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PubMed1992

Pulmonary venous infarction.

Pulmonary venous infarction, although rare, can develop in patients with the various pathologic conditions outlined. The triad of cough, dyspnea, and hemoptysis should raise clinical suspicion. The venous phase of pulmonary arteriography is the best way to document pulmonary venous obstruction, although MR imaging may also prove useful in the future. Treatment of patients with pulmonary venous infarction should be determined on the basis of the obstructing pathologic findings. Antibiotic therapy is important, as evidenced by the early experimental experience with this condition. It may be the only treatment available to patients with idiopathic fibrosing mediastinitis. Pulmonary resection, however, can be accomplished when a localized obstructing lesion is identified.

Animals↗
PubMed1988

Pulmonary haemorrhage, pulmonary infarction, and the lupus anticoagulant.

A patient with systemic lupus erythematosus developed pulmonary haemorrhage and pulmonary infarction as rare initial manifestations of her disease. The latter was associated with the presence of the circulating lupus anticoagulant. She recovered with pulse doses of methylprednisolone and plasmapheresis. Anticoagulants were not administered.

Adolescent↗
PubMed1985

Factors associated with pulmonary infarction. A discriminant analysis study.

To determine the relative importance of multiple interrelated factors that have been considered to contribute to pulmonary infarction, the authors performed a discriminant analysis on consecutively autopsied patients with pulmonary embolism. From the clinic records of 45 individuals, the authors tabulated the underlying illness, history of valvular or ischemic heart disease, right and left ventricular failure, sepsis, shock, malignancy, premortem functional status, and the clinician's suspicion of pulmonary embolism. At postmortem examination, the authors measured and recorded the extent of emphysema, pneumonia, neoplasia, pulmonary vascular atherosclerosis; thickness and dilatation of both cardiac ventricles; the presence of valvular heart disease; the number, diameter, and amount of occlusion of the pulmonary arteries that contained thromboemboli; the extension of the clot, the size of the infarct; the Reid-Index; and the thickness of pulmonary and bronchial arterial wall. The major determinants of infarction were as follows: poor premortem functional status, the number of lobes having emboli, left ventricular failure, and the presence of lung cancer. The authors then tested the equation generated from these patients on 21 additional patients. The discriminant function correctly classified 81% of first group and predicted the occurrence of infarction in new patients with 70% accuracy. The size of the infarct was most correlated with the use of vasodilators and the embolic burden.

Aged↗
PubMed1980

Pulmonary infarct: an unusual manifestation of fibrosing mediastinitis.

We have recently seen lung biopsy specimens showing pulmonary infarcts in two patients with fibrosing mediastinitis. The patients were young, and in each, the infarcts were the first manifestation of the underlying mediastinal fibrosis. The infarcts had several distinctive histologic features and may have been caused by constriction of major pulmonary veins by the fibrosis.

Adult↗
PubMed1994

Total lung collapse after pulmonary infarction.

A case is presented of total lung collapse secondary to intrabronchial blood clot as a complication of pulmonary infarction. The blood clot was removed at bronchoscopy with complete re-expansion of the lung.

Adult↗
PubMed1994

Cavitating pulmonary infarction in nephrotic syndrome.

A 6-year-old boy was admitted with anasarca due to relapse of nephrotic syndrome, non-productive cough, and dyspnea on exertion. On the 8th hospital day he manifested severe right shoulder and chest pain. A nodular opacity in the right lung that transformed into a cavitating lesion was documented by computerized axial tomography. Surgical biopsy of the affected area of the lung documented infarction due to pulmonary embolism. This case highlights the need to consider pulmonary embolism in the evaluation of nephrotic children with a cavitating pulmonary lesion.

Child↗
PubMed1977

False-positive cytological diagnosis of lung carcinoma in patients with pulmonary infarcts.

Cytological examination of specimens obtained from the tracheobronchial tree has become an integral part of the evaluation of pulmonary lesions. Cytological criteria for the diagnosis of carcinoma exist and are well defined. Certain benign processes, however, may possess features strongly suggestive of carcinoma of the lung. We report 3 patients in whom a positive cytological diagnosis of carcinoma of the lung was made by an experienced cytopathologist. At operation each patient was found to have pulmonary infarct and no evidence of carcinoma. Review of this experience has disclosed cytological and clinical features that should alert the clinician to the possibility that the cytological diagnosis of lung cancer may be misleading in certain nonmalignant diseases.

Adenocarcinoma↗
PubMed1981

[Tricuspid valve endocarditis with pulmonary infarction caused by central venous catheter (author's transl)].

Knowledge of common complications of central venous catheters is completed by a case of bacterial tricuspid endocarditis with recurrent pulmonary infarction. This rare, life threatening complication should be considered in differential diagnosis, when in case of central venous catheter sepsis, changing pulmonary infiltrations with pleural effusion as well as different auscultatory findings above the tricuspid valve do occur. The diagnosis can be supported by echocardiographic demonstration of tricuspid vegetations.

Catheterization↗
PubMedDate not supplied

Lung metastases manifesting as pulmonary infarction by mucin and tumor embolization: radiographic, high-resolution CT, and pathologic findings.

We present a case of lung metastasis manifesting as lung infarction by mucin and tumor embolization. The radiograph and high-resolution CT showed multiple focal consolidations with ground glass attenuation in subpleural areas of both lungs. Diagnosis was made by open lung biopsy, which revealed pulmonary infarction caused by intravascular adenocarcinoma with numerous mucus emboli in pulmonary arteries. Subpleurally located consolidations on high-resolution CT correlated well with the histologic findings of lung infarction by mucin and tumor emboli.

Humans↗