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SESSION TITLE: Autoimmune Diffuse Lung Disease Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Interstitial lung disease (ILD) associated with connective tissue diseases (CTD) present with varying degrees of severity and functional impairment. Patients with CTD-ILD may often initially present for pulmonary evaluation. Pulmonologists must be familiar with the spectrum of CTD syndromes, the associated serologic testing, and referral criteria to rheumatology. CASE PRESENTATION: A 62-year-old never-smoking female with prior mild COVID-19 infection, previously vaccinated, presented to clinic with a diagnosis of pulmonary fibrosis. She endorsed three years of progressive shortness of breath and dyspnea on exertion walking only eight blocks and with light household chores. The patient had worked as a professional chef in poorly ventilated kitchens. Review of systems was notable for morning stiffness and pain in bilateral hand joints with associated difficulty opening medication bottles secondary to symptoms. Previous computed tomography (CT) of the chest demonstrated peripheral, subpleural, and basal predominant reticulations accompanied by bronchiectasis and bronchioloectasis consistent with probable usual interstitial pneumonia (UIP). Envisia® genomic testing was performed and results were negative for idiopathic pulmonary fibrosis. Extensive serologic testing for CTD was performed, including rheumatoid factor and anti-cyclic citrullinated peptides which were normal. The patient was referred to rheumatology, and hand x-rays demonstrated diffuse MCP joint narrowing. The patient was diagnosed with seronegative rheumatoid arthritis (RA) with RA-ILD and started on treatment. DISCUSSION: Multiple society guidelines recommend serologic testing to rule out CTD-ILD in patients with new ILD. ILD has been reported to occur in 20-60% of patients with RA with multiple patterns. Patients with seronegative RA are more likely to develop extraarticular manifestations of RA including fibrotic lung disease. Patients who are asymptomatic from RA-ILD may be monitored clinically for worsening RA-ILD. The selection of patients for treatment with an immunosuppressive agent or glucocorticoids should be done with a multidisciplinary team. Patients with RA-ILD and a UIP pattern may not respond to immunosuppressive medications but are typically trialed on treatment for worsening lung disease. Randomized controlled trials that included patients with RA-ILD with fibrosis have suggested a role for nintedanib, an anti-fibrotic agent, in slowing the progression of forced vital capacity decline. CONCLUSIONS: CTD-ILD is a common diagnosis in pulmonary clinics, and ILD symptoms may be the chief complaint at presentation. Providers must be familiar with diagnostic criteria for CTD and obtain a detailed review of systems that might suggest the diagnosis of CTD. Early diagnosis of CTD-ILD and monitoring of disease activity is important to prevent progression of CTD-ILD. Reference #1: Yoo H, Hino T, Han J, et al. Connective tissue disease-related interstitial lung disease (CTD-ILD) and interstitial lung abnormality (ILA): Evolving concept of CT findings, pathology and management. Eur J Radiol Open. 2020;8:100311. Published 2020 Dec 16. doi:10.1016/j.ejro.2020.100311 Reference #2: Sahatciu-Meka V, Rexhepi S, Manxhuka-Kerliu S, Rexhepi M. Extra-articular manifestations of seronegative and seropositive rheumatoid arthritis. Bosn J Basic Med Sci. 2010;10(1):26-31. doi:10.17305/bjbms.2010.2729 Reference #3: Cottin V. Pragmatic prognostic approach of rheumatoid arthritis-associated interstitial lung disease. Eur Respir J. 2010 Jun;35(6):1206-8. doi: 10.1183/09031936.00008610. PMID: 20513909. DISCLOSURES: No relevant relationships by Brenda Garcia No relevant relationships by Zein Kattih No relevant relationships by Priyanka Makkar No relevant relationships by Jonathan Moore
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SESSION TITLE: Uncommon Presentations and Complications of Chest Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Cryptococcus is a ubiquitous fungus in the environment. Infections can occur in humans when Cryptococcus is aerosolized and inhaled. Severity of clinical presentation varies from asymptomatic pulmonary colonization to disseminated life-threatening infection such as meningitis. These infections usually occur with deficiencies in T-cell-mediated immunity, including those with HIV/AIDS and immunosuppression due to transplantation. Herein we present a case of isolated pulmonary cryptococcosis in an immunocompetent host. CASE PRESENTATION: The patient is a 36-year-old never-smoker male with history of recurrent left spontaneous pneumothorax status post VATS blebectomy, negative for alpha-1 antitrypsin deficiency and cystic fibrosis. A year later, he presented with fatigue, shortness of breath, and dry cough after a recent trip to Ohio. Viral panel including COVID-19 was negative. A chest x-ray showed a new 4 cm rounded opacity in the right middle lobe (RML). A CT scan of the chest showed 2 mass-like and nodular areas of consolidation with