Lower Lobe Opacity Research Articles

The "Origin" of the Lower Lobe Opacity.

The "Origin" of the Lower Lobe Opacity.

SINGLE CAVITARY LUNG LESION IN A HEALTHY YOUNG MALE

SINGLE CAVITARY LUNG LESION IN A HEALTHY YOUNG MALE

INCIDENTAL PRIMARY PULMONARY DIFFUSE LARGE B-CELL LYMPHOMA

INCIDENTAL PRIMARY PULMONARY DIFFUSE LARGE B-CELL LYMPHOMA

A CASE OF RETAINED ORAL CARE SPONGE IN THE BRONCHUS CAUSING PNEUMONIA IN CHRONICALLY VENTILATED PATIENT

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Aspiration of foreign bodies is not uncommon and mostly accidental with the highest prevalence in young children [1]. Occurrence in adults is rare and usually as a result of diminished consciousness, sedation, trauma, and neuromuscular disorders. We present a case of a 70 year old patient receiving chronic mechanical ventilation who had multiple episodes of hypoxia due to a dislodged oral care sponge. CASE PRESENTATION: A 70 year-old bedbound male with chronic mechanical ventilation (via tracheostomy?) after traumatic brain injury, and recurrent pneumonia was admitted for pneumonia. On admission, respiratory cultures grew Carbapenem resistant Acinetobacter Bumanii and Pseudomonas Aeruginosa with negative urinalysis and blood cultures. Chest radiograph showed bilateral lower lobe opacities. He was treated with vancomycin, polymyxin B, and meropenem. However, his FiO2 fluctuated between 40% and 60% and despite being on antibiotics he was persistently febrile. He continued to have copious secretions requiring frequent suctioning without any new infiltrates on repeat chest radiograph. A Computer tomography (CT) of the chest was performed which showed a tubular structure extending from the right main bronchus to the bronchus intermedius (Image 1). Bronchoscopy was done and the object was found to be the head of an oral care sponge. After foreign body removal his respiratory status improved and fevers resolved. DISCUSSION: Oral care in mechanically ventilated patients has been studied extensively and there are many guidelines recommend to minimize ventilator associated pneumonia. Extreme care must be taken by providers as defective products or aggressive technique can result in fragments being dislodged into the oral cavity and can result in aspiration especially in patients with chronic tracheostomy. In patients with tracheostomy, diminished airway protective mechanisms and a deflated balloon can result in an increased risk of foreign body aspiration. Aspiration of a foreign body is a significant cause of morbidity as it can cause asphyxiation or trauma to the airway resulting in pneumothorax, bleeding, and infections [2]. In patients with diminished consciousness the signs of foreign body aspirations can be subtle such a mild cough, fevers, frequent infections, or increasing oxygen and they may not be able to provide a proper history. CONCLUSIONS: This case highlights the need for vigilance regarding potential complications from providing oral care in the elderly who have diminished ability to protect their airway. REFERENCE #1: 1. Ding G et al., Tracheobronchial foreign body aspiration in children: A retrospective single-center cross-sectional study. Medicine (Baltimore). 2020 May 29;99(22):e20480. REFERENCE #2: 2. Aissaoui, N. H. Salem, and A. Chadly, "Unusual foreign body aspiration as a cause of asphyxia in adults: an autopsy case report," The American Journal of Forensic Medicine and Pathology, vol. 33, no. 3, pp. 284–285, 2012. DISCLOSURES: No relevant relationships by Kabu Chawla, source=Web Response No relevant relationships by Varun tej Gonuguntla, source=Web Response Speaker/Speaker's Bureau relationship with pfizer Please note: $1001 - $5000 by Yizhak Kupfer, source=Admin input, value=Consulting fee No relevant relationships by Sharad Oli, source=Web Response No relevant relationships by kiran para, source=Web Response No relevant relationships by Ankur Sinha, source=Web Response

ENDEMIC IN THE PANDEMIC: MURINE TYPHUS MASKING AS COVID-19 PNEUMONIA WITH PROFOUND HYPOXEMIA

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The presentation of fever, fatigue, myalgias, and acute hypoxemic respiratory failure is COVID-19 viral pneumonia until proven otherwise. However, findings like rash, photophobia, and unexplained lab abnormalities suggest an alternate diagnosis. We present a case of flea-borne (murine) typhus, causing acute illness with increasing prevalence in southern Texas and California. CASE PRESENTATION: In April 2020, a 32-year-old male presented to our emergency department (ED) with one week of fever, headache, progressive dyspnea, myalgias, and flank pain. Five days prior, COVID-19 PCR was negative;he was diagnosed with bilateral pneumonia on CT chest tomography and prescribed azithromycin. In the ED, he was found to be in acute hypoxemic respiratory failure needing high flow oxygen support prompting ICU admission. Vital demonstrated temperature of 103.4 degrees, heart rate of 130, respiratory rate of 26, and Spo2 of 96% oxygen saturation on 10L non-rebreather mask;Physical exam demonstrated dry mucous membranes, conjunctivitis, and labored respirations with accessory muscle use. Labs revealed hyponatremia, elevated liver function tests, hypoalbuminemia, thrombocytopenia, and elevated lactate dehydrogenase and procalcitonin. Repeat CT chest tomography showed posterior lower lobe opacities and concomitant ground glass opacities suggestive of atypical infection. Negative workup included two COVID-19 nasopharyngeal swabs, influenza A/B, RSV, HIV, streptococcus pneumoniae, and legionella urine antigen. He admitted recent travel to the Louisiana Gulf Coast with exposure to horses, chickens, and insect bites on the arm on further questioning. Vancomycin, ceftriaxone, and doxycycline were started on hospital day 2. A papular rash appeared on the lower back on hospital day 6. He still remained febrile and with significant hypoxemia for seven days. On day 9, Rickettsial typhus serologies returned IgM 1:512, and repeat tests confirmed both elevated IgM and IgG. The patient tapered off oxygen and was discharged home on doxycycline. DISCUSSION: Many cases of murine typhus are assumed to be a viral illness, but the clinical triad of fever, headache, and rash in endemic areas must raise suspicion. The exposure was likely insect bites (fleas), although it is not necessary, as endemic typhus has been identified in rural/suburban areas from possums, rats, or cats. In the COVID-19 pandemic, murine typhus with fever and acute hypoxemic respiratory failure was challenging to identify, but early diagnosis and treatment with tetracyclines provided a good outcome. CONCLUSIONS: The presentation of fever, headache, and rash with thrombocytopenia and transaminitis should trigger typhus workup and early treatment, which may otherwise progress to critical illness and death. REFERENCE #1: Afzal Z, Kallumadanda S, Wang F, Hemmige V, Musher D. Acute Febrile Illness and Complications Due to Murine Typhus, Texas, USA1,2. Emerg Infect Dis. 2017;23(8):1268-1273. doi:10.3201/eid2308.161861 REFERENCE #2: van der Vaart TW, van Thiel PP, Juffermans NP, van Vugt M, Geerlings SE, Grobusch MP, Goorhuis A. Severe murine typhus with pulmonary system involvement. Emerg Infect Dis. 2014 Aug;20(8):1375-7. doi: 10.3201/eid2008.131421. PMID: 25062435;PMCID: PMC4111165. DISCLOSURES: No relevant relationships by Philip Lavere, source=Web Response No relevant relationships by Dharani Kumari Narendra, source=Web Response

