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[Anatomoclinical study of pulmonary embolism in patients with or without pulmonary infarction].

The autopsy protocols of 560 patients were studied in order to detect the incidence of pulmonary embolism, 83 cases were found (15%). The clinical data was analyzed to establish the existence of differentiating points between subjects with pulmonary infarcts and those with embolism but without infarction. The necropsy findings were further scrutinized to determine the effect of the anatomic localization of the embolus upon the production of infarction. Pulmonary infarctions were present in 60% of the cases with pulmonary embolus. The presence of cardiac failure, valvular heart disease and left ventricular hypertrophy was significantly more frequent in patients with pulmonary infarcts. In subjects with or without infarction the age, sex and the presence of medical debilitating diseases, recent trauma, surgical interventions or postpartum, cardiac diseases, arteriosclerotic heart disease, clinical evidence of thrombophlebitis, prolonged bed rest and atrial fibriliation preceding the pulmonary embolism, did not evidenciate any significant difference. In the cases with infarction the pulmonary embolus was significantly more frequently located in the small and sublobar pulmonary artery branches, while when pulmonary infarction was not found the embolic process was more frequently located in the main, right or left pulmonary arteries; occlusion of the lobar arteries had approximately the same incidence in the two groups. The most common clinical signs of pulmonary thromboembolism were dyspnea, tachycardia, cough and shock. The presence of hyperthermia, cough, jaundice, bloody sputum, pleuritic pain, pleural friction rub and pleural effusion was significantly more frequent in those cases with pulmonary infarction; the last five features were present only in the presence of infarction. The electrocardiogram was strongly suggestive of pulmonary embolism in the 6% of all cases, while the chest X-ray in 30% of those with pulmonary infarct. The diagnosis was established antemortem in 40% of the cases with infarction and in 20% of the cases with embolus but without pulmonary infarction. In 23% adequate anticoagulant therapy was established.

Adult↗

Pulmonary cavitation following pulmonary infarction.

Cavitation following bland pulmonary infarction is not commonly considered in the differential diagnosis of cavitary lung disease. In a 4-year period we have found 10 cases of cavitating pulmonary infarction (CPI) by reviewing serial chest radiographs from autopsies with pulmonary infarction and in all cases with positive ventilation-perfusion lung scans. We have compared these cases to 31 previously reported cases in the English literature that met our criteria for CPI. In our 10 patients, there were 12 radiographic cavities; 5 in the upper lobes, 5 in the lower lobes and 2 in the middle lobe. This distribution was consistent with a relative upper-lobe predominance in the literature review. In nine patients the cavitation appeared rapidly (mean, 5 days) and was associated with fever, purulent sputum, and leukocytosis. Sputum cultures were obtained in eight patients, revealing Pseudomonas aeruginosa and Escherichia coli in three each and Proteus species in two. In four patients, pulmonary infarction was not considered and the diagnosis was made at autopsy, a situation also common in previously reported cases. We have seen a high incidence of CPI in a retrospective review of patients with pulmonary infarction, and we believe that it is important to consider this diagnosis when evaluating cavitary lesions.

Adult↗

The post-pulmonary infarction syndrome.

Following pulmonary infarction, three patients developed the classical signs and symptoms of the Dressler syndrome associated with persistent left pleural effusion. Each responded dramatically to corticosteroid therapy. While the pathogenesis of this "Post-Pulmonary Infarction syndrome," like the Dressler syndrome, is unclear, the response to corticosteroid therapy is both dramatic and diagnostic and may spare the patient prolonged discomfort and unnecessary diagnostic procedures.

Aged↗

[Pulmonary infarction associated with bronchogenic carcinoma].

Pulmonary infarction may be associated with bronchogenic carcinoma. Radiopathological correlation was performed in four patients. There were two cases of squamous cell carcinoma, one case of adenocarcinoma and one case of large cell carcinoma. Infarcts in patients with squamous cell carcinoma were obscured on plain radiographs by a large primary tumor or atelectasis of the affected lobe. Infarcts in adenocarcinoma and large cell carcinoma were clearly demonstrated on plain radiographs; 1 to 2 cm in size, round or polygonal in shape, blurred in margin, and located at the periphery of the same lobe as the primary tumor. Rapid appearance of infarcts was helpful in distinguishing from intrapulmonary metastasis. Invasion of the pulmonary artery, pulmonary vein and bronchial wall in hilar region was thought to be responsible for pulmonary infarction. Pulmonary infarct should be considered in patients with centrally invasive bronchogenic carcinoma, when a small ill-defined opacity appears at the periphery of the involved lobe over a short period.

