Left Lung Mass Research Articles

Clinical images: Pulmonary cryptococcoma in a 34-year-old woman

A previously healthy 34-year-old woman from Vancouver, British Columbia was referred for a left upper lobe lung mass. Main differential diagnoses were infection and malignancy. She underwent a bronchoscopy with endobronchial ultrasound-guided biopsy. Analysis of the bronchoscopic specimens revealed Cryptococcus gattii. Further investigations including neuroimaging and lumbar puncture for cerebrospinal fluid analysis excluded central nervous system involvement. Due to the size and proximity of the pulmonary cryptococcoma to the mediastinum, she was treated with Amphotericin and Flucytosine as induction therapy and oral Fluconazole as maintenance therapy. We review the clinical, radiological and pathological features of this disease entity in this report.

Primary pulmonary mucoepidermoid carcinoma: Cyto-histologic correlation and review of the literature

Preoperative fine needle aspiration diagnosis and cyto-histologic correlation of primary pulmonary mucoepidermoid carcinoma have rarely been described in detail in the literature. A 26-year old male presented at our institution with cough, bloody sputum, and a 4.3 cm left lower lobe lung mass. He was accurately diagnosed with pulmonary mucoepidermoid carcinoma on preoperative aspiration cytology. The patient subsequently proceeded to left lower lobectomy, confirming the diagnosis. In this article, we present a detailed report of primary pulmonary mucoepidermoid carcinoma describing the cytologic and histologic morphologic features, its differential diagnosis with review of the literature.

Medical image of the month: mucinous adenocarcinoma of the lung mimicking pneumonia

No abstract available. Article truncated after 150 words. Clinical Scenario: A 60-year-old man with a history of chronic obstructive pulmonary disease presented to the hospital with worsening shortness of breath over a period of 3 days. He had a 50-pack-year history of smoking, coronary artery disease, and a previous history of a left lung mass of unknown pathology status post left upper lobectomy. He was bought to the emergency room via ambulance after being found at home with oxygen saturations in the 60s. Upon arrival to the emergency room, he required continuous oxygen at 15 L/min to maintain his oxygen saturations above 88%. He had a progressive, markedly productive cough over the last few weeks prior to presentation. He had been treated for pneumonia with multiple courses of antibiotics over the last two months without any significant improvement. His blood work was significant for a leukocytosis with neutrophilia and an elevated D-dimer. He underwent a CTA of the …

Mycobacterium Avium Complex Presenting as a Lung Mass, Broncho-pleural Fistula and Empyema in an Immunocompetent Patient-A Case Report and Review of Literature

Mycobacterium avium complex (MAC) is a non-tuberculous mycobacteria (NTM) that causes subacute or chronic nodular bronchiectasis, cavitary or fibro-cavitary pneumonia in patients with chronic structural lung pathology including emphysema, chronic bronchitis, and bronchiectasis. It is also known to cause pulmonary and extrapulmonary infections in patients with impaired cell mediated immunity such as transplant recipients, (Acquired Immune Deficiency Syndrome) AIDS where it can cause disseminated infections. Empyema from MAC has been reported in immunocompromised patients and is a rare phenomenon. Here we report a patient who presented with chronic left pleural effusion and a left lower lobe lung mass that went undiagnosed for 2 years, despite extensive work-up. Later in his course, he presented with a large effusion complicated by a bronchopleural fistula and was diagnosed as MAC empyema. To our knowledge, this is the first case of MAC empyema, that presented as a chronic lung mass, complicated by a bronchopleural fistula. In this article, we present the clinical, laboratory, and radiological features, with emphasis on a combined medical and surgical approach in the management of MAC empyema. We also provide a brief overview of cases of MAC associated pleurisy and empyema that have been reported in literature.

A Rare Presentation of Cutaneous Metastases in Advanced Lung Adenocarcinoma

Patients with lung cancer may present with respiratory and systemic symptoms. However, cutaneous metastases from primary lung cancer is a rare phenomenon, especially in women, that signifies a poor prognosis. This paper reported a case regarding a 71-year-old woman who was first presented with a cutaneous nodule over the year. Her condition was further progressed to multiple lesions on the back and abdomen, dyspnoea, haemoptysis and weight loss. The results of the skin lesion biopsy exhibited metastatic lung adenocarcinoma with positive immunohistochemistry for thyroid transcription factor 1 (TTF1) and cytokeratin 7 (CK7). Computed tomography (CT) scan was conducted, and it revealed a left upper lobe lung mass. The patient was subsequently scheduled for additional management, but she had succumbed to complications of pulmonary embolism before the necessary interventions could be provided. In this particular case presentation, the biopsy of cutaneous lesions obtained had revealed an undiagnosed primary malignancy.