surrounding GGOs within the RML (Figure 1). He underwent navigational bronchoscopy with transbronchial biopsy (TBBx) of RML, BAL, and EBUS with transbronchial needle aspiration (TBNA). Cytology was negative for malignant cells. BAL showed rare yeast. Pathology of the TBBx showed the airway wall with chronic inflammation including granulomatous inflammation, positive for yeast, most consistent with Cryptococcus with positive Grocott methenamine silver (GMS) stain (Figure 2). Culture of the TBNA grew C. neoformans var. grubii. Other cultures were negative. Serum Cryptococcal antigen was positive. HIV test was negative. He started treatment with oral fluconazole with improvement of symptoms. DISCUSSION: Clinical presentation of pulmonary cryptococcosis can include a variety of symptoms in which immune status is critical for determining the course of infection. Infection can vary from asymptomatic infection to severe pneumonia and respiratory failure, and meningitis. Similarly, imaging findings can also vary and be characterized as pulmonary nodules, consolidations, cavitary lesions, and/or a diffuse interstitial pattern. The diagnosis of Cryptococcus is made using histology, fungal cultures, serum cryptococcal antigen, and radiography in the appropriate clinical and radiological context. Treatment recommendations are determinant on immune status of the patient as well as symptoms. Asymptomatic and localized disease in immunocompetent patients can be monitored and mild/moderate disease can be treated with fluconazole. Those with severe or disseminated infection warrant induction therapy with an amphotericin B and flucytosine CONCLUSIONS: Clinical and radiological presentation of cyptococcosis varies depending on immune status. Disease can occur in both immunocompromised and competent hosts. Immune status determines disease course and treatment. Reference #1: Huffnagle GB, Traynor TR, McDonald RA, Olszewski MA, Lindell DM, Herring AC, et al. Leukocyte recruitment during pulmonary Cryptococcus neoformans infection. Immunopharmacology. 2000 Jul 25;48(3):231–6. Reference #2: Kd B, Jw B, Pg P. Pulmonary cryptococcosis. Semin Respir Crit Care Med [Internet]. 2011 Dec [cited 2022 Apr 2];32(6). Available from: https://pubmed.ncbi.nlm.nih.gov/22167400/ Reference #3: Ms S, Rj G, Ra L, Pg P, Jr P, Wg P, et al. Practice guidelines for the management of cryptococcal disease. Infectious Diseases Society of America. Clin Infect Dis Off Publ Infect Dis Soc Am [Internet]. 2000 Apr [cited 2022 Apr 1];30(4). Available from: https://pubmed.ncbi.nlm.nih.gov/10770733/ DISCLOSURES: No relevant relationships by Mina Elmiry No relevant relationships by Brenda Garcia No relevant relationships by Zein Kattih no disclosure on file for Priyanka Makkar;No relevant relationships by Jonathan Moore
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TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Propofol-related infusion syndrome (PRIS) is a rare and serious effect of propofol infusion for sedation in critically ill patients. Though there has been an association seen with higher doses of propofol and prolonged infusion times, usually greater than 24 to 48 hours. CASE PRESENTATION: We present a case of an 86-year-old man with history of bradycardia and an implanted permanent pacemaker who was admitted for acute hypoxic respiratory failure caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia. Throughout hospital stay, this patient had progressively increasing oxygen requirements with appropriate escalation in level of care to the ICU. Due to increasing hypoxia despite non-invasive ventilation, the patient was intubated on day 4 of hospitalization, placed on vasopressors and started on sedation, which included continuous propofol infusion. On day 6 of hospitalization, the patient developed worsening hypotension requiring increased levels of sedation and significant lab abnormalities compared to labs collected the day prior. The patient was noted to have elevated potassium to 5.8 mmol/L, creatinine elevation to 2.41 mg/dL from 1.36 mg/dL, and elevated AST of 184 U/L and ALT of 95 U/L from normal levels. Lactate was 4.5, and creatinine kinase was 1317. Six hours later, repeat liver function tests revealed AST of 2078 U/L and ALT of 966 U/L. In the setting of sudden onset rhabdomyolysis, acute kidney injury, and lactic acidosis, there was concern for PRIS and propofol was discontinued. After extended discussion with the family, aggressive measures including dialysis were declined, and patient died. Of interest, the patient's pacemaker likely prevented the patient from developing bradycardia, classically seen in PRIS. DISCUSSION: Challenges with sedation of intubated patients with SARS-CoV-2 have been clinically observed and deeper sedation levels have been required to promote ventilator synchrony. Propofol continues to be a first-line sedative in critically ill patients, including SARS-CoV-2 patients. These patients require sedation higher infusion rates compared and are therefore at higher risk. Our patient was maintained on 20mcg/kg/min for 27 hours, then subsequently on 45 mcg/kg/min for 34 hours thereafter. Therefore, our patient was at increased risk of PRIS given propofol infusion at high doses was maintained for longer than 24 hours. Moreover, the concurrent use of vasopressors placed him at increased risk. CONCLUSIONS: Although propofol is recommended as a first-line anesthetic agent in critically ill patients with SARS-CoV-2 requiring sedation, the multiorgan failure resulting from PRIS is potentially fatal. Early recognition is crucial for management, which includes discontinuing propofol infusion and hemodialysis if indicated. REFERENCE #1: Hanidziar D, Bittner EA. Sedation of Mechanically Ventilated COVID-19 Patients: Challenges and Special Considerations. Anesth Analg. 