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

Environmental lung injury may take the form of acute tracheobronchitis, asthma, pulmonary edema, chronic bronchitis, emphysema, allergic pneumonitis, fibrosing alveolitis, pleurisy, and neoplastic disease. Environmental factors eliciting these responses include irritant gases and fumes, oxidants, organic allergens, inorganic dust, bacterial enzymes, and high partial pressures of oxygen. The basic pulmonary reactions to these toxic agents--bronchoconstriction, vasoconstriction, increased vascular permeability, inflammation, carcinogenesis--may be mediated, aggravated, or modulated by biologically active substances. These humoral agents include biogenic amines (e.g. histamine): peptides (e.g., bradykinin, vasoactive intestinal peptide, and spasmogenic lung peptide); enzymes (e.g., proteases, superoxide dismutase, and mixed function oxidases); and acidic lipids (e.g., prostaglandins, prostaglandin endoperoxides, and thromboxanes).
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PMID:Environmental injury of the lung: role of humoral mediators. 35 83

The Authors consider the global evaluation of clinical and functional data in patients with the following radiological features: 1) X-ray thoracic aspects characterized by marked broncho-vascular bundles and diffusion of reticular nodulation as in diffuse interstitial pulmonary fibrosis; 2) lack of ECG and clinical signs of heart failure. Since a reversibility of radiological alterations was considered a favourable reply to bleeding and diuretic acute and long term therapy the Authors suggest that these patterns should be related to a different distribution of hydric and haematic masses with a decreasing of interstitial pulmonary oedema which contributes to a full interlobar septa like "D" lines shadows, according to Kreel, (1975). The Authors, moreover, relate these clinical, functional and radiological aspects to the patterns of "wet lung" distinguished from the cardiac lung caused by congestive heart failure and from interstitial lung fibrosis.
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PMID:[Contribution to the study of "wet lung". Radiological and clinico-functional changes induced by depletion therapy in 5 patients with chronic bronchopulmonary disease]. 43 31

A follow up of pulmonary function has been performed on three patients having recovered from Mendelson's syndrome (between 1 and 70 months). In the 3 patients a syndrome of diffuse interstitial pulmonary fibrosis was observed. These perturbations disappeared relatively quickly. They were compatible with pulmonary oedema due to the disappearance of surfactant, consecutive to acid inhalation.
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PMID:[A follow up of pulmonary function after Mendelson's syndrome (author's transl)]. 49 9

Pulmonary tissue may be damaged by certain toxins or drugs in a dose-dependent way or by a hypersensitivity reaction. Pathological changes consist of a permeability pulmonary edema, an alveolar hemorrhage, an alveolitis and finally the formation of pulmonary fibrosis. Ingestion of the weed killer paraquat may induce a rapidly progressive and lethal form of fibrosing alveolitis, the inhalation of nitrous oxides may elicit lung edema. The most common drugs causing lung damage are cytotoxic agents, often used in combination, and the noncytotoxic drugs amiodarone and nitrofurantoin.
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PMID:[Toxic and drug-induced lesions of the pulmonary parenchyma]. 158 77

To provide a precise correlation between high-resolution computed tomographic (CT) findings and histologic studies of various parenchymal lung diseases, 20 fixed and inflated lungs were studied as follows: (a) Every lung was cut at the corresponding CT level into 1.5-mm-thick sections, (b) selected slices were cut into small blocks to prepare histologic slides, (c) each slide was photographed, and (d) the image of the entire lung section was reconstituted with the enlarged photographs (assembled as in a jigsaw puzzle). Results obtained in cases of normal lungs, pulmonary edema, alveolitis, hypersensitivity pneumonitis, emphysema, Pneumocystis carinii pneumonia, silicosis-asbestosis, and idiopathic pulmonary fibrosis demonstrated the method to be accurate in correlating high-resolution CT findings and the corresponding histologic data.
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PMID:High-resolution CT of parenchymal lung disease: precise correlation with histologic findings. 173 81

Methotrexate may cause pulmonary side effects. Two cases of methotrexate-induced fibrosing alveolitis are reported. One of the patients died from perforated gastric ulcer, the other was successfully treated with systemic steroids. The pulmonary side effects of methotrexate are reviewed. The most common clinical manifestation is fibrosing alveolitis. Pulmonary fibrosis and acute, non-cardiogenic pulmonary oedema are rare.
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PMID:[Methotrexate induced pulmonary disease]. 226 58