A RARE CASE OF DIAGNOSTICALLY CHALLENGING LUNG TUMOR

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Inflammatory myofibroblastic tumor (IMT) and pulmonary sarcomatoid carcinoma (PSC) are rare tumors and account for less than 1% of primary lung malignancies [1]. We present a diagnostically challenging case of lung neoplasm that was initially diagnosed as IMT but was later found to be PSC. CASE PRESENTATION: A 56-year-old Hispanic male with diabetes mellitus type 2, hypertension, and smoking history was found to have a left lung mass while undergoing treatment for STEMI. He reported diminished appetite, 12 lbs. weight loss, and cough with pink sputum over the last 4-5 months. Lab results showed prominent leukocytosis and normocytic anemia. Treatment with wide spectrum antibiotics was stated for obstructive pneumonia. CT of the chest revealed a necrotic appearing 9x8 cm mass in the left upper lobe of the lung extending to the left hilum with invasion to the left superior pulmonary vein and extension into the left atrium (Pictures 1,2). CT guided lung and mediastinum biopsy initially favored bronchoalveolar carcinoma, but further analysis indicated IMT negative for ALK and ROS markers. Hence, patient was referred for tumor resection but another CT guided lung biopsy at the referred hospital was inconclusive for IMT. A surgical lung biopsy then revealed PSC positive for CD56 marker (Image 3). Neoadjuvant chemotherapy with cisplatin and etoposide, and radiation were started. Debulking surgery was planned later. Six months later patient experienced complex partial seizures, and a 1 cm lesion in the right anterolateral frontal lobe was discovered on MRI (Image 4). Mass resection confirmed it as metastatic PSC. Numerous bilateral cerebral hemispheric hemorrhagic metastases were diagnosed in the following three months. Patient expired 10 months from the date of PSC diagnosis. DISCUSSION: While IMT is a benign mesenchymal neoplasm mixed with inflammatory cells, PSC is carcinoma with at least 10% mesenchymal sarcoma-like elements. Treatment for both is surgical resection, but while recurrence after surgery is rare for IMT (2%), PSC has a poor prognosis with a 5-year survival rate of 20%-36%, compared to 91% for IMT [1,4]. It is very difficult to diagnose PSC and IMT on small biopsy specimens because it may not contain the mesenchymal/heterologous component, resulting in under-detection of PSC [2,4], which was also the reason for multiple biopsies in our patient. Also, spindle cell subtype of PSC may have prominent inflammatory stroma that could be mistaken for IMT [3,5]. CONCLUSIONS: An adequate specimen through surgical resection is critical for diagnosis IMT and PSC due to the heterogeneous composition of the tumors. Inadequate biopsy specimen may lead to misdiagnosis and treatment delay. Reference #1: Weissferdt A. Pulmonary Sarcomatoid Carcinomas: A Review. Adv Anat Pathol. 2018;25(5):304–313. Reference #2: Borczuk AC. Uncommon Types of Lung Carcinoma With Mixed Histology: Sarcomatoid Carcinoma, Adenosquamous Carcinoma, and Mucoepidermoid Carcinoma. Arch Pathol Lab Med. 2018;142(8):914-921. Reference #3: Travis WD. Sarcomatoid neoplasms of the lung and pleura. Arch Pathol Lab Med. 2010 Nov;134(11):1645-58. Sagar AES, Jimenez CA, Shannon VR. Clinical and Histopathologic Correlates and Management Strategies for Inflammatory Myofibroblastic tumor of the lung. A case series and review of the literature. Med Oncol. 2018;35(7):102. Surabhi VR, Chua S, Patel RP, Takahashi N, Lalwani N, Prasad SR. Inflammatory Myofibroblastic Tumors: Current Update. Radiol Clin North Am. 2016;54(3):553-63. DISCLOSURES: No relevant relationships by Olga Grigorieva Olson, source=Web Response No relevant relationships by Faizan Malik, source=Web Response No relevant relationships by dushyant pawar, source=Web Response

AN UNUSUAL CASE OF PULMONARY CAVITARY LESIONS IN AN IMMUNOSUPPRESSED PATIENT

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The differential diagnosis of pulmonary cavitary lesions is broad. They can be categorized in to infectious and non-infectious diseases, including neoplasms. Among malignancies, squamous cell carcinoma is a common cause of lung cavitation (1). Herein, we report a rare case of primary pulmonary diffuse large B-cell lymphoma (DLBCL) in a patient with rheumatoid arthritis that presented with multiple cavitary lesions and hypercalcemia. CASE PRESENTATION: 83-year-old male presented with hemoptysis, dyspnea, confusion, and constipation for several weeks. His past medical history was significant for tobacco abuse and interstitial lung disease from rheumatoid arthritis (RA) treated with methotrexate. CT chest showed bilateral cavitary lung lesions, left-pneumothorax and pneumomediastinum, needing chest-tube placement. Pulmonary function test showed a mild restrictive defect with a severe reduction in diffusion capacity. Labs showed hypercalcemia of 13.7 mg/dl, suppressed parathyroid hormone (PTH), elevated PTH-related peptide (PTHrp), and 1-25(OH) 2 Vitamin-D level. Quantiferon gold, sputum acid-fast bacilli and cultures were negative. Blood cultures (1/4 bottles) grew Actinomyces viscosus that was treated with 6-weeks of piperacillin-tazobactam. Bronchoscopy with lavage was unrevealing; however, due to a suspicion for malignancy with elevated PTHrp level, a CT-guided biopsy of left lower lobe lung mass was performed that confirmed a diagnosis of DLBCL, non-germinal center B-cell type. DISCUSSION: Pulmonary lymphoma is very rare and presents with nonspecific pulmonary symptoms (2). The pathogenesis of primary pulmonary DLBCL remains elusive. Patients with autoimmune disorders and recurrent bacterial infections are at a higher risk for developing DLBCL. Chest imaging may show nodular lesions, consolidation or interstitial /mixed alveolar infiltrates (2). DLBCL presenting with multiple cavitary lesions, is rarely reported. In our patient hypercalcemia was mediated by elevation of both PTHrp and 1-25(OH)2 Vitamin-D, which is unusual. Most primary pulmonary lymphomas (PPL) are low-grade mucosa-associated lymphoid tissue (MALT)-type, compared to more aggressive pulmonary diffuse large B-cell lymphoma (DLBCL), which is very uncommon (3). Most likely, our patient's autoimmune disorder (RA) and chronic methotrexate use contributed in the development of his DLBCL. CONCLUSIONS: We report a rare case of primary pulmonary DLBCL that manifested with multiple cavitary lesions and hypercalcemia. DLBCL must be considered in the differential diagnosis of cavitary lung lesions particularly in immunosuppressed patients. Reference #1: Chaudhuri MR. Primary pulmonary cavitating carcinomas. Thorax. 1973;28:354-366 Reference #2: Fujita N, Ando M, Goto A, Sakata M, Ogata M, Usagawa Y, et al. Diffuse large B-Cell lymphoma arising from the lesion of chronic lobar atelectasis. Tohoku J Exp Med. 2020;250(2):129–35. Reference #3: Brown S, Horton J, Rosario D, Dorsey DA, Hetz S, King CS. High-grade primary pulmonary B cell lymphoma presenting as a Necrotic mass. Respir Care. 2011 Jun 1;56(6):871–3. DISCLOSURES: No relevant relationships by Haytham Adada, source=Web Response no disclosure on file for Mahmoud Amarna; No relevant relationships by Pavan Annamaraju, source=Web Response No relevant relationships by Camelia Chirculescu, source=Web Response No relevant relationships by Nino Nemsadze, source=Web Response No relevant relationships by Sana Yakoob, source=Web Response

