Pulmonary Tumor Embolism Research Articles

Burned-Out Testicular Carcinoma Presenting as Inferior Vena Cava Tumor Thrombus With Pulmonary Tumor Embolism on FDG PET/CT: A Case Report.

"Burned-out" testicular tumor is a very rare clinical phenomenon, which refers to the presence of a metastatic germ cell tumor with no clinical findings in the testicle due to spontaneous regression of the primary testicular lesion. We present an unusual case of burned-out testicular embryonal germ cell carcinoma presenting as an extensive inferior vena cava tumor thrombus with malignant pulmonary embolism in which FDG PET/CT played a pivotal role in detecting the extent and significance of the disease.

Case of Pulmonary Tumor Embolism due to Oropharyngeal Carcinoma Diagnosed by a Transbronchial Lung Biopsy.

Pulmonary tumor embolisms (PTEs) are primarily caused by adenocarcinoma. However, only a few cases of oropharyngeal carcinoma have been reported. We herein report a 47-year-old man who presented with a fever, cough, and dyspnea 6 months after treatment for stage II oropharyngeal carcinoma. Chest computed tomography revealed centrilobular granular and nodular shadows and subpleural consolidation. A transbronchial lung biopsy revealed a mass of squamous tumor cells forming emboli in the small vessels, resulting in the diagnosis of PTE due to oropharyngeal carcinoma. Therefore, PTE should be considered for patients with a history of hypoxia.

Morte súbita causada por embolismo tumoral em um cão

ABSTRACT: Tumor embolization is a well-described cause of unexpected death in human oncologic patients; however, it is poorly explored in veterinary medicine. We report a case of pulmonary tumor embolization in a dog with sudden death. During necropsy, a neoplastic mass was observed replacing the left adrenal gland and forming an intravascular thrombus within the central adrenal vein. A large embolus occluded the left pulmonary artery. The adrenal mass was histologically confirmed as a pheochromocytoma, and the embolus was constituted of neoplastic cells. Multiple smaller neoplastic emboli were observed within the pulmonary artery branches. Tumor embolization should be considered as a possible cause of sudden death in dogs, particularly in oncologic patients.

Pulmonary tumor embolism secondary to urothelial carcinoma of urinary bladder: case report and literature review

BackgroundTumor embolism is the least well-described cause of pulmonary embolism, taking into account the non-specificity of radiographic and nuclear imaging results, the necessity of anatomopathological evidence and the frequency of deep venous thrombosis in the course of solid tumors, suggesting thus thromboembolism.Case presentationWe report a rare case of urothelial carcinoma of the urinary bladder associated with persistent pulmonary embolism despite being on different anticoagulation regimens, the patient was ultimately found to have tumor thrombus in the pulmonary trunk secondary to tumoral extension. We provide a literature review as well about the diagnosis, evaluation and prognosis and of this rare clinical entity.ConclusionsOur case highlights the importance of keeping this unusual etiology in mind, particularly when faced with pulmonary embolism occurring in the context of a solid tumor and the ineffectiveness of various anticoagulation protocols. Furthermore, it emphasizes the pivotal role of cytology in confirming diagnosis and guiding therapy.

Intravascular Tumor Extension and Pulmonary Tumor Embolism in Children With Solid Malignancies: Is There a Role for Inferior Vena Cava Filters?

Intravascular tumor extension is an uncommon complication of solid malignancies that, when present in the inferior vena cava (IVC), can result in fatal pulmonary tumor embolism. Currently, neoadjuvant chemotherapy and surgery are the mainstays of treatment; however, there are no consensus guidelines for management. We describe three cases of pediatric solid malignancies with associated IVC extension and pulmonary tumor embolism. We hypothesize that there is scope for IVC filter placement in such cases to mitigate the risk of fatal pulmonary tumor embolism.

A Case of Fulminant Right Heart Failure Owing to Tumoral Pulmonary Hypertension

Tumoral pulmonary hypertension is a rare cause of pulmonary hypertension. We report a patient who was thought to have idiopathic pulmonary arterial hypertension, but later developed fulminant right heart failure ultimately leading to death. Autopsy revealed substantial pulmonary tumor embolism burden originating from liver adenocarcinoma. (Level of Difficulty: Advanced.)

