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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary infarction is a very uncommon cause of pneumothorax. The authors report two patients with pneumothorax arising as a complication of pulmonary infarction. One was a 72-year-old man who had hemoptysis, pleural effusion, and alveolar condensation. Four days later he developed a hydropneumothorax and pulmonary cavitation. He died of heart failure. The pulmonary infarction was not septic in this case. The other patient was a 12-year-old boy who suffered a septic embolism with cavitation as a result of an infected wound. He later developed a tension pneumothorax and died in a state of shock. The authors have found only 16 cases of pneumothorax as a complication of pulmonary infarction in the literature. It is surprising that, even though all infarctions are in contact with the pleural surface, the incidence of pneumothorax is not higher. The infarctions may or may not be septic. Cavitation is not necessarily present, though infarctions are usually cavitated before pneumothorax develops. Tension pneumothorax occurs in some cases.
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PMID:[Pulmonary infarction as a cause of pneumothorax: report of two cases (author's transl)]. 47 Apr 94

Two cases of chronic spontaneus chylothorax were successfully treated by small thoracotomy with parietal pleurectomy or decortication after unsuccessful needle aspiration and intercostal tube drainage with suction. In the one case the chylous effusion occurred spontaneously 29 years after extrapleural pneumothorax. The tuberculosis was long cured. In the other, apparently idiopathic case, the chylothorax on the left side disappeared completely after pleurectomy. Six months later a chylous effusion appeared on the right side. Mediastinoscopy then revealed an oatcell carcinoma in lymph nodes without a primary pulmonary tumor. One year after radiotherapy the patient died in heart failure. No primary tumor was found. Residual chylothorax was present only on the right side.
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PMID:[The spontaneous, non-traumatic chylothorax. Therapy by means of pleurectomy and decortication]. 83 98

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51

With the advent of modern therapeutic approaches, even patients with advanced Hodgkin's disease have high cure rates today. Therefore, more attention is gradually being focused upon the late complications of chemotherapy and irradiation, appearing long after the patient is in remission and thought to be cured. In this report, we review the incidence and presentation of some of the cardiovascular and pulmonary complications which may appear later in the course of the disease. Cardiovascular mishaps reviewed include pericardial manifestations, conduction abnormalities, cardiomyopathy, and premature coronary artery disease. Pulmonary complications discussed are lung fibrosis, spontaneous pneumothorax, pulmonary veno-occlusive disease, and hyperlucent lung. Three instructive cases from our recent experience, are also presented. One fatal case was due to cardiac failure because of radiation-induced pericarditis and coronary artery disease. Another patient with an almost fatal complication required lung transplantation because of severe bilateral radiation fibrosis of the lung and pulmonary veno-occlusive disease. The third instance was also life-threatening in nature, with radiation-induced arterial changes in the major arteries of the chest and neck, resulting in recurrent cerebral and ophthalmic thromboembolic disease. It is suggested that potentially severe cardiopulmonary complications be considered during the planning of the initial and subsequent management of patients with Hodgkin's disease, particularly in an era employing autologous and allogeneic bone marrow transplantation as part of therapy in some cases.
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PMID:Late cardiovascular and pulmonary complications of therapy in Hodgkin's disease: report of three unusual cases, with a review of relevant literature. 128 62