ATRIAL FLUTTERS AS AN INITIAL PRESENTATION OF LUNG CANCER CAUSING MALIGNANT PERICARDIAL EFFUSION

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pericardial effusion is a devastating cardiac condition, resulting from various etiology. Cardiac arrhythmia is an uncommon presentation of pericardial effusion, while atrial fibrillation is the most common arrhythmia found in this condition. Atrial flutter, as an initial presentation of malignant pericardial effusion, has not yet been reported. We presented a case of an elderly man with atrial flutter from malignant cardiac effusion from a newly diagnosed lung cancer. CASE PRESENTATION: An 81-year-old man, with chronic obstructive pulmonary disease and hypertension, presented with acute onset shortness of breath. He used albuterol MDI but his symptoms were not improved. On evaluation, he had heart rate 179 beats per minute (bpm), blood pressure 172/118 mmHg without pulsus paradoxus, and respiratory rate of 26. He had good mental status and did not have jugular venous distention. Lungs exam was normal. Heart exam revealed tachycardia without murmur. His blood test was unremarkable. His ECG showed atrial flutter with rapid ventricular rate and 2:1 block. He received intravenous Diltiazem 20 mg and his heart rate decreased to 90. Point of care ultrasound (POCUS) showed large pericardial effusion without tamponade physiology and no signs of pulmonary edema. Computed tomography (CT) chest illustrated large pericardial effusion with new left upper lung mass. Cytology from pericardial effusion revealed squamous cell carcinoma. He was diagnosed as malignant pericardial effusion from advance stage squamous cell lung cancer. His hospital course was complicated with septic shock and eventually death. DISCUSSION: Lung cancer is the most common metastasis cancer to the heart and pericardium because of the proximity of the tumor to the heart [1]. There are several possible explanations of malignant pericardial effusion pathogenesis. First, it can be a result of cardiac lymphatic drainage occlusion by the tumor [2]. Second, local or hematogenous spread of the tumor lead to venous blood flow obstruction and an increase in hydrostatic pressure causing pericardial effusion [3]. Third, neoplastic pericardial involvement stimulates an overproduction of pericardial fluid [3]. Pericardial effusion in cancer patients may arise from complications of treatment, including chemotherapy and radiation, and hypoalbuminemia from malignancy-related cachexia. Cytology analysis of pericardial fluid and pericardial biopsy should be performed to confirm the diagnosis. Management includes pericardiocentesis, pericardial window, pericardial sclerosis, and radiation therapy. CONCLUSIONS: We presented a rare case of atrial flutter secondary to malignant pericardial effusion from newly diagnosis of advanced-stage lung cancer. Clinicians should have pericardial effusion as a differential diagnosis of patients with atrial flutter as this is a catastrophic condition, requiring urgent management. Reference #1: DeCamp MM, et al. Malignant effusive disease of the pleura and pericardium. Chest. 1997;112(4 Suppl):2915-2955. Reference #2: Chiles C, et al. Metastatic involvement of the heart and pericardium: CT and MR imaging. Radiographics. 2011;21(2):438-449. Reference #3: Scheinin SA, Sosa-Herrera J. Cardiac tamponade resembling an acute myocardial infarction as the initial manifestation of metastatic pericardial adenocarcinoma. Methodist Debakey Cardiovasc J. 2014; 10:124–128. DISCLOSURES: No relevant relationships by Nehad Shabarek, source=Web Response No relevant relationships by Kulachanya Suwanwongse, source=Web Response

A CHALLENGING CASE OF DIFFUSE ALVEOLAR HEMORRHAGE

SESSION TITLE: Fellows Pulmonary Manifestations of Systemic Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is commonly seen in the intensive care unit and has a variety of causes including vasculitis. Most commonly, a vasculitis is linked to either antineutrophil cytoplasmic antibodies (ANCA) or an anti-glomerular basement membrane antibody. In rare cases, it manifests in a pauci-immune state. CASE PRESENTATION: 52-year-old male with a past medical history of biopsy confirmed IgA nephropathy, who presented with fatigue and hemoptysis. The patient was noted to be from Cambodia and recently visited his home country. During his hospitalization, patient was noted be hypoxic requiring oxygen supplementation. A CT chest was obtained revealing a left upper lung mass concerning for infection verses malignancy (Figure 1). CT guided biopsy by IR was performed, however, while waiting for the studies to return, patient decompensated and required ICU level of care secondary to massive hemoptysis. He was intubated and bronchoscopy revealed serial aliquots consistent with DAH (Figure 2). Transthoracic echocardiogram revealed severe mitral stenosis secondary to calcifications. Cardiology consultation recommended mitral valve replacement however, patient was in critical condition at this time. The patient’s CT guided left upper lobe biopsy returned positive for alveolar hemorrhage. There was no bacterial or viral infection noted. Additionally, vasculitis workup including ANA, ANCA, MPO, PR3, hepatitis panel, and HIV were all negative. Thoracic surgery was consulted and VATS of the left upper and right upper and lower lobe biopsy was performed. During his hospital course, the patient developed progressive AKI requiring hemodialysis. Open lung biopsies returned positive for focal active capillaritis. There was no specific staining noted for IgA, IgM, or IgG. The patient was started on pulse dose steroids and received seven days of plasma exchange therapy. His clinical status improved and he was discharged from the ICU. DISCUSSION: DAH can be caused from a variety of diseases. Interestingly, our patient had a history of IgA nephropathy and severe mitral stenosis, both of which can cause DAH, however, at the end of his workup and hospital course his diagnosis was pauci-immune vasculitis. This is a rare systemic disease that can cause pulmonary renal syndrome. Pulmonary renal syndrome is most commonly associated with ANCA associated vasculitis, however, in 10% this may be absent. Diagnosis is confirmed by open lung biopsy and immunosuppression is the mainstay of treatment. Patients with a negative ANCA were shown to have a worse renal outcome compared with those that had a positive ANCA, but similar survival rates. CONCLUSIONS: A careful evaluation of DAH must be performed even when the etiology is obvious. The gold standard for a definitive diagnosis is through open lung biopsy and should be performed if the patient can tolerate it. Reference #1: Saladi L, Shaikh D, Saad M, et al. Pulmonary renal syndrome: A case report of diffuse alveolar hemorrhage in association with ANCA negative pauci-immune glomerulonephritis. Medicine (Baltimore). 2018;97(23):e10954. doi:10.1097/MD.0000000000010954 DISCLOSURES: No relevant relationships by Alireza Nathani, source=Web Response No relevant relationships by Sean OConnor, source=Web Response No relevant relationships by Heath White, source=Web Response

