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

Based on a study of the literature and our own experience treating fisherman poisoned by mustard gas, this article outlines the clinical effects, and toxicological and mutagenic properties of the agent. Mustards are very persistent chemical agents that easily penetrate clothing. Mustard gas usually causes clinical symptoms after the liquid penetrates the skin or the vapor is inhaled. Skin lesions are similar to first- or second-degree burns and usually heal spontaneously in 4 to 6 weeks. Eye symptoms are photophobia and reduced vision. Following inhalation of the agent, pulmonary edema and long-term dyspnea may be seen. As mustard gas is an alkylating substance, it is conceivable that the risk of developing cancer may be increased, as observed in people who were involved with the production of mustard gas and in animals exposed to the gas. Also, transient significantly increased sister chromatid exchange rates have been found in fishermen exposed to mustard gas. Patients exposed to mustard gas must be treated immediately after exposure. Treatment should consist of cleaning of the exposed skin and clothes with an antigas powder and water and soap. The skin lesions should be treated as burns. Eye lesions and respiratory problems should be treated symptomatically.
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PMID:Mustard gas: clinical, toxicological, and mutagenic aspects based on modern experience. 331 37

Although pneumonia virus of mice (PVM) is ubiquitous among rodent colonies in the United States, it has not been reported to cause clinically apparent disease in euthymic mice. However, PVM has been reported to cause respiratory disease and death in experimentally infected euthymic and athymic mice. A group of nu/nu mice, housed in quarantine in a Trexler-type isolator, had weight loss and dyspnea. Gross necropsy findings included cachexia and diffuse pulmonary edema or lobar consolidation. Histologically there was diffuse interstitial pneumonia. Electron microscopy revealed filamentous virions budding from plasma membranes, and immunohistochemical staining of lung tissue was positive for PVM antigen. PVM was isolated from affected lung tissue in BHK 21 cells and mouse antibody production tests resulted in seroconversion to PVM. Experimental inoculation of athymic mice with lung homogenate from spontaneously infected mice resulted in clinically apparent respiratory disease and histologic lung changes similar to those in naturally infected mice. Inoculation of athymic mice with infected BHK 21 cell culture fluid resulted in pneumonia which was qualitatively similar to, but less severe than, that observed in mice with spontaneous disease. These findings indicate that naturally occurring PVM infection in athymic mice may cause respiratory disease and wasting.
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PMID:Respiratory disease and wasting in athymic mice infected with pneumonia virus of mice. 337 86

Over a 7-year period, 15 pregnant women admitted to Parkland Memorial Hospital for acute pyelonephritis developed respiratory insufficiency characterized by dyspnea, tachypnea, hypoxemia, and radiographic evidence of pulmonary infiltrates. Clinical manifestations usually appeared 24 to 48 hours after the patient was admitted and varied from mild respiratory distress to pulmonary failure in three; these three required tracheal intubation and mechanical ventilation. We found no evidence that pulmonary edema was caused by intravenous fluid overload. Oxygen therapy and ventilation were given to maintain the arterial PO2 at 80 mm Hg or greater, and erythrocyte transfusions were given to six women to correct anemia. Women with pulmonary injury were more likely to have multisystem derangement than a control group without respiratory involvement, but there were no clinical risk factors that were predictive at admission. This syndrome was probably caused by permeability pulmonary edema, likely mediated by endotoxin-induced alveolar-capillary membrane injury since other evidence of endotoxemia was common. Thrombocytopenia, hemolysis, intravascular coagulation, renal dysfunction, and transient cardiomegaly concomitant with hyperdynamic ventricular function are all explicable from endotoxin effects.
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PMID:Pulmonary injury complicating antepartum pyelonephritis. 357 94

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

Clinical studies were performed in 27 consecutive patients with high-altitude pulmonary edema who were transported from the mountains to Shinshu University Hospital, Matsumoto, Japan. The altitude of onset was 2,680 m to 3,190 m above sea level. Symptoms included marked dyspnea, cough, and stridor. Physical findings included cyanosis, tachycardia, and rales. Neurologic disturbances, which were seen in 17 patients, included headache, vomiting, memory disturbance, clouding of consciousness, or coma. Chest roentgenograms revealed patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern, and enlargement of the right ventricle. Hemodynamic studies by right cardiac catheterization showed that high-altitude pulmonary edema was noncardiogenic. Scintiscans of the lungs with technetium-99m-macroaggregated albumin (99mTc-MAA) performed in one patient showed decreased perfusion of 99mTc-MAA in the area of infiltrates. Pulmonary edema fluid collected through the endotracheal tube in two patients was rich in protein. Computerized tomograms of the brain showed small ventricles and cisterns, disappearance of sulci, and diffuse low density of the cerebrum, indicating cerebral edema in eight of nine cases. Retinal hemorrhage and papilledema were observed in five patients.
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PMID:Clinical features of patients with high-altitude pulmonary edema in Japan. 366 94

