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

Five patients are reported who developed evidence of acute lung damage after proved ingestion of paraquat. In two the lung changes resolved; in one an aspiration pneumonia occurred, which was successfully treated, while two developed fatal pulmonary oedema. These pulmonary complications after paraquat intoxication appear more common than the progressive pulmonary fibrosis previously described. It is suggested that acute pulmonary oedema is a response to large doses, usually of Gramoxone, that subclinical lung changes result from small doses, usually of Weedol, and that pulmonary fibrosis occurs after intermediate doses. Preliminary data on plasma paraquat concentrations suggest that these are of value in prognosis.
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PMID:Further clinical observations on the pulmonary effects of paraquat ingestion. 48 82

Accidental acute mercury vapor poisoning in three persons is reported. Three hours after exposure, symptomatology began by chills, vomiting, diarrhea and chest pain. Two patients, respectively 67 and 77 year old, presented severe pulmonary edema, then neurological symptoms with tremor and coma. This toxic pulmonary edema, which entailed artificial ventilation, was followed in both cases by an acute interstitial pulmonary fibrosis which led to death respectively after six and sixteen days. In the third case (a thirty eight year old patient) a skin rash, erythematous and pustuliform was observed. Analysis for total mercury by flameless atomic absorption showed very high mercury levels in blood and urine of the three patients. The effect of treatment by Dimercaptopropanol on renal excretion of mercury was studied. Optic and electron microscopy of the lung of the two patients who died showed the pulmonary changes of acute interstitial fibrosis.
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PMID:Accidental acute mercury vapor poisoning. 50 88

Ingestion or injection of the herbicide paraquat (1,1'-dimethyl-4,4'-dipyridylium dichloride) has caused more than 120 deaths in humans. Most have been due to respiratory failure caused by pulmonary edema, hemorrhage, and atelectasis, or subsequent pulmonary fibrosis. Paraquat is concentrated in lung tissue and is believed to cause superoxide radical formation in the presence of oxygen and suitable electron donors. Exposure to increased concentrations of oxygen has been reported to accelerate the toxicity of paraquat. The therapeutic efficacy of a reduced oxygen environment was investigated by exposing paraquat-poisoned mice to 10% oxygen after stepwise drops from 14% oxygen. Sixty-one mice were given intraperitoneal injections of 27 mg. per kg. of paraquat. The 25 mice in hypoxia for 7 days had a 32% mortality rate versus a 78% mortality rate for the remainder of the mice in room air, p less than 0.01. After a dose of 20 mg. per kg. of paraquat administered intraperitoneally, 24 mice in hypoxia had a 25% mortality rate versus 51% for 35 animals in room air. Brief exposures of the hypoxic group to "normoxia" (room air) led to pulmonary edema and death. The continuous exposure of paraquat-poisoned animals to hypoxic environments was protective. This approach may be useful in other oxidant lung injuries.
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PMID:Hypoxic protection in paraquat poisoning. 99 61

Paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride) has in the last decade gained popularity as an effective weedicide. It is marketed for commercial use as a liquid concentrate Gramoxone ICI (20% paraquat). Accidental or intentional ingestion of Gramoxone has caused 232 human deaths between 1964 and 1973 (Anon 1974). Most human patients suffer transient renal and hepatic insufficiency and pulmonary oedema followed after a latent period by progressive pulmonary fibrosis leading to death from respiratory failure (Harrison 1972). The clinical features of non-fatal paraquet poisoning in a cat and the clinical and pathological findings in fatal poisoning in a dog are reported.
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PMID:Paraquat poisoning in a dog and cat. 125 80