PAINFUL FINGERS AND TOES REVEAL A CASE OF NON-SMALL CELL LUNG CANCER

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: As a paraneoplastic syndrome, the association of hypercoagulability states (HCS) in cancer patients has been well established and can have an adverse effect on quality of life and survival. (1) The findings of HCS such as venous thromboembolism (VTE), embolic strokes, arterial thromboembolic events (ATE) and nonbacterial thrombotic endocarditis (NBTE) should make the clinician suspicious of an underlying malignancy. The deposition of thrombi on previously undamaged heart valves in the absence of bacterial infection is known as NBTE and is often discovered at time of autopsy or in late-stage cancer. (2) Here we describe a case of lung adenocarcinoma, who presented with multiple HCS at the time of diagnosis, including painful digits caused by ATE propagated by NBTE. CASE PRESENTATION: A 56 year old female with a 30 pack year smoking history presented with a myriad of complaints including dyspnea, fatigue, nausea, hematemesis and headache for one month. Most bothersome were her painful, blue-discolored fingers and toes (Fig. 1) that were cool to touch with palpable pulses. CXR identified a large left upper lobe lung mass and follow-up CT (Fig. 2) identified that the mass involved the pulmonary hilum with bilateral mediastinal lymphadenopathy. A bronchoalveolar lavage confirmed lung adenocarcinoma on cytology. MRI brain was performed which identified multiple infarcts of an embolic source. Lower extremity doppler studies revealed bilateral arterial and venous occlusions. She was treated with apixaban after EGD identified no source of bleed. Transesophageal echocardiography identified severe mitral regurgitation (MR) (Fig. 3) with small vegetations on both mitral valve leaflets consistent with NBTE—the source of her disseminated embolisms. She received mediastinal radiation and a chemotherapy regimen of carboplatin, pemetrexed, and pembrolizumab. For congestive heart failure (CHF) due to severe MR, she was discharged on metoprolol and furosemide. She returned one month later to the ICU in cardiogenic shock due to worsening CHF. She passed away one week later under hospice care. DISCUSSION: Since HCS have first been recognized in gastric cancer by Trousseau in 1865, multiple cancers, including lung cancer, have been associated with HCS. (3) Recommendations are that high-risk cancer patients (4) be offered prophylactic anticoagulation should no significant bleeding risk exist. (5) In general, NBTE and ATE were often reported after cancer diagnosis (6,7,8,9) and acute heart failure caused by NBTE is a rare clinical event reported only in a few case reports. (6,7) Our patient exemplifies the extensive findings of HCS as a manifestation of lung adenocarcinoma. CONCLUSIONS: This case shows a unique clinical presentation of NBTE, VTE, ATE, cerebral embolic infarction, and heart failure at the time of diagnosis of lung adenocarcinoma. Such HCS should be recognized as herald signs in underlying cancer. Reference #1: 1.Connolly GC, Francis CW. Cancer-associated thrombosis. Hematology Am Soc Hematol Educ Program. 2013;2013:684-691. doi:10.1182/asheducation-2013.1.684 2.el-Shami K, Griffiths E, Streiff M. Nonbacterial thrombotic endocarditis in cancer patients: pathogenesis, diagnosis, and treatment. Oncologist. 2007;12(5):518-523. doi:10.1634/theoncologist.12-5-518 3.Connolly GC, Dalal M, Lin J, Khorana AA. Incidence and predictors of venous thromboembolism (VTE) among ambulatory patients with lung cancer. Lung Cancer. 2012;78(3):253-258. doi:10.1016/j.lungcan.2012.09.007 Reference #2: 4.Khorana AA, Kuderer NM, Culakova E, Lyman GH, Francis CW. Development and validation of a predictive model for chemotherapy-associated thrombosis. Blood. 2008;111(10):4902-4907. doi:10.1182/blood-2007-10-116327 5.Key NS, Khorana AA, Kuderer NM, Bohlke K, Lee AYY, Arcelus JI, Wong SL, Balaban EP, Flowers CR, Francis CW, Gates LE, Kakkar AK, Levine MN, Liebman HA, Tempero MA, Lyman GH, Falanga A. Venous Thromboembolism Prophylaxis and Treatment in Patients With Cancer: ASCO Clinical Practice Guideline Update. J Clin Oncol. 2020 Feb 10;38(5):496-520. doi: 10.1200/JCO.19.01461. Epub 2019 Aug 5. PubMed PMID: 31381464. 6.Lee JM, Lim JH, Kim JS, Park JS, Memon A, Lee SK, Nam HS, Cho JH, Kwak SM, Lee HL, Kim HJ, Hong GJ, Ryu JS. Multiple hypercoagulability disorders at presentation of non-small-cell lung cancer. Tuberc Respir Dis (Seoul). 2014 Jul;77(1):34-7. doi: 10.4046/trd.2014.77.1.34. Epub 2014 Jul 31. PubMed PMID: 25114702; PubMed Central PMCID: PMC4127411. Reference #3: 7.Taniyama D, Yamamoto R, Kawasaki M, Kamata H, Miyamoto K, Mashimo S, et al. Nonbacterial thrombotic endocarditis leading to acute heart failure due to aortic stenosis in a patient with lung cancer. Intern Med 2013;52:1617-20. 8.Lopez JA, Ross RS, Fishbein MC, Siegel RJ. Nonbacterial thrombotic endocarditis: a review. Am Heart J. 1987;113(3):773-784. doi:10.1016/0002-8703(87)90719-8 9.Navi BB, Reiner AS, Kamel H, et al. Risk of Arterial Thromboembolism in Patients With Cancer. J Am Coll Cardiol. 2017;70(8):926-938. doi:10.1016/j.jacc.2017.06.047 DISCLOSURES: No relevant relationships by Milica Antic, source=Web Response No relevant relationships by Jeffrey Bloomer, source=Web Response No relevant relationships by Sara Ruiz Aguinaga, source=Web Response

