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

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.
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PMID:Suspected monensin toxicosis in feedlot cattle. 402 19

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions (PaO2 and PaCO2) were measured 24 hours after dosing was done and were correlated with clinical, biochemical, and pathologic changes. Three of the calves (No. 1, 2, and 3) showed acute respiratory distress syndrome 24 hours after the first 3-MI treatment, with a large increase in respiratory frequency, minute viscous work, and PaCO2 and a large decrease in tidal volume, dynamic lung compliance, and PaCO2. They died 36, 38, and 84 hours after dosing. Pulmonary function changes were compatible with the severe pulmonary edema and alveolar damage observed at necropsy. The 2 other calves, after they were given the 1st dose, showed only subacute respiratory distress syndrome with less severe changes in PF values recorded at 24 hours. Furthermore, they became progressively more tolerant to the 2nd, 3rd, and 4th weekly treatments, and showed base-line PF values after the 5th weekly treatment. Pathologic changes were not observed in lung biopsy material from these 2 animals at 2 and at 12 weeks after the 8th (or last) 3-MI treatment.
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PMID:Pathophysiologic study of 3-methylindole-induced pulmonary toxicosis in immature cattle. 403 88

Pulmonary oedema is caused by an excessive accumulation of interstitial fluid in the lungs: in the case of left ventricular failure, oedema arises due to an increase in capillary hydrostatic pressure. Non-cardiac oedema, on the other hand, is brought about by a change in alveolar capillary membrane permeability. Although the causes are different, namely respiratory distress syndrome in adults, altitude-induced pulmonary oedema, oxygen toxicity, medication, metabolic changes, etc., the result is the same, i.e. damage to the alveolar capillary membrane. This damage appears to be brought about by two factors: complement activation and damage to the blood clotting mechanism. The difference between cardiac and non-cardiac pulmonary oedema is difficult to gauge. If pulmonary cone pressure is normal or low, and if the oedematous fluid/plasma protein ratio is greater than 0.7, the oedema is non-cardiac in origin. Treatment is carried out with the aim of repairing the alveolar capillary membrane and preventing extension of the damage. Respiratory insufficiency is treated by a mechanical respirator, applying positive pressure at the end of expiration. Fluid administration is adjusted according to pulmonary cone pressure levels. Opinions are still divided over whether to administer crystalline or colloidal solutions, steroids or protease inhibitors.
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PMID:[Non-cardiac pulmonary edema: an enigma today]. 404 65

Non cardiogenic pulmonary edema (PE) is frequently observed during the postoperative period. 56 patients with postoperative PE were divided into two groups: ARDS, acute respiratory distress syndrom and NHPE, non hemodynamic PE. The incidence of primary pulmonary infection and pulmonary superinfection were investigated. Both groups were not different except for the level of PaO2 lower in ARDS. Mortality was higher in ARDS (80%) than in NHPE (42%). Pulmonary primary infection and superinfection were respectively observed in 33 and 10%, and 23 and 15% of ARDS and NHPE. Blood cultures were more frequently positive during abdominal sepsis than during pneumonia. Viral etiology was thrice noted in 13 pneumonitis. Value of diagnostic methods for respiratory infections is discussed.
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PMID:[Lung infection and acute adult respiratory distress syndrome during surgical resuscitation]. 405 51

Transfusion-related acute lung injury (TRALI) is an infrequent but life-threatening complication of hemotherapy. The findings in 36 cases are described. The typical clinical presentation includes acute respiratory distress characterized by hypoxemia and fulminant pulmonary edema. The onset is usually within 4 hours of transfusion and is accompanied by hypotension. In most patients (81%), recovery is rapid and complete. In 89 percent of cases, granulocyte or lymphocytotoxic antibodies are found in the serum of the implicated blood product which contained plasma. HLA-specific antibodies were identified in donor serums in 65 percent of cases evaluated. The passive transfer of these antibodies may promote complement activation and subsequent pulmonary injury. TRALI is an important cause of transfusion-associated morbidity and is probably often misdiagnosed. Blood banks need to identify donors whose plasma causes these reactions in order to prevent their recurrence.
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PMID:Diagnostic and pathogenetic considerations in transfusion-related acute lung injury. 407 3

