Abstract Studies using cardiopulmonary exercise testing (CPET) to evaluate persistent dyspnea following infection with COVID‐19 have focused on older patients with co‐morbid diseases who are post‐hospitalization. Less attention has been given to younger patients with post‐COVID‐19 dyspnea treated as outpatients for their acute infection. We sought to determine causes of persistent dyspnea in younger patients recovering from acute COVID‐19 infection that did not require hospitalization. We collected data on all post‐COVID‐19 patients who underwent CPET in our clinic in the calendar year 2021. Data on cardiac function and respiratory response were abstracted, and diagnoses were assigned using established criteria. CPET data on 45 patients (238.3 ± 124 days post‐test positivity) with a median age of 27.0 (22.0–40.0) were available for analysis. All but two (95.6%) were active‐duty service members. The group showed substantial loss of aerobic capacity—average VO2 peak (L/min) was 84.2 ± 23% predicted and 25 (55.2%) were below the threshold for normal. Spirometry, diffusion capacity, high‐resolution computed tomography, and echocardiogram were largely normal and were not correlated with VO2peak. The two most common contributors to dyspnea and exercise limitation following comprehensive evaluation were deconditioning and dysfunctional breathing (DB). Younger active‐duty military patients with persistent dyspnea following outpatient COVID‐19 infection show a substantial reduction in aerobic capacity that is not driven by structural cardiopulmonary disease. Deconditioning and DB breathing are common contributors to their exercise limitation. The chronicity and severity of symptoms accompanied by DB could be consistent with an underlying myopathy in some patients, a disorder that cannot be differentiated from deconditioning using non‐invasive CPET.

Background Sarcoidosis is a multisystem granulomatous disorder with unclear etiology. Morbidity and mortality vary based on organ involvement, with cardiac sarcoidosis (CS) associated with higher mortality; despite this, CS remains underdiagnosed. The Heart Rhythm Society (HRS) expert consensus statement recommends screening sarcoidosis patients for CS utilizing a symptom screen, EKG, and echocardiogram (TTE), while the American Thoracic Society (ATS) guideline recommends only EKG and symptom screening. These recommendations, however, are based on limited data with recommendations for further studies. Research question The purpose is to evaluate the prevalence of abnormal screening tests in patients with sarcoidosis and the correlation of these tests with the subsequent diagnosis of CS. A specific emphasis was placed on evaluating the sensitivity of the recommendations versus the sensitivity of a modified criteria. Study design and Methods: This study retrospectively evaluated a database of prospectively enrolled patients from a tertiary military academic center. All patients who underwent imaging with cardiac MRI and/or FDG-PET were identified. These results were correlated with screening studies (symptom screen, EKG, TTE, and ambulatory rhythm monitoring (ARM)) and used to calculate sensitivity, specificity, and positive and negative predictive values for each test. Using a clinical diagnosis of CS as the reference standard, the sensitivity and specificity of the HRS criteria were calculated and compared to a modified screening rubric developed a priori, consisting of minor changes to the criteria and the addition of ARM. Results This study evaluated 114 patients with sarcoidosis with 132 advanced imaging events, leading to a diagnosis of CS in 36 patients. Utilizing HRS screening recommendations, the sensitivity for CS was 63.9%, while the modified criteria increased sensitivity to 94.4%. Interpretation This study suggests that the HRS guidelines lack sensitivity to effectively screen for CS and that a modified screening model which includes ARM may be more effective.

