Primary cardiac synovial sarcoma originating from the atrial septum and associated pulmonary infarction: a case report.

BACKGROUND: Primary cardiac synovial sarcoma is a rare condition with limited treatment options for advanced stages. Surgery and chemotherapy are currently the mainstay treatments; however, survival rates remain low. CASE PRESENTATION: A 64-year-old woman presenting with symptoms of chest tightness and shortness of breath was found to have an obstructive right atrial mass, along with pulmonary infarction and metastasis. She was ultimately diagnosed with advanced primary cardiac synovial sarcoma. Following surgery, the patient's symptoms improved, and she underwent chemotherapy and anti-angiogenic therapy, but unfortunately, her survival time was only 8 months. CONCLUSION:  This case report aims to enhance clinicians' understanding of the diagnosis and treatment of primary cardiac synovial sarcoma. Enhancing both survival outcomes and quality of life in individuals with primary cardiac synovial sarcoma continues to present a significant challenge.

Pulmonary infarction caused by sarcoidosis vascular involvement: A case report.

Sarcoidosis is a systemic granulomatous disease. In pulmonary sarcoidosis, granulomatous vascular involvement is a common feature that occurs in all types of vessels, including large elastic arteries to venules, but sarcoidosis complicated with pulmonary infarction has not been reported. We report a case of a 60 years old female, who was operated on a clinical diagnosis of lung cancer, and histological examination revealed a pulmonary infarction and sarcoidosis. In the pulmonary elastic arteries, granulomas infiltrated the adventitia and media, and caused elastic fiber collapse and destruction. Arterial occlusion by granulomas was observed in the edge of the infarcted area. It was considered that the arterial sarcoidosis granuloma involvement was the cause of pulmonary infarction. Sarcoidosis is a significant risk factor for cardiovascular events. However, pulmonary infarction is an extremely rare complication of sarcoidosis. Our case suggests that sarcoidosis may cause vascular events in the lungs.

Pulmonary findings on high-resolution computed tomography in Takayasu arteritis.

OBJECTIVE: This study aimed to describe pulmonary high-resolution CT (HRCT) findings in Takayasu arteritis (TA) and to determine possible causes. METHODS: A total of 243 TA patients were enrolled from a prospective cohort after excluding patients with other pulmonary disorders or incomplete data. Patients were divided into two groups: those with normal lung HRCT and those with abnormal lung HRCT. Clinical characteristics were compared between groups and binary logistic regression analysis was applied to identify possible causes of the lung lesions. Follow-up HRCT (obtained in 64 patients) was analysed to study changes in pulmonary lesions after treatment. RESULTS: Of the 243 patients, 107 (44.0%) had normal lung HRCT while 136 (56.0%) had abnormal lung HRCT, including stripe opacity (60.3%), nodules (44.9%), patchy opacity (25.0%), pleural thickening (15.4%), pleural effusion (10.3%), ground-glass opacity (8.1%), pulmonary infarction (6.6%), mosaic attenuation (4.4%), bronchiectasis (3.7%) and pulmonary oedema (2.2%). Patients with abnormal HRCT were significantly more likely to have type II arterial involvement (25% vs 12.2%, P = 0.04), pulmonary arterial involvement (PAI; 21.3% vs 5.6%, P < 0.001), pulmonary hypertension (20.6% vs 8.4%, P = 0.01) and abnormal heart function (27.9% vs 7.6%, P < 0.001). Logistic regression analysis demonstrated that PAI, worsened heart function and age were associated with presence of pulmonary lesions. Pulmonary infarction, pleural effusion and patchy opacities improved partially after treatment. CONCLUSION: Pulmonary lesions are not rare in patients with TA. Age, PAI and worsened heart function are potential risk factors for presence of pulmonary lesions in TA.

Postoperative cavitating infarction following lobectomy: the importance of variant pulmonary anatomy.

