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At least 19 recordsLinked to original sources
PubMed1982

Pathogenesis of pulmonary infarction.

Pulmonary embolism discovered at autopsy is still as prevalent as previously reported in the last three to four decades. Only a certain percentage of pulmonary emboli result in pulmonary infarction. Recently published studies have suggested that importance of the size of the occluded pulmonary artery in the occurrence of infarction. Our study of 45 autopsy subjects in which there were pulmonary emboli shows a 31 percent incidence of pulmonary artery branches of 3 mm in diameter or less, but emboli in larger arteries may show frequent extensions into their smaller distal branches without producing infarct. Pulmonary infarction also occurs more commonly in patients dying of cardiovascular or malignant diseases than it does in those dying of other diseases, and the combination of shock and congestive left heart failure appears to be the most significant hemodynamic risk factor in the development of pulmonary infarction. However, the increased risk of pulmonary infarction in patients with malignancy may not be accounted for by the existence of these two hemodynamic risk factors alone.

Cardiomegaly↗
PubMed2004

Pure pulmonary arterial tumour embolism--a rare cause of pulmonary infarction.

Pulmonary vascular involvement in the natural course of spread of malignant tumours can produce respiratory distress and often manifests as lymphangitis carcinomatosis or carcinomatous arteriopathy. Pulmonary infarction due to arterial tumour embolism is infrequent. This is a report of a treated case of cervical cancer in middle-aged woman who presented after three years with infarction of the lungs following arterial tumour emboli.

Carcinoma, Squamous Cell↗
PubMed1998

[A case of systemic lupus erythematodes with hemosputum and pneumothorax probably resulting from pulmonary infarction and pulmonary angitis].

A 23-year-old man was admitted with fever, bloodysputum and consolidation in the bilateral lower lobes. Pulmonary infarction in the potla lower lobes was suspected because a lung perfusion scan showed a blood flow defect in the same places. Transbronchial biopsy was performed, and pulmonary hemorrhage and pulmonary angitis were demonstrated in the left lower lobe. His fever and bloodsyputum improved after steroid therapy, suggesting that pulmonary angitis may have been responsible for the bloodysputum. Subsequently pneumothorax occurred. In this case pulmonary infarction associated with pulmonary angitis may have been responsible for the pneumothorax.

Adult↗
PubMed1993

Sonographic observation of pulmonary infarction and early infarctions by pulmonary embolism.

Fifty-eight consecutive patients with clinical symptoms of pulmonary embolism/infarction were examined by ultrasound as the first imaging modality. The diagnosis was confirmed in 35 patients by ventilation-perfusion scintigraphy; 13 underwent pulmonary angiography for verification of clinical diagnosis. Seven patients died, necropsy was performed and the diagnosis of pulmonary embolism was confirmed in six cases; three patients were submitted to transthoracic lung biopsy. Intercostal space and an additional small pleural effusion in 48% of the examined patients served as a sonic window for the 5 MHz sector scanner. In 42 of the 54 cases with a final diagnosis of pulmonary embolism/infarction a total of 69, hypoechoic, lesions with a pleural basis were detected. These were conspicuous, predominantly triangular, of a mean size 4.6 x 3.7 cm (range 9 x 8 to 2 x 1.5). A hyperechoic structure with reverberation artefacts suggestive of air was frequently visible in the centre: a sign of segmental involvement. The ultrasound examination yielded a true positive result in 41 cases. The overall sensitivity was 98% and the specificity 66%. The prevalence of pulmonary embolism was 83% and the diagnostic accuracy 90%. This suggests that chest sonography can be an efficient technique in the detection of pulmonary infarction.

Adult↗
PubMed1990

Reflux pulmonary vein flow prevents pulmonary infarction after pulmonary artery obstruction.

Küttner showed in 1874 that simultaneous ligation of the pulmonary veins increased the frequency and severity of lung infarctions after pulmonary artery obstruction. The authors studied the possibility that a tidal pulmonary venous blood flow reflux from the left atrium could nourish the alveolar tissue. This could be driven by left atrial pressure transients and alternate expansion and compression of alveolar and extra alveolar vessels due to tidal lung volume changes. 5 anesthetized, closed chest goats were studied in the prone position after left pulmonary artery ligation and the obstruction of all bronchial blood flow to the left lung, checked by systemic microsphere injection. The inert, insoluble gas SF6 was infused into the left atrium and the exhaled gas from left and right lungs was collected separately. SF6 was found in the gas exhaled from the left lung, showing that left atrial blood had reached the alveolar tissues. The effective reflux blood flow was increased from control levels (no ventilation, normal left atrial pulses) by tidal volume changes, and by increased left atrial pressure transients (balloon induced mitral insufficiency). This venous reflux flow could explain why alveolar tissues do not suffer more severe injury when the pulmonary artery is obstructed.