Real Time F-18 FDG PET-CT-Guided Metabolic Biopsy Targeting Differential FDG Avidity in a Pulmonary Blastoma.

Pulmonary blastoma (PB) is a rare thoracic malignancy and preoperative diagnosis is challenging. A young man presented with dyspnea and chest pain for 3-4months and chest-computed tomography (CT) revealed large mass in the left lung upper lobe and pleural effusion. Repeated CT-guided fine-needle aspiration cytology from the lesion and pleural fluid aspiration was negative for malignancy. F-18-fluorodeoxyglucose positron emission tomography-computed tomography (FDG PET-CT) revealed heterogeneous tracer avidity in left lung mass with areas of necrosis. Real-time PET-CT-guided biopsy from metabolically active component of the lesion revealed biphasic PB on histopathology.

SAT-148 Ectopic ACTH Secretion Has Varied Presentation and Requires Individualized Treatment - One Size Does Not Fit All

Ectopic ACTH secretion (EAS) presents in myriad ways. We present five cases of EAS to highlight similarities and differences in presentation and treatment. The first woman with known metastatic lung neuroendocrine tumour (NET) for two years presented with facial fullness, proximal weakness, worsening hypertension and hypokalaemia. Random cortisol of 2742nmol/L (99.39mcg/dL), with adrenocorticotrophic hormone (ACTH) of 201ng/L (5-50), was in keeping with EAS. She received medical treatment followed by bilateral adrenalectomy with EAS resolution and development of adrenal insufficiency. She is doing well. The second woman with proximal weakness was evaluated by neurologists. All neurological tests were normal but facial fullness and easy bruising was noted. Random cortisol was 875nmol/L (31.71mcg/dL) and ACTH was 90 ng/L. Imaging revealed metastatic liver disease with unknown primary and biopsy confirmed NET. Cortisol rose despite medical treatment and she died within fifteen months. The third woman with significant smoking history presented with haemoptysis and breathlessness. A right lung mass was suspected on chest X-ray and confirmed with CT. Endobronchial ultrasound-guided biopsy revealed small cell lung cancer (SCLC). She developed generalised weakness and severe hypokalaemia. Random cortisol of 1645nmol/L (59.63mcg/dL) with ACTH of 282ng/L suggested EAS. Despite medical treatment, she died within two weeks. The fourth woman presented with confusion, hypertension and severe hypokalaemia. Morning cortisol of 8557nmol/L (310.19mcg/dL) and random ACTH of 73ng/L were suggestive of EAS. CT demonstrated left lung mass with widespread metastases. She deteriorated and died within 2 weeks. Our only man had incidentally discovered metastatic liver lesions on ultrasound. Further imaging revealed prostatic mass and biopsy showed small cell neuroendocrine cancer. He presented with severe hypokalaemia. Random cortisol was 1065nmol/L (38.61mcg/dL) and ACTH was 188ng/L. He was commenced on medical treatment but declined rapidly and died.All our patients had profound hypokalaemia and metastatic disease at presentation. Many patients do not exhibit classical cushingoid features as EAS tends to develop acutely and underlying malignancy drives weight loss. A high index of suspicion is required to make a diagnosis. EAS should be considered in patients with proximal myopathy, pigmentation, resistant or severe hypokalaemia or hypertension and known or suspected malignancy. Early and quick control of cortisol excess is essential to minimise cardiometabolic abnormalities, severe infections and thromboembolic complications. Prognosis depends upon age, frailty, comorbidity, nature of neoplasm and extent of hypercortisolaemia. Adrenolytics with or without bilateral adrenalectomy, reduction in tumour burden and management of complications are the mainstay of treatment.

Hydatid cyst of the lung in pregnancy: A rare case presentation

Hydatid cyst of the lung has been seen in 30% of the cases of hydatidosis in some series. In our case presentation, a 29-year old female, gravida 1, referred to the hospital with acute and severe pain in the lower left hemithorax, while she was in the 26th week of pregnancy. The pain was pleuritic and was accompanied with tachypnea. The patient was hospitalized with suspected pulmonary embolism. The chest X-ray and computed tomography showed a cystic mass in the lower left lung. After a diagnosis of hydatid cyst, the patient underwent surgery and all of her symptoms were resolved. As Albendazole is a medication from pregnancy category C, and since in our case, the patient underwent surgery and all of her symptoms were resolved, we can conclude that surgery is a safe and appropriate treatment for Hydatid cyst of the lung in pregnancy.