A 75-year-old woman was admitted to hospital with haemoptysis, fever and shortness of breath. She had undergone a right video-assisted thoracoscopic surgery upper lobectomy for an apical lung cancer 4 weeks earlier, and had been treated with antibiotics for 1 week prior to admission for a suspected postoperative lung abscess. Review of preoperative imaging found that she possessed a lobar pulmonary artery variant, with postoperative imaging confirming that the right lower lobe segmental pulmonary artery had been divided alongside the upper lobe vessels. The diagnosis of a lung abscess was thus revised to a cavitating pulmonary infarct. There are numerous variations of the pulmonary vasculature, all of which have the potential to cause a range of serious vascular complications if not appreciated preoperatively. Measures to mitigate the risk of complications resulting from vascular anomalies should be considered by both radiologists and surgeons, with effective lines of communication essential to safe working.

The "Survived Lung:" An Ultrasound Sign of "Bubbly Consolidation" Pulmonary Infarction.

Since the presence of "bubbly consolidation" (central lucencies) on a multi-slice computed tomography pulmonary angiography (MCTPA) is one of the highly specific imaging appearances of infarct secondary to pulmonary embolism, we investigated the ultrasound characteristics of these infarctions. In this study, 118 patients with MCTPA diagnosis of acute pulmonary embolism were enrolled. Pulmonary infarctions were detected in 21 patients (17.7%), of which 10 (47.6%) showed the typical appearance of bubbly consolidation on MCTPA. Lung ultrasound (LUS) was performed to evaluate the characteristics of the infarcts highlighted by MCTPA. The bubbly consolidations showed a very peculiar echographic aspect represented by a triangular hypoechoic consolidation with sharp margins, the absence of air bronchograms and a mostly central roundish hyperechoic area. Air lucencies within a pulmonary infarct is hypothesized to represent the coexistence of aerated non-infarcted lung with the infarcted lung in the same lobule. The ultrasound appearance confirms this hypothesis, so we named the roundish hyperechoic area the "survived lung." This picture was found in all patients with a diagnosis of bubbly consolidation on MCTPA (100%). Χ2 between MCTPA and LUS regarding the bubbly consolidation diagnosis is 17.18 (df = 1; p value = 0.00003). Bubbly consolidations show a very typical appearance on LUS. Their detection suggests further investigations (MCTPA or point-of-care multi-organ ultrasonography).

Pulmonary Infarction due to Paget-Schroetter Syndrome and Nephrotic Syndrome.

BACKGROUND Risk factors for venous thromboembolism can include a combination of genetic, anatomic, and physiologic factors, some of which are modifiable. Patients presenting to the hospital with venous thromboembolism may have multiple risk factors that require testing beyond the initial admission labs and hypercoagulability screening panel. CASE REPORT We describe a right-handed patient who lifts weights for exercise, who presented with pulmonary infarcts and clot in the right superior vena cava/subclavian vein. These were due to a combination of 1) an acquired hypercoagulability from minimal change disease and 2) dynamic anatomic narrowing of the subclavian vein, which is known as Paget-Schroetter syndrome. Despite normal serum levels of antithrombin, protein C and S, his serum albumin was low, which prompted workup for proteinuria. Testing revealed nephrotic range proteinuria as well as dynamic occlusion of the right subclavian vein on magnetic resonance venography only when the patient lifted and externally rotated his arms. CONCLUSIONS This case report highlights the need for a thorough history and physical examination, as well as additional testing in some patients beyond the initial admission laboratory tests and screening panel for hypercoagulability. Tests could include diagnostic imaging testing with provoking maneuvers, which can help elucidate dynamic physiology. Such testing, when appropriate, can help to inform the treatment plan and prevent recurrent thromboses.

Pulmonary Infarction with Pleural Effusion - Pathologic Surprise in the Oncological Patient.

