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Results for “Pulmonary Infarction”

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PubMed1979

Hemoptysis in patients with septic pulmonary infarcts from tricuspid endocarditis.

Three drug addicts with tricuspid valve endocarditis and pulmonary cavitation secondary to septic pulmonary infarcts developed massive hemoptysis. Two patients died of asphyxia and one survived. Both who died were improving clinically and had negative blood cultures when the fatal hemoptysis occurred. Therefore, however slight it may be, hemoptysis occurring in association with septic pulmonary infarcts associated with endocarditis may require prompt and aggressive measures.

Adult↗
PubMed1991

[A case of idiopathic hypereosinophilic syndrome (HES) complicated by pulmonary infarction].

We experienced a case of idiopathic hypereosinophilic syndrome (HES) associated with pulmonary infarction. The case was a 22-year-old woman with marked eosinophilia (16835/microliters) and peripheral edema and cyanosis. During hospitalization, she suddenly developed lower right chest pain, and infiltrative lesions with pleural effusions in the right lung were prominent. A diagnosis of pulmonary infarction was made after perfusion scan and angiography of the lung. Lupus anticoagulant was found to be positive and a transient increase of anti-cardiolipin antibody slightly in her serum was also observed. Recurrent thrombosis is known to be complicated by HES but its mechanism remains to be clarified. There has also been no study reported in the literature on the role of lupus anticoagulant in this process; its possible role in this patient is discussed.

Adult↗
PubMed1991

Magnetic resonance imaging in the diagnosis of pulmonary infarction.

We report for the first time, to our knowledge, MRI features which could differentiate noninvasively pulmonary infarction from pneumonia. Three subjects with angiographically proven pulmonary infarction showed high T1 weighted MRI signals located in the embolic territory. Three patients with pneumonia and one patient with emboli, but without infarction, did not have these T1 weighted images.

Diagnosis, Differential↗
PubMed2002

Frequency of myocardial infarction, pulmonary embolism, deep venous thrombosis, and death following primary hip or knee arthroplasty.

BACKGROUND: There is limited information about the frequency of perioperative complications after elective primary orthopedic total hip and knee arthroplasty in contemporary practice. The purpose of this study was to determine the frequency of clinically relevant myocardial infarction, pulmonary embolism, deep venous thrombosis, and death within 30 days after elective primary hip or knee arthroplasty treated according to contemporary perioperative management. METHODS: The authors examined the medical records of consecutive patients undergoing hip or knee arthroplasty at their institution in a 10-yr period. Prospectively collected databases were used to identify patients with the diagnosis of myocardial infarction, pulmonary embolism, deep venous thrombosis, or death using strict validation criteria and diagnostic-certainty categories. RESULTS: A total of 10,244 patients underwent primary total hip or knee arthroplasty in the period of study. Of these, 224 patients had one or more adverse events (overall event rate: 2.2%; myocardial infarction: 0.4%; pulmonary embolism: 0.7%; deep venous thrombosis: 1.5%; death: 0.5%). Most adverse events (myocardial infarction, pulmonary embolism, and death) increased in frequency with older age, particularly for patients aged 70 yr or older. Myocardial infarction occurred more frequently in male patients. There were no differences in the overall event frequency between types of procedure. However, pulmonary embolism was highest in patients undergoing bilateral knee operations. CONCLUSIONS: The overall frequency of serious complications within 30 days after primary total hip or knee arthroplasty with contemporary practice was 2.2%. Accurate knowledge of the perioperative risks associated with widely performed elective operations can be used to implement management strategies that may further improve patient outcomes and decrease cost.

Adult↗
PubMed1999

Pseudotumor due to pulmonary infarction diagnosed by video-assisted thoracoscopic surgery.

We report a case of pulmonary infarction in a 50-year-old man who was referred for an asymptomatic coin lesion in the periphery of the right lower lobe. Computed tomography of the chest demonstrated a subpleural solitary nodule with spicular radiation. Video-assisted thoracoscopic surgery was performed to obtain a histological diagnosis. Thoracoscopic examination showed that the tumor was dark purple and the central portion was gray, indicating blood retention in the lung and necrotic and fibrotic tissue in the central portion. This is the first case of pseudotumor due to pulmonary infarction that was diagnosed by video-assisted thoracoscopic resection.

