Development Of Acute Pulmonary Edema Research Articles

Transfusion-associated circulatory overload in orthopedic surgery patients: a multi-institutional study

Abstract Although recognized as a serious complication of hemotherapy, few data are available on the incidence of transfusion-associated circulatory overload (TACO). Detailed demographic and clinical information was obtained from records of 382 Medicare patients undergoing total hip or knee replacements (and receiving transfusions) from January 1992 to December 1993 at five Massachusetts hospitals. Seventy-eight percent of the patients were women with a mean age of 77 years. Thirty-two percent had co-morbidities including myocardial or coronary disease. Transfusion-related complications and comorbidities were identified and reviewed by transfusion experts. Patients were excluded from consideration if non-transfusion factors such as myocardial disease could have contributed to the development of acute pulmonary edema. Four (3 females, 1 male) patients (1.05%) developed TACO postoperatively. Mean age of these patients was 84 years (range, 75–101) versus 77 years for non-TACO. The mean intraoperative estimated blood loss was 375 mL. Each patient received only 1–2 units of red blood cells prior to onset of TACO, and in two cases only autologous blood was used. The mean positive fluid balance was 2,480 mL. The mean pretransfusion hematocrit prior to circulatory overload (CO) was 26.0 percent. symptoms were reversed with diuretics. Length of stay was significantly prolonged by these incidents. TACO is a frequent and serious event in an orthopedic surgical setting. It is associated with advanced age, increased health care costs, and may occur in the setting of modest transfusion volumes. The utilization of conservative transfusion criteria and fluid management in the perioperative setting may decrease the incidence of this complication in this population. Immunohematology 1996;12:87–89.

Comparative Toxicology of Ozone and t-Butyl Hydroperoxide on Isolated Rat Lung

Comparative studies were undertaken on the effects of ozone and t-butyl hydroperoxide (t-BuOOH) on alkane production, glutathione and lactate dehydrogenase (LDH) release from isolated rat lungs. Specifically, ethane and pentane production, as well as glutathione and LDH release were simultaneously determined at different time intervals from the isolated lung preparation in the absence and presence of toxic concentrations of ozone or t-BuOOH. When compared to control conditions, both toxic agents produced a marked decrease in the dry weight to wet weight ratios, reflecting the development of acute pulmonary edema. These toxic agents also caused a marked increase in the efflux of glutathione into the effluent. A much higher glutathione efflux into the effluent was observed during t-BuOOH perfusion in comparison to ozone exposure. In parallel with the enhancement of glutathione release a significant increase in ethane production was also observed during t-BuOOH perfusion. However, the production of either alkane by ozone inhalation was not significantly different from that in the control conditions. Unlike glutathione release, there was no marked increase of LDH release into the effluent following exposure to t-BuOOH or ozone. This suggests that the observed increase in glutathione release caused by t-BuOOH or ozone treatment was not associated with non-specific destruction of cell membrane integrity.

Acute Pulmonary Edema Resulting from Treatment for Premature Labor

The development of acute pulmonary edema in four pregnant women being treated for premature labor with betamimetic and glucocorticoid therapy is described. The radiological features and pertinent obstetrical literature concerning this adverse drug reaction are discussed.

Acute pulmonary edema resulting from treatment for premature labor.

The development of acute pulmonary edema in four pregnant women being treated for premature labor with betamimetic and glucocorticoid therapy is described. The radiological features and pertinent obstetrical literature concerning this adverse drug reaction are discussed.

Pulmonary Edema following Relief of Acute Upper Airway Obstruction

Five children, aged one to five years, with severe upper airway obstruction, three of whom had epiglottitis and two of whom had laryngotracheobronchitis, developed acute pulmonary edema after the obstruction had been relieved by placement of an artificial airway. Although major physiologic changes, such as hypoxemia and massive sympathetic discharge, play a significant role in the development of acute pulmonary edema, we have postulated a possible etiological cause for the development of pulmonary edema in these children which involves a series of physiologic events. The generation of very high transpulmonary pressure gradients during inspiration is opposed by a decreased venous return due to the obstruction during exhalation. Airway pressures then fall abruptly with the insertion of the artifial airway, resulting in a sudden increase in venous return to the central circulation and marked increase in the intravascular hydrostatic pressures. The final result of this series of events is the development of pulmonary hyperemia and edema. The prevention of this situation must begin the moment the airway is inserted and involves the application of moderate amounts of continuous positive pressure to the airway, thus allowing time for circulatory adaption to take place.