A CASE OF FANCONI SYNDROME SECONDARY TO LEGIONELLA PNEUMONIA

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Fanconi syndrome is a generalized dysfunction of the renal proximal tubules without primary glomerular involvement, characterized by wasting of phosphate, amino acids, or glucose by the proximal tubules. In addition, hypokalemia, hypouricemia, metabolic acidosis and proteinuria can be found (1, 2, 3). Acquired forms of Fanconi syndrome are caused by paraproteinemia, Sjogren syndrome, Primary Biliary Cirrhosis, and medications like cisplatin. Infectious diseases have not been reported as a common cause of Fanconi Syndrome (2). In this case report, we present an extremely rare case of Legionella pneumonia complicated by Fanconi syndrome. CASE PRESENTATION: A 42 year old woman with no past medical history was admitted to the hospital with fever, myalgias, diarrhea, and dyspnea. Vital signs on admission were; temperature 38.4 °C, blood pressure 114/57 mmHg, pulse 102 beats/min, respiration rate 20. Labs showed a white blood cell count of 10.9 x 10^3/ul, sedimentation rate of 126 mm/hr, procalcitonin 0.17 ng/ml, and C-reactive protein of 22.9 mg/dL. A CXR revealed a mild left lower lobe opacity compatible with pneumonia (figure 1). The patient tested positive for the Legionella urine antigen and was diagnosed with Legionella pneumonia. Multiple electrolyte abnormalities coexisted with the pneumonia including hypokalemia of 2.8mm/l, hypouricemia of 1.9mg/dl, hypophosphatemia of 1.8mg/dl and hypocalcemia of 8mg/dl. The patient's renal function was normal with no indication of metabolic acidosis. The urinalysis showed 4+ proteinuria, glucosuria and bilirubin with no WBCs. The patient was diagnosed with Fanconi Syndrome based on these findings. The patient was treated for Legionella pneumonia with Levaquin and improved clinically and serum electrolytes normalized. The repeat urinalysis after treatment revealed trace amounts of protein, negative glucose, decreased urobilinogen, and negative bilirubin. DISCUSSION: In this case because the electrolyte abnormalities disappeared after treatment for Legionella pneumonia and there was no evidence of other causes of Fanconi syndrome, it is most likely that Fanconi syndrome was associated with Legionella pneumonia. However, we are uncertain; (1) if Legionella pneumophila entered from basolateral/apical side of the renal proximal tubular cells and (2) why it specifically targeted the proximal tubular cells, developing reabsorption defects but not distal tubular cells. To our knowledge, only two cases (2, 3) have been reported in the literature linking Fanconi syndrome to Legionella pneumonia which makes our case exceedingly rare. CONCLUSIONS: This is an extremely rare case of Fanconi syndrome associated with Legionella pneumonia. Further studies are needed to understand the mechanisms responsible for electrolyte imbalances, which is important for the management of this potentially fatal infection. REFERENCE #1: Klootwijk ED, Reichold M, Unwin RJ, Kleta R, Warth R, Bockenhauer D. Renal Fanconi syndrome: taking a proximal look at the nephron. Nephrol Dial Transplant 30: 1456-1460, 2015. REFERENCE #2: Kinoshita-Katahashi, N., Fukasawa, H., Ishigaki, S., Isobe, S., Imokawa, S., Fujigaki, Y., & Furuya, R. (2013). Acquired Fanconi syndrome in patients with Legionella pneumonia. BMC nephrology, 14, 171. REFERENCE #3: Ryuge, A., Ito, Y., Yamakawa, T., Tanaka, H., Yasui, H., Mashimo, S., Watanabe, K., Nomura, R., Suganuma, N., & Maruyama, S. (2016). Fanconi Syndrome Associated with Hyponatremia in Two Patients with Legionella Pneumonia. Internal medicine (Tokyo, Japan), 55(23), 3479–3484. DISCLOSURES: No relevant relationships by Dilesha Kumanayaka, source=Web Response No relevant relationships by Richard Miller, source=Web Response No relevant relationships by Rutwik Patel, source=Web Response No relevant relationships by Bhavik Patel, source=Web Response

M413 COVID-19 IN A PATIENT WITH CVID AND CONTRAINDICATIONS TO SEVERAL POTENTIAL TREATMENTS

Despite nearly 18 million cases of SARS-CoV-2 thus far, there is minimal information regarding treatment in patients with common variable immunodeficiency (CVID), such as presented here. A 59-year-old male with CVID was receiving IVIG infusion when RN noted lethargy, fever, and cough. Chest Xray showed bilateral lower lobe opacities. Labs significant for lymphopenia to 0.5, CRP 4.9, CK 23, ESR 22. SARS-CoV-2 testing positive. Given history of atrial fibrillation, hypertension, severe back pain, and 10.5-pack-year smoking history, patient requested to be DNR/DNI. Patient eventually required high flow oxygen with 70% FiO2 at 35L/min. Hydroxychloroquine initiated, but Qtc became prolonged. He received vitamin C and enrolled in convalescent plasma trial. Patient’s respiratory status worsened with increasing hypoxia. D-dimer increased to 7.63, ferritin to 2862, and LDH to 533. Prone position poorly tolerated. BiPAP recommended, but patient increasingly anxious and declined, requesting to go home to die. Within 2 days of receiving plasma, mentation improved; within 9 days oxygen requirements decreased; discharge occurred after 24 days in the hospital. Patient subsequently admitted for severe back pain and found to be still SARS-CoV-2 positive, 8.5 weeks from initial test. However, he continued asymptomatic on room air with improved chest xray. This patient had contraindications to several potential medications, physical limitations with proning, and slow recovery after receiving convalescent plasma, though he did not require ventilator support. There was evidence of hyperinflammation secondary to COVID-19, and it is unknown to what degree immunodeficiency may have been protective against a severe cytokine storm. Further investigation necessary.