A flood source containing 25 mCi of technetium-99m (99Tcm) was used to measure thoracic tissue thickness (Tt) in 20 healthy subjects, 14 patients with cardiogenic pulmonary oedema, 8 patients with biopsy proven cryptogenic fibrosing alveolitis (CFA) and 10 subjects with radiographic evidence of severe, widespread emphysema. Unattenuated counts from the flood source were acquired first, and then with the subject seated between the flood source and the gamma camera, a second scan of transmitted counts was acquired. Assuming a constant linear attenuation coefficient of 0.135 cm-1, we calculated Tt per pixel of the gamma camera image, thus creating a profile of Tt throughout the length of the thorax. In normal subjects mean (S.D.) Tt at the base of the right lung was 10.8 (2.4) cm. In patients with pulmonary oedema, CFA and emphysema, mean (S.D.) values for Tt, in cm, were 12.9 (2.7) p less than 0.05, 14.4 (1.9) p less than 0.001 and 6.0 (1.1) p less than 0.0001 respectively. This simple, quick and inexpensive technique could be used to give regional measurements of Tt.
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PMID:Thoracic tissue thickness measured by transmission scintigraphy with 99Tcm. 235 68

Bone marrow transplantation is the treatment of choice of many haematological disorders but its success is limited by two major complications, graft-versus-host disease (GVHD) and pulmonary disorders. Of the first 31 patients transplanted at St. James's Hospital (1984-1986) 16 (52%) had a successful outcome. Of the 15 patients who died, two died of GVHD and one of recurrent leukaemia. All others had severe pulmonary disease either causing death directly (9 cases) or contributing to death from toxic encephalopathy, carditis or recurrent leukaemia (1 case each). The principal forms of pulmonary disease were cytomegalovirus pneumonitis (4 cases), acute haemorrhagic pulmonary oedema (4 cases) and pneumocystis carinii pneumonia (2 cases). There were single cases of staphylococcal pneumonia and idiopathic pulmonary fibrosis. Aspergillus was a second pathogen in two cases. Pulmonary damage due to conditioning chemoradiotherapy and to GVHD probably underlies this high incidence of pulmonary disease. T-cell depletion to limit the incidence of GVHD together with increased prophylaxis against CMV and pneumocystis carinii will probably substantially reduce these complications in the near future.
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PMID:Pulmonary disease following allogeneic bone marrow transplantation. 266 67

Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. It is evident that multisystem failure is responsible for death in many patients, as well as secondary pulmonary and extrapulmonary infections. Pathologic studies have provided descriptive information regarding the acute, subacute, and chronic phases of the syndrome, but little insight into the precise pathogenesis of the initial lung injury or the progressive fibrosing alveolitis and lung destruction that develops in some patients. There has been considerable circumstantial evidence from clinical studies implicating the neutrophil as a potentially important mediator of the early changes in lung endothelial and epithelial permeability. However, not all investigators have found the same alterations in neutrophil function in the circulation or in the lavage from the lungs of patients with ARDS. Also, the heterogeneous etiologies of ARDS make it difficult to be sure that there is a final common pathway for acute lung injury in all ARDS patients. In addition, there are a host of mediators, including products of complement activation and arachidonic acid metabolism, that may be important in amplifying the inflammatory response. Also, abnormalities of surfactant production and collagen turnover, as well as impaired host defenses in the lung, may contribute to the progressive respiratory failure that occurs in some ARDS patients, even though the acute, exudative phase of lung injury has resolved. Future human studies may provide useful information about the mechanisms of the acute lung injury through studies of circulating plasma markers, blood elements, and lavage fluids from high-risk patients. On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies? 333 57

The so-called ground glass pulmonary opacity is characterized by a slight increase in lung density, with persistent visibility of vascular structures and bronchial walls. If vessels are obscured, the term consolidation is preferred. This kind of pulmonary opacity, which may be patchy or diffuse, was well known in conventional radiology, but has been recently re-evaluated, following the increasingly widespread use of high resolution CT of the lung. Ground glass opacity is commonly observed in patients with early diffuse pulmonary infiltrative diseases. Though non-specific in itself, the sign is always very significant. Particularly, it could represent a useful sign of active and treatable abnormality in some diffuse pulmonary diseases, such as idiopathic pulmonary fibrosis and sarcoidosis. The ground glass opacity may also be observed in pulmonary edema, desquamative pneumonitis, Pneumocystis carinii pneumonia, alveolar proteinosis, hypersensitive pneumonitis and drug induced or radiation induced lung disease. This paper represents a contribution to the understanding of the pathologic bases of the ground glass pulmonary opacity and an introduction to its differential diagnosis.
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PMID:[Diffuse ground-glass opacity of the lung. A guide to interpreting the high-resolution computed tomographic (HRCT) picture]. 782 71


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