Fibrosis↗
PubMed1976

Pulmonary infarction following ligation of terminally shunted pulmonary artery.

The intracardiac repair of tetralogy of Fallot occasionally is complicated by the presence of a surgically created shunt between a systemic artery and the distal end of a divided pulmonary artery. Rarely, reconstruction of this pulmonary artery at the time of corrective operation is not technically feasible. Usually, this problem has been managed by obliterating the systemic-to-pulmonary arterial shunt, which has not previously been reported to result in complications in the involved lung. Two of our patients underwent intracardiac repair of tetralogy of Fallot, including ligation of a terminally shunted left pulmonary artery. Postoperatively they developed infarction of the left lung with resulting acute respiratory insufficiency. In both instances, conservative management ultimately achieved resolution of the pathological process and a good clinical result.

Adult↗
PubMed1993

Bronchial arteries in experimental pulmonary infarction: angiographic and morphometric study.

OBJECTIVES: The aim was to investigate (1) whether collateral bronchopulmonary circulation developing due to chronic pulmonary embolism could prevent the evolution of pulmonary infarction after induction of pulmonary venous outflow impairment; and (2) how collateral bronchopulmonary circulation developed after acute embolisation of the lung with impaired pulmonary venous outflow. METHODS: Fifty two mongrel dogs were studied. Thirty six dogs were experimental animals and 16 were in a control group. Unilateral impairment of pulmonary venous outflow was induced by constriction of the left pulmonary veins in two groups of experimental dogs: (1) three months after and (2) one hour before bilateral embolisation of the pulmonary artery. All animals were killed 12 days after constriction. The size of the bronchial arteries was evaluated from angiograms. The diameter and the wall thickness of the arteries were measured during histology. RESULTS: In all experimental dogs, haemorrhagic infarctions developed distally to emboli in the left lung regardless of whether the bronchial arteries were dilated before induction of pulmonary venous constriction or whether collateral circulation started to develop after pulmonary venous constriction. Constriction of the pulmonary veins was an essential factor for pulmonary infarction to develop as no infarction developed in the embolised regions of the right lungs with intact pulmonary venous outflow. Pulmonary venous constriction alone did not cause dilatation or hypertrophy of the bronchial arteries. After pulmonary artery embolisation, the same enlargement and hypertrophy of the bronchial arteries occurred both in the left lung with previously impaired venous outflow and in the right lung with intact pulmonary veins. CONCLUSIONS: Expanded bronchopulmonary circulation did not prevent the development of infarction in the embolised region of the lung with impaired pulmonary venous outflow. Development of collateral bronchopulmonary circulation was not influenced by previously impaired pulmonary venous outflow.

Animals↗
PubMed1979

What becomes of pulmonary infarcts?

In 32 patients, 58 angiographically proven pulmonary infarcts were followed for 3 months or longer by serial chest radiography. Complete clearing was seen in 29 (50%) of the infarcts on chest radiography. In the other 29 infarcts that left residual findings, linear scars were identified in 14, pleural diaphragmatic adhesions in nine, and localized pleural thickening in six; in all cases the features were diminutive when compared with the original abnormality. Follow-up perfusion lung images at similar time intervals to the chest films were available for 44 infarcts. Seven of these showed complete resolution and the other 37 showed a residual but much smaller perfusion defect. None of the patients had known preexisting pulmonary disease. The frequency of permanent radiographic scarring seemed to be the same at all ages.

Adolescent↗
PubMedDate not supplied

Experimental pulmonary infarction in dogs: a comparison of chest radiography and computed tomography.