STAPHYLOCOCCUS AUREUS PNEUMONIA AND EMPYEMA AS A COMPLICATION OF E-CIGARETTE USE

SESSION TITLE: Medical Student/Resident Tobacco Cessation and Prevention Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Electronic-cigarettes (e-cigarettes), popularized in the late 2000s, were introduced as a safer alternative to traditional tobacco cigarettes. However, emerging data suggests a considerable risk for developing pulmonary diseases in users of e-cigarettes. Despite this concern, e-cigarette use is on the rise with up to 20% of Americans aged 25 to 44 now using e-cigarettes [1]. We present an interesting case which explores the relationship between e-cigarettes and the development of methicillin sensitive Staphylococcus aureus (MSSA) pneumonia. CASE PRESENTATION: A 38-year-old female was admitted with a five-day history of fever, dyspnea, and a productive cough. Her medical history was only notable for daily use of nicotine products via an e-cigarette. Vital signs on arrival revealed a temperature of 37.9 degrees centigrade, tachycardia with a pulse rate of 133 beats per minute, and tachypnea with a respiratory rate of 26 breaths per minute. She was able to maintain appropriate oxygen saturations on room air. Physical examination was notable for diminished air movement in left lower lung base. Admission labs were notable for a white blood cell (WBC) count of 12.83 x10(9)/L, and a procalcitonin of 11.3 ng/mL. Notably, both urine streptococcus and legionella antigens were negative. A chest radiograph demonstrated a left lower lobe opacity with associated effusion [Figure 1], which was also present on a computed tomography scan of her chest [Figure 2A-B]. Therefore, a diagnostic thoracentesis was performed from which pleural fluid analysis revealed a pH of 6.6, lactate dehydrogenase of 1,478 units/L, protein of 4.7g/dL, and WBC count of 5,082 cells/mL. Subsequent cultures from both the pleural fluid and sputum grew MSSA. The patient was started on empiric antibiotics and had a left-sided chest tube inserted for drainage of her empyema. Given the presence of loculations, additional therapy with intrapleural dornase alpha and tissue plasminogen activator was initiated. The patient clinically improved, her chest tube was removed, and she was discharged home to complete four weeks of nafcillin. The patient reported continued recovery and success in quitting e-cigarettes at her subsequent follow up. DISCUSSION: As the long-term effects of e-cigarette use become more evident, it is clear that they pose significant risks to patients. E-cigarettes decrease host ability to fight infection by promoting virulence in bacterial colonizers of the airways and by increasing pro-inflammatory markers [2]. Furthermore, vapors from e-cigarettes have been implicated in increasing biofilm formation. Biofilms lead to an increase of virulence in a variety of lung pathogens, including Staphylococcus aureus [3]. CONCLUSIONS: Clinicians should be aware of an increase in virulence from bacterial pathogens (particularly MSSA) responsible for community acquired bacterial pneumonia amongst e-cigarette users. Reference #1: Hwang, John H., et al. “Electronic cigarette inhalation alters innate immunity and airway cytokines while increasing the virulence of colonizing bacteria.” Journal of molecular medicine 94.6 (2016): 667-679. Reference #2: Gilpin, Deirdre F., et al. “Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens.” Respiratory Research 20.1 (2019): 267. Reference #3: Shi, L., Wu, Y., Yang, C. et al. Effect of nicotine on Staphylococcus aureus biofilm formation and virulence factors. Sci Rep 9, 20243 (2019). https://doi.org/10.1038/s41598-019-56627-0 DISCLOSURES: No relevant relationships by Ethan Karle, source=Web Response No relevant relationships by Armin Krvavac, source=Web Response No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by SACHIN PATIL, source=Web Response No relevant relationships by Richard Swaney, source=Web Response