Roentgenographic Aspects of Narcotic Addiction

THE MEDICAL complications of narcotic addiction may be divided into two major categories: (1) untoward reactions to the drug itself, and (2) various infectious complications due to nonsterile equipment used for intravenous administration of narcotics. Drug Reactions The most conspicuous roentgenographic changes are encountered in the lungs, ie, the development of acute pulmonary edema (Fig 1 and 2). Although initially emphasized after intravenous use of heroin, the occurrence of pulmonary edema has also been noted with morphine, opium, methadone,1propoxyphene hydrochloride (Darvon), chlordiazepoxide hydrochloride (Librium),2and various other drugs. The roentgenographic findings typically consist of an alveolar pattern, with ill-defined, fluffy coalescent densities radiating from the lung roots peripherally, sometimes in a symmetric fashion, but often with localized variations. In milder cases, there may only be a coarse mottling of the lungs. Since physical findings of pulmonary edema after narcotic abuse may be absent, the radiologist can make

Death caused by fracture of Beall mitral prosthesis: Report of a case

Fracture of a strut of a Beall mitral prosthesis, model no. 105, occurred 151 days after its implantation. The fracture allowed escape of the disc occluder into the left ventricular cavity, resulting in the development of acute pulmonary edema, shock and death within 12 hours. Application of lateral force on the strut during handling of the prosthesis before or at implantation results in cracking of the carbon coat with subsequent stress fatigue and fracture of the underlying wire. This is the fourth known fatality due to this late complication of the model no. 105 Beall prosthesis. The possibility of fracture should be considered and looked for in patients with this prosthesis whenever symptoms of prosthetic malfunction develop. Emergency replacement of the fractured valve is mandatory.

Immaturity and Enhanced Susceptibility to Acute Hemodynamic Pulmonary Edema

The hypothesis that the immature lung is more susceptible than the mature lung to the development of acute pulmonary edema (PE), was tested by determining the transmural hydrostatic pressure in excess of whole blood colloid osmotic pressure (COP) necessary to produce PE in pups and adult dogs. Ten pups and ten adults were anesthetized with pentobarbital, parpalyzed with succinylcholine, and artifically ventilated. Transmural pulmonary artery wedge pressure (TPAWP) (as a reflection of vascular filtration pressure) was monitored continuously and whole blood COP intermittently. A balloon catheter in the thoracicaorta was inflated to produce an elevation of TPAWP in relation to COP that was maintained for 30 min by infusion of isosmotic dog blood to maintain a constant differential pressure (TPAWP-COP). Lungs were then removed and thed degree of PE assessed by gross microscopic appearance and determination of water content. Interstitial edema first appeared with thw following range odf values: Gross edema formed at higher differentiak pressures. Thus the pups developed minimal PE at lower TPAWP than would have been expected from their T.P. and COP. The data do not permit a choice of the several factors that might explain this finding. Similar susceptibility of the human fetus and newborn in relation to the adult would favor the development of PE during the perinatal period and might thus play a role in the pathogenesis of pulmonary problems of the newborn.

The mechanism of the development of acute pulmonary edema in lung surgery.

The mechanism of the development of acute pulmonary edema in lung surgery.

Some aspects of acute pulmonary edema with special reference to pulmonary hemodynamics.

PULMONARY edema has been produced by various agents and methods in experimental animals. Of particular importance to hemodynamic research is the consistent production of an acute pulmonary edema in a fairly large animal which will facilitate necessary determinations. The present report attempts to elucidate some hemodynamic aspects and importance of blood pressure regulation in the development of acute pulmonary edema in the dog.

