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At least 649 records · Page 36Linked to original sources
PubMed1990

[A case of pulmonary thromboembolism due to circulating lupus anticoagulant].

A 22-year-old man was admitted because of hemosputum and progressive dyspnea with 3 attacks of chest pain and dyspnea over the previous 4 months. Chest roentgenography showed pulmonary infarction of the left lower lobe, and the diagnosis was confirmed by pulmonary perfusion and inhalation scintigraphy and pulmonary arteriography. Thrombolytic therapy was performed, but no significant effect could be obtained and anticoagulant therapy was performed continuously. No deep-vein thrombosis could be seen. He was considered to have autoimmune hemolytic anemia with lupus anticoagulant on the basis of auto-antibody data. Lupus anticoagulant is an antibody to phospholipid, and it is suggested that a decrease in the production of prostanoid in the endothelium causes thrombosis. In this case, as the patient showed a low level of 6-keto-PGF1 alpha in the blood, it is suggested that one of the etiological factors of pulmonary thromboembolism is a disorder of prostacyclin production in the endothelium, causing thrombosis by lupus anticoagulant.

Adult↗
PubMed1993

Pulmonary tumor embolism to arterial vessels and carcinomatous lymphangitis. A comparative clinicopathological study.

A prospective study of 222 consecutive autopsies of cancer cases was undertaken to investigate whether carcinomatous lymphangitis and pure arterial tumor embolism of the lungs are different clinicopathological entities. The lungs were removed as a block and 15 sections (three from each lobe) were analyzed. A protocol containing clinical (ie, dyspnea, cyanosis, right ventricular failure, engorgement of jugular veins, and peripheral edema as main cause of death) and morphological (ie, right ventricle thickness and dilatation, vascular sclerosis, pulmonary infarct) data were carefully recorded in each case. Arterial tumor embolism was detected in 19 cases (8.5%) and carcinomatous lymphangitis in 44 cases (19.8%). We found no differences in relation to signs and symptoms of arterial tumor embolism and carcinomatous lymphangitis, but respiratory distress as the main cause of death was significantly more frequent in the cases with arterial involvement by tumor emboli. Morphologically, however, right ventricular hypertrophy-dilatation, histological signs of pulmonary hypertension, and hemorrhagic infarcts were more prevalent in the cases with arterial tumor embolism. This study permits us to conclude that although arterial tumor embolism and carcinomatous lymphangitis are clinically similar diseases, they are morphologically different entities. Our results suggest that the most probable pathogenesis of pulmonary endarteritis and subsequent pulmonary hypertension is the injury to the vascular endothelium caused by the arrest of tumor emboli.

Carcinoma↗
PubMed1977

Pharmacokinetics of digoxin.

The pharmacokinetics of digoxin, the most frequently used digitalis preparation, are reviewed. The dominate serum turnover time is about 34 hours, and is not affected by the route of administration. Excretion is largely as unchanged digoxin in the urine and this excretion is compromised in renal failure. Serum levels of digoxin (determined by radioimmunoassay) are generally available and are useful clinically in assessment of both toxicity and the state of underdigitalization, even though significant overlap exists. Special problems are presented in patients with myocardial infarction, pulmonary heart disease, and thyroid disease.

Acute Kidney Injury↗
PubMed1989

[Bedside cardiac catheterization. Advantages and disadvantages].

Three hundred patients submitted to bedside heart catheterization (BHC) from 1973 to 1985 were studied, in order to assess advantages and risks of the procedure. Two-hundred and sixty seven patients (89%) suffered a myocardial infarction (MI) and 146 of them were in functional class (Killip) II, 36 in FC III and 71 in FC IV. Thirty cases were submitted to BHC due to congestive heart failure. BHC was successful in 288 patients (96%) and the wedge pressure (WP) could be measured in 236 cases (78.7%). The WP was less than 18 mmHg in 47.2% of the patients in FC II, in 44.9% of the patients in FC III and in 35.3% of those in FC IV. Minor complications occurred in 33 cases (11.0%); balloon rupture in 12 (4.0%), transient arrhythmias in 11 (3.7%) and lumen obstruction in another 10 cases (3.3%). Forty five patients (15.0%) presented major complications related to the procedure: pulmonary infarction (PI) in 18 cases (6%), phlebitis in 15 cases (5%), sustained arrhythmias in 10 cases (3.3%), pulmonary artery rupture and endocarditis each in 1 case. The mean age between the group of patients with and without complications was similar the maintenance time as greater in the group of patients with complications: 3.4 +/- 0.2 vs 2.7 +/- 0.1 days (p less than 0.05). We concluded that many patients with clinical evidence of heart failure had WP smaller than 18 mmHg, emphasizing the value of the procedure in patients with complicated MI. The maintenance time was associated with the occurrence of complications, mainly PI and phlebitis.

Adult↗
PubMed1990

Unusual case of pacemaker lead migration.

Pulmonary artery migration of pacemaker lead is rare and may result in pulmonary emboli originating from the thrombus around the infected catheter and causing multiple pulmonary infarcts. We report an unusual case of pacemaker lead migration to the right pulmonary artery with septic pulmonary embolism. While being treated with intravenous Cefuroxamine, the patient had spontaneous migration of the lead to the left pulmonary artery with subsequent left pulmonary embolism.

