Diffuse Ground-glass Opacities Research Articles

M409 ELECTRONIC CIGARETTE OR VAPING PRODUCT USE-ASSOCIATED LUNG INJURY AMIDST THE COVID-19 PANDEMIC

Electronic cigarette or vaping product use-associated lung injury (EVALI) is currently a diagnosis of exclusion. Given the pro-inflammatory and partly immune-mediated pathogenesis, EVALI and SARS-CoV-2 infection share several clinical features, potentially posing a diagnostic challenge. A 24-year-old man without significant medical history presented with fever, worsening cough, dyspnea, vomiting and diarrhea during a local peak of COVID-19 cases. He required 10 liters of supplemental oxygen due to hypoxemic respiratory failure. Laboratory workup revealed: leukocytosis (ANC 15,200 cells/microliter), elevated ESR/CRP, ferritin-1030 ng/mL, d-dimer-791 ng/mL, procalcitonin-0.8 ng/mL, mild transaminitis, elevated IL-6 (173 pg/mL). Six nasopharyngeal PCR assays did not detect SARS-CoV-2 (2 prior to admission). Chest computed tomography delineated diffuse patchy ground glass opacities with shotty mediastinal and hilar lymphadenopathy. The working diagnosis was COVID-19 disease, however the patient subsequently admitted to frequent vaping of cannabis and THC-oils. He clinically improved after receiving antibiotics and steroids for treatment of EVALI. Similar to COVID-19, EVALI has a broad spectrum of pulmonary findings and may be accompanied by gastrointestinal or constitutional manifestations, elevated inflammatory markers and non-specific imaging. Leukocytosis with neutrophilic predominance is found in EVALI. The proposed immunopathology of lung damage in EVALI is via a cytokine cascade of IL-1, IL-6, and IL-13. COVID-19 may portend a detrimental cytokine storm syndrome. Elevated peripheral IL-6 levels can be detected in both diseases; this patient had a markedly elevated level suggesting a cytokine storm-like picture. The overall features of this case suggested EVALI, illustrating the importance of its consideration in the differential diagnosis of SARS-CoV-2 infection.

Characterizing e-cigarette vaping-associated lung injury in the pediatric intensive care unit.

Adolescent e-cigarette use has risen to epidemic levels in the US, revealing a new phenomenon of e-cigarette vaping-associated lung injury (EVALI). It is important to better characterize EVALI in critically ill adolescents as this is a vulnerable and rapidly growing demographic. This was a retrospective case series of patients ≤21 years old with confirmed or probable EVALI (as defined by the Centers for Disease Control) that resulted in admission to the pediatric intensive care unit (PICU) of a large tertiary academic children's hospital between August 2019 and January 2020. There were six eligible patients, with a median age of 17 years. All patients reported tetrahydrocannabinol as well as nicotine e-cigarette use. Half of the patients had a preexisting diagnosis of asthma and four patients had mental health comorbidities. All patients presented with respiratory alkalosis and chest radiography showing diffuse bilateral infiltrates; two patients had pneumomediastinum, subcutaneous air and/or pneumothorax. The lowest documented ratio of oxygen saturation to inspired oxygen (SpO2:FiO2 or S/F ratio) ranged from 146 to 296. Two patients required an arterial line, with the lowest ratio of arterial oxygen to inspired oxygen (PaO2:FiO2 or P/F ratio) of 197 and 165. Two patients tested positive for rhinovirus and respiratory cultures were negative for all patients. Four patients underwent chest computed tomography imaging, which showed diffuse ground-glass opacities. Every patient required noninvasive positive pressure ventilation, with one progressing to invasive ventilation. All patients received broad-spectrum intravenous antibiotics and steroids, though there was considerable variability in dose, frequency, and duration of steroids. The hospital length of stay ranged from 5 to 16 days (median 8.3 days) with PICU length of stay ranging from 4 to 10 days (median 5.5 days). Four patients had pulmonary function testing before discharge, two of which showed decreased diffusing capacity of the lung for carbon monoxide. There were no patient deaths. This single-center case series describes the presentation, course, and treatment of EVALI in a pediatric intensive care unit setting. Our results show nuanced differences in the presentation and management of the critically ill adolescent, and raise many questions about the long term implications on lung health, morbidity, and mortality. Importantly, these cases illustrate the critical care consequences of a public health phenomenon and should spur further research and policy to address the negative health effects of vaping.

STEROID DEPENDENT CHRONIC EOSINOPHILIC PNEUMONIA: A WIN FOR IL-5 ANTAGNONISM IN AN ACTIVE DUTY SERVICE MEMBER

SESSION TITLE: Fellows Diffuse Lung Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Chronic eosinophilic pneumonia (CEP) is characterized by a clinical syndrome which includes pulmonary symptoms, eosinophilia greater than 25% in bronchoalveolar lavage, and characteristic radiographic abnormalities. Corticosteroids are the mainstay of therapy. There is no standard alternative for steroid-refractory/dependent CEP, however, reports suggest anti-IL5 therapies may be an option. We present the case of a non-asthmatic, active duty service member with steroid dependent CEP who had a dramatic clinical response to mepolizumab. CASE PRESENTATION: A 47-year-old African American female presented to us for persistent productive cough and dyspnea despite multiple rounds of steroids and antibiotics for “recurrent upper respiratory infections”. Our evaluation was notable for thoracic lymphadenopathy and diffuse ground glass opacities on CT, a positive environmental allergy screen, IgE of > 4,000 IU/mL and an absolute serum eosinophil count of over 3,400. Pulmonary function testing, to include bronchoprovocation testing was normal. A diagnosis of allergic bronchopulmonary aspergillosis (ABPA) was excluded due to negative precipitins panel and lack of classic radiographic findings. Bronchoscopic evaluation revealed tissue eosinophilia with eosinophilic granuloma formation and no evidence of vasculitis. BAL from two separate lobes revealed a cell differential > 25% eosinophils with all infectious testing negative. An ANCA panel was positive for PR3, however, subsequent work up to include numerous biopsies of various sites, was not consistent with Eosinophilic Granulomatosis with Polyangitis (EGPA), especially in this non-asthmatic. We started steroid therapy for CEP which resulted in clinical improvement, however, our patient could not be weaned below 20mg daily without resulting in symptom relapse. For her steroid-dependent CEP we trialed mepolizumab, resolving her symptoms and radiographic findings, allowing cessation of all steroids DISCUSSION: IL-5 antagnosts, like mepolizumab, bind and neutralize IL-5 thereby inhibiting eosinophil production, activation and chemotaxis (1). They are used in eosinophilic asthma to relieve airway inflammation. In CEP, eosinophils also drive chronic inflammation. Steroids are classically considered the cornerstone of therapy for these patients and can generally be weaned, however, in this case the patient had steroid dependent disease necessitating consideration for alternative therapies. In the literature, anti-IL-5 therapy is non-asthmatics is discussed, however, to the best of our knowledge, there is only one published case documenting successful use of mepolizumab in CEP (2). CONCLUSIONS: Mepolizumab appears to be a promising therapy for patients with CEP and may be considered in patients who do not respond to, or are dependent on, steroids. More research must be done into such non-steroidal agents to reduce exposure to steroids and their side effects. Reference #1: 1. Garrett JK, Jameson SC, Thomson B, et al. Anti-interleukin-5 (mepolizumab) therapy for hypereosinophilic syndromes. J Allergy Clin Immunol. 2004;113(1):115-9. Reference #2: 2 To M, Kono Y, Yamawaki S, et al. A case of chronic eosinophilic pneumonia successfully treated with mepolizumab. J Allergy Clin Immunol Pract. 2018;6(5):1746-1748.e1. DISCLOSURES: No relevant relationships by Cyrus Askin, source=Web Response No relevant relationships by Tyson Sjulin, source=Web Response