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.
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PMID:Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings. 367 32

The intravenous injection of ethchlorvynol is an uncommon cause of noncardiac pulmonary edema. Two cases of intravenous ethchlorvynol-induced pulmonary edema are presented. The patients fell asleep after injecting the liquid contents of Placydil capsules (ethchlorvynol) and awoke several hours later with severe dyspnea. Arterial blood gases demonstrated marked hypoxia. Chest radiographs revealed bilateral diffuse alveolar densities. The patients' symptoms and radiographic findings resolved after several days of supportive care. Changes in the lung caused by ethchlorvynol may be the result of direct effect of the drug on the lung.
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PMID:Pulmonary edema induced by intravenous ethchlorvynol. 377 3

The clinical and autopsy records of 65 patients with either polymyositis (24) or dermatomyositis (41) and pulmonary disease were reviewed. Pulmonary symptoms were recorded in 43 of the cases and included dyspnoea in 31, cough in 23, and chest pain in six. Interstitial lung disease was noted at autopsy in 27 patients; almost half of these had arthritis. Bronchopneumonia was found in 35 patients, 31 of these had received prednisone. Dysphagia was present in a similar proportion of patients with and without pneumonia. Pulmonary vasculitis was seen in five patients; pulmonary symptoms, arthritis, and raised erythrocyte sedimentation rate were present in four of these cases and all five had associated interstitial lung disease. Other pulmonary manifestations included pulmonary oedema, primary pulmonary malignancy, diffuse alveolar damage, fibrinous pleuritis, pulmonary emboli, and diaphragmatic atrophy. The mean survival after disease onset was 29 months but was much less for those with interstitial lung disease and pulmonary vasculitis.
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PMID:Pulmonary disease in polymyositis/dermatomyositis: a clinicopathological analysis of 65 autopsy cases. 381 71

In this study, we report the case of a 48 year-old female patient showing a clinical picture after a month's evolution consisting of cough, moderate effort dyspnoea, asthenia, anorexia and loss of weight. One year before, she had been diagnosed with bronchial asthma and she had been treated for two years with policarpine collyrium for a glaucoma simplex. The exploration only showed the existence of iris synechias in the right eye and conjunctival hyperaemia on the same side, together with basal crepitant rales on auscultation. Once we had proved the existence of a peripheral eosinophilia superior to three thousand elements per mm3 and of peripheral pulmonary infiltrates with radiographic negative for pulmonary edema, the picture was included in the so-called P.I.E. syndrome whose various etiologies were discarded subsequently. Following a pharmacological survey, a study of parasites in faeces and cutaneous tests as well as provocative tests, the specific causes of P.I.E. were discarded. According to the transbronchial biopsy and the biopsies of skin, nerve and muscle, it was unlikely that the diagnosis would be granulomatosis and/or angiitis. No evidence was found of any of the affections in which P.I.E. is regarded as a minor component. In view of the above, we thought the correct diagnosis was chronic eosinophilic pneumonia, since all the characteristics defining this picture according to Carrington were fulfilled. The treatment was started with corticoids and a clear improvement of all clinical symptoms was observed, including the ocular findings and the disappearance of radiographic pulmonary infiltrates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Apropos of a case of chronic eosinophilic pneumonia associated with iridocyclitis and bronchial asthma]. 383 34

Hyperthyroidism was diagnosed in 4 cats with congestive heart failure. Dyspnea and anorexia were observed in 3 of the 4 cats. In each cat, a holosystolic left and/or right apical heart murmur was auscultated. In 3 cats, a prominent extra heart sound (gallop rhythm) was auscultated. All cats had a palpably large thyroid lobe(s) and weight loss. The laboratory and ECG changes were similar to those reported for feline hyperthyroidism. Moderate-to-severe pleural effusion and cardiomegaly were detected via radiography in all cats. Some cats had radiographic signs of pulmonary venous engorgement and pulmonary edema. Echocardiography revealed cardiac dilatation and low left ventricular shortening fraction (wall motion) in all cats. Three cats responded initially to cardiac drugs and propylthiouracil or thyroidectomy. One of these died later, presumably from an adverse reaction to propylthiouracil, and the others died from recurrent congestive heart failure (1) or postoperative cardiac arrest (1). One cat did not respond to treatment, and died 2 days after diagnosis.
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PMID:Congestive heart failure associated with hyperthyroidism in cats. 394 9


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