Betaadrenergics are the most important agents in the treatment of premature labour. Often they are used in combination with steroids which promote fetal lung maturation and prevent respiratory distress syndrome in preterm infants. Because PG synthesis inhibitors also reduce uterine contractions they have been used as tocolytics whenever beta adrenergics alone fail. Several cases of pulmonary edema in otherwise healthy pregnant women have been reported following a combined tocolytic treatment with betaadrenergic drugs and PG synthesis inhibitors. The inhibited synthesis and function of renal PGs may be a very important factor contributing to those fatal events. Both, the ADH stimulating effect of beta adrenergics and the inhibition of the negative feed back mechanism of PGs on ADH action by blockade of PG synthesis potentiates renal water retention, thereby increasing the risk of water intoxication. Concerning the effects of maternal tocolytic treatment on the fetus or newborn, there is good evidence that PG inhibitors like aspirin or indomethacin can lead to closure of the ductus Botalli prior to birth and persistent pulmonary hypertension of the newborn. Severe cardiopulmonary adaption disturbances may be the consequence. Routine clinical use of PG synthesis inhibitors in combination with adrenergic stimulants cannot be recommended on the basis of available information.
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PMID:[Risks of simultaneous tocolytic treatment with beta adrenergic and PG inhibiting agents]. 612 12

Neonates with respiratory distress requiring mechanical ventilation may be treated with muscular paralysis to improve oxygenation. This results in characteristic radiographic features that relate in part to the specific drug used. The radiographic signs are: bell-shaped chest, decreased bowel gas, and soft-tissue edema. When all three findings are present, the use of neuromuscular blockade can be suggested from the radiographs alone without the aid of clinical history. Radiographs of 57 infants treated with muscular paralysis and mechanical ventilation were compared to 20 infants treated with mechanical ventilation alone. In paralyzed patients, a characteristic bell-shaped chest was seen in 24 of 57 and decreased bowel gas in 46 of 52. Soft-tissue edema was seen in patients treated with metocurine, and the incidence increased with duration of therapy (18 of 25 treated for 5 or more days); it was not radiographically detected in patients treated with d-tubocurarine (0 of 13). Bell-shaped chest, decreased bowel gas, and soft-tissue edema occurred one, three, and one times, respectively, in 20 nonparalyzed control infants, and each time the findings carried significantly different clinical implications. All cases were reviewed to determine if pulmonary edema can result from mobilization of soft-tissue edema fluid after cessation of neuromuscular paralysis, and this was found not to occur.
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PMID:Therapeutic neuromuscular paralysis in neonates: characteristic radiographic features. 621 65

Nuclear medicine imaging procedures can play a significant role in evaluating the pulmonary complications that are seen in trauma patients. A quantitative method for measuring increased pulmonary capillary permeability that uses Tc-99m HSA allows early diagnosis of acute respiratory distress syndrome (ARDS) and accurately differentiates this condition from pneumonia or cardiogenic pulmonary edema. This technique may be of great value in following the response to therapy. The use of 133Xe to diagnose inhalation injury remains an important diagnostic tool, particularly at hospitals with specialized burn units. Regional decreases in ventilation-perfusion images reliably localize aspirated foreign bodies. Radionuclide techniques that are used to demonstrate gastropulmonary aspiration remain controversial and require further clinical evaluation. Pulmonary perfusion imaging, although nonspecific, may provide the earliest clue for correct diagnosis of fat embolism, air embolism, contusion, or laceration. Furthermore, the possibility of perfusion abnormality due to these uncommon conditions must be remembered whenever trauma patients are evaluated for pulmonary thromboembolism with scintigraphy. Occasionally, liver or spleen scintigraphy may be the most appropriate procedure when penetrating chest trauma also involves these subdiaphragmatic organs.
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PMID:Radionuclide evaluation of lung trauma. 622 97

The adult respiratory distress syndrome (ARDS) is an extreme form of noncardiogenic pulmonary edema associated with alveolar-capillary damage. Clinical features include acute respiratory distress, dyspnea and tachypnea, severe hypoxemia refractory to oxygen therapy, and diffuse bilateral pulmonary infiltrates. Any number of serious disorders can cause ARDS, but the processes leading to the alveolar permeability defect are not understood. Therefore, therapy remains nonspecific and supportive. Treatment includes positive end-expiratory pressure, careful fluid management, steroid therapy, and adequate nutrition. Unfortunately, even with the most sophisticated intensive care, the mortality of ARDS is still greater than 50%.
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PMID:The adult respiratory distress syndrome. 634 98

A primigravida with severe kyphoscoliosis developed cardio-respiratory failure in pregnancy. Cardiac arrest occurred 10 days after Caesarean section; gastric acid was aspirated then and was followed by the development of adult respiratory distress syndrome. Initial recovery, with clearing of peripheral oedema, was followed by a recurrence of respiratory distress associated with infection. Profound hypoxaemia and oliguria unresponsive to diuretics were relieved by the infusion of prostacyclin combined with fluid removal by ultrafiltration. This treatment may be of value in the management of respiratory distress syndrome when pulmonary oedema is the dominant feature.
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PMID:Use of prostacyclin and ultrafiltration in adult respiratory distress syndrome. 637 Oct 91


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