術後急性肺水腫に関する実験的研究

As one of the experiments to clarify the causes of the development of the post-operative acute pulmonary edema, 50 cc/kg saline solution was injected intravenously to 16 normal dogs and 6 dogs with hypoproteinemia at the rapid rate of 20 cc/m. These dogs were killed 2 hours after the transfusions and the influences of these transfusions on the development of the acute pulmonary edema were examined with following results.1) In normal dogs, the changes of circulatory blood volume and cardiac output and those of pulmonary arterial pressure by transfusions had a parallel relationship. Electrocardiographically, no disturbances of the heart muscle were observed. Histologically, pulmonary congestion and hemorrhages were found, but no lung edema.2) On the contrary, the following findings were observed by transfusions in the dogs with hypoproteinemia; decrease of circulatory blood volume, upset of pulmonary circulation caused by an abnormal rise in the pulmonary arterial pressure and a decrease in the cardiac output, signs of heart muscle disturbances in the E. K. G., and the picture of lung edemas in the microscopic examination.3) Congestion and hemorrhages were the main findings in the group of normal dogs. On the contrary, lung edemas were marked while congestion and hemorrhages were slight in the group of the hypoproteinemia-induced dogs.4) These findings suggested that the capillary permeability had increased more in the hypoproteinemia-induced dogs than in the normal dogs.5) A slight increase in the pulmonary arterial pressure and cardiac output had already been observable before transfusions in the hypoproteinemia-induced dogs, comparing with the normal dogs.6) It is considered from these results that hypoproteinemia which reduces the power of resistence to abrupt circulatory burden is in a preparatory state to the development of the pulmonary edema.

Development of acute pulmonary edema and death in dogs with aortic insufficiency following renal artery constriction.

A standardized type of experimental aortic insufficiency was produced in dogs by partial removal of the aortic ‘noncoronary’ valve. A transventricular approach was used to perform the valvulectomies. All dogs with this type of aortic insufficiency, when subjected to renal artery constriction died in 2 days on the average with acute massive pulmonary edema and congestion.

Development of acute pulmonary edema in mice and rats and interpretation.

ArticleDevelopment of Acute Pulmonary Edema in Mice and Rats and an InterpretationB. Cassen, and K. KistlerB. CassenFrom the Atomic Energy Project, School of Medicine, University of California at Los Angeles, California, and K. KistlerFrom the Atomic Energy Project, School of Medicine, University of California at Los Angeles, CaliforniaPublished Online:01 Jul 1954https://doi.org/10.1152/ajplegacy.1954.178.1.49MoreSectionsPDF (715 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of extreme elevations in venous pressure on reflection coefficient in the lungMicrovascular Research, Vol. 43, No. 1Mechanisms of neurogenic pulmonary edema.Circulation Research, Vol. 57, No. 1Das experimentelle LungenödemEdema of the lungs in albino rats and rabbits after injection of aconitine into the hypothalamusBulletin of Experimental Biology and Medicine, Vol. 63, No. 1ACUTE PULMONARY EDEMASTIMULATION EXPERIMENTS ON THE AMYGDALOID NUCLEAR COMPLEX AND RELATED STRUCTURES EFFECTS UPON THE RENAL VOLUME, URINARY SECRETION, MOVEMENTS OF THE URINARY BLADDER, BLOOD PRESSURE AND RESPIRATORY MOVEMENTSPsychiatry and Clinical Neurosciences, Vol. 11, No. 2 More from this issue > Volume 178Issue 1July 1954Pages 49-52 Copyright & PermissionsCopyright © 1954 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1954.178.1.49PubMed13180710History Received 5 November 1953 Published online 1 July 1954 Published in print 1 July 1954 Metrics

The induction of labor by rupture of the membranes

1.1. A series of 26 cases of induction of labor at or near term by stripping and rupture of the membranes is reported. The technic of induction included a preliminary course of castor oil, enema, and quinine.2.2. The results of this study show an efficiency of 80 per cent, maternal morbidity of 7.6 per cent, maternal mortality of 3.9 per cent, and a fetal mortality of 12 per cent. There was no fetal morbidity.3.3. The high maternal morbidity and mortality were chiefly due to the development of acute pulmonary edema in the two cardiac patients of the series.4.4. Although this method of induction of premature labor has certain advantages not possessed by other methods, its use in patients with organic heart disease appears to be rather dangerous.