Pulmonary tumour embolism and lymphangitis carcinomatosa: a case report and review of the literature

BackgroundPulmonary tumour embolism and lymphangitis carcinomatosa are complications of malignancy that may mimic the clinical presentation of pulmonary embolism.Case presentationWe present the case of a 52-year-old male patient with acute-onset right ventricular strain and dyspnoea with elevated D-dimer and without signs of pulmonary embolism on computed tomography pulmonary angiogram (CTPA) and ventilation/perfusion scintigraphy. The patient died eleven days after initial presentation. The diagnosis of pulmonary tumour embolism and lymphangitis carcinomatosa due to carcinoma of unknown origin was made post-mortem by immunohistochemical examination.ConclusionPulmonary tumour embolism and lymphangitis carcinomaosa are complications of malignancy and potential causes of acute right ventricular strain. Radiological signs are unspecific and the clinical course usually fatal. These differential diagnoses should be considered in patients with acute right ventricular strain, dyspnoea and positive D-dimer if there are no signs of pulmonary embolism on CTPA.

Successful resection of invasive thymoma directly invading the superior vena cava and right atrium with a pulmonary artery tumor embolus

Successful resection of invasive thymoma directly invading the superior vena cava and right atrium with a pulmonary artery tumor embolus

Pulmonary Tumor Embolism and Pulmonary Tumor Thrombotic Microangiopathy Causing Rapidly Progressive Respiratory Failure: A Case Series

Pulmonary tumor embolism (PTE) and pulmonary tumor thrombotic microangiopathy (PTTM) are rare etiologies for rapidly progressive dyspnea in the setting of undiagnosed metastatic cancer. They occur most frequently in association with adenocarcinomas, with PTE being most frequently associated with hepatocellular carcinoma and PTTM being most commonly reported with gastric adenocarcinoma. Pulmonary tumor embolism and PTTM appear to be a disease spectrum where PTTM represents an advanced form of PTE. Pulmonary tumor embolism and PTTM are mostly identified postmortem during autopsy as the antemortem diagnosis remains a clinical challenge due to the rapidly progressive nature of these rare diseases. We report 2 cases of rapidly progressive respiratory failure leading to death, due to tumoral pulmonary hypertension resulting from PTE and PTTM, diagnosed postmortem. Both of the patients were middle-aged females, nonsmokers, and had a gastrointestinal source of their primary malignancy.

P1‐32: A case report of a fatal pulmonary tumour emboli

P1‐32: A case report of a fatal pulmonary tumour emboli

Pulmonary tumor embolism: A retrospective study over a 30-year period

BackgroundPulmonary tumor embolism (PTE) is difficult to detect before death, and it is unclear whether the discrepancy between antemortem clinical and postmortem diagnosis improves with the advance of the diagnostic technologies. In this study we determined the incidence of PTE and analyzed the discrepancy between antemortem clinical and postmortem diagnosis.MethodsWe performed a retrospective autopsy study on patients with the history of malignant solid tumors from 1990 to 2020 and reviewed all the slides of the patients with PTE. We also analyzed the discrepancies between antemortem clinical and postmortem diagnosis in 1999, 2009 and 2019 by using the Goldman criteria. Goldman category major 1 refers to cases in which an autopsy diagnosis was the direct cause of death and was not recognized clinically, but if it had been recognized, it may have changed treatment or prolonged survival.ResultsWe found 20 (3%) cases with PTE out of the 658 autopsy cases with solid malignancies. Out of these 20 cases, urothelial carcinoma (30%, 6/20) and invasive ductal carcinoma of the breast (4/20, 20%) were the most common primary malignancies. Seven patients with shortness of breath died within 3–17 days (average 8.4±2.2 days) after onset of the symptoms. Pulmonary embolism was clinically suspected in seven out of twenty (35%, 7/20) patients before death, but only two patients (10, 2/20) were diagnosed by imaging studies before death. The rate of Goldman category major 1 was 13.2% (10/76) in 1999, 7.3% (4/55) in 2009 and 6.9% (8/116) in 2019. Although the rate of Goldman category major 1 appeared decreasing, the difference was not statistically significant. The autopsy rate was significantly higher in 2019 (8.4%, 116/1386) than in 2009 (4.4%, 55/1240).ConclusionsThe incidence of PTE is uncommon. Despite the advances of the radiological techniques, radiological imaging studies did not detect the majority of PTEs. The discrepancy between the antemortem clinical and the postmortem diagnosis has not improved significantly over the past 30 years, emphasizing the value of autopsy.