METASTATIC CAVITARY ADENOCARCINOMA OF THE LUNG IN A PATIENT WITH RECENT AGGRESSIVE SQUAMOUS CELL CARCINOMA OF THE CHEST WALL

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Simultaneous existence of two histologically different primary malignancies, although rare, has been reported in literature1. This represents a diagnostic dilemma especially when the first detected primary malignancy is aggressive, therefore, the second primary is often deemed to be a metastatic lesion, until proven otherwise on biopsy. We present a case of a 62 year old male, with a recent aggressive squamous cell carcinoma (SCC) of the chest wall, who developed metastatic cavitary adenocarcinoma of the lungs. CASE PRESENTATION: A 62-year old gentleman, with past medical history significant for basal cell carcinoma of the nose and a recent aggressive SCC of the chest wall, status post Mohs surgery, was referred to the outpatient pulmonology clinic after a CT scan of the chest showed persistent dense consolidation of the left upper lobe, multiple bilateral lung nodules with central necrosis and cavitation, and left sided hilar and mediastinal lymphadenopathy. He presented with low-grade fever and a productive cough, unresponsive to antibiotics, for the past three weeks prompting the CT scan of the chest. Diagnostic work-up, for infection (including fungal studies), vasculitis or any other autoimmune disorder, was started and urgent bronchoscopy was arranged. PET/CT scan showed a hyper-metabolic left upper lung mass, multiple hypermetabolic cavitary lung lesions. Bronchoscopy with endobronchial ultrasound revealed a reversible external compression of the right middle lobe bronchus with mediastinal lymphadenopathy. Bronchoalveolar lavage from the left upper lobe showed atypical cells, suspicious for malignancy while negative for fungal organisms. Fine needle aspiration of lymph nodes, station 7 and 4L, revealed non-small cell carcinoma with tumor cells being positive for CK-7 and TTF-1 and negative for CK20, CDX-2 and NKX3.1. With the recent aggressive SCC history and multiple cavitary lung lesions, biopsy of one of the cavitary lesions was recommended by the tumor board, to determine if they were SCC vs adenocarcinoma. Results of the biopsy were consistent with an invasive lung adenocarcinoma. DISCUSSION: Cavitary lesions shown on chest imaging can have several etiologies. Although various radiological features of these cavitations, including wall thickness, have been studied to differentiate benign from non-benign etiologies2, the final diagnosis in many instances is made on serological investigations or biopsy. 22% of primary lung cancers can cause cavitation with squamous cell carcinoma being the most common type of lung cancer associated with cavitary lesions followed by adenocarcinoma and large cell carcinoma3. CONCLUSIONS: Our case emphasizes that cavitary lesions on imaging, in patients with a prior history of malignancy, should prompt investigation for possible malignancy. Early biopsy, in such cases, becomes crucial for a timely and accurate diagnosis, and appropriate management. Reference #1: Jena A, Patnayak R, Lakshmi AY, Manilal B, Reddy MK. Multiple primary cancers: An enigma. South Asian J Cancer. 2016;5(1):29-32. Reference #2: Parkar AP, Kandiah P. Differential Diagnosis of Cavitary Lung Lesions. Journal of the Belgian Society of Radiology. 2016;100(1):100. DOI: http://doi.org/10.5334/jbr-btr.1202. Reference #3: Gill, R. R., Matsusoka, S. & Hatabu, H. Cavities in the lung in oncology patients: imaging overview and differential diagnoses. Applied Radiology 39, 10 (2010). DISCLOSURES: No relevant relationships by Huthayfa Ateeli, source=Web Response No relevant relationships by Mahum Shahid, source=Web Response

LEFT ATRIAL EXTENSION OF PRIMARY LUNG SARCOMA VIA THE PULMONARY VEIN

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Metastatic neoplasms to the heart are much more common than primary cardiac tumors.[1, 2] Primary lung tumors often invade the heart locally, spread to the heart via the blood, lymphatics, or both. However, extension of primary lung sarcoma to the left heart chamber via the pulmonary vein is a rare occurrence and has only been reported in limited cases.[1, 3-9] Here, we present a case of a primary lung sarcoma extending into the left atrium via the left superior pulmonary vein. CASE PRESENTATION: A 78-year-old F with a PMH of breast cancer s/p lumpectomy, radiation, and chemotherapy, hyperlipidemia, hypothyroidism, and left bundle branch block who presented to the ER for non-exertional chest pain and dry cough for six weeks. She also reported 9 lb unexplained weight loss in the last three months. Initial vital signs and physical exam was unremarkable. Lab workup revealed mild leukocytosis. EKG was non-ischemic and revealed LBBB, unchanged from prior. Chest x-ray showed a mass in left upper lobe. CT Chest revealed a 9.5cm x 8.5 cm x 7.2 cm left upper lobe mass with extension into the left atrium via left superior pulmonary vein. (Figure 1). TTE confirmed the left atrial tumor invasion. PET scan revealed large hypermetabolic left upper lobe lung mass with extension into the left atrium and anterior mediastinum (Figure 2). CT guided biopsy of the mass was performed, and pathology showed differentiated neoplasm. Immunohistochemistry analysis was suggestive of sarcoma. The patient remained afebrile and hemodynamically stable throughout the hospitalization, was treated with a short course of levofloxacin, and was discharged with outpatient Oncology follow up. DISCUSSION: Primary lung sarcomas are very rare, accounting for only 0.013 to 0.4% of lung tumors.[10] Extension of lung tumors into the left atrium via pulmonary veins occur most frequently in NSCLC; however, it is extremely rare in primary lung sarcomas. The clinical features of cardiac metastasis are variable and depend on the size of the tumor, location of the tumor, and the invasion of adjacent tissues. Patient may present with chest pain, shortness of breath, cough, hemoptysis, weight loss, and those of heart failure such as dyspnea on exertion and peripheral edema. These symptoms are often a result of the direct obstruction of cardiac or valve function, blockage of coronary blood flow, dysfunction of cardiac electrical system, and/or pericardial effusion.[11] Management of patients with cardiac metastasis should include a thorough assessment of all surgical options as these patients generally have poor clinical outcomes and high postoperative mortality.[12, 13] Usually, the treatment of choice is complete resection in combination with chemotherapy or radiotherapy.[14] CONCLUSIONS: Cardiac extension of lung sarcoma is possible via pulmonary vein and familiarity with it is of paramount importance to ensure proper management. Reference #1: Dogan, A., et al., Metastatic atrial sarcoma extending from the lung into the left atrium via a pulmonary vein. Exp Clin Cardiol, 2012. 17(2): p. 77-8. Reference #2: Paraskevaidis, I.A., et al., Cardiac tumors. ISRN Oncol, 2011. 2011: p. 208929. Reference #3: Shuman, R.L., Primary pulmonary sarcoma with left atrial extension via left superior pulmonary vein. En bloc resection and radical pneumonectomy on cardiopulmonary bypass. J Thorac Cardiovasc Surg, 1984. 88(2): p. 189-92. DISCLOSURES: No relevant relationships by Krishna Akella, source=Web Response No relevant relationships by Kashif Hussain, source=Web Response No relevant relationships by Gunjan Joshi, source=Web Response No relevant relationships by Howard Sklarek, source=Web Response