TOPIC: Disorders of the Pleura TYPE: Fellow Case Reports INTRODUCTION: Calcified pleural lesions have both benign and malignant etiologies. Benign lesions can originate from previous trauma, prior pleural infections, hemothorax, or asbestos exposures, and are often focal and limited1,2. Malignant lesions often involve metastatic disease from mesenchymal tumor origin, such as osteosarcoma, chondrosarcoma, or mesothelioma1,3. We describe a case of a patient with metastatic chondrosarcoma manifesting with extensive calcification of the parietal and visceral pleura. CASE PRESENTATION: A 67 year old man was referred to pulmonary for a new subcarinal soft tissue mass on chest CT. He had been previously diagnosed with chondrosarcoma in 2016 and underwent treatment via a radical right proximal humerus excision and shoulder arthroplasty, with final pathology revealing grade 2 conventional chondrosarcoma, mixed hyaline and myxoid, without metastatic foci.Screening chest CT in 2020 noted a new, partially calcified subcarinal soft tissue mass and adjacent lymphadenopathy with moderate hypermetabolism on a positron emission tomography scan (PET/CT). Bronchoscopy with endobronchial ultrasound transbronchial needle aspiration (EBUS-TBNA) subcarinal lymph node and adjacent posterior mass confirmed metastatic disease.He subsequently developed rapidly progressive dyspnea on exertion over the following month. Repeat chest CT revealed extensive development of circumferential nodularity and calcification of the right visceral and parietal pleura with a large pleural effusion. Thoracentesis improved dyspnea despite limited reexpansion of the lung and noted loculation of the effusion. Pleuroscopic evaluation of the complicated space was undertaken to remove loculations and optimize placement of an indwelling pleural catheter (IPC) for his malignant effusion. Despite difficulty with trocar insertion into the calcified pleural space, placement of the IPC was successful with improvement in his dyspnea. DISCUSSION: Metastatic pleural involvement of chondrosarcoma is rare, and can occur in the setting of direct extension in locoregional disease or hematogenous spread from other sites of primary involvement. Metastatic disease has been noted to be more prevalent in the dedifferentiated and mesenchymal subtypes4. Manifestations of metastatic pleural involvement are typically pleural calcifications that can be profound in the rapid evolution and extent of calcified involvement. Management is often palliative, as in this case, with drainage of any associated pleural effusions and attempts to mitigate accompanying dyspnea. CONCLUSIONS: This case of metastatic chondrosarcoma with extensive visceral and parietal pleural involvement is rare and infrequently noted in the literature. Palliative management with thoracentesis and IPC placement was complicated by the pervasive pleural calcification that prevented ultrasound imaging and made access to the pleural space difficult and dangerous. REFERENCE #1: Sureka B, Thukral BB, Mittal MK, Mittal A, Sinha M. Radiological review of pleural tumors. Indian J Radiol Imaging. 2013;23(4):313-320 DISCLOSURES: No relevant relationships by Robert Browning, source=Web Response, value=Grant/Research Support Removed 04/29/2021 by Robert Browning, source=Web Response No relevant relationships by Robert Browning, source=Web Response, value=Consulting fee Removed 04/29/2021 by Robert Browning, source=Web Response No relevant relationships by Robert Browning, source=Web Response, value=Consulting fee Removed 04/29/2021 by Robert Browning, source=Web Response No relevant relationships by Sean McKay, source=Web Response No relevant relationships by Philip Mullenix, source=Web Response No relevant relationships by Caitlin Nickens, source=Web Response No relevant relationships by John Shumar, source=Web Response

Progressive fibrosing interstitial lung disease (PF-ILD) describes a phenotypic subset of interstitial lung diseases characterized by progressive, intractable lung fibrosis. PF-ILD is separate from, but has radiographic, histopathologic, and clinical similarities to idiopathic pulmonary fibrosis. Two antifibrotic medications, nintedanib and pirfenidone, have been approved for use in patients with idiopathic pulmonary fibrosis. Recently completed randomized controlled trials have demonstrated the clinical efficacy of antifibrotic therapy in patients with PF-ILD. The validation of efficacy of antifibrotic therapy in PF-ILD has changed the treatment landscape for all of the fibrotic lung diseases, providing a new treatment pathway and opening the door for combined antifibrotic and immunosuppressant drug therapy to address both the fibrotic and inflammatory components of ILD characterized by mixed pathophysiologic pathways.