ALVEOLAR SARCOIDOSIS PRESENTING AS AN INCIDENTAL FINDING

SESSION TITLE: Medical Student/Resident Diffuse Lung Disease SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Sarcoidosis is protean in its presenting characteristics. The most common pulmonary manifestations are hilar adenopathy and interstitial infiltrates. The alveolar filling pattern is noted less frequently. Here we present of a case of 53-year-old woman who was diagnosed with alveolar sarcoidosis after an incidental finding on chest X-ray. CASE PRESENTATION: A 53-year-old woman was admitted to hospital for sepsis secondary to a urinary tract infection after presenting with fever, malaise and low abdominal pain. She had a 20-pack-year smoking history. On physical exam the chest was clear to auscultation. A routine chest X-ray (fig 1) showed an ill-defined density to the left hemithorax. She reported no cough, SOB, hemoptysis or other respiratory symptoms. CT chest showed a 2.9cm ground glass opacity in the superior segment of the left lower lobe (fig 2). Given the patient’s smoking history, suspicion was high for malignancy. A CT guided transthoracic needle biopsy was done which showed non-caseating granulomata and no evidence of malignancy. Tissue smears were negative for bacteria, AFB and fungi, antigen tests for histoplasma and blastomyces were negative. ACE levels were elevated at 89U/L. A CT scan done 8 weeks following initial imaging showed complete resolution of the left lower lobe opacity (fig 3). PET scan done at that time showed no areas of increased uptake. DISCUSSION: The diagnosis of sarcoidosis depends on clinical and radiological characteristics, the presence of non-caseating granulomas and excluding alternate diagnoses. The pattern of alveolar infiltrate noted in this case is a rare presentation seen in ∼1.8% of cases. Biopsy confirmed the presence of non-caseating granulomata, and infection and malignancy were ruled out. Supporting evidence was given by the elevated ACE levels, which, while not sensitive for sarcoidosis, have been reported having ∼89% specificity. Bronchoscopy, which can support diagnosis with an elevated CD4/CD8 ratio was deemed unnecessary as the patient had no pulmonary symptoms and the diagnosis was already confirmed. PET scanning, which has been useful in the monitoring of sarcoidosis was done at follow up to evaluate for other potential sites of active disease, but none were found. In the majority of cases, the inflammatory lesions of sarcoidosis resolve spontaneously, often in under 2 years. The 8-week interval to resolution appears unusually quick, however the initial time of onset of the lesion was not known. This case illustrates an unusual presentation of sarcoidosis and serves as reminder that this diagnosis must be kept in mind when evaluating asymptomatic lung masses. CONCLUSIONS: As sarcoidosis is variable in its presentation, a clinician must be aware of atypical presentations including the pattern of alveolar infiltrates on imaging, which can be asymptomatic. Reference #1: Valeyre D, Prasse A, Nunes H, Uzunhan Y, Brillet PY, Müller-quernheim J. Sarcoidosis. Lancet. 2014;383(9923):1155-67 Reference #2: Vettiyil B, Gupta N, Kumar R. Positron emission tomography imaging in sarcoidosis. World J Nucl Med. 2013;12(3):82-6 Reference #3: Ungprasert P, Carmona EM, Crowson CS, Matteson EL. Diagnostic Utility of Angiotensin-Converting Enzyme in Sarcoidosis: A Population-Based Study. Lung. 2016;194(1):91-5 DISCLOSURES: No relevant relationships by Muhammad Faiz, source=Web Response No relevant relationships by Jovan Gayle, source=Web Response No relevant relationships by Somshukla Ghosh, source=Web Response No relevant relationships by Natarajan Rajagopalan, source=Web Response

Generalizability of Deep Learning Tuberculosis Classifier to COVID-19 Chest Radiographs: New Tricks for an Old Algorithm?

Generalizability of Deep Learning Tuberculosis Classifier to COVID-19 Chest Radiographs: New Tricks for an Old Algorithm?

Lung Involvement in Gaucher Disease

Introduction: Gaucher Disease is an autosomal recessive lysosomal storage disease. Pulmonary involvement in Gaucher Disease is rare and often seen in the severe form of the disease with the worst outcome. Case Presentation: A 30-year-old man and known case of Gaucher Disease presented to our clinic with history of progressive dyspnea since 8 months ago. Pulmonary function test showed restrictive pattern. Chest CT scan revealed diffuse bilateral interlobular septal thickening and small interstitial nodules with ground glass opacities in lower lobes. Conclusion: Patients with Gaucher Disease that present with progressive dyspnea may have a manifestation of interstitial or alveolar lung disease.

RELAPSING CRYPTOGENIC ORGANIZING PNEUMONIA

SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Organizing pneumonia is a form of Interstitial lung disease. It has equal prevalence in men and women. Adults 40-60 years are most commonly affected. It can be idiopathic, called cryptogenic organizing pneumonia(COP), or secondary to other factors; secondary organizing pneumonia. CASE PRESENTATION: 77-year-old female with history of hypertension, CHF, COPD presented with 3 weeks of dyspnea. She was hospitalized 3 weeks prior and treated for CAP.CXR at that time demonstrated b/l upper lobe consolidations. She was discharged on 4L O2 and PO cefpodoxime. Pt reported subjective improvement, however she was not back to her baseline. CT chest revealed patchy consolidation in the b/l upper lobes, and multiple nodular opacities in lower lobes. On initial evaluation patient was afebrile, hypoxic, with PaO2:91 on non-rebreather saturating at 95%. WBC count of 8.9. Bronchoscopy was performed. BAL revealed WBC: 693, lymphocytes: 35%, cultures: negative. BAL analysis was supportive of a diagnosis of COP. Biopsy not done due to high FiO2 requirements and unstable condition. Patient was started on prednisone 40 mg x 4 weeks followed by 20 mg x 4 weeks. Patient was lost to follow up, and steroids stopped by PCP. 3 months later she was re hospitalized for hypoxia. CXR showed worsening opacities and she required 5 L O2 via NC. A tapering course of Prednisone was started. Patient seen on follow up at 3 months with resolution of symptoms. DISCUSSION: COP has an insidious onset. Risk factors include infections, connective tissue disease, malignancies, chronic recurrent aspiration, radiation, cocaine etc. The radiographic appearance of COP is variable. On chest CT scan patchy consolidation, is seen in 90% of patients. Nodules and irregular linear opacities or ground-glass attenuation may be seen. Diagnosis is made on history, Imaging, PFTs, Bronchoscopy with BAL and biopsy findings. PFTs may show obstructive vs restrictive defect. DLCO is usually decreased. Typical BAL findings include increases in lymphocytes (20 to 40 percent), neutrophils (5 to 10 percent), and eosinophils (5 to 25 percent). Foamy macrophages, mast cells, and a decreased CD4/CD8 T cell ratio may be seen. BAL neutrophilia (>10%) tends to correlate with relapse. Transbronchial/surgical lung biopsy provides a definitive diagnosis. Patients with minimal symptoms can be monitored without therapy as spontaneous remission may occur. For patients with severe disease: Long term course of steroids: 0.75-1 mg/kg/day for 4-8 weeks then 0.5 mg/kg/day for 4-8 weeks. Most patients respond to therapy with recovery usually occurring in two-thirds of patients. Approximately one-third of patients experience persistent symptoms, abnormalities on pulmonary function testing, and radiographic disease. CONCLUSIONS: Close monitoring is essential to ensure response and completion of therapy, as early discontinuation of steroids may result in recurrence of symptoms. Reference #1: 1. Cordier, J. F. "Cryptogenic organising pneumonia." European Respiratory Journal 28, no. 2 (2006): 422-446. Reference #2: 2. Drakopanagiotakis, Fotios, Koralia Paschalaki, Muhanned Abu-Hijleh, Bassam Aswad, Napoleon Karagianidis, Emmanouil Kastanakis, Sidney S. Braman, and Vlasis Polychronopoulos. "Cryptogenic and secondary organizing pneumonia: clinical presentation, radiographic findings, treatment response, and prognosis." Chest 139, no. 4 (2011): 893-900 Reference #3: 3. Epler, Gary R. "Bronchiolitis obliterans organizing pneumonia: definition and clinical features." Chest 102, no. 1 (1992): 2-6. DISCLOSURES: No relevant relationships by Siddique Chaudhary, source=Web Response No relevant relationships by Bhavna Sharma, source=Web Response No relevant relationships by Paul Kristan Valestra, source=Web Response