Adult↗
PubMed1999

Pulmonary tumor embolism from primary cardiac B-cell lymphoma.

We report the case of a 54-year-old man with pulmonary embolism during convalescence from "idiopathic" pericarditis. A transthoracic echocardiographic examination indicated a large mass within the right atrium. Subsequently, he died from refractory hypotension. On autopsy, two large whitish nodules were found in the right atrium; there was also nodular epicardial infiltration. Both lungs showed multiple, grossly visible tumor emboli with pulmonary infarction and no evidence of conventional thromboembolism. This is the first report of pulmonary tumor embolism due to large cell B-cell primary cardiac lymphoma. Refractory unexplained pericardial effusion, pulmonary embolism without risk factors for venous thrombosis, and/or the existence of a mass in the right heart should arouse clinical suspicion for this rare malignancy.

Echocardiography↗
PubMed2005

Acute pulmonary edema complicating myocardial infarction: is colour M-mode Doppler of the mitral valve a valuable tool?

OBJECTIVE: To assess the value of colour M-mode Doppler of the mitral valve in patients with acute myocardial infarction complicated by pulmonary edema. DESIGN: Case-control, clinical. SETTING: Coronary care unit in a university hospital. PATIENTS/SUBJECTS: 28 patients admitted because of acute myocardial infarction, and who developed pulmonary edema (group P, cases); 39 patients with uncomplicated myocardial infarction (group C, controls). RESULTS: Patients in group P showed higher E wave (77+/-20 vs. 64+/-16 cm/s, p=0.007), E/A ratio (1.5+/-1.0 vs. 1.0+/-0.4, p=0.014), lower time of deceleration of the E wave (153+/-40 vs. 196+/-53 ms, p=0.001) and lower Ejection Fraction (35+/-10 vs. 49+/-11, p<0.001). There were no differences in the velocity of the colour M-mode Doppler of the mitral valve (Vp: 36.2+/-11 vs. 34.0+/-12 cm/s). Excluding patients with abnormal relaxation or restrictive pattern of the pulsed Doppler, Vp was identical (group P 34+/-10, group C 34+/-12). CONCLUSIONS: M-mode colour Doppler of the mitral valve was not useful to differentiate patients with acute pulmonary edema complicating myocardial infarction. Measurement of Vp is not warranted as a routine in these patients.

Acute Disease↗
PubMed2004

Pulmonary haemangiosarcoma with main pulmonary artery thrombosis imitating subacute pulmonary embolism with infarction.

We report a patient with subacute pulmonary hypertension caused by unilateral massive pulmonary artery thrombosis due to a pulmonary haemangiosarcoma of the lower lobe with pulmonary arterial and bronchial invasion. The patient was misdiagnosed as having subacute pulmonary embolism and underwent thrombolytic therapy complicated by severe pulmonary haemorrhage. The imaging features of pulmonary artery thrombosis with underlying malignancy and their differential diagnosis are discussed.

Aged↗
PubMedDate not supplied

[Pulmonary function in chronic ischemic cardiopathy].

Twenty patients with heart disease were prospectively studied. Seven of them had an old myocardial infarction and thirteen, ischemic symptoms without infarction. Pulmonary function was studied focusing on small airway disease and gas exchange abnormalities. Our results showed that a mild degree of abnormality exists as reflected by bronchial obstruction with origin in small airways, V/Q disturbed and hypoxemia. In 88% these seem to be related to left ventricular disfunction. Twenty four hours after pulmonary function test all patients underwent left heart catheterization with coronarography and ventriculography.

Coronary Disease↗
PubMed1984

Endoarterial pulmonary metastasis of malignant trophoblast associated with a term intrauterine pregnancy.

A previously healthy gravida 4, para 3, developed preclampsia and progressive dyspnea at the 37th gestational week and had bilateral pulmonary infiltrates on chest roentgenogram. She delivered a healthy, term, male infant with a normal appearing placenta. Postpartum, her respiratory status gradually worsened. A lung biopsy on the 20th postpartum day revealed intravascular trophoblasts, diffuse arteriolar thrombosis with pulmonary infarction, and subacute interstitial pneumonitis. Combination chemotherapy was instituted, but the patient died from respiratory insufficiency.

Adult↗
PubMed2005

Pulmonary pathology of severe acute respiratory syndrome in Toronto.

The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein-Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5-108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.

Adult↗
PubMed1990

Occult fatal pulmonary embolism with disseminated intravascular coagulation. An unusual case masquerading as miliary tuberculosis.

We report a fatal case of occult pulmonary embolism complicating bronchogenic carcinoma which presented with rapidly progressive pulmonary miliary shadows and respiratory failure. A clotting profile abnormality compatible with disseminated intravascular coagulation was noted. Postmortem examination showed extensive clots occluding the major pulmonary vessels and areas of pulmonary infarcts. Histologic examination revealed fibrin deposition in the microvasculature compatible with DIC. Cases of pulmonary embolism with DIC have previously been reported, but this is the first case with pathologic confirmation. Thus, unusual presentation with diffuse lung shadow and DIC should not deter the clinician from correct diagnosis so that appropriate treatment can be promptly started.

Adult↗