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.

Atypical pattern of lung involvement in pacemaker endocarditis.

Pacemaker endocarditis has a high rate of morbidity and mortality and is associated with substantial health-care cost. To maximize the effectiveness of treatment, diagnosis of pacemaker endocarditis should be made as early as possible. Medical treatment alone is not successful, and the removal of the entire artificial pacing system is often required. We present a case of a female patient with a permanent transvenous pacemaker, recurring episodes of fever and chills, general malaise, and a computed tomography image of a solitary tumor-like lesion indicating pneumonia. The symptoms subsided with empirical antibiotics but without improvement in the radiologic images. A wedge resection of the lesion by thoracotomy was performed, revealing a necrotic lung lesion compatible with pulmonary infarct. Transesophageal echocardiography showed a mass that was adherent to the pacemaker lead. The therapeutic approach consisted of surgical removal of the complete pacing system along with long-term antibiotic therapy and implantation of a new device with an epicardial lead. Serial follow-up echocardiograms for a 1-y period did not show any recurrence, and the subsequent course was uneventful.