Cardiac metastasis from liposarcoma to the right ventricle complicated by massive pulmonary tumor embolism.

Cardiac metastasis from liposarcoma to the right ventricle complicated by massive pulmonary tumor embolism.

The diagnostic challenge in pulmonary tumour embolism in cancer: a case report and literature review

Pulmonary tumour embolism is a rare condition without specific symptoms or pathognomonic features. Pulmonary tumour embolism can occur as the first manifestation of cancer, but because of diagnostic difficulties, it is often wrongly recognised as a more common cardiopulmonary disease. We present a case of a 46-year-old Caucasian male with no prior malignancy diagnosis, admitted because of progressing dyspnoea and cough. Based on radiological and clinical presentations, sarcoidosis, silicosis and lymphangitic carcinomatosis were considered in the differential diagnosis. Histopathological analysis of lung biopsy revealed that multiple emboli of atypical epithelial cells found in the pulmonary vessels were of gastrointestinal origin. Further pathological examination of the gastric biopsy led to the final diagnosis of the signet-ring cells gastric adenocarcinoma. The patient was referred for chemotherapy. After a short-term partial remission, he died within two months after the final diagnosis. The presented case illustrates challenges posed by the diagnostic process of pulmonary tumour embolism.

Primary mesenchymal chondrosarcoma of the kidney without HEY1-NCOA2 and IRF2BP2-CDX1 fusion: A case report and review.

Mesenchymal chondrosarcoma (MC) of the kidney is rare. To the best of our knowledge, the current report is the first case of a giant extraskeletal MC that arose primarily from the right kidney and mimicked renal cell carcinoma at the locally advanced stage (cT3bN0) with vena cava thrombus and multiple pulmonary arterial tumor emboli. Additionally, the literature on renal EMC is reviewed and the possibilities of oncogenic heterogeneity are discussed. A 64-year-old woman was admitted to Yamagata University Hospital for sudden onset of asymptomatic gross hematuria. CT revealed a 90 mm renal mass without calcification in the right kidney and tumor thrombus extending to the inferior vena cava. Radical nephrectomy with thrombectomy was performed. Lung metastasis was detected 2 months later. The patient received systemic chemotherapy, which was only marginally effective. She died of the malignancy 8 months after surgery. Microscopic examination of the tumor revealed typical histology of MC and a lack of HEY1-NCOA2 and IRF2BP2-CDX1 gene fusions in the tumor tissues. Not all MC patients may exhibit chromosomal alterations in the tumor, suggesting the presence of genetically heterogeneous pathways of MC oncogenesis. Further studies are required to confirm the present findings and reinforce the molecular diagnosis of MC.

An autopsy case of massive pulmonary tumor embolism due to undiagnosed prostatic adenocarcinoma

Adenocarcinoma of the prostate is occasionally associated with pulmonary embolism, occurring as a result of secondary hypercoagulable states or cancer-associated emboli. The objective of this study was to provide a review of clinical, histopathological and immunohistochemical features of poorly differentiated prostatic adenocarcinoma, emphasizing the relevance of undiagnosed malignancy as a cause of pulmonary embolism. The current study describes the case of a 78-year-old male who experienced remarkable clinical symptoms suggestive of pulmonary embolism. Following several diagnostic examinations, the patient was diagnosed with pulmonary embolism, which led to the detection of prostatic adenocarcinoma. Poorly differentiated adenocarcinoma with a Gleason's score of nine was set as a definite diagnosis. Multiple tumor emboli within small and medium-sized pulmonary blood vessels were found in all specimens taken from lung tissue. Immunohistochemical analysis showed diffuse and strong positivity of tumor cells within pulmonary arteries. Hidden malignancy is a diagnostic challenge that should be considered in the differential diagnosis of pulmonary embolism. Laboratory and radiological findings with additional histopathological evaluation are needed for the definite diagnosis.

