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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of early postoperative thrombosis of a Starr-Edwards mitral valve prosthesis in a 36 year old female who had undergone closed heart surgery nine years previously for tight mitral stenosis. Severe restenosis led to mitral valve replacement in 1980, and the insertion of a Starr-Edwards prosthesis. On the 8th postoperative day thrombosis of the prosthesis presented with pulmonary oedema and a change in the prosthetic valve sounds which regressed with therapy. The diagnosis was confirmed on the 9th postoperative day by left heart catheterisation and angiography. Fibrinolytic treatment was instituted on the 10th postoperative day with 4500 u/Kg of Urokinase for 24 hours. Pulmonary oedema regressed at the 6th hour of treatment and the prosthetic valve sounds reverted to normal. No significant complication was observed. The good result has been maintained up to the 6th postoperative month. This case demonstrates the possibility of using fibrinolytic therapy in the early postoperative period after valve replacement: this should be weighed in the balance against the mortality of reoperation in such cases of early thrombosis of prosthetic heart valves.
Arch Mal Coeur Vaiss 1982 Mar
PMID:[Early postoperative (10th day) thrombosis of a Starr mitral prosthesis. Successful fibrinolytic treatment]. 680 52

The authors report three cases of unilateral pulmonary oedema following the re-expansion of a spontaneous pneumothorax. The importance of the duration of the pneumothorax and the use of too negative pressure while re-expanding the lung were both underlined. The different physiopathological hypotheses responsible for the appearance of pulmonary oedema were discussed, notably altered mechanical properties of the lung and alveolar-capillary permeability. The numerous precautions to take to avoid the appearance of oedema, as well as the therapeutic measures to adopt for severe pulmonary oedema were reviewed.
Rev Fr Mal Respir 1981
PMID:[Unilateral pulmonary oedema after re-expansion (author's transl)]. 732 2

The aim of this prospective study was to analyse the contribution of the measurement of alveolar arterial gradients of CO2 during forced expiration in the diagnosis of pulmonary emboli occurring in chronic airflow obstruction (COPD) as a result of smoking. The study was carried out on 178 patients: Group 1: 54 subjects without emboli (14 controls, 33 COPD and 7 patients with chest pain); Group 2: 72 patients with proved emboli (49 non COPD, 23 COPD); Group 3: 52 patients COPD presenting with varied non-embolic broncho-pulmonary pathology (pneumonia, bronchospasm, pulmonary oedema, bronchial neoplasm). The diagnosis of pulmonary emboli was confirmed by scintigraphy in patients with non COPD or angiography (in patients with COPD). The maximal fraction of CO2 was measured using a capnologue during a forced expiration which was long and prolonged until residual volume was achieved. The PaCO2 was measured simultaneously by an analysis of arterial blood gases. The D index was calculated according to the formula [(PaCO2-PEM CO2)/PaCO2] x 100. The D index was significantly lower in Group 1 (3.42 +/- 3.8% p < 0.0001) than in Group 2 (20.8 +/- 10%) and Group 3 (17.6 +/- 11.7%) (not significant between Groups 2 and 3). In patients with COPD the specificity and sensitivity and the predicted positive and negative value were 100% for a D limit of 7%. In COPD patients these values were respectively 82, 95, 75 and 96% for a D limit of 7%; on the other hand for a D below 5% the values were 60, 100, 64 and 100% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Mal Respir 1995
PMID:[The significance of maximal expiratory concentrations of CO2 (MEC CO2) in the negative diagnosis of acute pulmonary embolism in chronic obstructive bronchopneumopathies]. 789 65

Mechanical ventilation may have adverse effects on the lung. The appearance of extra-alveolar air, either as a pneumothorax or as subcutaneous emphysema along with other manifestations, is a complication of barotrauma which has been known for a long time. Recent experimental studies have clearly shown that mechanical ventilation can also lead to alterations in the blood gas barrier. Mechanical ventilation with high inflation pressure and elevated tidal volumes induces pulmonary oedema; the genesis of which results principally from anomalies of alveolar capillary permeability. These anomalies are made as a result of pulmonary distension and not as a result of elevated pressures in the airways, thus justifying the term "volume traumatism". The existence of previous acute pulmonary injury considerably worsens the deleterious pulmonary effect of mechanical ventilation. Although the direct clinical implications of these experimental studies are difficult to confirm, these latter have nevertheless lead to profound changes in ventilatory strategy during the course of acute pulmonary disease such as the adult respiratory distress syndrome.
Rev Mal Respir 1995
PMID:[Deleterious effects of mechanical ventilation on the lower lung]. 867 49