S2262 A Rare Manifestation of Cryptogenic Organizing Pneumonia in a Patient With Ulcerative Colitis Being Treated With an Anti-TNF Biosimilar

INTRODUCTION: Ulcerative colitis (UC) is an inflammatory bowel disorder (IBD) resulting in continuous mucosal inflammation from the rectum with variable extension to the proximal colon. Symptoms can include abdominal pain, hematochezia, or tenesmus. Anti-tumor necrosis factor (anti-TNF) therapy has been recognized as a treatment modality for moderate to severe UC. Extraintestinal manifestations of IBD have been well documented, with pulmonary manifestations being an uncommon presentation. One such manifestation is cryptogenic organizing pneumonia (COP). The most common finding is diffuse ground glass opacities and bilateral infiltrates on CT. In addition, COP has been described as a noninfectious complication associated with anti-TNF therapy. Here we present a case of COP in a patient being treated with an anti-TNF biosimilar for moderate to severe UC. CASE DESCRIPTION/METHODS: A 38 year-old female with left-sided UC presented to the hospital complaining of 2 weeks of progressively worsening shortness of breath. She had been on Inflectra and mesalamine for 2 years without complications. A chest CT revealed bilateral infiltrates concerning for organizing pneumonia. Bronchoscopy with bronchoalveolar lavage (BAL) was negative for fungal, pneumocystis jirovecii, bacterial, or viral etiologies. The patient was eventually discharged, however, she still required supplemental oxygen. She was started on prednisone and Bactrim for pneumocystis pneumonia prophylaxis. She was referred to gastroenterology for a concern of a possible association between Inflectra and COP. Mesalamine and Inflectra were stopped and the patient developed fecal urgency and rectal bleeding. The patient was started on vedolizumab and prednisone with an eventual prednisone taper, in addition to levalbuterol for her ongoing dyspnea. After two months of vedolizumab therapy, the patient noted significant improvement in her gastrointestinal symptoms as well as her pulmonary symptoms. DISCUSSION: There have been case reports detailing COP in patients undergoing therapy with Infliximab, however, this is the first known case of COP with a biosimilar. The improvement in pulmonary symptoms with discontinuing Inflectra, which was controlling her UC, and starting vedolizumab to continue control of the UC with subsequent improvement in her COP suggests the biosimilar, Inflectra, as opposed to an extra intestinal manifestation of UC, was the cause of COP.

A MATTER OF FLUX: A CASE REPORT ON ARC WELDER'S LUNG

SESSION TITLE: Medical Student/Resident Occupational and Environmental Lung Disease SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Occupational diseases are a major cause of individual health deterioration We present a case of occupational exposure to metal fumes resulting in Arc Welder’s Lungs (AWL). CASE PRESENTATION: A 63-year old male presented with shortness of breath and productive cough for 8 days. He was a welder for 27 years. He never smoked and was not taking any medications. He was afebrile, hypoxic at 78% O2 saturation, respiratory rate was 31, pulse of 97 and blood pressure of 172/90 mmHg. He had diffuse rhonchi most prominent in the bibasilar lung fields. Labs revealed a leukocytosis of 14.2 K/uL, normal liver and chemistry panels and a procalcitonin of 0.1 ng/mL. Chest X Ray showed perihilar and basilar multifocal consolidation.(Image A) A chest CT angiography was negative for pulmonary embolism but showed extensive bilateral focal consolidation and diffuse ground glass opacities with an enlarged main pulmonary artery.(Image B) He was started on antibiotics, steroids and required 6L of nasal cannula. Transthoracic echocardiography showed severe left ventricular hypertrophy, an ejection fraction of 70% and an estimated pulmonary artery pressure of 91 mmHg. His symptoms progressively worsened and oxygen requirements escalated. Viral panels, autoimmune serologies, amyloid workup and cultures were all negative. A right heart catheterization showed right atrial pressure of 6 mmHg, right ventricular pressure of 75/5 mmHg, pulmonary capillary wedge pressure of 10 mmHg, a cardiac index of 3.9 L/min/m2 and pulmonary vascular resistance of 5.3 WU suggesting a potential arteriopathy component in the setting of acute pulmonary inflammation. A bronchoscopy with lavage showed numerous hemosiderin laden macrophage with positive iron staining and positive oil red O stain. A transbronchial biopsy was not pursued due to potential bleeding risk in setting of pulmonary hypertension. Serum ferritin level was 2163 ng/mL. Based on occupational history and bronchoscopy findings, the patient was diagnosed with AWL. Given the acute inflammatory parenchymal process, pulse dose steroids were initiated with subsequent clinical improvement. DISCUSSION: AWL can present in different forms of lung disease.[1] Cases are usually “benign” without residual effects, however there are reports of symptomatic presentations with underlying fibrosis.[2] We describe the first welder’s lung case with an acute inhalational pneumonitis responsive to pulse dose steroids. Three months interval CT scan showed significant improvement of ground glass component with residual areas of underlying reticular and fibrotic changes in the bases, possibly suggestive of desquamative interstitial pneumonia.(Image C) CONCLUSIONS: Our case highlights the implications of occupational diseases which can be preventable and the possible variability in presentations. Physicians should be aware of AWL and include it in their differential diagnosis Reference #1: Riccelli MG, Goldoni M, Poli D, Mozzoni P, Cavallo D, Corradi M. Welding Fumes, a Risk Factor for Lung Diseases. Int J Environ Res Public Health. 2020;17(7):2552. Published 2020 Apr 8. doi:10.3390/ijerph17072552 Reference #2: M. P. Cosgrove, Pulmonary fibrosis and exposure to steel welding fume, Occupational Medicine, Volume 65, Issue 9, December 2015, Pages 706–712, https://doi.org/10.1093/occmed/kqv093 DISCLOSURES: No relevant relationships by Youssef Abouleish, source=Web Response No relevant relationships by Mit Patel, source=Web Response No relevant relationships by Anthony Quaranta, source=Web Response

Clinical study of 34 patients with cytomegalovirus pneumonia after allogeneic hematopoietic stem cell transplantation

目的分析异基因造血干细胞移植（allo-HSCT）后巨细胞病毒（CMV）肺炎的临床特点及预后。方法对2016年3月1日至2019年6月30日在上海市第一人民医院血液科接受allo-HSCT后并发CMV肺炎的患者进行回顾性分析。结果①全部411例allo-HSCT患者中，34例（8.3％）移植后发生CMV肺炎，其中男18例，女16例，中位年龄32（8～62）岁；急性髓系白血病14例，急性淋巴细胞白血病10例，骨髓增生异常综合征5例，非霍奇金淋巴瘤3例，再生障碍性贫血2例。②CMV肺炎中位发病时间为移植后53（36～506）d，主要症状为咳嗽（26例，76.5％）、发热（23例，67.6％）及气促（14例，41.2％），仅17.6％（6/34）的患者有咯痰，2例（5.9％）患者早期无明显症状而在常规胸部CT检查时发现。28例（82.4％）患者的影像学表现为小叶中心结节、弥漫毛玻璃影等典型间质性肺炎改变，6例（17.6％）表现为斑片、结节以及实变样不典型影像学改变。③26例（76.5％）患者血浆CMV-DNA阳性，拷贝数低于同期BALF检测结果［1.70×107（5.44×105～4.45×109）拷贝/L对1.45×108（1.10×107～1.10×1011）拷贝/L，P＝0.004］。④13例（38.2％）CMV肺炎患者合并其他下呼吸道病原体感染（真菌10株，细菌6株，腺病毒1株）。⑤所有患者中位随访时间12.8（0.4～46.5）个月，总生存率为58.82％，年龄≥40岁、接受高流量通气是CMV肺炎患者独立预后不良因素（P＝0.049，P＝0.009）。结论气管镜肺泡灌洗液检测有助于提升allo-HSCT后CMV肺炎病原学诊断的准确性。年龄≥40岁及接受高流量通气是CMV肺炎患者独立预后不良因素。