COR PULMONALE RESULTING FROM PULMONARY TUMOR MICRO EMBOLI

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: Pulmonary tumor microemboli is a rare entity, often missed and diagnosed on autopsy. It leads to elevated pulmonary pressures, cor pulmonale and death. We present a case of a young man with dyspnea and sudden right ventricular failure found to have metastatic adenocarcinoma and tumor microemboli on autopsy. CASE PRESENTATION: A 42 year old man with cough, intermittent hemoptysis, dyspnea, night sweats, and 25 pound weight loss for 6 months. He was cachectic appearing and hypoxemic. Chest computed tomography (CT) revealed bilateral ground glass opacities, tree in bud opacities, mediastinal and hilar lymphadenopathy, without pulmonary embolism (PE). Echo showed normal left ventricular ejection fraction, mildly dilated right ventricle with elevated right sided pressures. Infectious workup was negative. He underwent bronchoscopy with endobronchial ultrasound (EBUS) and transbronchial needle aspiration of the subcarinal lymph node. Bronchoalveolar lavage showed numerous AFB. Treatment for both tuberculosis and Mycobacterium avium complex (MAC) was started and he was discharged home while waiting for cytology results. Two days later presented with worsening dyspnea and hypoxemia. CT chest showed progression of lung opacities in the right upper lobe. Final cytology from the needle aspiration showed metastatic adenocarcinoma. Abdominal CT demonstrated gastric wall thickening with retroperitoneal and perigastric lymphadenopathy. On echocardiogram, the RV was dilated with severely reduced systolic function and elevated pressures, without shunting. Patient deteriorated quickly and suffered cardiac arrest, likely sequelae of acute right ventricular failure due to severe pulmonary hypertension. Autopsy revealed extensive tumor cell microthrombi in the pulmonary vasculature, consistent with pulmonary tumor emboli, and lymphangitic carcinomatosis. The gastric body had multiple ulcers with nodular borders, which were consistent with gastric adenocarcinoma with extensive lymphatic involvement. AFB sputum cultures grew MAC. There was no evidence of pulmonary granulomatous infection in the autopsy. DISCUSSION: Pulmonary tumor microemboli are exceedingly rare. The condition has been reported with multiple malignancies but more commonly in gastric adenocarcinoma. The diagnosis often goes unrecognized given vague symptoms at presentation, as in our patient. Obstruction of the pulmonary vasculature with emboli leads to elevated pulmonary pressures and cor pulmonare. RV failure tends to be rapid, thus early identification is necessary. CONCLUSIONS: Pulmonary tumor emboli should be considered in patients with malignancy presenting with hypoxemia out of proportion to their imaging findings and elevated pulmonary pressures. Mortality is high and the majority of the cases are diagnosed post-mortem. Early diagnosis and chemotherapy may improve outcome. Reference #1: Hirata, K., Miyagi, S., Tome, M., Asato, H., Uechi, N., Kunishima, N. Cor Pulmonale due to Tumor Cell Microemboli. Arch Intern Med 1988; 148:2287-2289 Reference #2: Roberts, K., Hamele- Been, D., Saqi, A., Stein, C.A., Cole, R. Pulmonary Tumor Embolism: A Review of the Literature. Am J Med. 2003;115:228 –232. Reference #3: Liang, Y-H., Kuo, S-W., Lin, Y-L., Chang, Y-L. Disseminated microvascular pulmonary tumor embolism from non-small cell lung cancer leading to pulmonary hypertension followed by sudden cardiac arrest. Lung Cancer 72 (2011) 132–135. DISCLOSURES: No relevant relationships by Louis Buja, source=Web Response No relevant relationships by Sujith Cherian, source=Web Response No relevant relationships by Rosa Estrada-Y-Martin, source=Web Response No relevant relationships by Maryam Kaous, source=Web Response No relevant relationships by Michelle McDonald, source=Web Response

