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

Several recent reports have documented the efficacy of surfactants replacement therapy in the neonatal respiratory distress syndrome (RDS). The surfactants tested in these trials were obtained from animal lungs or human amniotic fluid. In general, such natural preparations seem to be superior to entirely synthetic surfactants, although promising results have recently been obtained in animal experiments with artificial surfactant based on isolated apoproteins and synthetic phospholipids. Furthermore, surfactant replacement therapy seems to be more effective when the exogenous material is administered at birth, before the first breath, than when surfactant is instilled into the airways after a period of ventilation. This discrepancy may be due to maldistribution of the exogenous material, or to the rapid development of epithelial lesions in the immature lung, with leakage of surfactant-inhibiting proteins into the airspaces. A transient beneficial response to surfactant replacement may also be due to circulatory problems, especially reversal of the shunt through a patent ductus arteriosus, with overloading of the lung circulation leading to pulmonary oedema and recurrent respiratory failure. Additional, properly randomized clinical trials are required to evaluate the benefits and potential hazards of surfactant replacement therapy in neonatal RDS.
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PMID:Surfactant replacement in the management of the neonatal respiratory distress syndrome. 332 64

Four children, aged 1 to 3 1/2, were first seen with cor pulmonale, pulmonary edema and severe respiratory distress due to chronic upper airway obstruction secondary to adenoidal or tonsillar hypertrophy or both. Arterial blood gas values, electrocardiograms and chest x-ray films were compatible with cor pulmonale. Echocardiography (four cases) and radionuclide angiography (two cases) showed severe right ventricular and right atrial dilation with reduced right ventricular ejection fraction. Following surgery, all four children improved; their echocardiographic and radionuclide findings returned to normal. Cardiac catheterization, traditionally performed in such cases, was unnecessary. The diagnosis and follow-up of this syndrome are adequately performed noninvasively.
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PMID:Cor pulmonale due to adenoidal or tonsillar hypertrophy or both in children. Noninvasive diagnosis and follow-up. 333 41

Intravenous isosorbide-5-mononitrate (IS-5-MN) was administered to 24 patients, mean age 73, with severe respiratory distress after pulmonary edema and acute left heart failure. The condition was due to ischemic cardiopathy in 18 patients (4 with acute myocardial infarctions), congestive cardiomyopathy in 3, hypertensive cardiopathy in 2, and mitral valvular disease in 1. Therapy consisted of an intravenous (i.v.) bolus dose of IS-5-MN, followed by a continuous infusion (mean 8 mg/hour over 24 hours) of i.v. furosemide and additional oxygen. Clinical data were recorded as well as blood gas values and repeated chest radiographs. All patients survived and improved markedly; only 6 needed mechanical ventilation. Most patients had fast respiratory relief, with no untoward reaction, except a brief decrease of blood pressure in a ventilated patient taking morphine. These data indicate that i.v. IS-5-MN is effective and safe for the management of severe acute cardiogenic pulmonary edema.
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PMID:Emergency treatment of severe cardiogenic pulmonary edema with intravenous isosorbide-5-mononitrate. 334 37

A diffuse lesion in the alveolar-capillary membrane appears as an initial pathological event which preludes the emergence of an Acute Respiratory Distress (ARDS) with pulmonary oedema. The implication of polymorphous nuclear cells (PMN) as the cells initiating this lesion remains solidly established. The activation of the complement system has been established in numerous circumstances associated with the risk of the development of an ARDS. This activation can be exogenous and leads to the generation of inflammatory agents, stimulating different types of cells such as the PMN, the monocytes and mastocytes by intermediation of specific receptors, and activate important function of locomotion, adhesion, aggregation, degranulation, etc. Authors describe here the behaviour of C5a and the aggregability of PMN in such patients with a risk of ARDS.
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PMID:IVth International Meeting of Clinical Biology CH Sainte-Ode, Baconfoy, Belgium May 23-24th, 1987 clinical biology in intensive care medicine. Leukocyte aggregation and complement activation in respiratory distress syndrome (ARDS). 338 80

