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

When patients present with suspected prosthetic valve dysfunction, investigation is usually instituted to delineate the site and cause thereof. Precordial cross-sectional echocardiography is often helpful in this respect, but in the patient with acute pulmonary edema, imaging may be impaired because of discomfort and respiratory distress. The information obtained may also be suboptimal as a result of concomitant obesity, chest wall deformity, and pulmonary disease. In addition, further difficulties may relate to the acoustic shadowing produced by the metallic portion of the valve and its sewing ring, especially with valves in the mitral position. In such patients, cardiac catheterization may cause further decompensation and is associated with a recognized increase in morbidity and mortality. Angiography does not accurately site regurgitant jets in relation to the prosthetic valve concerned and will not detect the presence of vegetations. Transesophageal echocardiography circumvents many of these imaging difficulties and we evaluated its use in five patients with prosthetic heart valves who presented acutely ill, in severe pulmonary edema and suspected prosthetic heart valve failure. In each case, the diagnosis of valve dysfunction was established, and precise information regarding the site and cause of the failure was obtained. No complications or deterioration in patient condition resulted from the procedure and the findings were confirmed at surgery performed within 24 hours in all five patients. Transesophageal echocardiography should be included in the assessment of acute prosthetic heart valve failure.
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PMID:The value of transesophageal echocardiography in the investigation of acute prosthetic valve dysfunction. 239 17

In this experiment, rabbit model with smoke inhalation injury was used. The study was designed to observe the dynamic changes of elastase activities of polymorphonuclear leukocytes (PMN), alveolar macrophages (AM) and bronchoalveolar lavage fluid (BALF); and trypsin inhibitory capacities of serum and BALF (STIC & BTIC). The relationships between these changes and acute lung injury, as well as the concomitant changes of arterial blood gas levels, lung water volume and pathomorphology of trachea and lung tissues were also observed. It was found that after injury the elastase activities of PMN and AM were markedly reduced, and the elastase activity of BALF was rapidly increased. STIC was also reduced. PaO2 progressively dropped and PaCO2 progressively increased. Animals showed respiratory distress. Pathomorphological phagocytes aggregations in lungs, pulmonary edema and pneumorrhagia were found. There were serious destructions of capillary endothelial cells, alveolar epithelial cells, basement membranes and interstitial fibers. The number of elastic fibers of parenchyma decreased. The lung water volume was markedly increased, and there was a significant correlation between the increment of extravascular lung water and the rising of elastase activity of BALF. On the basis of our observation, it is proposed that the imbalance of elastase-antiprotease may play an important role in the development of acute lung injury after smoke inhalation.
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PMID:[Experimental study of dynamic changes in elastase-antiprotease in rabbits in the early stage of inhalation injury]. 251 41

The treatment of premature labor with beta-adrenergic substances is complicated by side effects. Although most human control mechanisms are pulsatile, therapy is usually administered continuously. We designed a microprocessor-controlled pump to allow pulsatile tocolytic infusion, hoping to reduce the total dose and thus the side effects. In 33 patients pulsatile bolus tocolysis was compared with continuous tocolysis in a control group of 38 patients. Bolus tocolysis required considerably less beta-sympathomimetic agent for comparable therapeutic success (median dosage 3.0 versus 15.9 mg, p less than 0.001). Duration of therapy under bolus tocolysis was also significantly shorter (p less than 0.05). Birth weight was higher after bolus tocolysis (median 3070 versus 2580 gm, p = 0.05). Additional indicators favored bolus tocolysis but were not statistically significant: a longer gestational period, fewer infants weighing less than 2500 gm, and a lower incidence of respiratory distress syndrome. Pulmonary edema occurred in one patient during continuous tocolysis.
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PMID:Bolus tocolysis: treatment of preterm labor with pulsatile administration of a beta-adrenergic agonist. 256 41

Animal models of cardiogenic edema, overhydration edema and respiratory distress syndrome (RDS) were established in 12 rabbits, radiography and CT of the chest were taken in supine position and compared with pathology. In cardiogenic and overhydration edema, the lesion is located at the posterior part of the lungs and around the hili both on CT image and the pathologic specimen. On the radiograph the lesion was projected onto the middle and inner zones of the lungs. In RDS, both CT and pathology showed that the peripheral and posterior parts of the lungs were involved, while on radiograph, the hazy shadows were situated at the periphery of the lungs or in a diffuse pattern. The authors were of the opinion that CT can demonstrate the lesions more clearly than radiography. The underlying mechanism for different distribution of lesions in pulmonary edema and RDS was discussed.
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PMID:[CT, radiologic and pathologic correlative study of pulmonary edema and respiratory distress syndrome in animal model]. 258 12

