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

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.
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PMID:Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice. 1 87

Non cardiogenic pulmonary edema is caused by an increase of alveolocapillary permeability, due to different etiologies: fat embolism, multiple trauma, septic shock, influenza pneumonia, aspiration syndrome... Chest radiographs exhibit interstitial and/or alveolar pattern, severity of injury is assessed by the magnitude of intra-pulmonary shunting. Pulmonary wedge pressure is normal, and increased pulmonary vascular resistance is sometimes evidence in prolonged evolutions, especially in fatal cases. Treatment consists in the suppression of hypervolemia, and ventilation with positive and expiratory pressure (PEEP). Extra-corporeal membrane lung oxygenation remains since now rather unsuccessful.
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PMID:[Non cardiogenic pulmonary edema (author's transl)]. 22 Jul 23

The analysis of most important publications and the authors' own data on the pathological anatomy and pathogenesis of influenza are presented. Severe complicated forms of influenza are characterized by the development of acute bacterial tracheobronchites which are the source of staphylococcal aspirations into the lungs. The degree of severity of developing pneumonias is determined to a large extent by destructive changes in the lungs. The destruction of osmiophilic bodies in the alveolar epithelium and the disturbance of the surfactant system is conducive to pulmonary edema. An important role in the involvement of the lungs and other organs is played by viralstaphylococcal toxicity. Lymphoid-macrophage and leukocyte reactions responsible for the production of antibody, interferon, and other factors of resistance are very important for protection against influenza. During epidemics, particular attention should be paid to combinations of influenza with cardio-vascular diseases.
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PMID:[Pathological anatomy and pathogenesis of influenza]. 90 14

We report the case of a 24-year-old white female in need of tocolysis during the 25th week of pregnancy with i.v. hexoprenaline, while suffering from a discrete influenza-like syndrome with nasal discharge and sinusitis. A few hours later fulminant acute adult respiratory distress syndrome (ARDS) developed. ARDS is a rare (0.5-5%) but feared complication of tocolysis with beta-2 mimetic agents and magnesium sulfate. Its physiopathology is obscure, but iatrogenic hyperhydration and lesions of the alveolar-capillary membrane are suspected. In this case both factors were involved, but lesions of the alveolar-capillary membrane were predominant. A direct toxic effect of beta-2 mimetic agents on the alveolar-capillary membrane has not been demonstrated and other factors favoring pulmonary edema during tocolysis with beta-2 mimetic agents, especially infections, are discussed.
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PMID:[Lesional pulmonary edema associated with tocolysis by hexoprenaline sulfate]. 153 26

Of several toxins examined, only staphylococcal alpha and gamma toxin, endotoxin, and diphtheria toxins were lethal for 5-day-old ferrets. Their toxicities were enhanced in animals infected at 1 day old with influenza virus, from 3-fold with staphylococcal gamma toxin through 14-fold for staphylococcal alpha toxin, 84-fold for endotoxin, and 219-fold for diphtheria toxin. No increased viral replication occurred in any tissue; thus the effects of the toxins were exacerbated by the infection, not vice versa. Neonates died suddenly without clinical symptoms as in human babies dying from the sudden infant death syndrome (SIDS). Pathologic examination showed inflammation in the upper respiratory tract, lung edema and collapse, and early bronchopneumonia in the toxin- and influenza virus-treated animals but not in those treated with toxin or virus alone. Thus, bacterial toxins could play a role in SIDS, this being more likely with a concomitant influenza virus infection.
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PMID:Exacerbation of bacterial toxicity to infant ferrets by influenza virus: possible role in sudden infant death syndrome. 198 74

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Inhalation of fumes from pyrolysis of polytetrafluoroethylene (Teflon) is known to cause polymer fume fever, a mild syndrome of influenza-like symptoms of short duration. Occasionally more severe reactions occur. Several cases of pulmonary edema have been reported, only one of which was fatal. We report a case history of pulmonary edema and pericarditis following inhalation of fumes from grinding a Teflon coated surface. Pericarditis has not been reported previously in connection with polymer fume reactions. We discuss various aspects of such reactions, with reference to the case and to selected literature.
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PMID:[Pulmonary edema and pericarditis after inhalation of Teflon fumes]. 292 20

Three recent cases from one institution using the total artificial heart (TAH) before transplantation are reviewed. The first patient was implanted for 12 hours with the pneumatic Phoenix total artificial heart after failure of a donor heart 1 day after transplant. Following retransplantation the patient died from severe pulmonary edema, pulmonary hypertension, right ventricular failure, and Pseudomonas septicemia. The second patient was implanted with the Jarvik-7 total artificial heart for rapidly deteriorating idiopathic cardiomyopathy. Major complications during the 9 1/2-day implant consisted of severe pulmonary edema for the first 4 days and a multifocal cerebral embolic event on the seventh day after implantation from which he fully recovered. Major problems after transplant included disseminated toxoplasmosis and two mild episodes of rejection. The patient was discharged 68 days after surgery and remains well. The third patient was a 40-year-old woman with rapidly progressing acute influenza A viral myocarditis. Despite immunosuppressive and antiviral therapy, cardiogenic shock with multiple organ failure developed. The 70 ml Jarvik-7 was implanted for 4 1/2 days. Acute humoral rejection from autoantibodies and alloantibodies led to a cardiac arrest on the second day after transplantation. A second 70 ml Jarvik-7 implant was followed by severe multisystem and infectious complications. After prolonged intensive care support, the patient recovered and is now awaiting transplantation. Nearly 100% cytotoxic antibody reactivity caused by multiple antigenic stimuli is preventing ready access to donor hearts for this patient. We view the current role of the total artificial heart as a tool to preserve life until a suitable donor heart can be found, reverse the end-organ effects of progressive heart failure and low output, and restore transplant candidacy in selected patients with temporary reversible contraindications to transplantation.
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PMID:Three recent cases of the total artificial heart before transplantation. 330 69

A patient with probable hydrochlorothiazide-induced pulmonary edema is described. A 70-year-old woman experienced nausea, diaphoresis, and severe respiratory distress approximately 1/2 hour after taking an Aldactazide tablet. She had experienced a flu-like syndrome after taking a single tablet two weeks previously. The patient was mildly tachycardic with a blood pressure of 74/0 mm Hg. A chest X-ray revealed cardiomegaly and bilateral pulmonary edema suggestive of congestive heart failure. The pulmonary capillary wedge pressure was normal. It was felt that the patient had developed a noncardiac pulmonary edema possibly secondary to hydrochlorothiazide ingestion. Nine other cases reported in the literature also are described. Pharmacists should be aware of this potential life-threatening reaction and avoid patient reexposure to the drug.
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PMID:Hydrochlorothiazide-induced pulmonary edema. 669 86

The effect of remantadine on the development of viral toxicosis caused in mice by original and remantadine-resistant strains of influenza virus was studied. A definite reduction of the antitoxic effectiveness of remantadine was demonstrated in passages of toxigenic influenza A virus strain in its presence. Prophylactic administration of remantadine protected mice from the development of toxic pulmonary edema and death caused by inoculation of a massive dose of influenza B virus. Passages of influenza B virus in the presence of remantadine produced a strain causing toxicosis in mice the course of which was not affected by remantadine any longer.
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PMID:[Effect of remantadine on the development of toxicoses caused by different strains of influenza virus]. 733 81


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