TOPIC: Imaging TYPE: Medical Student/Resident Case Reports INTRODUCTION: Superior vena cava (SVC) syndrome can be a complication of malignancy compressing the SVC, resulting in facial or arm swelling, dyspnea, cerebral edema, or thrombosis. SVC occlusion from malignancy is treated with endovascular stenting, with adjunctive chemo-radiotherapy as appropriate [1,2]. We describe a case of a patient whose SVC syndrome treated with endovascular stenting was complicated by stent migration to the right atrium (RA) of the heart, and was treated with systemic anticoagulation instead of endovascular correction. CASE PRESENTATION: A 71 year-old man with non-small cell lung cancer developed facial and right arm swelling and dyspnea with imaging findings of a right para-tracheal mass compressing the SVC, consistent with SVC syndrome. He received SVC stenting with symptom relief. One month later, he presented to the emergency room for chest pain and was admitted with subsequent development of hypoxic respiratory failure secondary to hemoptysis requiring endotracheal intubation and bronchial artery embolization. A computed tomography (CT) chest angiogram showed bilateral pleural effusions, infiltrates, and a right upper lung cavitary lesion that was treated empirically with vancomycin and piperacillin-tazobactam before transitioning to meropenem after sputum cultures demonstrated pseudomonas resistant to ceftazidime, levofloxacin, and piperacillin-tazobactam. The CT also noted partial SVC stent thrombosis and RA migration, which was also visualized on point-of-care ultrasound (POCUS). Cardiothoracic surgery and interventional radiology deemed the patient to not be a surgical candidate and the stent retained some patency, so it was left in place. The thrombus was not easily accessible, and the risk of catheter-directed thrombolysis was considered too high given his hemoptysis risk from his lung mass. He was ultimately treated with systemic anticoagulation. DISCUSSION: No randomized controlled studies compare endovascular stenting and chemo-radiotherapy in the management of malignancy-related SVC syndrome, but a Cochrane database review showed stenting relieves SVC obstruction better than chemotherapy or radiotherapy [1]. The major complication rate of stenting is about 4% and includes stent migration, bleeding, infection, thrombosis, SVC rupture, pericardial tamponade, heart failure, and arrhythmia [1]. RA stent migration occurs in about 2% of cases and can cause arrhythmia, conduction abnormalities, valvular damage, endocarditis, and cardiac perforation [2]. Stent migration is generally treated with endovascular snaring or SVC-to-inferior vena cava bridging stent, and the role of systemic anticoagulation is unclear. CONCLUSIONS: This case of SVC stent migration to the RA represents the diagnostic utility of POCUS and reveals an area of future study as patient outcomes in endovascular correction of migration compared to systemic anticoagulation are unclear. REFERENCE #1: Warner P, et al. Superior vena cava stenting in the 21st century. Postgrad Med J. 2013;89(1050):224-230. doi:10.1136/postgradmedj-2012-131186 REFERENCE #2: Taylor JD, Lehmann ED, Belli AM, et al. Strategies for the management of SVC stent migration into the right atrium. Cardiovasc Intervent Radiol. 2007;30(5):1003-1009. doi:10.1007/s00270-007-9109-3 REFERENCE #3: Uberoi R. Quality assurance guidelines for superior vena cava stenting in malignant disease. Cardiovasc Intervent Radiol. 2006;29(3):319-322. doi:10.1007/s00270-005-0284-9 DISCLOSURES: No relevant relationships by Andrew Goodwin, source=Web Response No relevant relationships by John Shumar, source=Web Response No relevant relationships by Joseph Zeman, source=Web Response