RECURRENT HYPOXIA: ACUTE PULMONARY EMBOLI IN PATIENTS RECOVERING FROM COVID-19

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: New York has been the epicenter of the COVID-19 pandemic in the United States. As potential treatment options are investigated, discussion revolves around the thrombotic nature of this novel virus. We present two COVID-19 positive patients in an NYC hospital, whose recoveries were complicated by pulmonary emboli despite receiving anticoagulation. CASE PRESENTATION: Patient 1: A 66-year-old female with coronary artery disease presented with dyspnea, cough, and fever. She was hypoxic, with labwork notable for elevated D-dimer of 1.83. She was initiated on hydroxychloroquine, dexamethasone, and prophylactic-dose enoxaparin. Initial CT angiogram (CTA) of the chest was negative for PE. Her symptoms improved, inflammatory markers down-trended, and she was discharged. Three days later, she returned with worsened dyspnea, tachycardia, hypoxia to 70%, and increased D-dimer, now greater than 20. Repeat CTA demonstrated a new saddle pulmonary embolus extending to lobar, segmental, and subsegmental branches bilaterally with evidence of right heart strain. She was treated with therapeutic enoxaparin, with gradual improvement in symptoms. Patient 2: A 48-year-old female with obesity presented with dyspnea, non-productive cough, and fever. She was hypoxic, with initial CTA showing bilateral ground-glass opacities and no evidence of PE. Labs revealed elevated inflammatory markers, including D-dimer of 2.2. She was started on hydroxychloroquine, azithromycin, dexamethasone, tocilizumab, and prophylactic-dose enoxaparin. Inflammatory markers continued to rise, so she was switched to therapeutic-dose enoxaparin and high-flow nasal cannula. Two days later, she developed heavy bleeding due to menses and was switched back to prophylactic enoxaparin. She subsequently developed worsening hypoxia requiring BiPAP. Repeat CTA now demonstrated central emboli in the left pulmonary artery. She was given alteplase and started on therapeutic unfractionated heparin with transition to coumadin. CTA three weeks after admission demonstrated resolution of pulmonary emboli, but the patient’s diffuse ground-glass opacities and hypoxia persisted. DISCUSSION: These patients raise concerns about the thrombotic nature of COVID-19 and suggest that prophylactic doses of anticoagulation may not be enough to prevent thrombotic events. Trending D-dimers in combination with monitoring changes in oxygen requirements may be useful tools when suspecting new PEs and deciding when to start therapeutic anticoagulation. CONCLUSIONS: While more data is needed on the thrombotic nature of COVID-19, therapeutic doses of anticoagulation may be necessary to prevent major thrombotic events in COVID-19 patients at low risk of bleeding. Reference #1: Levi M, Thachil J, Iba T, Levy JH. Coagulation abnormalities and thrombosis in patients with COVID-19. Lancet Haematol. 2020;7(6) DISCLOSURES: No relevant relationships by Tiffany Chen, source=Web Response No relevant relationships by Justin Gasper, source=Web Response No relevant relationships by Adam Rothman, source=Web Response No relevant relationships by Frederick Rozenshteyn, source=Web Response

S1973 Achalasia With Diffuse Esophageal Dilation Causing Tracheal Compression and Severe Asthma

INTRODUCTION: Achalasia is a rare esophageal disorder that is caused by the lack of relaxation of the lower esophageal sphincter, causing loss of peristalsis and a dilated esophagus. Patients present with various upper gastrointestinal complaints. Here, we present the case of a 16-year-old female with history of uncontrolled asthma, including intubation at age 14 for status asthmaticus, who was found to have a massively dilated esophagus causing compression of the trachea. Peroral endoscopic myotomy (POEM) was performed and she experienced complete regression of her asthma symptoms. CASE DESCRIPTION/METHODS: 16-year-old female with history of uncontrolled asthma presents to pulmonology clinic. Pulmonary function testing (PFT) demonstrates severe obstruction (FEV1 33%, FEV1/FVC 45%) with little improvement following a 5-day course of oral steroids. She endorses mild, nonproductive cough. She appears well, speaking full sentences and ambulating without difficulty. She has diminished breath sounds bilaterally. Labs reveal only mild normocytic anemia. She is started on intravenous steroids and inhaler therapy. CT chest without contrast shows diffusely distended esophagus filled with liquid and food debris, exerting mass effect on the trachea and proximal mainstem bronchi, as well as diffuse groundglass opacities and scattered pulmonary nodules. Upon further assessment, the patient endorses occasional dysphagia with solid foods. She has infrequent vomiting episodes but denies odynophagia or weight loss. Eckardt score is 5. EGD reveals dilation in the entire esophagus; EndoFLIP reveals decreased distensibility and absent contractility consistent with type I achalasia. The following day, POEM procedure is performed. Post-procedure Eckardt score is 0. She is discharged home on lansoprazole 30 mg twice daily for 2 months. Over the next 6 months, she experiences complete remission of her asthma symptoms and inhaler therapy is discontinued. She also has complete resolution of dysphagia and gains 50 pounds. DISCUSSION: In our case, the patient had worsening PFT despite adequate treatment for asthma. Chest CT found a dilated esophagus, which may have been present 2 years prior when she was intubated for status asthmaticus. Her respiratory symptoms regressed completely after POEM for achalasia. This case demonstrates the importance of diagnostic review, especially in cases of primary treatment failure. Maintaining a broad differential can help clinicians think critically and correct potential reversible causes.Figure 1.: Chest CT shows diffusely dilated esophagus, likely secondary to achalasia.Figure 2.: Dilated esophagus causing compression of proximal mainstem bronchus.Figure 3.: Liquid and food debris in dilated esophagus near the LES.

REPEAT PRESENTATION OF A FEBRILE RESPIRATORY ILLNESS SECONDARY TO HYPERSENSITIVITY PNEUMONITIS

SESSION TITLE: Medical Student/Resident Occupational and Environmental Lung Disease SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Dyspnea is one of the most common reasons for presentation to the hospital. Antigen mediated lung diseases are an important cause of dyspnea however due to the wide variation in clinical presentation, the large number of possible antigens, and a lack of diagnostic tests identification can be difficult.1 Thus, a high index of suspicion must be maintained to prevent missed or delayed diagnosis. CASE PRESENTATION: A 44-year-old nonsmoker with an insignificant past medical history originally presented to an outpatient urgent care with an acute onset of fever, dyspnea, productive cough, and myalgias. He was empirically treated for bacterial pneumonia with an oral antibiotic. After initial improvement, his symptoms progressed and he ultimately presented to the emergency room with fever and worsening dyspnea. He was admitted with acute hypoxic respiratory failure and sepsis secondary to presumed post-influenza pneumonia (standard chest radiograph showed left lower lobe infiltrate). He was fluid resuscitated and received broad spectrum antibiotics. With antibiotics his fever dissipated although he continued to remain hypoxic and was discharged on hospital day seven on three liters of oxygen via nasal cannula. At hospital follow up one week later he continued to endorse dry cough and severe dyspnea (being only able to ambulate household distances with oxygen prior to having to rest). Exam was significant for crackles in the bilateral lung bases along with hypoxia (oxygen saturation dropped to 83% with removal of his nasal cannula during rest). Further history revealed the patient owned seven parakeets which were kept in the same room that the patient slept. He also endorsed unintentional 12-pound weight loss over the past 3 months. CT imaging was pursued which showed diffuse ill-defined centrilobular micronodularity and ground glass opacities throughout both lungs. Based upon this new information serum hypersensitivity pneumonitis screen was performed and ultimately returned negative for the presence of six antigens (only bird antigen on the screen was pigeon serum). Based upon the patient meeting five out of six clinical criteria for a validated clinical predication rule a diagnosis of hypersensitivity pneumonitis was established (92% Likelihood).2 He was advised to avoid further exposure to his birds and outpatient pulmonology consultation was arranged. After a short course of prednisone and avoiding further exposure the patient's symptoms resolved. DISCUSSION: Hypersensitivity pneumonitis is an important disease to keep on the differential for a patient presenting with dyspnea. CONCLUSIONS: Early diagnosis is of the upmost importance as with avoiding further exposure early lung disease can be potentially completely reversed. This case also illustrates the importance of taking a complete history and how routine use of validated clinical predication rules can help you make a diagnosis. Reference #1: 1. Riario Sforza, G.G., Marinou, A. Hypersensitivity pneumonitis: a complex lung disease. Clin Mol Allergy. 2017; 15, 6. Reference #2: 2. Lacasse Y, Selman M, Costabel U, Dalphin JC, Ando M, Morell F, Erkinjuntti-Pekkanen R, Muller N, Colby TV, Schuyler M, Cormier Y. Clinical diagnosis of hypersensitivity pneumonitis. Am J Respir Crit Care Med. 2003;168(8):952. DISCLOSURES: No relevant relationships by Catherine Cheney, source=Web Response No relevant relationships by Chris Morris, source=Web Response

