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

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.
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PMID:[Examinations to phenomenon of shock-lung (author's transl)]. 0 60

So-called "shock lung" has typical pathological findings; radiologically it is characterised at first by interstitial, late by alveolar pulmonary oedema. This has been shown by a number of case reports. In addition to shock, however, certain intoxications and all forms of left heart failure produce the radiological changes of pulmonary oedema. Transient hyperhydration of the lungs following infusion therapy causes signs of pulmonary oedema which disappear as soon as the fluid balance becomes normal. The radiographic findings of pulmonary oedema correlate well with the intensity and extent of the pathological changes. The radiologist is therefore in a position to evaluate the severity of the shock lung; this is a valuable addition to the clinical findings and the results of physiological tests and blood gas analysis. It has to be emphasised that the radiological changes appear at an early stage, in any case much sooner than the clinical features. Radiological findings may be present without abnormalities on oscultation or percussion. Radiographs of the lungs are therefore indicated in all patients who may be subject to shock lung, particularly if they suffer from undiagnosed hyperventilation.
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PMID:[The radiological diagnosis of shock lung (author's transl)]. 1 30

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
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PMID:Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome. 37 80

The spectrum of pulmonary complications in 28 of 66 burn victims is analyzed according to time of onset and resultant radiographic features. Immediately recognizable pulmonary abnormalities are usually due to chemical pulmonary edema and inhalation pneumonitis. Complications manifested 2-5 days after injury include pulmonary microembolism, adult respiratory distress syndrome, and atelectasis. Delayed complications are major pulmonary embolism, pneumonia, and adult respiratory distress syndrome. In this series, 25 patients (89%) developing pulmonary complications died. The critical role of serial chest radiographs in the evaluation and management of burn victims is emphasized.
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PMID:The radiographic spectrum of pulmonary complications in burn victims. 40 38

Many causes for the adult respiratory distress syndrome (ARDS) have been reported, all with common pathologic, pathophysiologic and biochemical end results. The final common pathway may involve changes in lung content of a critical enzyme, superoxide dismutase, or alterations in surfactant metabolism, or both. The early assumption that the disorder is partially due to oxygen toxicity from inspired oxygen concentrations greater than 60 percent is consistent with findings of recent biochemical studies. Although the lung normally maintains its alveoli dry, during ARDS increased permeability of small pulmonary vessels results in primary pulmonary edema, in contrast to edema from increased vascular pressure. These data have been obtained mainly in animals; whether they apply to humans with ARDS is not certain. Tissue oxygenation is improved by increasing end-expiratory pressure in an animal model of ARDS, more effectively during spontaneous breathing than during mechanical ventilation. During spontaneous breathing, adverse ventilatory effects were caused by stimulation of pulmonary reflexes.
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PMID:Adult respiratory distress syndrome. 42 3

The clinical course and radiographs of 30 patients with fat embolism syndrome were reviewed. In all cases the classic triad of neurologic dysfunction, respiratory insufficiency, and petechiae were present. Three responses to embolized fat were noted. The hyperacute response was seen in two patients with paradoxical embolization of fat to the systemic circulation. A "classic response" was noted in 18 patients with transient respiratory compromise and variable radiographic findings. The two deaths in the group responding in the classical manner were attributed to massive pulmonary emboli. The third response, noted in ten patients, consisted of a chest radiograph compatible with pulmonary edema in the clinical setting of the adult respiratory distress syndrome. In this group the degree of respiratory dysfunction and pulmonary damage correlated with the development of disseminated intravascular coagulation. Pathologic correlations are presented and the mechanisms by which embolic fat produces tissue damage are discussed.
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PMID:The three syndromes of fat embolism: pulmonary manifestations. 45 28

We observed two patients with aspirin (ASA) ingestion (blood levels of 87 and 56.5 mg/100 ml) who presented with noncardiogenic pulmonary edema (adult respiratory distress syndrome. To determine if ASA had a direct effect on the alveolar epithelial membrane, we established an in vitro isolated lung model and perfused it with platelet free plasma. T1/2 (in minutes), the time for 50% equilibration between the plasma and the saline filled lung, was determined before and after 500 mg salicylate infusion for various molecular weight dextrans. T1/2 decreased significantly (p less than 0.05) as follows: 3000 MW dextran, 2273 +/- 932 to 961 +/- 375; 40,000 MW dextran, 4059 +/- 1550 to 733 +/- 275; 70,000 MW dextran, 11,730 +/- 2750 to 7700 +/- 2230. Histamine levels in plasma and lung liquid did not change significantly with ASA infusion. We conclude that ASA directly increases alveolar epithelial permeability to dextrans less than 70,000 MW.
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PMID:The effect of salicylate infusion on the alveolar epithelial membrane in the isolated perfused lung. 65 22

Sudden death after subcutaneous injection of silicone has been described. However, there are no cases in the literature of clinically diagnosed noncardiogenic pulmonary edema. In the patient reported here, progressive hypoxemia and diffuse pulmonary infiltrates occurred following intramammary injection of a material presumed to be silicone. The presence of birefringent particles in the alveolar macrophages implies entrance of this material into the vascular compartment, its embolization to the lung and migration across the damaged alveolar-capillary membrane. Large volume subcutaneous injections of silicone should be added to the differential diagnosis of the etiology of the adult respiratory distress syndrome.
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PMID:Adult respiratory distress syndrome following mammary augmentation. 66 14

Pulmonary shock syndrome may be better understood by comparing morphological and patho-physiological alterations in different stages. In the very early stage only fine structural tracer studies in experimental animals elicit morphological alterations of the microcirculation in the alveolar wall. These findings can be related to changes of ventilatory and blood-gas parameters. After a short interval microscopic and radiological features correspond. Interstitial pulmonary edema is the main syndrome of shock lung.
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PMID:[Pathological and roentgenographic morphology in different stages of pulmonary shock (author's transl)]. 70 34

An assessment of morbidity in near-drowning was made from a review of emergency room and hospital records of 72 patients, ages 9 months to 20 years, who suffered near-drowning during the period January 1972 through June 1974. Fifteen patients (21% evidenced severe anoxic encephalopathy; the remainder had no detectable neurologic deficits. Hypoxemia was demonstrated in 56 patients. Severe acidosis was not present unless respiratory failure occurred. Neither electrolytes, red blood cell hemolysis, nor cardiac arrhythmias presented a problem. Respiratory complications included pulmonary edema, aspiration pneumonia, atelectasis, shock lung, pneumothorax, and pneumomediastinum. All children requiring cardiopulmonary resuscitation in the emergency room suffered anoxic encephalopathy. The occurrence of seizures, fixed and dilated pupils, flaccid extremities, and lack of response to deep pain in the emergency room had almost universal correlation with resultant severe anoxic encephalopathy, as did a submersion period of six or more minutes. The morbidity of near-drowning is significant with regard to the number of children affected and the severity of the central nervous system insult received. The statement by the American Heart Association that resuscitative efforts in children should be continued for periods longer than ten minutes needs reevaluation, since neurologic recovery did not occur in any child requiring cardiopulmonary resuscitation (CPR) in the emergency room. More importantly, new methods of cerebral resuscitation need to be developed and established. In short, medical personnel need to think in terms of cardiopulmonary cerebral resuscitation (CPCR) rather than in terms of CPR.
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PMID:Morbidity of childhood near-drowning. 84 May 54


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