We present the case of a 49 years-old female treated 10 years ago for a breast cancer (mastectomy followed by radio- and chemotherapy), referred to our unit for a recurrent pleural effusion with no response to medical treatment (pleural liquid - total proteins 4,1 g%, glucose 100 mg%, LDH 493 U/l, abundant cellularity with 30% eosinophils but no obvious neoplastic cells). The CT examination showed a loculated pleural effusion and a thickened irregular pleura, raising the suspicion of malignancy. Intraoperatively we found a loculated effusion - Fraser Gourd decortication and 7 subpleural pulmonary tumors with a diameter between 0,5 and 5 cm which we considered to be pulmonary metastases and performed non-anatomical resections with pulmonary reconstruction. The postoperative course was favourable, with discharge on postoperative day 16.The pathologic examination showed an inflammatory infiltrated pleura with no atypia and pulmonary infarction in all the 7 pulmonary resection specimens. Standard coagulation tests were normal but a detailed analysis of the coagulation status was not available, while postoperative cardiac and peripheric venous ultrasound did not show any abnormality explaining the pulmonary infarction. After the definitive diagnosis, the patient was treated with antiaggregants and dicumarinic oral anticoagulation, the later being abandoned due to poor compliance. At the 26 months follow-up the patient showed no signs of recurrence but she died at 32 months after surgery due to a stroke. The case is interesting due to the illustration of the diagnostic difficulties encountered in the oncological patients with pleural effusions; considering this case as "inoperable" would have resulted in anuseless chemotherapy and progression towards a more severe pleuro-pulmonary suppuration.

Symptomatic bilateral pulmonary embolism without deep venous thrombosis in an adolescent following arthroscopic anterior cruciate ligament reconstruction: a case report and review of the literature.

BACKGROUND: Venous thromboembolism, specifically pulmonary embolism, is a rare complication following elective pediatric orthopedic surgery. Bilateral pulmonary embolism with associated pulmonary hemorrhage/infarct without concomitant deep vein thrombosis has never been reported following routine anterior cruciate ligament reconstruction in an adolescent. CASE PRESENTATION: A 16-year-old white girl presented with acute onset shortness of breath and pleuritic chest pain 6 days following elective anterior cruciate ligament reconstruction. After performing a thorough work-up, she was diagnosed as having provoked bilateral pulmonary embolism with associated pulmonary hemorrhage without concomitant deep vein thrombosis. She was treated successfully with 3 months of anticoagulation therapy with daily Lovenox (enoxaparin) injections. CONCLUSIONS: Symptomatic bilateral pulmonary embolism may have a good prognosis if it is diagnosed early and treated appropriately. It is important to appreciate the risk of provoked thromboembolic events in healthy adolescents undergoing arthroscopic knee surgery.

Aggressive Renal Angiomyolipoma in a Patient With Tuberous Sclerosis Resulting in Pulmonary Tumor Embolus and Pulmonary Infarction.

Renal angiomyolipoma (AML) is the most commonly encountered mesenchymal tumor of the kidney which can present spontaneously or in association with tuberous sclerosis complex. Rarely, renal AMLs may demonstrate aggressive features such as renal vein invasion. This common entity and its uncommon complications are diagnosed based on physical examination and computed tomography results. Here we report imaging findings of a renal AML with renal vein and inferior vena cava invasion resulting in pulmonary tumor embolus and pulmonary infarction.

Pulmonary Infarction: In the Beginning: The Natural History of Pulmonary Infarction.

BACKGROUND: Massive pulmonary emboli can cause an abrupt onset of symptoms simultaneous with large pulmonary artery occlusions. In contrast, the temporal relationship between pulmonary vascular occlusion by smaller emboli and the development of symptoms of pulmonary infarction is unknown. We describe the time interval between embolization and the onset of clinical symptoms and signs compatible with pulmonary infarction. METHODS: We examined the records of 56 patients with hereditary hemorrhagic telangiectasia (HHT) who underwent therapeutic balloon embolization of pulmonary arteriovenous malformation (PAVM) in a single center after noting that some of them experienced symptoms and signs compatible with pulmonary infarction. Because both the times of embolization and the onset of clinical symptoms were documented in medical records, we were able to calculate the time interval between embolic occlusion of vessels and the onset of symptoms. RESULTS: The records of 56 patients who underwent therapeutic embolization for HHT were examined. Five patients experienced a single episode of pleuritic pain postembolization, and one patient experienced episodes of pleuritic pain after each of two separate embolization procedures. Four of these pleuritic pain events evolved into a complex compatible with pulmonary infarction. The time intervals between embolization and the onset of pleuritic pain in those experiencing the infarction symptoms and signs were 24 hours, 48 ± 4 hours, 65 hours, and 67 hours, respectively. CONCLUSIONS: The clinically silent time interval between embolization of a pulmonary artery and the onset of symptoms and signs compatible with lung infarction is 24 hours or greater.