SESSION TITLE: Medical Student/Resident Pulmonary Manifestations of Systemic Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: As an extra pulmonary manifestation of sarcoidosis, male genitourinary involvement is rare, with only an estimated 60 cases described in the literature. Amongst those patients with genitourinary sarcoidosis, epididymal involvement is most common, followed by the testis and vas deferens[1]. We describe a case of a patient with an 8 year history of sarcoidosis with cutaneous manifestations who presented to his primary care physician (PCP) with dysuria and a painless scrotal mass, initially concerning for malignancy but found to be consistent with genitourinary sarcoidosis after partial orchiectomy revealed non-caseating granulomas. CASE PRESENTATION: A 43 year old African American man with an 8 year history of sarcoidosis with cutaneous manifestations without prior or current treatment presented to his PCP for evaluation of one week of dysuria. A physical exam revealed a 3 cm firm, non-tender lesion superior to the left testis. A testicular ultrasound revealed a 2 cm left epididymal mass and a 1 cm hypoechoic, irregular right intratesticular mass. Given these findings, he was referred to the urology service. Serum tumor markers (AFP, hCG, and LDH) were not elevated. Further imaging was obtained via a CT chest / abdomen / pelvis and subsequent PET scan, which showed focal hypermetabolism in the left epididymis, absent hypermetabolism in the right testis, and diffuse lymphadenopathy, most notable in the inguinal chains. He subsequently underwent a partial right orchiectomy with inguinal lymph node exploration. Intraoperative frozen specimens of the right testis and left epididymis showed non-caseating granulomas without evidence of malignancy, consistent with genitourinary sarcoidosis. He had an uneventful postoperative course, and was initiated on glucocorticoid therapy with prednisone followed by maintenance hydroxychloroquine. The left sided epididymal mass resolved completely with treatment. DISCUSSION: Sarcoidosis is a chronic, multisystem disease defined by the presence of non-caseating granulomas affecting any organ system. Genitourinary involvement of sarcoidosis is rare, with an estimated prevalence of around 0.2%[1]. The clinical presentation is often a unilateral, nodular, painless scrotal mass, which in this population is highly concerning for a primary testicular malignancy[2]. Thus, the immediate priority is to evaluate for malignancy while ensuring the preservation of fertility[1]. Imaging does not differentiate between genitourinary sarcoidosis and malignancy, so a tissue sample is required and often occurs with inguinal exploration as well as partial orchiectomy[1,2]. CONCLUSIONS: This presentation of bilateral genitourinary sarcoidosis occurring many years after initial diagnosis represents an exceedingly rare case and one that highlights the importance of ruling out malignancy in these clinical situations and always keeping sarcoidosis on the differential. Reference #1: Rao PK, Sabanegh ES. Genitourinary sarcoidosis. Rev Urol. 2009;11(2):108-13. Reference #2: Chierigo F, Alnajjar HM, Haider A, Walkden M, Shaikh T, Muneer A. Testicular pain as an atypical presentation of sarcoidosis. Ann R Coll Surg Engl. 2019;101(4):e99-e101. DISCLOSURES: No relevant relationships by Tyler Church, source=Admin input No relevant relationships by Sean Dooley, source=Admin input No relevant relationships by Arthur Holtzclaw, source=Admin input No relevant relationships by John Shumar, source=Web Response

A 70-year-old African–American woman with a history of biopsy-proven sarcoidosis with pulmonary and cutaneous manifestations diagnosed 20 years ago presented to her primary care physician (PCP) for an evaluation after two recent falls at home. Given the acute nature of these changes, her PCP

We present an adult patient with Crouzon syndrome manifesting with facial deformities and panhypopituitarism. Crouzon syndrome is a rare, autosomal dominant genetic disorder characterized by facial bone deformities, such as a prominent nose, frontal bossing, and ocular proptosis, as well as headaches, seizures, and developmental delay.

SESSION TITLE: Pulmonary Manifestations of Systemic Disease SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/23/2019 8:45 AM - 9:45 AM INTRODUCTION: Osseous involvement in sarcoidosis is quite rare, with an estimated prevalence of around 3-13% among all patients with sarcoidosis[1]. Most cases of osseous involvement are identified at the initial diagnosis, with the majority demonstrating axial skeleton involvement[2]. Here we describe a case of a patient with longstanding pulmonary and cutaneous sarcoidosis diagnosed with osseous involvement of the axial skeleton and calvarium nearly twenty years after initial presentation. CASE PRESENTATION: A 70 year old African American woman with a twenty year history of sarcoidosis with pulmonary and cutaneous manifestations presented to her primary care physician for evaluation of recent falls. A CT scan of the head revealed numerous lytic lesions within the calvarium. Given these findings, a prior CT scan of the chest from two weeks prior was reviewed retrospectively and also significant for new multifocal lytic lesions in the cervical and thoracic spine suggestive of malignancy, notably multiple myeloma. SPEP, UPEP, serum free light chains, and peripheral smear were ordered but all were without adverse findings. She was up to date with age appropriate cancer screenings with no significant findings. Ultimately, she underwent a PET/CT, revealing innumerable lytic lesions concerning for osseous sarcoidosis given her otherwise negative workup. A right iliac crest biopsy was performed, significant for granulomatous inflammation consistent with osseous sarcoidosis. DISCUSSION: Sarcoidosis is a systemic inflammatory disease defined by the development of non-caseating granulomas affecting any organ system. Osseous involvement is relatively rare and infrequently described in the literature. Most of these cases are identified at initial diagnosis but can also be discovered incidentally on imaging during the investigation of another complaint. Unfortunately, there is no classic imaging finding for osseous sarcoid which can be described as permeative, destructive, or lytic, and is often radiographically indistinguishable from malignancy.[2] As a result, late presenting osseous sarcoidosis can be a clinical dilemma, often leading to a high concern for malignancy and stress for the patient and typically requires a biopsy for confirmation and delineation of the underlying pathology. CONCLUSIONS: This case of severe osseous sarcoidosis presenting twenty years after initial diagnosis is an exceedingly rare presentation of a rare disease and is a pertinent reminder of the pervasive nature of sarcoidosis and its potential to affect any organ system at any time. Reference #1: 1. James DG, Neville E, Siltzbach LE. A worldwide review of sarcoidosis. Ann NY Acad Sci. 1976;278:321-34. Reference #2: 2. Sparks JA, Mcsparron JI, Shah N, et al. Osseous sarcoidosis: clinical characteristics, treatment, and outcomes--experience from a large, academic hospital. Semin Arthritis Rheum. 2014;44(3):371-9. DISCLOSURES: No relevant relationships by Tyler Church, DO, source=Admin input No relevant relationships by Arthur Holtzclaw, source=Web Response No relevant relationships by John Shumar, source=Web Response No relevant relationships by Joseph Zeman, source=Web Response