Natural surfactant (Surfactant TA, Survanta, CLSE, SF-RI 1, Curosurf and human surfactant obtained from amniotic fluid) therapy for RDS in very premature infants has been evaluated in 17 controlled clinical trials. Uniformly intratracheal surfactant administration caused a decreased intensity of mechanical ventilation during the first hours (reduced inspiratory pressure, reduced oxygen requirements) as an immediate effect of surfactant administration. Metanalysis reveals barotraumatic pulmonary complications mainly, pneumothorax and pulmonary interstitial emphysema to occur less frequently in surfactant-treated infants in virtually all trials; an increased incidence of survival without bronchopulmonary dysplasia following surfactant treatment was observed in 10 controlled clinical trials. The incidence of other complications of prematurity (intracranial hemorrhage, patent ductus arteriosus and necrotizing enterocolitis) was unchanged following natural surfactant treatment. Dosing of natural surfactant is still under investigation, however recent data indicate that the initial dose should not be less than 100 mg/kg b.w. and retreatment should be given to infants with unsatisfactory response (i.e. fraction of inspired oxygen (FiO2) > 40%). Timing of surfactant treatment still remains controversial. Prophylactic treatment shortly following birth has been compared with rescue-treatment, i.e. surfactant administration to infants suffering from manifest RDS in most studies 4-8 h after birth. Conflicting data from 5 controlled trials may be interpreted as follows: prophylactic treatment seems to be favourable for extremely premature infants (GA < or = 26 weeks) and rescue treatment seems to be adequate for infants of 27-30 weeks of gestation. Intratracheal surfactant instillation in very premature infants did not result in an improved lung function for 24 h to 48 h in all patients. Ten--25% of study infants were reported to be "non-responders", i.e. infants without sustained decrease in oxygen requirements (i.e. FiO2 > 40%). Various factors may be operative including congenital bacterial infections (sepsis or pneumonia), lung hypoplasia and cardiac failure. Inactivation of surface properties of natural surfactant caused by a leakage of proteins across the alveolar-capillary membrane was observed in experimental and clinical studies. Current investigations focus on a combination of postnatal steroids and surfactant treatment to improve lung function and outcome in "non-responders". As long as any controlled clinical studies are being published, this approach remains experimental. Up to now, any controlled clinical trials have been performed to assess different modes of artificial ventilation (e.g. high frequency oscillating ventilation versus conventional ventilation) combined with surfactant therapy. Data obtained from premature animals given natural surfactant indicate any advantage with respect to gas exchange and lung histology to result from high frequency ventilation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural surfactant for neonatal respiratory distress syndrome in very premature infants: a 1992 update. 129 66

Three children with suppurative arthritis and osteomyelitis are described to emphasise that delayed or incorrect diagnosis may lead to serious cardiopulmonary complications. In two patients, bilateral bronchopneumonia developed with pneumatocoeles, pneumothorax and empyema. The other had cardiac failure from septic pericarditis. In one case, disarticulation of the knee was needed as a life-saving measure, and the other leg developed an infected pseudarthrosis of the tibia. The causative organism in each case was staphylococcus aureus and no evidence of immunodeficiency was demonstrated.
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PMID:Complications of suppurative arthritis and osteomyelitis in children. 174 34

Assessing the short-term prognosis of bronchopulmonary dysplasia (BPD) (duration of mechanical ventilation, of O2 therapy, and risk of death) is often uncertain at the early stages of the disease. From a retrospective study of 124 cases of BPD, we made a search for factors of poor prognosis which could be recognized early. Among the 124 BPD, 56 (45%) had a severe disease (mechanical ventilation for greater than 3 months and/or O2 for greater than 4 months), and 24 of them (20%) died. Two types of factors have been identified as linked to a poor prognosis (risk of evolution towards a severe disease in a proportion of 70 to 90%): some respiratory events (refractory hypoxemia, recurrent pneumothorax, interstitial emphysema, no improvement of hyaline membrane disease at 3-4 days of life in babies less than 32 weeks gestational age) and hemodynamic failures (cardiac failure due to persistent ductus arteriosus, collapse following infection or anoxia). We have also defined different values of a ventilatory index (I = mean airway pressure x FiO2) which allows the neonatologists to estimate the final prognosis of BPD during the first two months of life.
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PMID:[Evaluation of short term prognosis of bronchopulmonary dysplasia]. 207 7