We report the case of a young patient of 37 presenting with two attacks of pulmonary oedema which revealed an underlying pheochromocytoma. The diagnosis was suggested by the raised level of vanyl-mandelic acid in the urine and the abdominal CT scan. After an adrenalectomy the outcome was satisfactory. Pheochromocytoma should be considered in the differential diagnosis of the acute respiratory distress syndrome in the adult linked to the action of the circulating catecholamines on the pulmonary capillaries.
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PMID:[Pheochromocytoma revealed by pulmonary edema]. 260 19

The authors compared the clinical and pathological findings between adult respiratory distress syndrome (ARDS), and infant respiratory distress syndrome (IRDS). In ARDS, the most common causes were injury, infection, shock and acidosis. The clinical course was longer. The weight of the lungs increased markedly, the hyaline membrane formation in the alveoli was late in the clinical course, and the degree of edema in the interstitium of the lungs and microthrombosis within the blood vessels was more serious. The pathogenesis of ARDS was related to the activation of the complements and neutrophils by inflammation in which proteinase, oxygen radical, thromboxane, leukotriene and prostaglandin were released. Thus the endothelial cells of the blood vessels and capillary-alveoli membrane were damaged by these mediators. On the other hand, the main contributory factors of IRDS were suffocation of premature fetus by various reasons in the uterus and aspiration of meconium during delivery by the infant. The clinical course was shorter, alveolar hemorrhage and collapse were severe and hyaline membrane in alveoli was formed in early stage of the clinical course. Insufficiency of surfactant in premature fetus, damage of the surfactant system by hypoxia, aspiration of foreign materials and defect of the epithelial cells of infant were the pathogenic factors of IRDS, they resulted in increase of permeability of fluid and, as a result, led to pulmonary edema and atelectasis.
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PMID:[Clinical and pathologic comparison of adult respiratory distress syndrome and infant respiratory distress syndrome]. 263 70

Neurogenic pulmonary edema (NPE) is a serious complication associated with various central nervous system insults. Experimental and clinical data support the occurrence of pulmonary edema as a result of neurogenic factors. Patients with NPE have increased intracranial pressure and respiratory distress, and their care presents a challenge to critical care nurses. The pathophysiology of this disease is not well understood. We discuss the current theories of NPE, its signs and symptoms, and the nursing management for patients with NPE.
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PMID:Pulmonary complications in the patient with acute head injury: neurogenic pulmonary edema. 268 17

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

This study was designed to test whether intraperitoneally injected sodium hydrosulfide (NaHS) would mimic the pulmonary alterations induced by lethal peracute exposure to an atmosphere containing hydrogen sulfide. Groups of five Sprague-Dawley rats were exposed to an atmosphere of either 2317.6 +/- 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were injected intraperitoneally with a solution containing 30 mg kg-1 sodium hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of the air and saline groups were killed by cervical dislocation. All rats exposed to H2S or injected with NaHS died within 3 min; however, only rats exposed to H2S showed severe respiratory distress in the agonic phase preceding death. In addition, rats in the H2S group had a notable discharge of serous fluid from the mouth and nostrils. At necropsy, all rats in the H2S group had gross and histologic evidence of pulmonary edema characterized by massive extravasation of eosinophilic fluid into the bronchoalveolar space. In contrast, the lungs of rats injected with NaHS or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of H2S in the lungs cannot be reproduced by injection of NaHS. The severity of lung edema induced by a peracute exposure to H2S was extensive enough to account for death.
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PMID:Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. 271 35

Acute lung injury was produced by intravenous injection of oleic acid. After oleic acid injection, PaO2 was decreased, dogs were involved in respiratory distress. Histological examination indicated aggregation of leukocytes in microvasculature, interstitial and intraalveolar pulmonary edema and congestion in the lung. Using radioimmunoassay technique, changes in arterial and venous plasma levels of stable metabolite of thromboxane A2 (TXA2), thromboxane B2 (TXB2) have been observed. After oleic acid administration, plasma 6-keto-PGF1alpha level was markedly elevated with two peaks. 6-keto-PGF1alpha level in arteries was higher in concentration than in veins. It was suggested that the lung might synthesis a great quantity of prostacyclin entering the systemic circulation. TXB2 was markedly elevated in plasma, which was more in veins than in arteries. A significant arteriovenous difference suggests that there might be extrapulmonary sources contributing to the elevation of plasma TXB2 in oleic acid induced lung injury in dogs. After treatment with large dose of anisodamine (654-2), platelets and leukocytes aggregation could be inhibited as well as the synthesis of TXA2 and prostacyclin. 654-2 might play a role of cyclo-oxygenase inhibitor. It was suggested that 654-2 reduce synthesis of the precursors of TXA2 and prostacyclin, reduce pulmonary edema and might be a therapeutical effect to lung injury.
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PMID:[The study of thromboxane A2 and prostacyclin in oleic acid-induced lung injury in dogs]. 273 67


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