeks. Despite receiving only 1 dose of COVID-19 vaccine (Moderna) 5 months ago, patient tested positive for COVID-19 on PCR test at the urgent care 4 days prior. Her symptoms progressed despite initial outpatient treatment with steroids and antibiotics. Initial emergency department chest computed tomography (CT) revealed dense bilateral consolidations, with hypoxic respiratory failure, patient was admitted for treatment of presumed COVID-19 pneumonia, and guideline directed treatment was initiated. Despite maximal medical management, that included steroids, broad spectrum antibiotics, remedisivir, patient failed to improve, with repeat CT chest revealing worsening consolidations. Bronchoscopy was performed 12 days into the admission revealed thick white secretions, with cultures growing blastomyces dermatitidis. At this point patient development of septic shock with multiorgan failure. Patient was subsequently intubated, and due to significant renal failure, initiated on hemodialysis (HD). Anti-fungal treatment was initiated with amphotericin B, and transitioned to itraconazole afterwards. Patient required several HD sessions, after which her renal function fully recovered. Patient was successfully extubated 7 days later, but required additional 22 days of medical care and physical therapy before being ready for discharge to rehabilitation facility. On the outpatient follow up 6 weeks after discharge, patient continues to slowly recover. Repeat CT chest still with significant bilateral consolidations. Patient will require at least 12 months of itraconazole therapy. DISCUSSION: PB can mimic bacterial and viral pneumonia symptoms. (1) In the widespread COVID-19 pandemic, clinicians can be misled by COVID-19 positive test in patient with bilateral pneumonia, and initiate guideline directed therapy. Immunosuppression agents can lead to adverse outcomes in patients with underlying PB. Questionable is the significance of COVID positive PCR test in semi-vaccinated individual. Potentially even mild COVID-19 infection could predispose patient for PB. Early diagnosis of PB is important, as delay in treatment and medical immunosuppression can lead to worse outcomes. CONCLUSIONS: PB should be suspected even in patients presenting with positive COVID-19 PCR test. Guideline directed therapy for COVID-19 can worsen underlying PB. Reference #1: https://www.cdc.gov/fungal/covid-fungal.html Reference #2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8503152/ DISCLOSURES: No relevant relationships by Dovile Baniulis No relevant relationships by Dovile Cerkauskaite No relevant relationships by Igor Dumic No relevant relationships by Momcilo Durdevic No relevant relationships by Dragana Durdevic No relevant relationships by Ashutossh Naaraayan No relevant relationships by Ankita Subedi