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

Four patients developed an acute respiratory distress syndrome characterised by clinical and radiological signs of pulmonary oedema, a protein-rich oedema, severe hypoxemia refractory to oxygen therapy, contrasting with normal left ventricular filling pressures and indicating increased permeability of the alveolo-capillary membrane, 24 to 72 hours after the onset of acute myocardial infarction. After having excluded the usual causes of the acute respiratory distress syndrome, the authors suggest that acute myocardial infarction, especially when extensive, may cause a lesion of the alveolo-capillary membrane by an unknown mechanism. Treatment consisted in mechanical ventilation with positive expiratory pressures in 3 cases and with continuous positive pressure during spontaneous respiration in the third patient and in relay with controlled ventilation in the other two. These techniques of ventilation improved the hypoxemia and led to complete cure in all cases without evolution to pulmonary fibrosis. In addition to mechanical ventilation, all patients were given systematic antibiotic therapy because of the possibility of an infectious etiology while waiting for the results of microbiological and serological testing and because of the high risk of superinfection which plays an essential part in the outcome of the condition. The immediate response to treatment was favourable in all cases. One patient died suddenly of cardiogenic shock two weeks after this episode. The other patients are still alive 39, 38 and 20 months after infarction. The importance of the diagnosis of the acute respiratory distress syndrome in the acute phase of myocardial infarction resides in its therapeutic implications which are quite different to those of cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress syndrome in the initial phase of myocardial infarction in adults]. 212 17

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Cytotoxic agents may cause interstitial or eosinophilic pneumonitis, alveolar proteinosis, pulmonary venous occlusive disease, pulmonary fibrosis, pneumothorax, or pulmonary oedema. These agents may also potentiate lung injury caused by radiotherapy or high oxygen fractions in inspired air. Clinical and roentgenological features of lung damage induced by cytotoxic drugs are usually non-specific, and differential diagnoses include progression of the malignant disease and a plethora of opportunistic infections. Monitoring of blood gases and carbon monoxide transfer factor may facilitate early detection of drug induced lung injury. Fiberoptic bronchoscopy, bronchoalveolar lavage, transbronchial biopsy, or open lung biopsy may be necessary for reliable diagnosis. Early detection of lung damage and immediate withdrawal of the responsible agent(s) are essential. Steroids may be of therapeutic value in some patients.
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PMID:Pulmonary toxicity of cytotoxic and immunosuppressive agents. A review. 218 2

Methotrexate, an antifolate cytotoxic drug, is used in anticancer chemotherapy as well as an immuno suppressive in rheumatoid arthritis. It is responsible for numerous secondary effects, amongst which is a characteristic acute pneumonia known since 1969. This pneumonitis has been described in detail, up to the present time in 78 cases gathered in this review. The prevalence of this complication is estimated at around 7%. This pneumonia may occur whatever the age, indication for which methotrexate is prescribed, the route of administration of the product (including the intra-thecal route) and the dose. It includes dyspnoea, fever, (sometimes quite marked) and frequently an acute reversible respiratory failure. Radiologically the opacities are usually diffuse interstitial and symmetrical with a basal predominance with sometimes some confluence and occasionally a pleural reaction. In a small number of cases a transient mediastinal adenopathy has been described. Respiratory function tests show a rapidly developing restrictive syndrome accompanied by hypoxia and hypocapnia. Broncho-alveolar lavage is characterised by hypercellularity with a frank and apparently transitory lymphocytosis. Histologically the most frequent lesion sighted is an extensive acute granulomatous reaction with or without oedema. Most often the outcome is favourable (75% of cases). However 6 deaths due to respiratory failure have been reported. Even though there has not been any formal test, steroid therapy in high dosage seems to accelerate recovery. Progress to an irreversible pulmonary fibrosis is possible but rare. The mechanism of this drug related acute pneumonia is not known but would seem to resemble that of other granulomatosis. Besides this rapidly progressive pneumonitis, methotrexate is responsible for a very small number of cases of severe pulmonary oedema and of acute painful pleurisies.
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PMID:[Pneumopathy caused by methotrexate]. 225 35

A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
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PMID:Lung fibrosis induced by Thorotrast. 225 23


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