A CASE OF E-CIGARETTE VAPING-ASSOCIATED INTERSTITIAL LUNG DISEASE WITH CRYPTOGENIC ORGANIZING PNEUMONIA

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: E-cigarette/Vaping-associated lung injury (EVALI) is a relatively new term that was described in 2019, since then more than 2000 new cases have been reported in USA.(1) Usual cases present with cough/dyspnea associated with hypoxemia and bilateral air-opacities in the Chest X-Ray. (2) Further research is still needed since the histopathologic pattern is not specific and variable. CASE PRESENTATION: We present a case of a 52-year old female with a history of vaping who presented with dyspnea and cough. Patient was tachypneic and hypoxic at 58% on room air. Chest x-ray (CXR) showed bilateral airspace opacities with perihilar and basilar distribution; Chest CT showed diffuse bilateral ground glass opacities (Figure 1). Patient was intubated due to worsening tachypnea and hemodynamic instability on BiPAP; she was started empirically on broad-spectrum antibiotics, and methylprednisolone. She was successfully extubated after 4 days but required re-intubation for persistent respiratory distress. Bronchoalveolar lavage was attempted but due to insufficient sample Video-assisted thoracoscopic surgery with biopsy was performed. Lung biopsy showed cryptogenic organizing pneumonia, (Figure 1) which in this clinical setting suggested a diagnosis of EVALI (Figure 2). Patient was successfully extubated 10 days after the second intubation. She was discharged home with a 6-week course of methylprednisolone. Patient presented to the Emergency department 3-weeks later with acid reflux, and routine CXR was done showing complete resolution of bilateral opacities and no respiratory distress. DISCUSSION: EVALI is a diagnosis of exclusion that usually presents with cough and dyspnea in a patient with a positive screen for vaping-specific history. Chest Imaging can show nonspecific bilateral ground glass opacities or bilateral infiltrates. As per literature review, only 17 patients amongst the thousands with clinical EVALI have an open lung biopsy confirming the presence of acute lung injury with various histopathologic patterns such as acute eosinophilic pneumonia, cryptogenic organizing pneumonia or lipoid pneumonia. (1) Physicians must be able to recognize EVALI as a probable diagnosis, even in community hospitals, since this condition can response to steroids and could be prevented with patient education. CONCLUSIONS: EVALI is becoming a common pathology. This means that physicians in every setting of patient care must be aware of the possibility of EVALI in patients presenting with cough/dyspnea, typical chest imaging and vaping history. Providers should also be familiar with prevention, structured diagnostic approach and treatment of EVALI. (1) Reference #1: Henry TS, et al. Imaging of vaping-associated lung disease; N Engl J Med 2019;381:1486-1487 Reference #2: Hartnett KP, et al. Syndromic Surveillance for E-Cigarette, or Vaping, Product Use–Associated Lung Injury; N Engl J Med. 2019 Dec 20 DISCLOSURES: No relevant relationships by Jorge Cedano, source=Web Response No relevant relationships by Syed Kazmi, source=Web Response No relevant relationships by Anuraag Sah, source=Web Response

COCCIDIOIDES KILLS: A CASE REPORT

SESSION TITLE: Fellows Lung Pathology Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coccidioidomycosis immitis is a dimorphic fungus that infects the host via inhalation of spores found in the soil of endemic areas such as the southwestern United States. In immunocompetent patients it usually presents as a flu like illness. In patients that are immunocompromised it can lead to disseminated disease affecting numerous organs. CASE PRESENTATION: A 32-year-old male with a history of asthma presented to the ED with fevers, back pain, shaking chills, shortness of breath, and a nonproductive cough for two weeks. A CT chest was performed that revealed diffuse bilateral ground glass opacities (Figure 1). His respiratory status worsened despite treatment for pneumonia and he was subsequently intubated. MRI of the thoracic spine was performed given his back pain, which showed T8-T12 paravertebral abscess (Figure 2). It was also noted while gathering history that he played football in Arizona and lived in that area for some time. Aspiration of the paraspinal abscess was performed. Patient was placed on empiric amphotericin B as he developed worsening acute respiratory distress syndrome (ARDS). Despite being on lung protective strategies, he was difficult to oxygenate and placed on ECMO. Infectious workup for other organisms was also performed including bacterial and viral co-infection in the blood, cerebrospinal fluid (CSF), and bronchial fluids. His spinal cultures and CSF grew Coccidioides immitis along with spherules noted in his bronchial washings. He was also found to have cutaneous disseminated lesions on his upper extremity (Figure 3). Despite best efforts, patient continued to decompensate. Palliative care was consulted and withdrawal of support was performed after patient was noted to have multiple cardiac arrests. DISCUSSION: Symptomatic patients with coccidioidomycosis typically present with community acquired pneumonia. Uncommonly, in about 1% of infections, hematogenous, extra pulmonary dissemination can occur to the spine, meninges, joints, and skin. Coccidioidomycosis is commonly diagnosed in disease-endemic areas but frequently overlooked in disease-nonendemic areas because of a low index of suspicion among physicians. Individuals at risk of dissemination have suppressed cellular immunity, including those with advanced HIV infection, transplantation recipients, and those receiving chronic immunosuppressive medications such as glucocorticoids. Interestingly, this patient had no such risk factors, but the key in his case was obtaining travel/living history as it increased suspicion of coccidioidomycosis infection earlier. Unfortunately, in his case, this did not change his outcome. CONCLUSIONS: Although coccidioidomycosis is rare in non-endemic areas, physicians must keep it in mind when evaluating patients who have traveled or lived in endemic areas even without immunosuppression. Reference #1: Ramanathan D, Sahasrabudhe N, Kim E. Disseminated Coccidioidomycosis to the Spine-Case Series and Review of Literature. Brain Sci. 2019 Jul 7;9(7). doi: 10.3390/brainsci9070160. PubMed PMID: 31284663; PubMed Central PMCID: PMC6680672. DISCLOSURES: No relevant relationships by Alireza Nathani, source=Web Response No relevant relationships by Sean OConnor, source=Web Response No relevant relationships by Chhaya Patel, source=Web Response No relevant relationships by Jorge Velazco, source=Web Response

SMOKE EVERYWHERE, FROM LUNGS TO SPINE!