ACUTE FIBRINOUS AND ORGANIZING PNEUMONIA: A RARE CAUSE OF INTERSTITIAL LUNG DISEASE

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Acute fibrinous and organizing pneumonia (AFOP) is a rare cause of interstitial lung disease that is commonly misdiagnosed in patients presenting with diffuse alveolar opacities. Here we present a case of a 60-year-old previously healthy man who presented with fevers, shortness of breath and cough and was eventually diagnosed with steroid-responsive AFOP. CASE PRESENTATION: A 60-year-old otherwise healthy man presented to the hospital with shortness of breath, dry cough and recurrent fevers as high as 40C of two weeks duration. Physical exam was significant for a respiratory rate of 22, oxygen saturation on room air of 94% and bibasilar crackles. Lab work-up revealed elevated white blood cell count at 12K, erythrocyte sedimentation rate and C-reactive protein were highly elevated at >120mm and 190 mg/L, respectively. Respiratory viral panel and atypical respiratory bacterial culture were negative. Chest x-ray showed left basilar and right lower lobe opacities. After 4 days of broad-spectrum antibiotics, the patient failed to improve with paroxysmal high fevers and hypoxemia, requiring 3-5L of oxygen with nasal cannula. A high-resolution CT of the chest (Figure 1) showed worsening multi-focal parenchymal consolidation in the lower lobes and new patchy involvement in the upper lobes. Antibiotics were discontinued after bronchoscopy & bronchoalveolar lavage showed the absence of infectious organisms. Work-up for collagen vascular disease was negative. Biopsy of the lung parenchyma was done and showed prominent intra-alveolar fibrin, scattered inflammatory cells, and patchy intraluminal connective tissue consistent with AFOP. The patient was started on high dose oral prednisone of 80mg daily with a plan for a prolonged taper over 8 weeks. Over the next few days, his symptoms, oxygen requirements and chest X-ray findings all improved. The patient was discharged home with no oxygen supplementation. DISCUSSION: One of the rare histologic interstitial pneumonias, AFOP was first reported in 2002 (1). It is defined as a subgroup of idiopathic interstitial lung disease with acute lung injury characterized by intra-alveolar fibrin deposition and organization of loose connective tissue (2). Patients with AFOP tend to present with pulmonary as well as extra-pulmonary symptoms. Cough, both productive and non-productive, has been found to be the most common symptom, followed by dyspnea and fever. While AFOP can present as an idiopathic disease process, it has been found to be associated with other disease processes as well including autoimmune, infectious and connective tissue diseases.Treatment consists of systemic glucocorticoids and immunosuppression (3). CONCLUSIONS: AFOP is a rare histopathological diagnosis that requires a high degree of clinical suspicion for diagnosis. Increasing awareness of this entity might lead to earlier diagnosis and more prompt initiation of appropriate therapy. Reference #1: Beasley MB, Franks TJ, Galvin JR, et al. Acute fibrinous and organizing pneumonia: a histological pattern of lung injury and possible variant of diffuse alveolar damage. Arch Pathol Lab Med 2002;126:1064. Reference #2: Travis WD, Costabel U, Hansell DM, King TE Jr, Lynch DA, Nicholson AG, et al. An official American Thoracic Society/European Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med 2013;188(6):733–48. Reference #3: Bhatti S, Hakeem A, Torrealba J, et al. Severe acute fibrinous and organizing pneumonia (AFOP) causing ventilatory failure: successful treatment with mycophenolate mofetil and corticosteroids. Respir Med 2009;103:1764. DISCLOSURES: No relevant relationships by Shameek Gayen, source=Web Response No relevant relationships by Xiang Liu, source=Web Response No relevant relationships by Mahmoud Madi, source=Web Response

A BLACK DIAGNOSIS OUT OF THE BLUE: BRONCHIAL ANTHRACOFIBROSIS

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Bronchial anthracofibrosis (BAF) indicates blackening of the airways with concomitant scarring often due to exposure from cooking over an open fire. It often presents late in life with a COPD-like syndrome in non-smokers. BAF is progressive and can lead to obstruction of the bronchial tree. Here we present a case of BAF secondary to years of cooking over a charcoal stove. CASE PRESENTATION: A 74-year-old Turkish woman presented with a four month history of cough, hemoptysis, and dyspnea on exertion. She was a non-smoker, but reported she had cooked for many years over a charcoal stove in her home. A chest x-ray showed a right lower lobe opacity. A chest CT showed a right hilar obstructing peribronchial mass concerning for neoplasm. She was then referred to pulmonology for bronchoscopy. Initial bronchoscopy noted dark anthracotic-like pigment throughout the right bronchial tree and bronchial obstruction. Washes were negative for infectious or malignant etiologies. A repeat bronchoscopy with endobronchial ultrasound with fine needle aspiration of a pretracheal-subcarinal lymph node revealed abundant anthracotic pigment and no evidence of malignancy. She was started on inhaled corticosteroids and supplemental oxygen. Her symptoms slowly improved, and follow up imaging showed very slow progression of the obstruction. She did have positive interferon gamma release assay testing and was treated with INH. DISCUSSION: Anthracosis was initially associated with lung disease in coal miners, but has been associated with smoke exposure from open fire cooking and dust. Darkening of airway mucosa can be seen in smokers and tuberculosis as well. The presentation of bronchial anthracofibrosis is similar to COPD, with patients noting dyspnea on exertion, cough, and sometimes hemoptysis. It generally affects older patients, predominantly women. Pulmonary function testing generally reveals obstruction with normal DLCO. Imaging will often show airway obstruction as in malignancy and generally leads to bronchoscopy. Bronchoscopy reveals bluish-black pigmented mucosa and bronchial stenosis. Lymph nodes with a hypoechoic, scattered nodular pattern are unique to anthracosis. BAF can appear similar to tuberculosis, therefore patients should have complete workup and treatment for this. There are no clear treatment studies, but BAF is typically managed similarly to COPD. CONCLUSIONS: Bronchial anthracofibrosis should be suspected in older patients with COPD-like symptoms without history of tobacco use, but with exposure to biomaterials such as smoke and dust. Patients with BAF should also be ruled out for active tuberculosis. Reference #1: Mirsadraee M. Anthracosis of the lungs: etiology, clinical manifestations and diagnosis: a review. Tanaffos. 2014;13(4):1-13. DISCLOSURES: No relevant relationships by Gopal Punjabi, source=Web Response No relevant relationships by Lauren Thornton, source=Web Response