PULMONARY TUMOR THROMBOTIC MICROANGIOPATHY: A RARE CAUSE OF PULMONARY HYPERTENSION

SESSION TITLE: Monday Fellow Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: We present a case of a 64 year old male who was admitted to the hospital for rapidly progressive dyspnea. Imaging revealed bilateral mosaic attenuation, septal thickening and ground glass opacities. After an extensive work-up, the patient was diagnosed with pulmonary hypertension related to pulmonary tumor emboli mircoangiopathy(PTTM). CASE PRESENTATION: A 64-year-old male with a history of atrial fibrillation and OSA presented with dyspnea on exertion associated with hemoptysis and hematuria. The patient was in his usual state of health until the summer when he was diagnosed with atrial fibrillation as a part of his work physical. After of which he was referred to a cardiologist who attempted multiple unsuccessful cardioversions while on different anti-arrhythmic agents. During this time, he was also continued on rivaroxaban for anticoagulation. After his last cardioversion he was maintained in normal sinus rhythm but this unfortunately did little to help resolve his profound dyspnea on exertion. He then underwent a right heart catheterization as an outpatient and had a right atrial pressure of 3 mmHg, pulmonary artery pressure of 67/19 and a pulmonary capillary wedge pressure of 3 mmHg. As he was quickly worsening from a respiratory stand point, he was then referred to the emergency department for admission and pulmonary was consulted. Physical exam demonstrated clear lungs bilaterally with no palpable lymphadenopathy. Chest x-ray on admission showed clear lung fields with no infiltrate, effusions, or masses. CT chest revealed multiple ground glass opacities, mosaic attenuation and septal thickening. Differential diagnosis at the time included inflammatory, vasculitis, autoimmune, and malignant etiologies. Extensive lab work that included auto-immune serologies were all negative. Given radiologic findings and right heart catheterization report there was concern of an occlusive disease and the patient underwent a VATS wedge resection. Pathology showed metastatic poorly differentiated carcinoma involving pulmonary arteries and vein with immunohistochemical findings suggest urothelial carcinoma. DISCUSSION: Pulmonary hypertension in PTTM presents with rapidly progressive dyspnea and develops due to progressive vascular fibrointimal stenosis and occlusion. A unique abnormality that can be found on lab work in patients with PTTM is a ‘compensated DIC’ in which there is a slow consumption of clotting factors and platelets. This along with progressive RV dysfunction can clue a diagnostician to preform a RHC with a pulmonary artery wedge aspiration for cytology. This has a reported sensitivity of 80-88% and 82-94% specificity respectively. CONCLUSIONS: In patients where the severity of pulmonary hypertension is otherwise not explained by the severity of heart or lung disease, PH due to pulmonary artery obstruction needs to be considered in the differential diagnosis. Reference #1: Uruga, Hironori, et al. "Pulmonary tumor thrombotic microangiopathy: a clinical analysis of 30 autopsy cases.” Internal Medicine 52.12 (2013): 1317-1323. Reference #2: Roberts, Kari E., et al. "Pulmonary tumor embolism: a review of the literature.” The American journal of medicine 115.3 (2003): 228-232. Reference #3: Price, Laura C., Athol U. Wells, and Stephen J. Wort. "Pulmonary tumour thrombotic microangiopathy.” Current opinion in pulmonary medicine 22.5 (2016): 421-428. DISCLOSURES: no disclosure on file for Eliot Friedman; No relevant relationships by Kriti Pathak, source=Web Response No relevant relationships by Noor Salam, source=Web Response

Cover Image: Volume 34 Issue 10

Front Cover Caption: The cover image is based on the Original Article Pulmonary tumor embolization as early manifestation in patients with renal cell carcinoma and tumor thrombus: Perioperative management and outcomes by Giuseppe Serena et al., https://doi.org/10.1111/jocs.14182.

Pulmonary tumor embolization as early manifestation in patients with renal cell carcinoma and tumor thrombus: Perioperative management and outcomes.