Six cases of leptospirosis with pulmonary complications are reported. Three cases were accompanying an hepato-nephritis due to L. icterohaemorrhagiae. The first patient died with massive hemoptysis. The second, presenting a bilateral pneumopathy predominant on the left side, recovered after plasma exchange and hemofiltration. The third case concerned a pulmonary edema complicating a vascular refilling in a shock syndrome it simply recovered. The three other cases were observed in an anicteric leptospirosis: in two cases, L. Australis was responsible; in the last, L. icterohaemorrhagiae was involved. The first patient had a radiologic picture simulating miliary tuberculosis. The second had pulmonary edema complicating a vascular refilling in a shock syndrome. The last was an acute respiratory distress syndrome, treated with artificial ventilation with penicillin therapy and corticotherapy. All these 3 patients recovered. The diagnostic, physiopathologic and therapeutic problems of these pulmonary complications of leptospirosis are discussed. The lesional nature of the pulmonary edema is proved by the low pulmonary wedge pressures observed with the Swan-Ganz Catheter.
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PMID:[Respiratory complications of leptospirosis. Apropos of 6 cases, 3 of which show hemodynamic studies]. 340 72

Pulmonary edema and/or hemorrhage (PEH) induced by IV injection of norepinephrine was demonstrated in six rats by In-111 chloride lung/heart imaging. The anesthetized rats were positioned under a gamma camera using a pinhole collimator. After In-111 chloride IV injection, analog thorax images were obtained and dynamic data were recorded at 30 seconds/frame for 20 min before and after induced PEH. The gamma camera was interfaced to a computer which generated the curve of the lung/heart radioactivity ratio which rose from 0.4-0.5 at baseline to 1.0-1.4 at the end of the study. The image after IV norepinephrine injection showed a reversal of the lung/heart radioactivity concentration. In-111 chloride instantly binds to plasma transferrin yielding an excellent intravascular imaging agent. Leakage of this tracer into alevoli indicates loss of aveolar membrane wall competence. Pulmonary edema, as in acute respiratory distress syndrome, is difficult to diagnose radiographically and this In-111 chloride lung/heart imaging technique may be potentially useful.
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PMID:Detection of pulmonary edema and hemorrhage using indium-111 chloride images: rat model. 340 9

The non-hemodynamic pulmonary oedema by increase alveolo-capillary permeability or Adult Respiratory distress Syndrome (ARDS), has many causes and determine an acute insufficiency respiratory who needed mechanic ventilation. It can above all progressing to interstitial fibrosis after deadly. The writer present lesional pulmonary oedema case which evolved to fibrosis in a 17 old patient. This patient has been operated for duodenal ulcer with bi-vagotomy and antrectomy and presented a post operatory shock. The particularity of this observation is The fibrosis evolution to an cartilaginous metaplasia. The lesional pulmonary oedema has usually serious prognosis because the mortality is from 50 to 80% in the literature review.
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PMID:[Apropos of a case of lesional pulmonary edema advancing to fibrosis with cartilage metaplasia]. 344 42

Inhalation injury has emerged as the number one cause of fatality in the burn patient. Fiberoptic bronchoscopy and 133Xe scanning complement traditional clinical signs of inhalation injury and have led to discovery of a higher incidence of these injuries among patients with burns. Patients with inhalation injury typically demonstrate three stages: acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia, all of which carry at least 50 per cent mortality rates. The major early pathophysiologic changes in the lungs of burned patients are related to upper-airway obstruction and lower-airway permeability edema. Treatment consists of intubation for signs of respiratory distress, pulmonary toilet, humidification of inspired air, and antibiotics for documented infection.
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PMID:Pulmonary injury in burned patients. 354 66

The potential hazards to maintenance personnel cleaning hot-spring reservoirs are reported following two severe and unusual episodes of acute hydrogen sulfide poisoning involving seven workers. In the first episode, five victims lost consciousness immediately after climbing down a manhole to the bottom of a reservoir disregarding a strong odor of rotten eggs. One of them died immediately. Of the four who lived, three developed hemorrhagic keratoconjunctivitis and aspiration pneumonia, but no sequelae were observed 2 years later. In the second episode, two workers had been cleaning the reservoir for about 2 hours when one collapsed and his companion went to seek help. Both died of acute respiratory distress syndrome due to pulmonary edema within 12 hours. Since hot-spring bathing is a popular recreation in Taiwan, other accidents of hydrogen sulfide poisoning may have occurred but have not been reported. Such clinical information is helpful to enable regulators to initiate proper precautions to safeguard those workers involved.
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PMID:Hydrogen sulfide poisonings in hot-spring reservoir cleaning: two case reports. 357 97

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


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