SAVED BY THE BAL: A CASE OF ACUTE EOSINOPHILIC PNEUMONIA AFTER METHYL-NALTREXONE INJECTION

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Eosinophilic pneumonia (EP) can result as an adverse effect of many drugs. Methyl-naltrexone injection has become increasingly popular this case serves to bring attention to a rare, but potential adverse effects. CASE PRESENTATION: A 44-year-old male with history of alcohol use disorder was brought to the emergency department (ED) by ambulance in acute respiratory failure. He received his monthly naltrexone injection three days prior. The following day, he started having lip swelling, rash, and two days later, had dyspnea. Upon arrival to the ED, he was given two doses of IM epinephrine, as well as methylprednisolone 125 mg IV, and he required BiPAP, after what was thought to be an anaphylactic reaction to naltrexone. Chest x-ray revealed stable bilateral lower lobe opacities, possibly related to aspiration pneumonia, patient was placed on ampicillin-sulbactam. CBC demonstrated increased absolute levels of eosinophils (700k/mm3), anaphylaxis was ruled out with tryptase level of 2.8 (normal <11.5). Patient’s symptoms slightly improved, however patient's eosinophil count continued to trend upwards, as high as 2500k/mm3 four days after presentation. CTA of chest demonstrated no evidence of pulmonary embolism, but did reveal diffuse ground glass opacities consistent with acute infiltrates. Bronchoscopy with bronchoalveolar lavage (BAL) was performed and BAL yielded fluid with eosinophils making up greater than 50% of the WBC's and the fluid was negative for malignant cells. Eosinophilic pneumonia diagnosis was established and steroids were initiated with improvement of symptoms. DISCUSSION: Acute eosinophic pneumonia is characterized by acute onset febrile illness, hypoxemia, diffuse bilateral infiltrates on imaging, and pulmonary eosinophilia with more than 25% eosinophils in BAL. EP is characterized by symptoms lasting less than 1 month and usually less than 1 week. EP will respond rapidly to steroid therapy but early recognition remains important to choose appropriate therapy given mimics such as infection. Several medications have historically been shown to cause EP, in one review of the literature the most commonly cited drugs include antibiotics or anti-inflammatories. Imaging findings typically include bilateral reticular ground-glass opacities that expand as the disease progresses. Methyl-naltrexone is increasingly utilized as an effective treatment for alcohol dependence disorder. Its possible association with EP was initially noted in a large randomized control trial published in JAMA by Garbutt et al. In our review of the literature there have been only four other cases of naltrexone induced eosinophilic pneumonia. CONCLUSIONS: This case demonstrates a likely outcome of eosinophilic pneumonia in a patient receiving methyl-naltrexone injections for alcohol use disorder. It is important to recognize naltrexone as a possible etiology for eosinophilic pneumonia due to its increasing use. Reference #1: Carmi Bartal, MD, MHA, Iftach Sagy, MD, and Leonid Barski, MD. Medicine (Baltimore). 2018 Jan; 97(4): e9688. Published online 2018 Jan 26. Drug-induced eosinophilic pneumonia: A review of 196 case reports Reference #2: Kim H, Ali M, Buch K. Eosinophilic Pneumonia Induced by Injectable Naltrexone. Am J Respir Crit Care Med. 2014;189:A2283 Reference #3: Garbutt JC, Kranzler HR, O'Malley SS, Gastfriend DR, Pettinati HM, Silverman BL, Loewy JW, Ehrich EW; Vivitrex Study Group. Efficacy and tolerability of long-acting injectable naltrexone for alcohol dependence: a randomized controlled trial. JAMA. 2005 Apr 6;293(13):1617-25 DISCLOSURES: No relevant relationships by Anthony Esposito, source=Web Response No relevant relationships by benison lau, source=Web Response

Pulmonary tuberculosis and pneumocystis jirovecii concurrent pneumonia in HIV infected patients at a resource limited setting in Eastern India: A case series

Pneumocytis jirovecii pneumonia (PJP) and Pulmonary TB (PTB) both are common opportunistic infections among HIV infected individuals. But concurrent infections pose a diagnostic challenge owing to similar clinical features. Data suggests a high prevalence of such concurrent infections in developing countries but limited diagnostic modalities especially in resource constraint setup limits accurate diagnosis. At our centre we came across 6 newly diagnosed PTB patients among HIV infected ones had persistent shortness of breath (SOB) and hypoxia despite starting anti-tuberculous treatment (ATT). We excluded concomitant bacterial pneumonia by imaging, sputum examination and blood culture. Serum lactate dehydrogenase (LDH) was estimated and hypoxia by arterial blood gas (ABG). We found all 6 patients had elevated serum LDH, hypoxia and imaging suggestive of PJP were offered sputum for Geisma stain and standard treatment for PJP in form of Bactrim-double strength and steroid. 1 patient had PJ cysts in sputum. 5 patient's classical radiologic findings in form of ground glass opacities in lower lobes along with bilateral infiltrates and 1 had honeycombing. Serum LDH was elevated all 6 subjects. 5 were newly diagnosed HIV and 4 had CD4 count below 50 cells/mm3 and 2 had below 200 cells/mm3.1 patient had developed bilateral pneumothorax as complication. 4 patients responded to treatment and 2 (33.3%) died of respiratory failure during treatment. We were able to diagnose only severe PJP cases as concurrent infection with PTB as there was no availability of broncho alveolar lavage (BAL) as well as direct fluorescent antigen (DFA) test for PJ detection. A high index of suspicion for PJP even in PTB patients with low CD4 count will guide to appropriate therapy for both infections and eventually reduces morbidity and mortality.