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: E-Cigarette/Vaping associated Lung Injury (EVALI) has presented with no pattern of disease progression.Availability of e-cigarettes since 2007 in the US have seen a rise in demand in younger age group, reported use by 20.8% high schoolers in 2018. (1) CASE PRESENTATION: 19-year-old male presented with nausea, vomiting, diarrhea, dyspnea, chest pain.Physical examination-saturation 77% on room air, decreased bilateral breath sounds, crackles and sinus tachycardia. Initial chest x-ray(CXR) showed bilateral pneumothorax, pneumomediastinum, extensive subcutaneous emphysema to neck, upper back. CT chest was consistent with CXR and diffuse bilateral ground glass opacities on lower lobes. No evidence of recent travel, infections, drug use, smoking history was reported. Boerhaave syndrome from vomiting was ruled out with CT oral contrast without esophageal leak. He eventually admitted to vaping tetrahydrocannabinoid (THC) products three times daily for last 3-4 weeks. Started on high dose methylprednisone 125 mg every 6hours. He worsened to severe acute respiratory distress syndrome requiring bilateral 32Fr chest tubes, with PaO2/FiO2 69 while on ventilatory support with PEEP of 10cm of water, FiO2 100%.CT head and spine showed air in the subcutaneous tissues of skull base, neck, orbits and epidural space of spinal canal confirming to our knowledge the first ever case of Pneumorrhachis secondary to EVALI. DISCUSSION: EVALI is worldwide phenomenon with more concentration in Illinois and Wisconsin.EVALI is diagnosis of exclusion in absence of infectious/autoimmune causes and direct correlation with vaping THC with/without nicotine.Different combinations used are nicotine, THC, dank vapes, dabbing, cannabinoid oil.[1,2]Unregulated THC products contain Vitamin E acetate which is the culprit agent. An accurate pathophysiology is still to be determined but possibility of lipoid pneumonia,subacute bronchial toxicity,respiratory bronchiolitis–interstitial lung disease, bronchiolitis obliterans organizing pneumonia, diffuse alveolar hemorrhage, acute eosinophilic and acute hypersensitivity pneumonia have been discussed.[3]Although controversial due to nonspecific,evidence of macrophages with lipid deposition in bronchoalveolar lavage(BAL) is seen.Urine has higher sensitivity compared to BAL for THC analysis.CT ranges from infiltrates, consolidations, air bronchograms, ground glass opacities more in lower lobes. Pneumorrhachis, an extremely rare phenomenon of air in the spinal canal, is likely result of high-pressured alveolar rupture.This however, is likely the first ever reported case of pneumorrhachis secondary to EVALI. Like EVALI,no guidelines exist for pneumorrhachis due to rare incidence but conservative course has been reported previously. CONCLUSIONS: These findings in a healthy young male show, vulnerability and unpredictable disease course of EVALI, with no recommended guidelines for management yet. Reference #1: Dinardo P, Rome ES. Vaping: The new wave of nicotine addiction. Cleve Clin J Med. 2019;86(12):789-798. doi:10.3949/ccjm.86a.19118 Reference #2: Kalininskiy A, Bach CT, Nacca NE, et al. E-cigarette, or vaping, product use associated lung injury (EVALI): case series and diagnostic approach. Lancet Respir Med. 2019;7(12):1017-1026. doi:10.1016/S2213-2600(19)30415-1 Reference #3: Ghinai I, Pray IW, Navon L, et al. E-cigarette Product Use, or Vaping, Among Persons with Associated Lung Injury - Illinois and Wisconsin, April-September 2019. MMWR Morb Mortal Wkly Rep. 2019;68(39):865-869. Published 2019 Oct 4. doi:10.15585/mmwr.mm6839e2 DISCLOSURES: No relevant relationships by Habiba Hussain, source=Web Response No relevant relationships by Matthew Sehring, source=Web Response No relevant relationships by Deepak Taneja, source=Web Response

MICROSCOPIC POLYANGIITIS PRESENTING AS DIFFUSE PULMONARY HEMORRHAGE AND ACUTE TYPE-1 RESPIRATORY FAILURE

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: Microscopic polyangiitis is one of the causes of pulmonary-renal syndrome, a grave diagnosis with high mortality rate. Pulmonary symptoms include chest pain, dyspnea, and hemoptysis, with imaging showing diffuse pulmonary infiltrates. High degree of suspicion is required for timely diagnosis and management as delay in treatment increases mortality rate. CASE PRESENTATION: 59-year-old white Caucasian male with multiple comorbidities was admitted with acute type one respiratory failure requiring intubation due to diffuse pulmonary hemorrhage. During intubation, copious bloody secretions within the airway were noted, making intubation technically difficult. Patient was not taking any anticoagulant prior to admission and prophylactic anticoagulation was not initiated due to profound anemia on admission and concerns of airway hemorrhage.His clinical course was complicated by hemorrhagic shock, ischemic hepatitis, and worsening acute kidney injury that required dialysis, patient was treated with pulse steroid therapy, erythropoeitin was given in an attempt to improve anemia. Physical examination at presentation showed diffuse bilateral coarse breath sounds on auscultation. Pertinent blood work was hemoglobin of 6.8 gm/dl, Creatinine of 2.1 mg/dl, ALT of 1369 U/L, AST of 1812 U/L, positive MPO antibody with ANCA titer of 1:40, and low C3 complement level, pulmonary-renal syndrome was suspected with hemorrhagic airway and worsening kidney injury. CT scan of chest without contrast showed diffuse bilateral ground-glass opacities. Patient's family refused blood products due to religious beliefs and had continued worsening. Unfortunately, the patient did not respond to treatment and passed away. DISCUSSION: Microscopic polyangiitis (MPA) is an ANCA positive small vessel vasculitis and one of the causes of pulmonary-renal syndrome. MPA is associated with a 90% positive ANCA antibody and causes necrotizing vasculitis of small vessels without granuloma formation. Despite appropriate management, ANCA vasculitis remains a grave diagnosis with a mortality rate of 10% at one year.Intubating a patient with suspected alveolar hemorrhage can be technically difficult, placing a large diameter ETT considered safe, elective intuabtion of non-bleeding lung if bleeding lung can be indetified using bronchoscopy. Double lumen ETT is less preferable and comes with serious consequences of poor positioning and limiting bronchoscopy due to smaller-diameter lumen.Patients who declines blood transfusion can be challenging. Minimizing blood loss, reducing blood draws as well as optimizing RBC cell production along with reducing oxygen demand, improving oxygen delivery and using erythyroipesis stimulating agents have been used to improve anemia in such patients. CONCLUSIONS: Clinicians should be aware of the possibility of pulmonary-renal syndrome in a patient presenting with hemoptysis, hypoxia, and renal impairment. Reference #1: https://www.ncbi.nlm.nih.gov/pubmed/25984050 Reference #2: https://www.ncbi.nlm.nih.gov/pubmed/32185342 Reference #3: https://www.ncbi.nlm.nih.gov/books/NBK554372/ DISCLOSURES: No relevant relationships by Adel El Abbassi, source=Web Response No relevant relationships by Mahmoud El Iskandarani, source=Web Response No relevant relationships by Ibrahim Haddad, source=Web Response No relevant relationships by Sajin Karakattu, source=Web Response No relevant relationships by Lana Makahleh, source=Web Response No relevant relationships by Rasheed Musa, source=Web Response

