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

A case is reported of fatal recurrent unilateral reexpansion pulmonary edema following thoracentesis in a woman with stage IV ovarian adenocarcinoma. Reexpansion pulmonary edema is a rare complication resulting from reexpansion of a collapsed lung after treatment of pleural effusion, pneumothorax, or atelectasis. The etiology is unknown, and there are no guaranteed measures of prevention. The clinical presentation varies from asymptomatic to rapidly progressive fatal pulmonary edema. The diagnosis is established by chest x-ray. Depending on the severity of the clinical symptoms, treatment varies from monitoring with serial chest x-rays to mechanical ventilation. Reexpansion pulmonary edema is fatal in 20% of cases. Gynecologists should be aware of this rare entity because it may require immediate diagnosis and aggressive treatment.
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PMID:Fatal recurrent reexpansion pulmonary edema. 276 41

Thoracic CT for patients in intensive care is cumbersome but provides important additional information in the presence of complicated lung changes. Total opacification of a lung field visualised on conventional portable films may be due to infiltration and/or fluid and/or collapse by using the clinical information in conjunction with densitometric measurements. CT may help in the differentiation of pulmonary oedema, particularly in the presence of ARDS and its complications. It is also possible to accurately localise abscesses and empyemas in the presence of extensive consolidation. This makes it possible to drain abscesses or empyemas, or pleural fluid in unusual situations, which has become loculated, or to aspirate a pneumothorax.
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PMID:[Computerized tomography of the thorax in intensive care patients]. 303 34

Unilateral reexpansion pulmonary edema (RPE) is a rare complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. Although RPE generally is believed to occur only when a chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid, in this review 15 of 47 cases of RPE available for assessment occurred when the pulmonary collapse was of short duration or when the lung was reexpanded without suction. The pathogenesis of RPE is unknown and is probably multifactorial. Implicated in the etiological process of RPE are chronicity of collapse, technique of reexpansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant, and pulmonary artery pressure changes. Since the outcome of RPE was fatal in 11 of 53 cases reviewed (20%), physicians treating lung collapse must be aware of the possible causes and endeavor to prevent the occurrence of this complication.
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PMID:Reexpansion pulmonary edema. 327 31

Pulmonary edema after re-expansion of a pneumothorax occurs within a maximum of 3 days of the pneumothorax and manifests by intense clinical signs (cough, abundant foamy expectoration, major cyanosis), marked hypoxia and a "white lung" radiologic image. The outcome was rapidly favorable in the case reported, despite the severity of the initial symptomatology. Currently accepted physiopathologic mechanisms implicate numerous factors in the genesis of edema due to re-expansion. The lesional pulmonary edema can be explained by alteration in alveolar capillary permeability, by the atelectasis, hypoperfusion and stretching during revascularization, and possibly by the action of free radicals. A hemodynamic edema also exists as a consequence of the reduction in pulmonary interstitial pressure. Possible prophylactic measures are discussed, the most appropriate appearing to be very progressive evacuation of the pneumothorax.
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PMID:[Reexpansion pulmonary edema after pneumothorax. Apropos of a case. Review of the literature]. 328 64

Re-expansion pulmonary oedema is a rare complication to follow the treatment of pneumothorax or pleural effusion. A unique case is described here which occurred in a young man immediately after the surgical repair of a ruptured diaphragm. The possible causative mechanisms are discussed.
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PMID:Acute localised pulmonary oedema. Re-expansion pulmonary oedema following the surgical repair of a ruptured hemidiaphragm. 274 10

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.
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PMID:Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood. 347 56

Complications were noted in 83% of patients with an associated trauma of the chest. Bilateral pneumonia was the most frequent complication (57.7%), then were traumatic pulmonitis (15.9%) and total pulmonary edema (18%). The adequate anesthesia, liquidation of a disturbance of the chest carcass, timely elimination of hemo- and pneumothorax are thought to be the most effective measures of struggle against pulmonary complications in patients in the early period of the trauma disease. The complex treatment has given 1.5 times less amount of pulmonary complications.
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PMID:[Prevention and treatment of pulmonary complications in patients with combined injuries of the chest accompanied by shock in the early period of trauma]. 372 6

A case of unilateral pulmonary oedema (UPO) caused by rapid re-expansion after drainage of a spontaneous pneumothorax is reported. If acute respiratory failure is noted at the moment of re-expansion the condition can be brought within safe limits by careful clinical observation and if necessary the use of assisted respiration.
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PMID:[Unilateral pulmonary edema due to rapid re-expansion in pneumothorax]. 380 90

Re-expansion pulmonary oedema may develop if diagnosis and treatment of pneumothorax are delayed. This condition may be fatal if inappropriately managed.
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PMID:Re-expansion pulmonary oedema: a potentially serious complication of delayed diagnosis of pneumothorax. 392 82

1. Action potentials have been recorded from single laryngeal motor fibres, with expiratory or inspiratory phases, in cats anaesthetized with pentobarbitone and breathing through a tracheal cannula.2. Pneumothorax increased the discharge of both inspiratory and expiratory units, the inspiratory response being greatly reduced by bilateral vagotomy below the origin of the recurrent laryngeal nerves.3. Addition of a ;viscous' resistance to breathing, or asphyxial rebreathing through an added dead space, increased the activity of inspiratory units and decreased that of expiratory units.4. Induction of pulmonary oedema decreased the discharge of inspiratory units and increased that of expiratory units. After vagotomy the response of inspiratory units was reversed.5. Intravenous injections of potassium cyanide increased the activity of both types of unit.6. Chemical irritation of the laryngeal mucosa decreased the discharge of inspiratory units and increased that of expiratory units, whether the vagi were intact or cut.7. It is concluded that expiratory unit discharge can be correlated with expiratory laryngeal resistance, but that inspiratory unit discharge does not correlate so well with inspiratory laryngeal resistance.8. The relationship between laryngeal motor-fibre activity and the contractions of the inspiratory and expiratory muscles of breathing is discussed.
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PMID:Reflex control of discharge in motor fibres to the larynx. 441 12


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