POTT'S DISEASE: A RARE BUT CRITICAL DIAGNOSIS

SESSION TITLE: Chest Infections 1 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Pott’s disease is the most common form of skeletal tuberculosis (TB) which often affects the thoracic and lumbar spines. In 2013, it represented only 2.3% of all United States TB cases. However, it is important for clinicians to include this differential diagnosis to prevent delays of diagnosis and treatment. CASE PRESENTATION: An 82-year-old male with a history of non-compliance to Mycobacterium Avium-Intracellulare (MAI) treatment and atrial fibrillation presented after notification of “bone biopsy positive for TB”. Previously, he presented to another hospital for worsening lower back and bilateral hip pain for the past three months associated with unintentional twenty-pound weight loss within the last six months and night sweats for the past two to three years. Chest X-Ray showed a right lower lobe opacity. Magnetic Resonance Imaging (MRI) revealed abnormal signal intensities/ enhancements and discitis/ osteomyelitis at the thoracic and lumbar vertebrae. It also showed a small epidural abscess/ phelgmon causing moderate to severe spinal canal stenosis at the L2/L3 level and bilateral psoas muscle abscesses. Following a Computed Tomography (CT) guided biopsy of the paraspinal collection and L2- L3 disc space, he received empiric osteomyelitis treatment with Vancomycin and Meropenem. Despite being Quantiferon positive, he was deemed as having latent TB after three negative Acid-Fast Bacillus (AFB) by sputum. Three weeks later, he presented to our hospital after notification of the biopsy results. AFB smear was negative, but culture revealed growth of AFB detected in broth and Mycobacterium tuberculosis complex by DNA probe. Further history revealed he had emigrated from China ten years ago and recently visited China for one month a year ago. Subsequently, Pott’s disease treatment was initiated with Isoniazid, Rifampin, Pyrazinamide, Ethambutol and Pyridoxine. DISCUSSION: Pott’s disease presents as back pain with muscle spasms and rigidity, but rarely constitutional symptoms. Diagnosing skeletal TB presents with challenges such as not including it as a differential diagnosis due to the subtle presentation, lack of active pulmonary disease, and slow disease progression. It is diagnosed by clinical presentation, radiologic imaging with MRI as the most sensitive diagnostic modality, and biopsy. Biopsy limitations include slow culture growth of 6 to 8 weeks, needing 10 – 100 bacilli for culture recovery, and sometimes inconclusive histopathology. Delays in diagnosis lead to complications including vertebral collapse, cord compression, and paraplegia. CONCLUSIONS: It raises the importance of a proper and thorough history in order to include an appropriate differential diagnosis. Since extra-pulmonary tuberculosis is more common in immigrants from endemic areas, our patient who was from China with complaints of back pain should have elicited a higher suspicion of Pott’s disease. Reference #1: McDonald M and Sexton D. Skeletal tuberculosis. UpToDate. July 2017. Available at https://www.uptodate.com/contents/skeletal-tuberculosis?source=search_result&search=potts%20disease&selectedTitle=1∼13#H6 . Accessed August 15, 2017 Reference #2: Ansari S, Amanullah F, Ahmad K, Rauniyar R. Pott’s Spine: Diagnostic Imaging Modalities and Technology Advancements. N Am J Med Sci. 2013 Jul; 5 (7): 404-411. Reference #3: Kumar M, Kumar R, Srivastva AK, et al. The efficiency of diagnostic battery in Pott’s disease: A prospective study. Indian Journal of Orthopedics. 2014; 48 (1) : 60-66 DISCLOSURES: No relevant relationships by Adam Hines, source=Web Response No relevant relationships by Roxana Lazarescu, source=Web Response No relevant relationships by Jennifer Tom, source=Web Response

Rare Presentation of Esophageal Duplication Cyst in Adult

Introduction: Esophageal duplication cyst (EDC) is an unusual mediastinal cyst which commonly presents with pulmonary infection, dyspnea or dysphagia due to compression of adjacent structures during childhood. In very few cases, it can remain asymptomatic until adolescence, eventually needing intervention due to symptoms and complications. We present a rare case of EDC in an adult who was admitted with pneumonia. Case Description:A 57 year old woman with no significant past medical history came to the emergency department with productive cough for one week associated with fever of 102°Fahrenheit. On examination, she had crackles in the right lower lobe of the lung. Her labs were only significant for white blood cell count of 12300 cells/uL. Chest X-ray showed right paratracheal mass and right lower lobe infiltrate. Computed tomography (CT) scan of chest revealed right lower lobe opacities and right large fluid-filled paratracheal cyst compressing esophagus and trachea. Barium swallow examination demonstrated leftward deviation of proximal esophagus without any communication with the cyst. Mediastinal mass was further evaluated by endoscopic ultrasound (EUS) which exhibited a 5cm homogeneous anechoic cystic structure contained within the third layer of esophagus with no blood flow, consistent with an EDC [figure 1]. She was started on Ceftriaxone and Azithromycin for management of community acquired pneumonia with improvement in symptoms over the next three days. On stabilization, she underwent video assisted thoracoscopic resection of the cyst and appeared to be doing well on one month follow up. Discussion: EDC is diagnosed in childhood in up to 80% of the cases and less than 7% remain asymptomatic until adolescence. It can cause local compressive symptoms as well as complications like hemorrhage, rupture into pleura and progression to malignancy. Diagnosis is usually made by EUS which can help in the differentiation of solid from cystic lesions. EDC should be promptly treated in symptomatic patients and resection can be performed through open thoracotomy or video-assisted thoracoscopic surgery. Biopsy and aspiration of the asymptomatic cyst is not recommended because of the potential for complications and cyst infection. Physicians should be aware of this rare condition to facilitate early diagnosis and treatment.1733 Figure 1 No Caption available.