The pathology of drug-induced pulmonary toxicity in children is poorly understood and probably under-estimated, in the absence of any prospective studies evaluating in a systematic fashion the side effect of medication on the respiratory apparatus. The pulmonary toxicity of thoracic irradiation has markedly receded with more restricted indications for this sort of treatment. Three clinical patterns are most commonly encountered in drug induced lung disease in children: interstitial lung disease, hypersensitivity lung disease and non-cardiogenic pulmonary oedema. The diagnosis is a diagnosis of exclusion and rests on a group of clinical arguments and also on the progress of the disease. Broncho-alveolar lavage rules out infectious disease. Respiratory function tests show non-specific anomalies. A lung biopsy may be indicated. The mechanism of the pulmonary toxicity are associated with disequilibrium of the oxidant/antioxidant and protease/antiprotease system as well as disturbance of the immune response or alteration of the pulmonary matrix by disease of the collagen system. Increased toxicity may be seen in children because of a very significant cumulative dose. The cytotoxic drugs which are most often implicated in causing this are bleomycin, methotrexate, cyclophosphamide and busulfan. Other drugs which are responsible for toxic lung disease are nitrofurantoin, sulfasalazine, D-penicillamine, betalactams, Diphenyl-hydantoin and carbamazepine. Acute post-radiation lung disease is rare. Post-radiation fibrosis is found six months after irradiation and hinders thoraco-pulmonary growth in the child. It is important to assess lung function in all children before any chemotherapy or thoracic irradiation. Cytotoxic drugs are the most common cause of toxic lung disease. This iatrogenic disease requires a multi-discipline approach to ensure the quality of care for these children.
Rev Mal Respir 1996 Jul
PMID:[Pulmonary toxicity of drugs and thoracic irradiation in children]. 876 15

One hundred patients operated for left atrial myxoma in the same surgical department underwent clinical and anatomical assessment at long-term from 1959 to July 1995 (66 women and 34 men, average age 52.2 years). The clinical presentation was related to mitral valve obstruction in half the cases (dyspnoea, cough, pulmonary oedema), the presentation in the other half of cases being very variable. The widespread use of echocardiography has relegated other investigations to a subsidiary role: auscultation, radiology, ECG (9 cases diagnosed by echocardiography performed for another indication). Serious complications of left atrial myxoma include systemic embolism : 37 cases out of the 100 in this series, including 10 plurifocal but mainly cerebral (19 cases including 11 isolated cerebral emboli). Surgical treatment is well established, should not be deferred and gives excellent results (2 early postoperative deaths out of 100 cases in the early years of the study). There were 6 cases of recurrences including 3 cases of Carney's syndrome. Clinico-pathological correlations showed that mitral stenotic effects occurred when the tumour diameter exceeded 5 cm and embolism was associated with tumours having multiple villositi. Histopathological analysis distinguished between active and inactive tumours, differentiated or not, and enabled the elaboration of hypotheses on the rate of growth of the tumour and on the absence of true metastases. Histopathological techniques also show the presence of lymphoplasmocytic infiltration, the sign of secretion of interleukin 6 by the myxoma, a cytokine involved in the general inflammatory process and which explains the unusual clinical presentation sometimes observed.
Arch Mal Coeur Vaiss 1996 Sep
PMID:[Myxoma of the left atrium, Clinical outcome of 100 operated patients]. 895 35

Currently transplantation constitutes the only treatment for terminal heart, liver or renal failure. Post-transplantation complications remain numerous and sometimes fatal. The rejection of the organ, acute or chronic, and secondary infections due to immunosuppression are the most frequent complications that are observed. Added to this are the complications of the surgery itself and also the non-infectious complications of the immunosuppressive drugs. Pulmonary complications contribute an important factor to the post-graft morbidity and mortality. The majority of heart and liver transplants develop pulmonary complications principally in the first six months after graft. The immediate post-operative complications such as atelectasis, pleural effusion and pulmonary oedema are the most frequent but the infectious complications are much the most serious and are responsible for a significant part of the mortality. In renal transplantation pulmonary complications are above all infectious and are much less common than in cardiac or hepatic transplantation. An early diagnosis of the type of complication constitutes a major prognostic factor in immunodepressed patients. Thus, the practising pneumologist must thoroughly know the principal respiratory complications of solid organ transplant.
Rev Mal Respir 1996 Nov
PMID:[Lung pathology in heart, liver and kidney transplantation in adults]. 901 13