Chemotherapy-induced diarrhoea (CID) is a risk of antineoplastic regimens, often associated with 5-fluorouracil (5-FU), irinotecan and capecitabine. Current treatment guidelines for CID include the use of loperamide and octreotide but do not account for other therapies, including budesonide. Small case reports have shown benefit with budesonide in CID secondary to 5-FU and irinotecan, but there is no literature base addressing budesonide use in CID secondary to capecitabine. We describe a case of a patient with severe capecitabine-induced diarrhoea that was refractory to guideline based therapy but resolved with the use of budesonide.

Presentations of drug-induced liver injury (DILI) are highly variable. Although biochemical evidence of cholestasis is common, the extent of aminotransferase elevations and patterns of liver injury vary. Patients may be asymptomatic, and many cases may never be diagnosed. We describe a case of memantine-induced hepatotoxicity in an elderly patient with Alzheimer's dementia, with probable causality for drug-induced liver injury, as assessed using the Roussel Uclaf Causality Assessment Method (RUCAM) score.

Chemotherapy induced diarrhea (CID) is a risk of anti-neoplastic regimens, often associated with 5-fluorouracil (5-FU), irinotecan, and capecitabine. Current treatment guidelines for CID include use of loperamide and octreotide, but do not account for other therapies, including budesonide. Small case reports have shown benefit with budesonide in CID secondary to 5-FU and irinotecan, but there is no literature base addressing budesonide use in CID secondary to capecitabine. An 81 year old woman with T3M0N0 Stage IIA rectal adenocarcinoma on neoadjuvant chemoradiation with capecitabine presented to the ED with four days of severe diarrhea not amenable to loperamide, representing a grade III toxicity for which capecitabine was discontinued. The patient was admitted to the hospital and started on loperamide and octreotide. After multiple days, she demonstrated no response even to maximum dosing. Tincture of opium was trialed, complicated by the acute onset of a severe ileus, and after several days of conservative management, the ileus resolved with return of diarrhea. A flexible sigmoidoscopy was performed, which revealed edematous colonic mucosa with biopsies showing focal cytomegaly and endothelial hypertrophy, consistent with chemotherapy-associated injury. She was discharged home with less frequent diarrhea and tolerating an oral diet. At a close follow-up appointment, she reported persistence of diarrhea. Due to her continued symptoms, she was started on a trial of budesonide. The diarrhea improved significantly within days of initiation of budesonide 9mg by mouth daily, and within two weeks had complete resolution. The budesonide dose was tapered over four weeks with continued formed stools over the following months. CID can be a debilitating side effect of chemotherapy. The mainstays in treatment of CID are loperamide and octreotide; however, these are not without complications, as seen with the patient's atypical transition from diarrhea to severe ileus. Whereas loperamide and octreotide focus on disordered bowel motility, budesonide exerts an anti-inflammatory effect on the bowel itself. The success of budesonide therapy in this patient likely represents this anti-inflammatory effect precipitating remission of bowel wall edema from the toxic effect of capecitabine. Considering the success of the budesonide and ultimate remission of her treatment-resistant CID, this case suggests an increased role for budesonide in the treatment guidelines for CID.