A RARE MALIGNANCY

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Ewing's sarcoma is a malignant neoplasm which arises from the skeletal bones. It most commonly affects children and young adults with a female preponderance. Ewing’s sarcoma of the rib is a rare enity as long bones are usually affected . CASE PRESENTATION: A 24 year-old male presented with complaints of shortness of breath , cough and left chest pain for 1 month. He also had episodes of seizures since last 3 years. He had multiple soft cutaneous nodules and macular patches over chest , back and upper limbs. There was bulging of left anterior chest wall with shifting of trachea as well as apex beat to right. There was increased vocal fremitus as well dull percussion note on left. There were reduced breath sounds with increased vocal resonance on left. Routine blood investigations were within normal limits. Chest X -ray revealed a homogeneously white left hemithorax with shifting of mediastinum to the right. Pleural fluid cytology had features suggestive of small round cell tumor. CECT thorax revealed a large heterogeneous mass in the left hemithorax with shifting of mediastinum to right and lytic destruction of left 6 th rib. There was minimal left pleural effusion with nodular pleural deposits. USG guided trucut biopsy from the left lung mass revealed small cell neuroendocrine carcinoma. The tumour was CD 99, Synaptophysin, CD 56 , FLI-1 - positive and negative for CK, CK7, TTF-1 and chromogranin. Dermatology opinion favoured the skin nodules to be neurofibromatosis. So a final diagnosis of Ewing’s sarcoma left sixth rib with Neurofibromatosis and seizure disorder was made. The patient received Vincristine , Adriamycine and Cyclophosphamide (VAC),alternating with Ifosfamide and Etoposide as well as was planned for radiotherapy DISCUSSION: Ewing sarcoma is an uncommon disease, which usually arises from the skeletal bones. It constitutes approximately 10 % of all primary malignant bone tumours. Only 40 % of such cases are seen in flat bones like innominate, ribs, scapula and sterum #1.A characteristic chromosomal translocation, (11; 22) (q24; q12) can be detected in 90% of cases .Patients with Ewing's Sarcoma of the ribs present with breathlessness, weight loss and painful chest wall mass. #2 pleural effusion as in our case, is an unusual finding #3 . The tumour has propensity to spread inwards towards the thoracic cavity and thus,may manifest as an extra pleural mass.our case unique in a wayas it had several other associated finding like neurofibromatosis,seizure disorder as well as skin lesion although such association are not commonly reported CONCLUSIONS: This case showcases the significance of IHC an important tool in diagnosis of lung malignancies and lays stress on excluding extrathoracic involvement in all such cases. Reference #1: MirraJM. Bone tumors: clinical, radiologic, and pathologic correlations. Philadelphia: Lea&Febiger, 1989; 1087-1117. Reference #2: Gladish GW, Sabloff BM, Munden RF, Truong MT, Erasmus JJ, Chasen MH. Primary thoracic sarcomas. Radiographics 2002 May-Jun;22(3):621-637 Reference #3: Wolf G, Aigner RM, Schwarz T. Massive pleural effusion with dyspnea in a 17-year-old boy as the first sign of ewing sarcoma. J Pediatr Hematol Oncol 2002 Jun-Jul;24(5):420 DISCLOSURES: No relevant relationships by UMER AHMED SYED, source=Web Response

Pleural fluid secondary to pulmonary cryptococcal infection: a case report and review of the literature

BackgroundPulmonary Cryptococcosis (PC) is diagnosed with increasing incidence in recent years, but it does not commonly involve the pleural space. Here, we report a HIV-negative case with advanced stage IIIB non-small cell lung cancer (NSCLC) treated with radiation therapy presented with dyspnea, a new PET-positive lung mass and bilateral pleural effusion suspecting progressive cancer. However, the patient has been diagnosed as pulmonary cryptococcal infection and successfully treated with oral fluconazole therapy.Case presentationA 77-year-old male with advanced stage non-small cell lung cancer treated with combined chemo-radiation therapy who presented with progressive dyspnea, a new PET-positive left lower lobe lung mass and bilateral pleural effusions. Initial diagnostic thoracentesis and bronchoscopy yielded no cancer, but instead found yeast forms consistent with cryptococcal organisms in the transbronchial biopsies of the left lower lobe lung mass. Subsequent to this, the previously collected pleural fluid culture showed growth of Cryptococcus neoformans. The same sample of pleural effusion was tested and was found to be positive for crytococcal antigen (CrAg) by a lateral flow assay (LFA). The patient has been treated with oral fluconazole therapy resulting in gradual resolution of the nodular infiltrates.ConclusionPC should be considered in immunosuppressed cancer patients. Additionally, concomitant pleural involvement in pulmonary cryptococcal infections may occur. The incidence of false positive 18FDG-PET scans in granulomatous infections and the use of CrAg testing in pleural fluid to aid in diagnosis are reviewed.

Neonatal lung growth in congenital diaphragmatic hernia: evaluation of lung density and mass by pulmonary MRI.