Renal cell carcinoma (RCC) with tumor thrombus extending into the inferior vena cava (IVC) occurs in 4%-10% of cases. Within this subset, pulmonary tumor embolism (PTE) appears in approximately 0.9%-2.4% of cases. We wanted to review our experience in managing patients with RCC with IVC involvement and a preoperative diagnosis of PTE. A total of seven patients presented at our center between January, 2005 and January, 2015 with RCC, IVC involvement, and PTE (diagnosed either by chest computerized tomography angiography or preoperative transesophageal echocardiogram). Each patient underwent a radical nephrectomy and tumor thrombectomy using an organ transplant-based approach. Surgical removal of the PTE was performed in three patients (tumor embolectomy in two cases, right lower lobe resection in one case); the PTEs in four patients were considered to be too small to undergo surgical resection. PTE pathology found neoplastic cells in each patient that had surgical removal. No postoperative complications were observed in any of the seven patients. All four patients who were metastasis-free preoperatively (with 2/4 having tumor embolectomy performed) developed distant metastasis; median time-to-developing metastatic disease was 6.5 months. With a median follow-up of 19 months, three deaths because the disease have occurred. Although RCC with IVC tumor thrombus complicated by PTE may not be catastrophic in most cases, it appears to be associated with an increased risk of developing metastatic disease. In addition, as the PTEs appear to contain neoplastic cells, pulmonary artery embolectomy at the time of nephrectomy should be performed whenever possible.

MON-344 A Large Adrenal Mass with Neuroendocrine Features Presenting as Pulmonary Embolism: A Case Report

Background: Adrenocortical Carcinoma (ACC) is a rare disease that has a bimodal distribution. 60% of ACC presents with symptoms and signs of adrenal steroid hormone excess [1] while non-functional ACCs present less conspicuously with abdominal mass or other nonspecific symptoms making diagnosis challenging. The usual sites of metastasis are the lung (71%), lymph node (68%), liver (42%), and bone (26%) [1]. According to literature, there has been few reported cases of ACC extending to the inferior vena cava and right atrium presenting with pulmonary embolism. Clinical Case: Patient is a 38 year old male admitted due to dyspnea, BP elevation and weight loss. Initial CXR was done showing canon ball lesions. On work up, Chest CT scan revealed pulmonary metastasis and pulmonary embolism. Abdominal CT scan showed a large right suprarenal mass with tumor infiltrating the inferior vena cava, hepatic and portal veins. 2 d echo revealed a large pedunculated mass attached to the free wall of the right atrium. The patient was started on anticoagulation. Diagnostic work up for adrenal function was done. Plasma renin and aldosterone in supine position were 3.30ng/mL/hr (reference range 0.3-1.9), and 23.28 ng/dL (reference range: 3.78-23.3) respectively with an ARR 7. 8 am cortisol was 12.30 ug/dL (reference range: 3.7-19.4ug/dL), 24 hour urine metanephrine 0.43 (reference range: 0-1) and plasma free metanephrine 36.75 pg/mL (reference range <65pg/mL) were all normal. Chromogranin A was normal at 90.71 ng/mL (reference range: <100ng/mL) however, DHEAS was 3x elevated at 1,406.00 ug/dL (Reference Range: 139.70–484.40 ug/dL). The patient underwent FNAB of the lung nodules revealing a malignant neoplasm with neuroendocrine features. Since the etiology of the adrenal mass was still uncertain, a functional imaging with 68Ga-DOTATATE PET-CT scan was done. However, the large right suprarenal mass was mostly necrotic with a small 68Ga-DOTATATE-avid focus. During admission, patient had sudden onset of chest pain, diaphoresis, hypotension and desaturation. He deteriorated and eventually expired. Post mortem examination revealed adrenocortical carcinoma with neuroendocrine features; hemorrhagic infarction secondary to massive pulmonary tumor embolism. Conclusion: Adrenocortical carcinoma is a rare cancer with varied initial presentation. A rare presentation is pulmonary embolism. In advanced stage diseases, with distant metastases, ACC has a poor prognosis. Multimodality approach with radiotherapy, aggressive surgical resection and mitotane can be offered as treatment options. Reference: 1. Kim, KH, et al. "A case of non-functioning huge adrenocortical carcinoma extending into inferior vena cava and right atrium."