Transcatheter electrocoagulation of the pulmonary artery was used to successfully create experimental pulmonary infarcts in 15 to 16 dogs. The animals were evaluated from one to 13 weeks by chest radiography, computed tomography (CT), angiography, and pathologic examination. The abnormal densities in the dogs' lungs cleared in two to three weeks. The majority of the chest radiographs were normal in two weeks, and all were normal after three weeks. Prior to sacrifice, CT showed abnormal densities in the lungs in only two of eight animals. CT proved to be more sensitive than chest radiography for showing the densities in the lungs due to pulmonary infarction.

Angiography↗
PubMed1979

Pulmonary infarction in sickle cell trait.

A young black man presented with unexplained pleuritic chest pain. A hematologic evaluation revealed sickle cell trait, Chest roentgenograms, ventilation/perfusion lung scanning and a pleural-parenchymal lung biopsy documented pulmonary infarction. Sickle cell trait with resultant pulmonary infarction should be considered in black subjects with unexplained pulmonary diseases.

Adult↗
PubMed1989

[A case of nephrotic syndrome associated with pulmonary infarction and renal vein thrombosis. (A review of literature)].

A case of nephrotic syndrome found by pulmonary infarction associated with renal vein thrombosis was reported. The renal biopsy showed the presence of membranous glomerulonephritis. The patient had the increase of serum level of the coagulation factor II, V, fibrinogen and FDP, and the level of urine FDP. These laboratory data suggested that the hyper coagulation state of his blood caused by nephrotic state, induced his multiple thromboembolism. We surveyed 47 case report abstracts of nephrotic syndrome patients having thromboembolism on the Japanese Journal of Nephrology published from 1974 to 1986. The histopathology of their renal biopsies showed the high incidence of membranous glomerulonephritis, followed by minimal change nephrotic syndrome and focal glomerular sclerosis. Renal vein thrombosis was the most common thromboembolism in the reports, followed by thrombosis of cerebral vessels, peripheral vessels and pulmonary artery. Some patients died of pulmonary infarction or myocardial infarction. These data showed that we must keep in mind of the possibility of thromboembolism in the treatment of nephrotic syndrome.

Glomerulonephritis, Membranous↗
PubMed2000

Ruptured pulmonary infarction: a rare, fatal complication of thromboembolic disease.

We describe 2 men, ages 69 and 49 years, who experienced fatal rupture of pulmonary infarcts. Both patients had documented prior thromboembolic events and subsequently had abrupt deterioration in cardiorespiratory function. Autopsies showed massive unilateral hemothorax in both patients. Rupture of a pulmonary infarct may occur spontaneously or iatrogenically due to aggressive anticoagulation. This may be difficult to distinguish from secondary hemothorax with an intact pleura, but rupture typically has a considerably more rapid clinical evolution. Treatment should include immediate withdrawal of thrombolytic or anticoagulant medications and evacuation of the pleural space. Surgical intervention can be considered, although the utility of that approach must await prospective trials.

Aged↗
PubMed2004

False-positive sputum cytology in a case of pulmonary infarction.

Sputum cytology is an important diagnostic tool in pulmonary medicine, but it can yield a false-positive diagnosis of malignancy. We describe such a case, which involved a 70-year-old man who presented with chest pain, hemoptysis, and bilateral pulmonary infiltrates. In the initial evaluation of hemoptysis, multiple sputum samples demonstrated cytological abnormalities consistent with adenocarcinoma, but bronchoscopy found no evidence of malignancy. He was ultimately found to have pulmonary thromboembolic disease with infarction. Follow-up radiographs showed resolution of the pulmonary infarcts, and the absence of malignancy was proven during postmortem examination. Pulmonary infarction is one of many diseases that can produce sputum cytological findings falsely indicative of malignancy.

Adenocarcinoma↗
PubMed1990

Pulmonary infarction presenting as aseptic cavitation.

A case of pulmonary infarction presenting as aseptic cavitation was reported. Basically, the patient suffered from rheumatic heart disease, mitral stenosis and insufficiency, and atrial fibrillation with predominant right heart enlargement. Hemoptysis, chest pain and dyspnea were present. Chest film simulated a thin wall lung abscess. The clinical picture suggested aseptic cavitation, which was confirmed by 99mTc-MAA lung scan.

Aged↗