2020;131(1):e40-e41. doi:10.1213/ANE.0000000000004887 REFERENCE #2: Payen JF, Chanques G, Futier E, Velly L, Jaber S, Constantin JM. Sedation for critically ill patients with COVID-19: Which specificities? One size does not fit all. Anaesth Crit Care Pain Med. 2020;39(3):341-343. doi:10.1016/j.accpm.2020.04.010 REFERENCE #3: Yamamoto K. Risk of propofol use for sedation in COVID-19 patient. Anaesthesiology Intensive Therapy. 2020;52(4):354-355. doi:10.5114/ait.2020.100477. DISCLOSURES: No relevant relationships by Sravani Gajjala, source=Web Response No relevant relationships by Oki Ishikawa, source=Web Response No relevant relationships by Stacey Jou, source=Web Response No relevant relationships by Zein Kattih, source=Web Response No relevant relationships by Vinayak Shenoy, source=Web Response
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TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) myocarditis has recently been described in case reports. A systematic review in early 2021 found fourteen case reports of myocarditis or myopericarditis secondary to this viral infection. We describe an interesting case of proven non-ischemic cardiac dysfunction in the setting of acute infection. Despite steroid treatment, which has been suggested to have favorable outcomes, our patient did not survive. CASE PRESENTATION: We present a case of a 77-year-old man with extensive electrophysiologic and ischemic cardiac disease who presented to the hospital for generalized weakness, malaise, and shortness of breath. The patient's cardiac history was significant for atrial flutter s/p ablation, coronary artery disease s/p coronary artery bypass graft in the distant past, peripheral artery disease s/p right lower extremity revascularization, and carotid stenosis s/p carotid endarterectomy. SARS-CoV-2 PCR test was positive. The patient had increasing hypoxia which required non-invasive ventilation and eventually, tracheal intubation and mechanical ventilation. The hospital course was complicated by the development of persistent chest pain associated with elevated cardiac enzymes. EKG showed diffuse ST-segment depressions. An echocardiogram revealed diffuse left ventricular hypokinesis and a reduced ejection fraction of 20% which was not present previously. In this setting, the patient was ruled in for acute coronary syndrome and underwent cardiac catheterization. Cardiac catheterization demonstrated patent grafts and no significant obstructive disease. A presumptive diagnosis of myocarditis was made. The patient's clinical status deteriorated despite optimal medical treatment, and he developed hemodynamically unstable atrial fibrillation that did not respond to pharmacologic treatment or cardioversion and resulted in cardiogenic shock and, ultimately, his death. DISCUSSION: SARS-CoV-2 myocarditis has been described in select case reports internationally. Many of these cases are described in patients with no previously identified comorbid conditions. This case suggests that in patients with underlying electrophysiologic dysfunction, SARS-CoV-2 myocarditis is associated with poor outcomes. CONCLUSIONS: The mechanism of the effect of SARS-CoV-2 on the heart is unclear and includes myocarditis or myopericarditis. In our patient, cardiac catheterization which was performed during his hospitalization confirmed no ischemic disease and suggested the presence of myocarditis which was ultimately fatal in the setting of refractory cardiogenic shock. Further research is needed into the optimal management of myocarditis associated with SARS-CoV-2. REFERENCE #1: Sawalha K, Abozenah M, Kadado AJ, et al. Systematic Review of COVID-19 Related Myocarditis- Insights on Management and Outcome. Cardiovasc Revasc Med. Feb 2021;23:107-113. REFERENCE #2: Purdy A, Ido F, Sterner S, et al. Myocarditis in COVID-19 presenting with cardiogenic shock: a case series. Eur Heart J Case Rep. Feb 2021;5(2):ytab028. REFERENCE #3: Fried JA, Ramasubbu K, Bhatt R, et al. The Variety of Cardiovascular Presentations of COVID-19. Circulation. 2020;141(23):1930-1936. DISCLOSURES: No relevant relationships by Sravani Gajjala, source=Web Response No relevant relationships by Stacey Jou, source=Web Response No relevant relationships by Zein Kattih, source=Web Response No relevant relationships by Rosaline Ma, source=Web Response No relevant relationships by Akhilesh Mahajan, source=Web Response No relevant relationships by Vinayak Shenoy, source=Web Response