A 21-YEAR-OLD MALE WITH A DEADLY COUGH

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coccidioidomycosis, commonly known as Valley Fever, is caused by Coccidioides immitis/posadasii species endemic to the Southwestern United States. Infection most commonly is asymptomatic, but rarely (1-4.7%) disseminated disease can occur, with mortality as high as 70%. The use of extracorporeal membrane oxygenation (ECMO) has rarely been reported, and never with a duration exceeding 90 days. CASE PRESENTATION: A 21-year-old African American male without significant past medical history, presented with one week history of dyspnea, back pain, and 10 lb weight loss. Chest X-ray showed diffuse bilateral interstitial infiltrates, and the patient was treated for community acquired pneumonia. However, the patient clinically deteriorated. Whole body CT revealed lytic bone lesions (multiple vertebrae, sacral, left scapula, and ribs) with diffuse pulmonary ground-glass and nodular opacities. A rib biopsy diagnosed disseminated coccidioidomycosis. Antifungal therapy was initiated, but the patient continued to worsen and developed acute respiratory distress syndrome (ARDS). He was failing conventional ventilator strategies and was eventually stabilized on ECMO. The patient underwent multiple surgeries to achieve source control. The patient was able to overcome the infectious process, with eventual lung recovery. He was decannulated after 90 days of ECMO and was discharged on life-long triazole therapy. He is currently finishing is college degree. DISCUSSION: Disseminated endemic fungal diseases, although rare, can be devastating. Despite antifungal therapy, our patient failed to improve. This was likely due to the severity of dissemination, particularly his osseous lesions. Surgical debridement is recommended for osseous lesions as antifungal therapy alone is likely to fail. Due to the severity of respiratory involvement, our patient also had to be supported on ECMO, which required continuous systemic anticoagulation to avoid circuit thrombosis. However, he had multiple spinal lesions that required debridement. Need for neurosurgery has previously been considered a relative contraindication to ECMO, however with careful management of anticoagulation these procedures can be done safely with minimal complications. Our patient underwent multiple neurosurgical procedures while on ECMO without significant hemorrhagic complications. CONCLUSIONS: There is a paucity evidence in the literature regarding the use of ECMO as salvage therapy for disseminated endemic fungal infections. Furthermore, surgical intervention has been considered a relative contraindication to ECMO, particularly neurosurgical intervention. Our case shows that not only can ECMO be used as a salvage therapy for ARDS due to disseminated coccidioidomycosis, but surgical interventions with high hemorrhagic risks can be performed with deliberate and strategic anticoagulation planning. Reference #1: Galgiani, J. N. Coccidioidomycosis. West J Med. 1993; 159:153-171. Reference #2: Studemeister, A., Studemeister, L. Brun, F. The role of extracorporeal membrane oxygenation in severe pulmonary coccidioidomycosis. Heart Lung. 2018; 47(3), 261–263. Reference #3: Combes, A., Hajage, D., Capellier, G., et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. 2018; 378:1965–1975. DISCLOSURES: No relevant relationships by Andrew Berglund, source=Web Response No relevant relationships by Thomas Lee, source=Web Response no disclosure on file for Phillip Mason; No relevant relationships by Michael Moulton, source=Web Response No relevant relationships by Whittney Warren, source=Web Response No relevant relationships by Joseph Yabes, source=Web Response

DOING THE RIGHT THING CAN HARM: DIFFUSE ALVEOLAR HEMORRHAGE SECONDARY TO HYDRALAZINE USE

SESSION TITLE: Fellows Pulmonary Manifestations of Systemic Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Hydralazine-induced vasculitis results from anti-MPO antibody formation and fibrinoid necrosis, leading to disruption of alveolar basement membrane with resultant hemorrhage.1 Rarely does this vasculitis cause diffuse alveolar hemorrhage (DAH).1 Presented is a case where long-term compliance with hydralazine led to the fatal outcome of DAH. CASE PRESENTATION: A 59 year old male with history of HFpEF, HTN, DM, CKD 4 presented with hemoptysis. He was recently admitted for dyspnea and abdominal pain and was discharged the day prior. He had taken hydralazine 100mg BID for 10 years and hydralazine-induced vasculitis was diagnosed at that time with renal biopsy showing pauci-immune glomerulonephritis. On physical exam, a copious amount of blood was present in the mouth. The patient was intubated and admitted to ICU. Bronchoscopy revealed DAH diagnosed by progressively bloodier bronchial alveolar lavages. Treatment consisted of high dose steroids, plasmapheresis, and rituximab with little improvement. The patient continued to have hemoptysis and episodes of oxygen desaturation requiring multiple bronchoscopies to retrieve blood clots and mucous plugs. Lab studies revealed an ANA with a 1:640 titer, anti-MPO antibody greater than 800 unit/mg, and a positive dsDNA with a 1:20 titer. CT thorax demonstrated diffuse bilateral ground-glass opacities. Cyclophosphamide was started due to severe disease resistance to the previously described treatments. The patient initially had good improvement with cyclophosphamide, however, his ICU course was later complicated by profound neutropenia leading to septic shock with multi-organ failure due invasive aspergillosis and recurrent duodenal ulcer bleeding. On hospital day 25, the patient passed away due to these complications. DISCUSSION: Hydralazine-induced vasculitis is a rare entity, occurring in 10 cases per million.2 Majority of cases occur in African-American females around age 70.2 It commonly presents with fever, rash, and joint pain. Renal failure may occur, but pulmonary complications are extremely rare.3 Our case is amongst only a few cases reported of alveolar hemorrhage attributed to hydralazine. Some patients studied achieved remission, with severe cases amenable to rituximab.2 Our patient had multiple rituximab treatments, along with plasmapheresis, steroids, and cyclophosphamide, but progressed to multi-organ failure and eventual death. CONCLUSIONS: Even with proper treatment, patients may progress to ARDS, as seen in our patient. Early diagnosis is imperative to prevent fatal complications. By sharing our case, we hope to increase awareness and prompt further research into a rare but serious complication of a commonly used drug, as fatality rates have increased despite management with current guidelines. Reference #1: Aeddula NR, Pathireddy S, Ansari A, et al. Hydralazine-associated antineutrophil cytoplasmic antibody vasculitis with pulmonary–renal syndrome. Case Reports 2018;2018:bcr-2018-227161. Reference #2: Timlin H, Liebowitz JE, Jaggi K, Geetha D. Outcomes of hydralazine induced renal vasculitis. Eur J Rheumatol. 2018;5(1):5–8. https://doi.org/10.5152/eurjrheum.2017.17075 Reference #3: Thakur, K. et al. “Hydralazine Induced Vasculitis Manifesting in Alveolar Hemorrhage” Crit Care Med. 2014; vol. 42, https://doi.org/10.1097/01.ccm.0000458649.47284.46. DISCLOSURES: No relevant relationships by Fatima Anjum, source=Web Response No relevant relationships by Alex Diaz, source=Web Response No relevant relationships by Aamna Hassan, source=Web Response No relevant relationships by Javed Iqbal, source=Web Response No relevant relationships by James Kang, source=Web Response No relevant relationships by Hyfaa Mashaal, source=Web Response No relevant relationships by Rezwan Munshi, source=Web Response No relevant relationships by José Russe-Russe, source=Web Response