Patients with idiopathic pulmonary fibrosis (IPF) inevitably experience declines in functional status that are most frequently due to progressive pulmonary fibrosis. However, the cause of the clinical deterioration is often uncertain, and disease progression is difficult to distinguish from disease-associated complications or adverse effects of therapy. In studies of the clinical course of IPF, mortality is most frequently due to respiratory failure (38.7%); other causes of death include heart failure (14.4%), bronchogenic carcinoma (10.4%), ischemic heart disease (9.5%), infection (6.5%), and pulmonary embolism (3.4%). Other, usually nonfatal, disease-associated complications include pneumothorax, corticosteroid-induced metabolic side effects and myopathy, and therapy-related immunosuppression. In evaluating clinical deterioration in patients with IPF, disease-associated complications and adverse effects of therapy should be distinguished from progressive pulmonary fibrosis. The cause of clinical deterioration will alter the therapeutic intervention required and will influence patient prognosis and duration of survival. This article examines the causes of clinical deterioration in patients with IPF and the diagnostic procedures for assessing disease-associated complications and staging IPF progression.
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PMID:Clinical deterioration in patients with idiopathic pulmonary fibrosis: causes and assessment. 218 1

Between April 1985 and July 1989, 125 cases with pleural effusion were admitted to our department. The causes of pleural effusion were carcinomatous pleurisy in 47 cases, infection without tuberculosis in 34 cases, tuberculous pleurisy in 17 cases, cardiac insufficiency and hypoproteinemia in 11 cases, trauma and pneumothorax in nine cases, collagen disease in two cases and unknown origin in five cases. Carcinomatous pleurisy and tuberculous pleurisy, the differential diagnosis of which is very important, comprised 37% and 14% of all cases, respectively. These diseases can be definitively diagnosed by pleural biopsy, effusion cytology and/or effusion culture. In July 1987, we introduced thoracoscopy to improve the ratio of definitive diagnoses. The ratio for carcinomatous pleurisy in the previous term, when thoracoscopy was not being used, was 59%, while that in the latter term, when it was used, was 73%. The ratio for all cases with tuberculous pleurisy was 47%. Prior to June 1987, pleural biopsies in our department were performed with a Cope needle. Using that procedure, a low positive ratio of 50% was obtained. For thoracoscopic pleural biopsies, a high positive ratio of 84% was achieved (in carcinomatous pleurisy, 13 out of 15 cases; in tuberculous pleurisy, three out of four cases). This procedure was performed with minimal patient discomfort and no serious complications. Therefore, thoracoscopic pleural biopsy is recommended as a diagnostic procedure for cases with pleural effusion.
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PMID:[The role of thoracoscopy in pleural biopsy in cases with pleural effusion]. 221 27

While fifty years ago 20 p. 100 of cystic fibrosis patients only reached the age of one year, more than 50 p. 100 of the patients now live more than twenty years. The clinical manifestations of cystic fibrosis are more diverse in adults than in children, so that the diagnosis might concern several specialties. In actual fact, only 3 to 7 p. 100 of cystic fibroses are diagnosed after thirteen to sixteen years, and in half the cases the symptoms had been present before the age of one year. In adults, the respiratory manifestations of cystic fibrosis are predominant, whereas the gastrointestinal manifestations tend to be blurred. Radiography of the chest shows interstitial lesions (opacities, cystic images, disorders of ventilation), principally located in the right side and the apex. The most common functional defect is an obstructive syndrome corresponding to a gradual involvement of the peripheral airways. A number of complications may develop, including recurrent Pseudomonas infection of the lung, pneumothorax, heart failure, malnutrition, liver cirrhosis, episodes of intestinal occlusion, etc. The longer life span of these patients raises the problems of diabetes with its vascular complications, infertility or pregnancy, social and professional insertion, and so forth. The prognosis of cystic fibrosis in adults depends on the date the diagnosis was made, on the therapeutic follow-up and on the creation of specialized centres. The control of Pseudomonas infections and the development of lung transplantation are the main advances to be expected.
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PMID:[Cystic fibrosis in adults]. 236 14


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