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

Serious pulmonary complications are often associated with acute pancreatitis. The destruction of pulmonary surfactant by the action of pancreatic phospholipase A2 (PLA2), together with pulmonary edema, is considered an important etiopathogenic factor of acute respiratory insufficiency. This experimental study was undertaken to elucidate the destruction of pulmonary surfactant in acute pancreatitis using the lung pressure volume curve (P-V curve). Acute hemorrhagic pancreatitis was induced in mongrel dogs by a retrograde injection of Na-taurocholate into the main pancreatic duct. Pulmonary surface tension was measured by P-V curve and the effect of PLA2 on pulmonary surfactant was assessed by the ratio of lysolecithin and lecithin, which are essential components of pulmonary surfactant (Ly/Le) in lung wash. Extravascular lung water volume (Ww/Dw) and blood gases were also measured. The value of Ly/Le and serum PLA2 rose significantly from the 3rd hour. On the contrary, no significant differences were seen on P-V curve until the 12th hour but after 20 hours surface tension increased significantly. Ww/Dw and A-aDO2 increased after 3 and 12 hours, respectively. These findings, the degradation of lecithin and the elevation of surface tension accompanied with an increase of serum PLA2, suggest that pulmonary surfactant is destroyed in severe acute pancreatitis, and that the increased capillary permeability of the lung precedes the deterioration of surface tension as the cause of pulmonary insufficiency.
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PMID:[Experimental study on the pathogenesis of pulmonary insufficiency in acute pancreatitis and changes in the pulmonary surfactant]. 322 26

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

Neonatal pulmonary diseases may require mechanical ventilation and supplemental oxygen therapy. These supportive measures can damage the immature lung or distort the normal maturation processes of the developing lung. The formation of hyaline membranes occurs acutely, often complicated by left-to-right cardiac shunts. Pulmonary edema occurs next, followed by interstitial fibrosis and finally by parenchymal emphysema. This process is termed bronchopulmonary dysplasia. Significant morbidity and mortality are associated with this developmental pulmonary dysplasia, particularly during the first two years of life. A delay in normal growth and development is often present, acute episodes of pulmonary insufficiency are seen, and multiple episodes of pulmonary infection occur. Subsequently, the radiographic appearance and the clinical symptoms improve. Therapy is mainly supportive throughout the course of the disease and the bronchopulmonary dysplasia tends to resolve slowly. Residual pulmonary dysfunction is usually mild or absent.
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PMID:Bronchopulmonary dysplasia. 361 5

The clinical fat embolism syndrome consisting of progressive pulmonary insufficiency, cerebral disfunction, and petechiae is rare. Following severe skeletal trauma, fat droplets appear in the circulating blood and embolize the capillaries of the lungs and other organs. Whether fat droplets are of mechanical or chemical origin remains controversial. These fat droplets cause mechanical occlusion of lung capillaries followed by chemical changes associated with hydrolysis of the neutral fat to free fatty acids. The free fatty acids produce a toxic and inflammatory reaction resulting in pulmonary edema, hemorrhage, and microatelectasis. The clinical and radiographic abnormalities appear after an initial latent period of 12 to 72 hours. The chest radiographic findings are nonspecific and consist of bilateral patchy or diffuse alveolar and interstitial lung densities. With aggressive management the survival has markedly improved, and mortality is now rare.
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PMID:The fat embolism syndrome. 361 20

1. With improvements in treatment of burn shock and wound sepsis, inhalation injury has emerged as the number one cause of fatality in the burn patient; it accounts for 20 to 84 per cent of burn mortality. 2. Only steam is capable of inflicting direct thermal damage; most injury is caused by incomplete products of combustion, the most important being aldehydes. 3. More accurate diagnostic techniques, including fiberoptic bronchoscopy and 133Xe scanning, have been added to the traditional clinical signs of inhalation injury, such as facial burns, singed nasal vibrissae, and closed space injury, and have led to a new estimation of a 30 per cent incidence among patients with major burns. 4. Patients with inhalation injury typically pass through three stages, those of acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia. 5. The major early pathophysiologic changes seen in the lungs of burned patients related to edema. With inhalation injury this is probably mediated by the products of activated neutrophils. Later changes are the result of the reduction of surfactant and thus lung compliance. 6. Treatment consists of intubation at the first hint of respiratory distress; the issue of tracheostomy versus endotracheal intubation has not been scientifically resolved, but most centers employ prolonged nasotracheal intubation. Prophylactic antibiotics or steroids are not of benefit. Further care is only supportive and includes CPAP, PEEP, vigorous pulmonary toilet, humidification of inspired air, and antibiotics for documented infection. 7. Further advances await the development of pharmacologic methods of affecting the lung's response to injury, which includes altered capillary permeability and decreased immune function.
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PMID:Pulmonary injury in burned patients. 391 76