PULMONARY CAPILLARY HEMANGIOMATOSIS: A RARE CASE OF STABLE DISEASE WITHOUT TREATMENT

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension caused by extensive proliferation of pulmonary capillaries within parenchymal, vascular, and bronchial tissue. Typically, PCH progresses rapidly with a median time to lung transplantation of two years post diagnosis. To our knowledge, we present the longest case of biopsy proven PCH that has been stable without treatment for seven years. CASE PRESENTATION: A healthy 23-year old non-smoking male presented to the emergency department (ED) with a 2-week history of hemoptysis associated with intermittent left-sided pleuritic chest pain, fatigue, and dyspnea. His physical exam, routine lab work, and chest X-ray were unremarkable. He was discharged home and prescribed clarithromycin for suspected bronchitis. He returned to the ED months later with ongoing symptoms and was referred for urgent outpatient consultation to pulmonology. Bronchoscopy was performed with no blood on bronchoalveolar lavage analysis. Further serum rheumatologic and vasculitis panels were negative. A non-contrast computed tomography (CT) scan of his chest revealed subtle bilateral upper lung predominant centrilobular ground-glass opacities. (Figure 1) With worsening hemoptysis, he returned to the ED six months later. A CT Chest angiogram was performed and showed progressive bilateral airspace opacities. (Figure 2) The patient was referred to Thoracic Surgery for lung biopsy. This demonstrated septal proliferation of capillaries consistent with PCH without evidence of vasculitis, venous occlusion or microorganisms. Immunofluorescence staining was also negative. (Figure 3) The patient remains stable with no signs of progression or pulmonary hypertension on echocardiogram. His enhanced CT and pulmonary function tests remain normal seven years from his initial presentation. DISCUSSION: The typical presentation of PCH includes progressive dyspnea, cough with or without hemoptysis, chest pain, and fatigue. (1) Chest X-ray can be normal or progress to demonstrate bilateral opacities in keeping with diffuse alveolar hemorrhage (DAH). CT chest often shows diffuse centrilobular ground-glass opacities. (1) Bronchoscopy may not reveal erythrocytes if the patient is not actively bleeding. Diagnosis of PCH is essential, as vasodilators used in pulmonary hypertension can cause hemodynamic instability in PCH. (2) Interestingly, an autopsy case series found incidental cases of PCH in patients who were asymptomatic during life. (3) This raises the possibility that subclinical cases of PCH may exist which do not require urgent referral for lung transplantation. CONCLUSIONS: This case represents the longest active case of PCH after confirmation with biopsy without treatment. Re-evaluating the expected prognosis for individuals diagnosed with PCH is important, as median survival may be longer than currently reported in the literature. Reference #1: O'keefe MC, and Post MD. Pulmonary Capillary Hemangiomatosis: A Rare Cause of Pulmonary Hypertension. Archives of Pathology & Laboratory Medicine, 2015;139(2):274–277. Reference #2: Almagro P, Julia J, Sanjuame M, Gonalez G, Casalots J, Heredia JL, et al. Pulmonary Capillary Hemangiomatosis Associated with Primary Pulmonary Hypertension. Medicine. 2002;81(6):417–24. Reference #3: Havlik DM, Massey LW, Williams WL, and Crooks LA. Pulmonary Capillary Hemangiomatosis- like foci: an autopsy study of 8 cases. Anatomic Pathology. 2000;113(5):665-662. DISCLOSURES: No relevant relationships by Meredith Chiasson, source=Web Response No relevant relationships by Jasper Johar, source=Web Response No relevant relationships by Daria Manos, source=Web Response No relevant relationships by Matthew Nunn, source=Web Response

ACTINOMYCOSIS MIMICKING LUNG CANCER: A CASE REPORT

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary actinomycosis is a rare disease that can be challenging to diagnose and is associated with multiple risk factors such as poor oral hygiene, alcoholism, and chronic underlying lung diseases. Actinomycosis can often be misdiagnosed as lung abscess, tuberculosis, or malignancy with radiologic findings that might be misleading. Here we present a case with initial chest CT finding concerning neoplasm but diagnosed as pulmonary actinomycosis on further evaluation. CASE PRESENTATION: 55-year-old male with past medical history of HTN presented with right sided upper back pain and 6 pounds of unintentional weight for 4 weeks. He did not report any symptoms of cough, hemoptysis, shortness of breath, or chest pain. He was a heavy smoker with 45 pack years of smoking and a history of chronic alcoholism with 30 ml of 3-4 vodka shots twice a week for the last 30 years. Patient’s laboratory studies were pertinent for WBC count of 19.6 X 10 3. CT of the chest showed 4.6 x 3.4 cm thick-walled cavitary mass in the right lower lobe concerning for neoplasm with the extension of mass to the right paravertebral region and diffuse right pleural metastases, pathologic lymphadenopathy, and trace right pleural effusion. He underwent BAL with bronchial brushing which showed significant endobronchial inflammation. Microbiological examination of samples obtained from BAL showed Gram-positive filamentous bacteria. Treatment was given with IV clindamycin and he was discharged home on PO Clindamycin for 4 weeks with a repeat chest X-ray in 2 weeks. He was readmitted after 2 weeks with worsening shortness of breath, was found to be hypoxic with SpO2 of 65% on RA and RR of 40/min, he was intubated. Repeat CT chest showed diffuse right pleural thickening and ground-glass opacity of the right upper and middle lung. He was started on broad-spectrum antibiotics with IV vancomycin, IV Zosyn and IV Penicillin but he remained critically ill and a decision was made by the family to withdraw care. The patient was terminally extubated. DISCUSSION: Actinomycosis is a chronic, granulomatous disease mostly caused by A. israelii which is a normal commensal of human oropharynx, GI tract, and female genitalia. Pulmonary actinomycosis accounts for 15% of total disease burden and is usually caused by aspiration of the oropharyngeal or gastrointestinal secretion especially in patients with chronic alcoholism and poor dentition, facial or dental trauma1. CONCLUSIONS: Diagnosis of actinomycosis can be challenging given that presentation and radiologic findings might resemble various other conditions. Pulmonary actinomycosis if diagnosed and treated early has an excellent prognosis, the clinician should have high levels of suspicion in patients with risk factors such as chronic alcoholism, poor dental hygiene, prompting further evaluation with radiology and confirmation of diagnosis with histology and microbiology. Reference #1: 1. Mabeza GF, Macfarlane J. Pulmonary actinomycosis. Eur Respir J. 2003;21(3):545-551. doi:10.1183/09031936.03.00089103 DISCLOSURES: No relevant relationships by Sotirios Doukas, source=Web Response No relevant relationships by Leena Kavali, source=Web Response No relevant relationships by Shashank Nuguru, source=Web Response

S2457 Histoplasma Hepatitis Presenting as Mirizzi Syndrome

INTRODUCTION: Hepatitis secondary to Histoplasmosis is a pathology that is complex and difficult to diagnose. We report a case that presented as Mirizzi syndrome with respiratory dysfunction that proved to be disseminated histoplasmosis with hepatic involvement. CASE DESCRIPTION/METHODS: A 50 y/o female on adalimumab for rheumatoid arthritis presented with right-upper quadrant pain, a 5-day history of jaundice, fever and shortness of breath. Liver chemistries were elevated with alkaline phosphatase of 733 IU/L, total bilirubin of 7 mg/dl, AST 612 IU/L and ALT 202 IU/L. Abdominal ultrasonography revealed gallstones and mildly dilated common bile duct. A chest CT showed diffuse bilateral groundglass opacities. Based on the complex presentation and timing (mid March, 2020) the working diagnoses were gallstone disease with potential SARS-CoV2 infection. Endoscopic Retrograde Cholangiopancreatography exposed Mirizzi syndrome and a long-stent was placed into the bile duct. COVID-19 testing was negative. Liver enzymes showed minimal improvement and respiratory symptoms continued to worsen. Other laboratory tests as well as a detailed toxin intake (including alcohol) were negative. Due to the lack of improvement the patient underwent bronchoscopy and liver biopsy. The former showed buddying yeast in the lungs and the latter liver granulomas with PAS positive yeast consistent with Histoplasma. Liver biopsy cultures were positive for Histoplasma capsulatum. The patient was placed on Itraconazole and discharged home upon improvement. Eight weeks post discharge her liver enzymes have almost completely normalized and symptoms have resolved. DISCUSSION: Disseminated histoplasmosis affecting the liver is a relatively rare and often lethal complication of this infection. The confirmation of extra pulmonary disease is critical as the length of therapy extends from several weeks to one year. Histoplasma hepatitis has been reported in individuals undergoing immunosuppression, such as our patient, and a consistently reported characteristic has been a high AST to ALT ratio which can lead to an initial suspicion of alcoholic hepatitis. This should be kept in mind if the provided history is not compatible with toxin-related (alcohol) liver disease. Our patient also had a clinical presentation compatible with Mirizzi syndrome further obscuring the diagnosis. In this regard, alternative diagnoses should be thought if there are no dramatic improvements of liver chemistries following recanalization of the bile duct.