Animals↗
PubMed1996

Chronic solitary pulmonary nodule due to unsuspected pulmonary infarction from silent pulmonary embolism.

A case of pulmonary embolism showing a longstanding solitary pulmonary nodule is presented. An asymptomatic 57 year-old man with a solitary nodule in the right lower lobe was referred to our hospital. A pulmonary perfusion-ventilation scan following a sudden onset of dyspnoea established the diagnosis of recurrent pulmonary embolism. The nodule gradually disappeared after anticoagulant treatment, indicating that the nodule was pulmonary infarction from silent pulmonary embolism. Although the incidence of pulmonary infarction is low in Japan, this case suggests that pulmonary infarction from silent pulmonary embolism should be considered as one important cause of a solitary pulmonary nodule.

Chronic Disease↗
PubMed1997

Pulmonary infarcts can mimic pulmonary metastases from renal cancer.

PURPOSE: Spontaneous regression of pulmonary metastases from renal cell carcinoma is a rare but well documented event. We present 2 recent cases that were radiographically consistent with pulmonary metastases from renal cell carcinoma but were pathologically shown to be pulmonary infarcts with no evidence of metastatic cells. Stable pulmonary infarcts can be misconstrued as metastatic disease in patients with renal cell carcinoma while resolving pulmonary infarcts may represent a subpopulation of patients with apparent spontaneous regression. Clinical implications of these findings are discussed. MATERIALS AND METHODS: Clinical and pathological data from 2 patients with large primary renal tumors, venous thrombi and lung masses were reviewed. Data from these cases, as well as pertinent urological and pathological literature, are presented. RESULTS: Although preoperative assessment was consistent with stage IV renal cell carcinoma, pathological examination of the lung masses in these patients showed no evidence of tumor cells. CONCLUSIONS: Pulmonary infarcts may mimic resolving or stable pulmonary metastasis in patients with renal cell carcinoma. Accurate clinical staging is crucial for the prognosis and treatment of renal cell carcinoma. Mistaking pulmonary infarcts for metastatic lesions can lead to inaccurate prognoses and inappropriate treatment.

Carcinoma, Renal Cell↗
PubMed1977

Unsuspected pulmonary emboli in well persons: the incomplete pulmonary infarction syndrome.

Pulmonary embolization from occult venous thrombosis in the lower extremities occurs in previously well individuals of all ages. Incomplete or hemorrhagic pulmonary infarction may result. The incomplete pulmonary infarction syndrome (IPIS) is characterized by sudden onset of pain in the lower chest, knife-like and stabbing in quality and accentuated by breathing, with pathognomonic abnormalities on chest x-rays. The physician should hospitalize the patient, begin heparinization and confirm the diagnosis with daily chest x-rays in multiple views. Failure to promptly diagnose and treat IPIS may lead to catastrophic, massive pulmonary embolism and death, or to recurrent embolism with pulmonary hypertension and chronic cor pulmonale, resulting in incapacitating dyspnea on exertion, and disability.

Adolescent↗
PubMed1987

Left atrial myxoma: pulmonary infarction caused by pulmonary venous occlusion.

Atrial myxomas are the most common primary cardiac tumors. Typical complications include congestive heart failure, systemic emboli, or vasculitic type syndromes. Presented is a case of postpartum congestive heart failure in a 17-year-old girl. Echocardiography revealed a left atrial mass. Intraoperatively this mass was found to be extending into and occluding the left pulmonary veins. Left pulmonary infarction had occurred, and left pneumonectomy was required to completely remove the lesion. This case thus represents an unusual complication of left atrial myxoma.

Adolescent↗
PubMed1978

[Contribution to the differential diagnosis of lung infarct, pulmonary tuberculosis and lung neoplasms].

It is reported on the rare case of a symptom-free, atypically localised haemorrhagic pulmonary infarction without provable cause in a 52-year-old male. The patient became conspicuous on account of a plum-sized focal shadow in the right lateral upper field detected during a mass examination. The state was regarded as bronchial. carcinoma. Operation and following histological investigation of the resection preparation finally resulted in the diagnosis.

Diagnosis, Differential↗
PubMedDate not supplied

[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↗