The medical records and radiographs of 62 patients admitted for smoke inhalation were reviewed to determine the value of the plain chest radiograph in the early detection of inhalation injury. Pulmonary edema resulting from the inhalation injury often leads to pulmonary insufficiency, and its early diagnosis is crucial to the management of patients with this condition. In addition to the usual presentation of pulmonary edema, subtle radiographic findings of interstitial edema such as perivascular fuzziness and peribronchial "cuffing" were observed. Of 56 patients with significant inhalation injury, 35 (62.5%) had radiographic findings attributed only to smoke inhalation. These abnormalities often had a characteristic distribution in the lungs, and in the majority of patients they appeared in the first 24 hours after the injury. The radiologic diagnosis of inhalation injury may be made at a time when findings of other diagnostic tests are still equivocal or mildly abnormal, thus alerting the clinician to impending pulmonary failure.
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PMID:Smoke inhalation: radiologic manifestations. 662 80

Experimental investigations in the rabbit were aimed at solving the question whether the development of a pulmonary oedema during tocolytic therapy with beta 2-sympathomimetics can be explained by hyperhydration, since myocardial necroses are not likely to be the cause of a pulmonary-oedema at the standard clinical dosage level. Fenoterol is infused over a period of 24 hours in combination with low (2.5 mgl/h) and high (30 ml/h) supply of liquid (isotonic solution, Sterofundin). Essential changes in the measured parameters occur only if the quantity infused is high. The following findings were established: 1. an increase in the liquid content of the lung and heart from 80 to 90%. 2. blood gas analysis revealed marked signs of a ventilatory disturbance, 3. histologically, the lungs showed partly massive changes pointing to the presence of an interstitial and intraalveolar oedema. Since no myocardial necroses can be histologically identified, the pulmonary insufficiency cannot be due to cardiac decompensation as a result of myocardial necroses.
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PMID:[Occurrence of pulmonary oedemas without myocardial necroses under beta 2-sympathomimetic therapy with fenoterol (experimental investigations in the rabbit (author's transl)]. 679 6

In a clinical study the applicability and effectiveness of breathing therapy with intermittent positive pressure in cases of incipient or already established pulmonary complications are evaluated. The case material was divided into four groups: 1. Imminent respiratory complications (haemorrhagic shock, flail chest); 2. acute postoperative pulmonary insufficiency in old patients; 3. postoperative alveolar or interstitial pulmonary oedema; 4. postoperative pneumonia. Individual respiratory training succeeded in all patients in significantly improving the arterial blood gases; prolonged artificial ventilation could be dispensed with. The method and its limitations and indications for its use are reviewed.
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PMID:[Respiratory training with intermittent positive pressure in acute respiratory disturbances (author's transl)]. 679 79

It is suggested that pulmonary microembolism, due to intravascular platelet aggregation, is an important pathogenetic factor in the development of acute post-traumatic pulmonary insufficiency. Changes in blood flow, vessel wall injury and/or changes in the composition of the blood may all induce aggregation of the circulating platelets. Platelet aggregates are then trapped in the pulmonary microcirculation. Experimentally induced intravascular platelet aggregation causes pulmonary vasoconstriction and increases pulmonary vascular resistance. The vasoconstriction has predominantly a precapillary localization. It has also been demonstrated that intravascular platelet aggregation will increase transiently the hydraulic conductivity of pulmonary exchange vessels. Thus, edema development is facilitated, although platelet aggregation per se cannot induce fulminant lung edema. In parallel with the vascular changes, platelet aggregation causes constriction of both peripheral and central airways, as reflected in a decreased dynamic compliance and an increased pulmonary resistance. The central airways are at least partly constricted secondary to nervous reflexes mediated through bronchomotor, parasympathetic nerve fibres in the vagal nerve. If a persistent and long-lasting intravascular aggregation of platelets is induced, the changes in respiratory mechanics described will impair gas exchange and precipitate a severe respiratory insufficiency. This pulmonary insufficiency is, however, dependent on an ongoing activation and aggregation of platelets. When the experimentally induced platelet aggregation is stopped, gas exchange function returns rapidly to normal.
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PMID:The role of platelets in post-traumatic pulmonary insufficiency. 693 94

Injury to the respiratory tract from inhalation of steam, although rare, often leads to acute pulmonary insufficiency. The injury to the alveolar epithelium results in increased pulmonary capillary permeability, pulmonary oedema and interfering abnormalities in gas exchange. Vigorous treatment should be instituted in these patients to obtain optimal outcome.
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PMID:Burns and inhalation injury caused by steam. 878 28


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