Outcomes of infants with congenital diaphragmatic hernia (CDH) are primarily dependent on the severity of pulmonary hypoplasia. It is previously unknown whether postnatal lung growth in infants with CDH represents true parenchymal lung growth or merely an expansion in volume of the existing tissue. We hypothesized that lung volume growth in CDH infants will be accompanied by an increase in lung mass and that CDH infants will demonstrate accelerated catch-up growth of the more hypoplastic lung. We used fetal and post-CDH repair MRI of 12 infants to measure lung volume and density, which was used to calculate lung mass. The average increase in right lung mass was 1.1 ± 1.1 g/week (p = 0.003) and the average increase in left lung mass was 1.8 ± 0.7 g/week (p < 0.001). When the ratio of left-to-right lung mass of the prenatal MRI was compared to post-repair MRI, the ratio significantly increased in all infants with average prenatal and post-repair ratios of 0.30 and 0.73, respectively (p = 0.002). Lung growth in infants with CDH is indeed growth in lung mass (i.e. parenchyma), and the lungs demonstrate catch-up growth (i.e., increased rate of growth in the more hypoplastic ipsilateral lung).

Primary Pulmonary Synovial Sarcoma: Is it Worth All the Hard Work?

Synovial sarcoma (SS) is highly malignant tumor that occurs mainly in adolescents and young adults and is usually seen in the extremities. However, primary SS arising from the lung is extremely rare, accounting for 0.3% to 1.3%. Primary pulmonary SS (PPSS) is an extremely aggressive malignant tumor that can invade adjacent organs or give distant metastases. Besides clinical evaluation and imaging methods for definitive diagnosis, immunohistochemical examination is must. We report a case of elderly male with left lung mass lesion invading into the pericardium and left-sided pleural effusion with a history of smoking. Positron emission tomography (PET)–computerised tomography (CT)-guided trucut biopsy from lung mass lesion led to the diagnosis, and thoracoscopic pleural biopsy showed the pleural involvement with final diagnosis of PPSS (monophasic type). There are no guidelines for optimal treatment due to the rarity of such tumors. Current treatment includes resectional surgery and adjuvant chemotherapy and/or radiotherapy. But because of advanced age and poor performance status, our patient was not candidate for any treatment but palliation.

A RARE CASE OF ERDHEIM-CHESTER DISEASE MASQUERADING AS METASTATIC LUNG CANCER

SESSION TITLE: Lung Cancer 3 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Erdheim-Chester Disease (ECD) is a non-Langerhans histiocytosis characterized by xanthomatous infiltration by CD68 positive, CD1a and S100 negative foamy histiocytes causing multi-system involvement. It was first identified in 1930, however, there have only been approximately 500 reported cases. Concomitant pituitary involvement, multiple axial skeletal lesions, and lung involvement is suggestive of ECD. Diagnosis typically involves histopathological studies in the appropriate clinical and radiological context. Here we present a case of ECD diagnosed during investigation of diabetes insipidus (DI) and a lung mass. CASE PRESENTATION: A 63-year-old female with a history of hyperlipidemia presented to the Endocrinology clinic for evaluation of polydipsia which was later diagnosed as DI. Extensive serum evaluation for etiology was unremarkable. MRI brain showed thickened infundibulum with increased enhancement suggestive of an inflammatory or infiltrative process. As part of her routine health maintenance, she had CTA coronaries done which showed a 2.1 cm spiculated left lung mass. Further investigations with repeat chest CT, PET scan and a bone scan confirmed malignant appearing left lung lesion along with body-wide skeletal lesions involving bilateral femurs, tibias, and left humerus, concerning for metastatic lung cancer. She underwent biopsy of the lung mass followed by lobectomy. Pathology findings were consistent with adenocarcinoma of the lung with immunostaining positive for TTF-1 and napsin-A. Subsequently, the patient underwent open biopsy of the left humeral lesion, which showed extensive fibrosis, focal lymphoplasmacytic infiltration, and scattered histiocytes. Immunostaining was negative for S100 and CD1a and positive for CD68. Pituitary involvement, DI, the presence of multiple skeletal lesions and staining profile is highly suggestive of ECD. Peripheral blood cytometry was positive for BRAF-V600 mutation. We are awaiting tissue studies for mutational analysis prior to treatment initiation. DISCUSSION: Patients with ECD are usually males of age 40-70 years; our patient had atypical features with female gender and late age of onset. DI associated with pituitary stalk thickening represents the most common neurological symptom, along with long bone involvement. Given the rarity of the disease, there are no clear guidelines regarding treatment approach; consensus guidelines recommend a treatment tailored for organ predominance and clinical severity to help facilitate treatment of “high risk” groups. CONCLUSIONS: Currently, the 5-year survival is less than 70%. However, the discovery of activating mutations of BRAF in 54% of the ECD patients has led to a modified therapeutic approach. A recent study suggests Vemurafenib (BRAF inhibitor) has prolonged efficacy in patients with BRAF V-600 mutant ECD and warrants consideration as the new standard of care for these patients. Reference #1: Cives, M., Simone, V., et.al. (2015). Erdheim–Chester disease: A systematic review. Retrieved March 03, 2018, from https://doi.org/10.1016/j.critrevonc.2015.02.004 Reference #2: Diamond, E. L., Subbiah, V., et.al. (2017). Vemurafenib for BRAF V600-Mutant Erdheim-Chester Disease and Langerhans Cell Histiocytosis: Analysis of Data From the Histology-Independent, Phase 2, Open-label VE-BASKET Study. Retrieved March 03, 2018, from https://www.ncbi.nlm.nih.gov/pubmed/29188284 DISCLOSURES: No relevant relationships by Nayla Ahmed, source=Web Response No relevant relationships by Ayushi Chauhan, source=Web Response No relevant relationships by Prashant Grover, source=Web Response No relevant relationships by Joerg Rathmann, source=Web Response No relevant relationships by Parin Shah, source=Web Response No relevant relationships by Aniket Sharma, source=Web Response No relevant relationships by John Thayer, source=Web Response