A CONFUSING CASE OF PNEUMONIA IN A PATIENT WITH HUMAN IMMUNODEFICIENCY VIRUS

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The incidence of acquired immunodeficiency syndrome (AIDS) related opportunistic infections has declined dramatically following the introduction of potent antiretroviral therapy. However, pulmonary infections remain a significant cause of morbidity and mortality (1). The spectrum of pulmonary disease that can affect patients with human immunodeficiency virus (HIV) is wide and includes opportunistic infection with many bacterial, fungal, viral, and parasitic organisms (2). Herein, we present a rare case of pneumonia caused by four different pathogens: Strongyloides Stercoralis, Pneumocystis Jirovecii (PCP), Cytomegalovirus (CMV) and Pseudomonas Aeruginosa. CASE PRESENTATION: A 65-year-old female from Mexico with a past medical history of HIV presents to the emergency department with subacute dyspnea, mild hemoptysis, melena, and fatigue. She was non-compliant with her anti-retroviral therapy. Her CD4 count was <20 cells/uL with a HIV PCR of 1,690,000 copies/mL. CBC demonstrated normocytic anemia (hemoglobin: 6.0 g/dl); hemolysis was excluded. Her Pa02 was 60 mmHg on room air. A computed tomography (CT) scan of the chest with contrast (image) revealed diffuse bilateral ground-glass opacities with diffuse interlobular septal thickening. Severe enteritis and colitis were seen on the CT abdomen/pelvis with contrast. The patient was empirically started on levofloxacin, metronidazole, intravenous (IV) trimethoprim-sulfamethoxazole and prednisone. Sputum cultures were positive for pan sensitive Pseudomonas Aeruginosa. Bronchoalveolar lavage (BAL), upper and lower endoscopy were performed. Blood and BAL CMV PCR were positive. She was subsequently started on IV ganciclovir. BAL PCP PCR was high. Several days later, numerous Strongyloides Stercoralis larvae were seen in the BAL and on the duodenal biopsy. Daily ivermectin was initiated. The patient progressed to septic shock requiring IV norepinephrine and her oxygenation worsened. The patient refused escalation of care and decided to proceed with comfort measures. The patient passed away within a few hours. DISCUSSION: Prior to the era of potent antiretroviral therapy, parasitic pulmonary infections were more commonly seen than they are today (2). Immunocompromised patients are at high risk for systemic strongyloidiasis which presents as either disseminated strongyloidiasis or hyper infection syndrome (3). Aside from HIV, our patient was empirically started on prednisone for PCP treatment which might have contributed to worsening systemic strongyloidiasis and therefore worsening clinical status. For severe disease, patients should be started on daily ivermectin along with empiric antibiotic therapy with activity against gram-negative bacteria. CONCLUSIONS: We describe a rare case of HIV related pneumonia caused by four different pathogens. Reference #1: Boyton RJ. Infectious lung complications in patients with HIV/AIDS. Curr Opin Pulm Med. 2005 May;11(3):203-7. Reference #2: Skalski JH, Limper AH. Fungal, Viral, and Parasitic Pneumonias Associated with Human Immunodeficiency Virus. Semin Respir Crit Care Med. 2016;37(2):257. Reference #3: Celedon JC, Mathur-Wagh U, Fox J, Garcia R, Wiest PM. Systemic strongyloidiasis in patients infected with the human immunodeficiency virus. A report of 3 cases and review of the literature. Medicine (Baltimore). 1994;73(5):256 DISCLOSURES: No relevant relationships by Ahmad Al-Shyoukh, source=Web Response No relevant relationships by Laith Derbas, source=Web Response No relevant relationships by Ashraf Gohar, source=Web Response No relevant relationships by Raed Qarajeh, source=Web Response No relevant relationships by Moustafa Younis, source=Web Response

METASTATIC PULMONARY CALCIFICATION: A RARE CAUSE OF PULMONARY HYPERTENSION

SESSION TITLE: Fellows Pulmonary Vascular Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Metastatic calcification is seen at autopsy in 60-75% of CKD patients on hemodialysis (HD) due to increased calcium phosphate product (normal 40 mg2/dl2; MPC >70 mg2/dl2) (1,2). Metastatic pulmonary calcification associated with pulmonary hypertension (PH) is rare. We present a case of MPC associated combined postcapillary and precapillary PH (CpcPH). CASE PRESENTATION: A 58-year-old woman with SLE, CTD-ILD (FVC 64%, TLC 56 %), ESRD on HD since 2008 and diastolic heart failure was admitted to the hospital with worsening dyspnea, leg edema and orthopnea. Her calcium phosphate product was 61. CT chest showed diffuse ground glass opacity with mosaic perfusion, enlarged pulmonary artery (PA 4.3 cm) and chest wall calcifications. Echocardiogram showed grade 3 diastolic dysfunction, severely dilated left atrium and elevated right ventricular systolic pressure. Heart catheterization showed mean PA pressure 62 mm Hg, PA wedge pressure 29 mm Hg, transpulmonary gradient (TPG) 33, diastolic pulmonary gradient (DPG) 11, pulmonary vascular resistance 9 WU, LV end diastolic pressure 27 mm Hg, cardiac output 3.6, cardiac index 2.1. Given her severe PH, low CI and NYHA functional class IV, she was started on inhaled treprostinil with improvement in leg edema and orthopnea at 6-month follow up. DISCUSSION: Hyperphosphatemia in ESRD causes increased calcium phosphate product leading to calcium crystallization. Metastatic calcifications are usually seen in lamina propria of stomach, lung alveoli, renal tubules and interstitium(2). Acidosis between HD sessions causes leaching of calcium from bone, leading to deposition during post dialysis alkalosis. Uremia alters the configuration of tissue protein, rendering them more calcifiable. Three main CT patterns of MPC include centrilobular ground glass nodules, dense consolidation and small dense nodules(1). It is usually peripheral in distribution with upper lung zone dominance due to increased alkalinity (higher V/Q ratio causing low PaCO2) causing calcium salt deposition. Vascular calcification in chest and abdominal wall is a common finding as noted in our case. 30-50% of CKD and ESRD patients have PH. Vascular calcification can affect pulmonary arterial capacitance (low PAC in our case 0.81) and increase RV afterload. In this case, contributing factors to her PH are elevated LVEDP, ILD and ESRD (WHO group II, III and V). TPG >12 and DPG >7 suggested pulmonary vascular remodeling from shear stress and downstream pressure. This is an interesting case of MPC with associated PH. Initiation of the pulmonary vasodilator treprostinil reduced her PVR allowing for a better coupling of the RV-PA system. CONCLUSIONS: Treatment of MPC includes intensification of HD sessions and use of calcium and phosphate binders. In this case, inhaled pulmonary vasodilators for treatment of CpcPH after medical treatment optimization of other co-morbidities led to symptomatic improvement. Reference #1: Metastatic pulmonary calcification: HRCT findings in 23 cases, Radiol Bras.2017 Jul-Aug; 50(4): 231–236 Reference #2: Metastatic pulmonary calcification: State-of-the-art review focused on imaging findings, Respiratory Medicine Feb 2014 (108): 668-676 Reference #3: Pulmonary hypertension with extensive calcification in small pulmonary vessels and alveolar capillary wall in a chronic hemodialysis patient, Journal of Cardiology Cases 8 (Feb 2013) e13–e16 DISCLOSURES: No relevant relationships by Moises Cossio, source=Web Response No relevant relationships by Domingo Franco-Palacios, source=Web Response No relevant relationships by Kushagra Gupta, source=Web Response No relevant relationships by Shahzad Hussain, source=Web Response No relevant relationships by Venkateswara Kollipara, source=Web Response No relevant relationships by Toribiong Uchel, source=Web Response