The usual causes of pulmonary edema are left ventricular dysfunction, mitral valve disease or left atrial myxoma. Obstruction to pulmonary venous drainage is a rare and unrecognised diagnosis which should be considered when the usual investigations are unproductive. The authors report four cases in which transesophageal echocardiography showed pulmonary edema to be due to compression of one or more pulmonary veins by a mediastinal mass (2 cases), by the false lumen of dissection of the aorta (1 case) and postoperative stenosis of the pulmonary veins (1 case). These cases underline the diagnostic value of this technique which rapidly provides diagnostic information with privileged visualisation of the pulmonary veins and abnormalities of acceleration of blood velocities in the Doppler mode due to obstruction.
Arch Mal Coeur Vaiss 1997 Jan
PMID:[Unexplained pulmonary edema: demonstration of obstruction to pulmonary venous return by transesophageal echocardiography. Apropos of 4 cases]. 913 17

One hundred and eleven patients with severe left ventricular dysfunction (EF < or = 25%) underwent coronary bypass surgery between January 1984 and December 1994. The selection criteria were based on the measurement of an EF < or = 25%, LVEDP and CI. All patients had angina and 83 had signs of pulmonary oedema or episodes of congestive failure. Patients with valvular disease, left ventricular aneurysms, reoperations, surgery for arrhythmias and prior angioplasty, were excluded. The coronary disease usually involved all three vessels. Seventeen patients had lesions of the left main stem associated with lesions of the right coronary artery. The average number of bypass grafts was 2.6 +/- 1.6 per patient. The average duration of aortic clamping was 60 +/- 19 minutes. Operative mortality (first month after surgery) was 10 patients (9%). The operative risk factors were: gender, stage of cardiac failure, emergency surgery, LVEDP > 23 mmHg (p < 0.05), CI < 21/min/m2 (p < 0.05). The mean follow-up period was 42 +/- months (3 lost to follow-up). Late mortality was 42 patients. The one year actuarial survival was 88 +/- 5.3%, 76 +/- 9% at 3 years, and 56 +/- 18% at 6 years. Long-term functional results were related to: preoperative stage of cardiac failure (NYHA stage IV) and the association of raised LVEDP and low CI. Surgical results remained satisfactory, however, and the surgical indication was justified in selected patients despite severe left ventricular dysfunction in cases usually with stable invalidating or unstable angina, in the knowledge that myocardial deterioration is progressive in the medium-term with a high incidence of cardiac failure.
Arch Mal Coeur Vaiss 1997 Apr
PMID:[Coronary bypass in patients with severe left ventricular dysfunction (EF < or = 25%). Apropos of 111 patients]. 923 60

There are frequently respiratory complications with cancer particularly in primary lung carcinoma. Among these are bronchopulmonary infections with or without endobronchial obstruction, carcinomatous lymphangitis, thromboembolic disease and haemorrhagic disease as well. Radiotherapy and chemotherapy may induce various respiratory complications which diagnosis can be of varying shades of difficulty. The classical post radiation pneumonitis occurring exclusively in the field of radiation hardly poses any problem unless it could be masking a recurrence. Certain clinical manifestations address very difficult problems of differential diagnosis by their lack of specificity and by their often unforeseeable character (except for bleomycin fibrosis which is perfectly dose dependent). Moreover patients often have multiple treatments and the identification of the single responsible agent becomes very difficult. We will not discuss here the infectious or secondary haemorrhagic complications of radiotherapy or chemotherapy but rather the anaphylactic manifestations, diffuse interstitial pneumonia with lymphocytic alveolitis or fibrosis, eosinophilic pneumonia, non-cardiogenic pulmonary oedema, bronchiolitis obliterans with organising pneumonia and the rare pulmonary vascular disorders such as pulmonary veno-occlusive disease.
Rev Mal Respir 1997 Nov
PMID:[Radiation- and chemically-induced respiratory manifestations]. 948 Apr 78


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