Aged↗

[Acute pulmonary embolism and pulmonary infarction].

32 cases of pulmonary embolism were reported, 18 cases had been autopsied (massive pulmonary embolism 9 cases. moderate pulmonary embolism 23 cases). The incidence risk factors pathogenesis, clinical manifestations of pulmonary embolism were presented. The relation between pulmonary embolism and pulmonary infarction and treatment of massive pulmonary infarction were discussed.

Acute Disease↗

[Preliminary therapeutic observation in 82 cases of pulmonary infarction].

The therapeutic effects on pulmonary infarction in 82 cases were reported. The cases were divided into 2 groups: trial group of 60 cases treated with heparin and Chinese herbal medicine Qing Fei decoction (QFD) and control group with antibiotics, cough-remedy, expectorant and treatment for symptomatic relief. The results showed that the resolution rate of pulmonary infarction in the trial group was higher than that of the other group (P less than 0.01). The fading phase of the infarction appeared earlier in the trial group than that in the control group (P less than 0.01). Thrombophlebitis and venous thrombosis were cured simultaneously and the recurrence rate was lower in the trial group than that in the control. Evidences showed that heparin combined with QFD has a excellent effects on the treatment of pulmonary infarction.

Diagnostic Errors↗

Causes and presenting features of pulmonary infarctions in 43 cases identified by surgical lung biopsy.

BACKGROUND: Although pulmonary infarction is usually associated with pulmonary thromboembolism, it can occur with other disorders such as vasculitis, angioinvasive infections, sickle-cell disease, tumor embolism, and pulmonary torsion. STUDY OBJECTIVE: To identify causes and presenting features of pulmonary infarctions diagnosed by surgical biopsy in a consecutive series of patients encountered at a single institution. DESIGN: Retrospective review. SETTING: Tertiary care, referral medical center. PATIENTS: Forty-three patients with pulmonary infarction identified on surgical lung biopsy over a period of 7 years, January 1996 through December 2002. RESULTS: The median age of these 43 patients was 55 years (range, 22 to 85 years); 17 patients (40%) were women, and 26 patients (60%) were men. Thirty-five patients (81%) had a smoking history. Twenty-eight patients (65%) presented with solitary or multiple lung nodules/masses of undetermined etiology. The underlying cause was identifiable in 31 cases (72%) based on a review of clinical, laboratory, radiologic, and histopathologic data. The two most common causes were pulmonary thromboembolism (18 cases, 42%) and pulmonary infections (5 cases, 12%). Thromboembolic pulmonary infarctions typically presented as solitary or multiple nodules located in the subpleural regions. Other causes included diffuse alveolar damage in two cases (5%), pulmonary torsion in two cases (5%), and one case each of lung cancer, amyloidosis, embolotherapy, and catheter embolism. In 12 cases (28%), the underlying cause was not directly identifiable but was probably due to previous pulmonary thromboembolism. CONCLUSION: We conclude that although pulmonary thromboembolism is the most common cause of pulmonary infarction identified by surgical lung biopsy, a variety of other causes are clinically encountered, including infections, inflammatory or infiltrative lung diseases, pulmonary torsion, malignancy, and nonthrombotic embolism. Pulmonary infarction should be considered in the differential diagnosis of peripheral lung nodules or masses.

Adult↗

Pneumothorax complicating aseptic cavitating pulmonary infarction.

This report documents a pulmonary infarction secondary to an angiographically proven pulmonary embolus with complicating aseptic cavitation and pneumothorax. These two rare complications of pulmonary infarction have not previously been clinically or radiographically documented to occur simultaneously. The patient recovered uneventfully.

Adolescent↗

Clinicoradiological features of pulmonary infarctions mimicking lung cancer.