Clinical Relevance of Pleural Effusion in Patients with Pulmonary Embolism.

BACKGROUND: Data regarding pleural effusion due to pulmonary embolism (PE) are limited. OBJECTIVES: The aim of this study was to investigate the clinical characteristics of PE patients with pleural effusion caused by PE. METHODS: Patients with PE were retrospectively analyzed and divided into 2 groups based on computed tomography: a group with pleural effusion due to PE (effusion group) and a group without pleural effusion (control group). Clinical characteristics were compared between the 2 groups. RESULTS: The study population consisted of the effusion group (n = 127) and the control group (n = 651). Serum C-reactive protein (CRP) level was significantly higher in the effusion group than in the control group. The percentages of high-risk Simplified PE Severity Index (57 vs. 47%, p = 0.008), central PE (84 vs. 73%, p = 0.013), right ventricular dilation (45 vs. 36%, p = 0.053), and pulmonary infarction (40 vs. 8%, p < 0.001) were higher in the effusion group than in the control group. Multivariate analysis demonstrated that pulmonary infarction (odds ratio [OR] 6.20, 95% confidence interval [CI] 3.49-10.91, p < 0.001) and CRP level (OR 1.05, 95% CI 1.101-1.09, p = 0.023) were independent predictors of pleural effusion due to PE. The presence of pleural effusion was not a predictor of short-term outcomes or length of hospital stay. CONCLUSIONS: Patients with more severe PE are likely to have pleural effusion caused by PE. However, pleural effusion was not a proven predictor of short-term outcome or length of hospital stay. Pulmonary infarction and CRP levels were independent risk factors for the development of pleural effusion.

Infarction of the lingula following left upper lobe trisegmentectomy.

Anatomical segmentectomy has emerged as the procedure of choice for early-stage non-small-cell lung cancer, especially in the presence of poor cardiopulmonary reserve. The most common postoperative complications are pneumonia, persistent air leak, and rarely, vascular compromise of the remaining lobe. We report the case of a 74-year-old woman who underwent thoracotomy and left upper lobe trisegmentectomy for T1bN0Mo squamous cell carcinoma and subsequently developed infarction and hepatization of the remaining lingula. A completion left upper lobectomy was performed and the patient made a full recovery.

Allergy and Venous Thromboembolism: A Casual or Causative Association.

Allergic diseases are very frequent conditions worldwide. The pathogenesis of allergic reactions and venous thromboembolism (VTE) shares several risk factors and predisposing conditions. In particular, the concentration of immunoglobulin E (IgE) is considerably increased in patients with allergic diseases, and this immunoglobulin exert many prothrombotic and antifibrinolytic activities, especially through interaction with mast cells. Therefore, this narrative review is aimed to provide an overview of the current scientific evidence supporting a potential relationship between allergy and the risk of VTE. Although no prospective studies have been published so far, the evidence provided by six large cross-sectional studies and several case reports support the existence of an unquestionable epidemiological association between different allergic diseases (especially atopy, asthma, and celiac disease) and venous thrombosis. Two additional investigations reported that the concentration of IgE might predict the onset of severe complications of pulmonary embolism such as pulmonary infarction and pleural fluid accumulation. Therefore, the existence of a convincing epidemiologic link between allergy and VTE paves the way to future investigations aimed to establish whether the prevention or treatment of allergic diseases might be regarded as an effective measure to lower the risk of VTE.