PURULENT PERICARDIAL EFFUSION AND CARDIAC TAMPONADE: UNUSUAL PRESENTATION IN AN ANTIBIOTIC ERA

SESSION TITLE: Chest Infections 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Bacterial pericarditis with cardiac tamponade due purulent pericardial effusion is rare in the modern antibiotic era. It is a rapidly progressive and highly fatal infection and is often diagnosed postmortem in majority of the cases. We present a case of purulent pericardial effusion due to streptococcus pneumoniae in an immunocompromised patient with PLAID (PLCG2 associated antibody deficiency and immune dysregulation) syndrome. PLAID is a complex dominantly inherited disease, characterized almost universally by cold urticaria, autoimmunity and skin granuloma formation. CASE PRESENTATION: A 28-year-old male, with past medical history significant for PLAID syndrome associated with cutaneous malignancies and asthma presented with a weeklong history of increased cough with productive sputum and pleuritic chest pain. Upon admission, he was hemodynamically stable except for tachycardia and exam showed muffled heart sounds and crackles at left lung base. Labs were significant for leukocytosis of 45,000 and CXR showed left lower lobe opacity consistent with pneumonia. He was therefore started on antibiotics but since he continued to deteriorate clinically, CT scan was ordered which revealed bilateral multifocal pneumonia, a large multiloculated left pleural effusion, and a large pericardial effusion. A subsequent echocardiogram in conjunction with physical exam findings of pulsus paradoxus of 28mm of Hg was consistent with early tamponade physiology, and the patient underwent an uncomplicated sub-xiphoid pericardial window with placement of drain. Chest tube was placed for left posterior pleural effusion. Pleural fluid and blood, and pericardial fluid cultures grew Streptococcus pneumonia. The pericardial drain was removed. The patient eventually had a pulmonary decortication of the lung tissue secondary to dense, copious adhesions and has recovered well. DISCUSSION: Purulent pericarditis, especially from streptococcus pneumonia is a rare entity in the developed world. Following the introduction of antibiotics and more recently the pneumococcal-conjugate vaccine, the incidence of bacterial pericarditis from streptococcus pneumonia has drastically decreased. Diagnosis is therefore challenging due to low clinical suspicion. It generally presents with acute cardiovascular decompensation and a sepsis-like appearance. Our case was unique as initial course of illness was indolent, which could be related to patients immunodeficiency. If untreated, this condition has a mortality rate of up to 100%. CONCLUSIONS: Purulent pericarditis secondary to streptococcus pneumoniae is rare, however, a high index of suspicion is needed for early diagnosis to instate appropriate therapy with drainage and antibiotics given the risk of life-threatening tamponade. Reference #1: J. Sagrista-Sauleda, J.A. Barrabes, G. Permanyer-Miralda, J. Soler-SolerPurulent pericarditis: review of a 20 year experience in a general hospitalJ Am Coll Cardiol, 22 (1993), pp. 1661-1665 DISCLOSURES: No relevant relationships by Timothy Ford, source=Admin input No relevant relationships by Sriharsha Gowtham, source=Web Response No relevant relationships by adithya kattamanchi, source=Web Response No relevant relationships by Saptak Pandita, source=Web Response No relevant relationships by Vikrant Tambe, source=Web Response

NSAID-INDUCED EOSINOPHILIC PLEURAL EFFUSION: A RARE CASE

SESSION TITLE: Disorders of the Pleura 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 pm - 02:15 pm INTRODUCTION: Non-steroidal anti-inflammatory drugs (NSAIDs) are known to induce systemic eosinophilia, and rare case reports have linked them to eosinophilic pneumonia. The literature, however, does not clearly associate NSAIDs with an eosinophilic pleural effusion. In this case, we present an unusual presentation of an eosinophilic pleural effusion secondary to NSAID use. CASE PRESENTATION: A 49 year-old homeless man with chronic hepatitis C, cholelithiasis, active alcohol and tobacco abuse, and depression, presented to the emergency department with cough and left-sided pleuritic chest pain. Chest x-ray (CXR) showed left lower lobe opacity and he was discharged with a course of azithromycin for presumed community-acquired pneumonia. He then returned for persistent symptoms, and a chest computed tomography (CT) confirmed left lower lobe pneumonia with pleural thickening. He was hospitalized, placed on broader antibiotics, and was given ibuprofen for pleuritic pain. Over the following month, he had several more presentations for persistent symptoms. Serial imaging revealed accumulation of left pleural effusion and laboratory studies were significant for serum eosinophilia ranging from 6.6% to 14.3%. Two separate thoracenteses were performed, yielding blood-tinged exudative effusions with normal pH and an eosinophil-predominance (up to 43% on the cell count differential). Extensive workup for bacterial, mycobacterial, viral, fungal and parasitic causes, as well as pulmonary embolism, and underlying rheumatologic disorders were all negative. He was instructed to discontinue his ibuprofen and was scheduled to follow up in the pulmonary clinic. After a month, repeat serum cell counts with differentials normalized (eosinophil 1.2 %), and the pleural effusion improved. DISCUSSION: Eosinophilic pleural effusions are known to be caused by a variety of medications such as valproic acid, nitrofurantoin, dantrolene, warfarin, and fluoxetine. Upon literature review, it is noted that ibuprofen can cause systemic eosinophilia and also eosinophilic pneumonia. Our patient likely had underlying pleural inflammation from his recent pneumonia. Following the initiation of NSAIDs, the elevated systemic eosinophils likely caused further inflammation to the pleural space, leading to the eosinophil-predominant pleural effusion. CONCLUSIONS: 49 year old male presenting with ibuprofen induced recurrent pleural effusion with eosinophilia resolving with cessation of medication. Further investigation between ibuprofen effects on pleural effusion development should be explored. We recommend caution when prescribing NSAIDs in patients with systemic eosinophilia. Reference #1: Bartal, C., Sagy, I., & Barski, L. (2018). Drug-Induced Eosinophilic Pneumonia. Medicine,97(4), 1-6. Retrieved February 02, 2018, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5794373/. Reference #2: Huggins, J. T., & Sahn, S. A. (2004). Drug-Induced Pleural Disease. Clinics in Chest Medicine,25(1), 141-153. Retrieved February 10, 2018, from https://www.sciencedirect.com/science/article/pii/S0272523103001254?via%3Dihub. DISCLOSURES: No relevant relationships by Angela Love, source=Web Response No relevant relationships by Tetsuro Maeda, source=Web Response No relevant relationships by Adam Rothman, source=Web Response No relevant relationships by Reza Samad, source=Web Response No relevant relationships by Gorav Sharma, source=Web Response