OBJECTIVE: To describe presenting features of pulmonary infarction that may simulate those of lung cancer. PATIENTS AND METHODS: We reviewed the medical records of 43 patients with pulmonary infarction diagnosed by surgical lung biopsy at the Mayo Clinic in Rochester, Minn, from January 1, 1996, to December 31, 2002. Of 16 patients presenting with an undiagnosed solitary pulmonary nodule or mass, 6 had features suggestive of lung cancer on additional imaging, including abnormalities on contrast-enhancement computed tomography (CT), positron emission tomography (PET), or nonsurgical lung biopsy before surgical resection. We examined the presenting symptoms, epidemiological, clinical, and radiological features, and clinical course of these 6 patients. RESULTS: All 6 patients, ranging in age from 41 to 85 years, had a history of smoking and underlying cardiopulmonary disease. In 5 of the 6 patients, CT showed a nodule in the subpleural region of the lung. Three patients had abnormalities on contrast-enhancement CT, 2 had abnormalities on PET, and 1 had abnormal cytologic findings on a transthoracic needle biopsy of the lung; all these studies showed abnormalities suggestive of lung cancer. Surgical resection of the nodule or mass revealed pulmonary infarction associated with organizing thrombi in all 6 patients. CONCLUSIONS: Pulmonary infarctions can closely mimic the clinicoradiological characteristics of lung cancer, an association not reported previously. Furthermore, cytologic changes that occur in pulmonary infarctions may produce malignant-appearing cells on needle biopsy of the lung. The possibility of pulmonary infarction should be considered in the differential diagnosis of a solitary lung nodule or mass located in the subpleural region, even in the absence of clinically recognized venous thromboembolism.

Adult↗

Saprophytic invasion of infarcted pulmonary tissue by Aspergillus species.

Saprophytic invasion of infarcted pulmonary tissue has received only passing reference in published reports. Five patients with colonisation of pulmonary infarcts by aspergillus are described, with discussion of the clinical and histopathological features. The characteristic features were widespread invasion of dead tissue by fungal hyphae, in three cases with liquefaction resulting in the production of a cavitated lesion. There was no evidence that the vascular thrombosis and the consequent infarction present in four cases were caused by the fungus. In two cases the lesions were resected as possible peripheral cavitated tumours, and in two they were incidental findings at necropsy in patients who had had carcinoma and received radiotherapy. In the fifth case the clinical diagnosis was pneumococcal pneumonia but the possibility of primary aspergillus pneumonia was raised.

Aged↗

Cavitary pulmonary infarct in immunocompromised hosts.

Pulmonary disease in immunocompromised patients is common, but cavitary lung disease is less common and is usually associated with a fungal or mycobacterial infection. Pulmonary embolism is a noninfectious cause of a cavitary pulmonary process. Pulmonary embolism causes infarction in fewer than 15% of cases, and only about 5% of infarctions cavitate. Herein we describe two cases of cavitary infarcts in immunocompromised patients and review the clinical aspects of pulmonary infarcts and cavitation. Cavitary pulmonary infarction has been reported only rarely in immunocompromised patients. It is a dangerous but treatable pulmonary disease that must be considered in the differential diagnosis of immuno-compromised patients with lung disease.

Aged↗

[Tumor embolism of pulmonary arteries and subsequent pulmonary infarction observed in two hepatocellular carcinoma cases].

Tumor emboli of the pulmonary arteries are infrequent and premortem detection of this lesion is rare. We encountered two cases of hepatocellular carcinoma associated with tumor emboli of the pulmonary arteries and subsequent pulmonary infarctions. Plain radiographs and CT demonstrated multiple metastatic pulmonary nodules as well as pleural-based pulmonary consolidations representing pulmonary infarctions. Postcontrast CT also showed filling defects in the main pulmonary arteries. These radiographic and CT features are considered to be characteristic of tumor emboli of pulmonary arteries and subsequent pulmonary infarction. In one patient whose initial symptoms were chest pain and bloody sputum, CT was useful in detecting the primary site of tumor emboli of the pulmonary arteries. It should be kept in mind that neoplasm with a tendency to venous invasion can cause tumor emboli of the pulmonary arteries and subsequent pulmonary infarction.

Aged↗

Clearing patterns of pulmonary infarction and slowly resolving pneumonia.

Previous authors have suggested that the radiographic clearing pattern of pulmonary infarction is specific and permits differentiation from pneumonitis. Pulmonary infarcts are said to "shrink" or "melt" and pneumonitis consolidations to clear diffusely. Chest radiographs of 4 patients with angiographically confirmed pulmonary infarction and 5 with slowly resolving pneumonitis were examined, in random case order, by three independent radiologists unaware of the diagnosis. All observers found the shrinking pattern in 3 of the 4 cases of pulmonary infarction and in 1 case of pneumonitis. The shrinking pattern is not specific for pulmonary infarction; it may be related to fibrotic organization of pulmonary consolidation.

Diagnosis, Differential↗