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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Environmental lung injury may take the form of acute tracheobronchitis, asthma, pulmonary edema, chronic bronchitis, emphysema, allergic pneumonitis, fibrosing alveolitis, pleurisy, and neoplastic disease. Environmental factors eliciting these responses include irritant gases and fumes, oxidants, organic allergens, inorganic dust, bacterial enzymes, and high partial pressures of oxygen. The basic pulmonary reactions to these toxic agents--bronchoconstriction, vasoconstriction, increased vascular permeability, inflammation, carcinogenesis--may be mediated, aggravated, or modulated by biologically active substances. These humoral agents include biogenic amines (e.g. histamine): peptides (e.g., bradykinin, vasoactive intestinal peptide, and spasmogenic lung peptide); enzymes (e.g., proteases, superoxide dismutase, and mixed function oxidases); and acidic lipids (e.g., prostaglandins, prostaglandin endoperoxides, and thromboxanes).
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PMID:Environmental injury of the lung: role of humoral mediators. 35 83

Although most new 'high tech' industrial processes are developed in industrialized countries, many of these technologies are eventually transferred to the industrializing countries. Many of these new technologies are associated with the use of respiratory toxins. However, there has been little study of acute or chronic health effects of work in these industries. The semiconductor industry illustrates many of these issues. The past decade has been increasing globalization of semiconductor manufacturing. Semiconductor manufacturing uses many chemicals with extremely high respiratory toxicity, including gases such as arsine and phosphine, strong acids and bases, dopants and photoactive chemicals. In semiconductor manufacturing, gases and chemicals are strictly controlled, but little is known about the occurrence of respiratory symptoms or disease in this industry. Potential acute respiratory effects of these exposures include mucous membrane irritation, tracheobronchitis, pulmonary edema and death. Chronic effects may include airway sensitization and possibly respiratory cancer. Movement of 'high tech' industries to less industrialized countries may not be accompanied by the same degree of attention to the control of workplace exposures. The shortage of adequately trained health and safety personnel, greater attention to safety than to health issues, and the unorganized and unskilled workforce in industrializing countries may exacerbate this situation. More research is needed on the health effects of exposures in rapidly changing industries such as semiconductor manufacturing, and the results of this research must be communicated and safe practices implemented worldwide.
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PMID:Occupational lung diseases in the industrializing and industrialized world due to modern industries and modern pollutants. 132 47

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

During summer-like outdoor temperature, a seven-month old female infant was put into a sleeping bag, wrapped up with a blanket and tied up by her mother and a friend of hers because of unrest and continuous screaming. Prior to that, between 0.30 a.m. and 0.45 a.m., occurred the rectal measurement of temperature: 37.5 degrees C. The infant died one to two hours later. At 10.00 a.m., about 8 hours after death, in the criminal investigations of the police measurements of temperature were made: rectal 38.1 degrees C; in the pharyngeal cavity 29.5 degrees C; surrounding temperature 22.2 degrees C. In the forensic autopsy, symptoms of maltreatment were noticed: hematoma of the skin at buttock and legs, no essential change of organs. The histological investigation showed an interstitial pulmonary oedema, an acute catarrhal tracheobronchitis and hyperaemic inner organs. Concerning the complete investigation results, an acute cardiac insufficiency and circulatory failure due to hyperthermy after wrapping up and immobilisation of the child were assumed to be the cause of death. In consequence of the avowal of the maltreater they were accused of murder and convicted for bodily injury with death. The difficulties of the differential diagnosis SIDS by hyperthermy and mortal hyperthermy due to maltreatment will be discussed. The necessity of a close cooperation between police and forensic physicians is emphasized as prerequisite to clarify such events.
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PMID:[The differential diagnosis of sudden infant death or child abuse--a case of fatal hyperthermia]. 281 99

The case report of a fatal result in an abortion requested because X-ray diagnostic studies of the gallbladder and intestine had been made during an undiagnosed early pregnancy is presented. A uterine vacuum aspirator had not been purchased by the hospital. A portable laboratory vacuum pump with an appropriate suction trap was used. The apparatus had been used previously in several abortion cases. After dilatation of the cervix and insertion of the aspirating cannula, the pump was turned on. A sudden massive effusion of bloody froth issued from around the cannula. The cannula was removed immediately. It was found that the tubing had been incorrectly connected. The aspirator tube was connected with the pressure outlet of the pump. The tubing was then correctly placed and the uterus emptied. The patient was given succinyl choline, intubated, placed in the Trendelenburg position, and monitored cardiographically. About 30 seconds after the uterine insufflation blood pressure became unobtainable. The pulse slowed to 50 beats/minute and respiration diminished. Cardiac ausculation revealed no sounds. Respiration was maintained using oxygen through an endoctracheal tube. The pulse was still palpable and the EKG showed abnormal QRS complexes. Cyanosis then became evident. Closed chest cardiac massage was used for 1 minute but the patient became pulseless and QRS complexes were bizarre. Then the chest was opened and each ventricle was needled. From each ventricle of the distended heart air hissed under pressure through the needle vent site. The ascending aorta was needled and air escaped under pressure. Cardiac color and action improved when aided by massage. Iv isoproterenol and intracardiac epinephrine were given. An electric defibrillator converted the cardiac rhythm to a sinus rhythm. Norepinephirne brought about hypertension. Blood and albumin were given iv. The patient never regained consciousness. Tracheostomy and a feeding gastrostomy were required. Urinary and respiratory infections followed and the patient died after 2 1/2 months. Autopsy revealed tracheobronchitis, bronchopneumonia, and pulmonary edema. The brain showed extensive cerebral cortical necrosis. The heart was normal. This maternal death was preventable.
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PMID:Air embolism and maternal death from therapeutic abortion. 502 50

In recent years, pulmonary complications have become a major cause of death in burn victims. Familiarity with the spectrum of these complications leads to an earlier and more specific diagnosis based on chest radiographs. We reviewed the medical records and chest radiographs of 239 patients admitted to our burn unit over a one-year period. Pulmonary complications were categorized on the basis of their anatomic location in the respiratory tract and on whether they were the result of direct chemical injury from smoke inhalation, or were secondary to inhalation injury with or without cutaneous burns. Tracheobronchitis, chemical pulmonary edema, and adult respiratory distress syndrome (ARDS) resulted from direct injury. Pneumonia, ARDS, pulmonary congestion, atelectasis and pulmonary emboli were the main complications secondary to the injury. Pulmonary complications developed in 76 patients (31.8%) and, of these, 57 died (75%). Patients involved in a closed space fire and those who had a burn involving 50% or more of their surface area seem to be at the greatest risk of developing pulmonary complications.
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PMID:Pulmonary complications in burn patients. 666 83

Incidence and extent of pulmonary complications were evaluated retrospectively in 101 patients with hepatic coma (34 patients with acute liver failure, 57 patients with hepatic encephalopathy and 10 patients with mixed forms). 76 patients (73.3%) had pulmonary complications (pulmonary edema 57 cases, pneumonia 20 cases, tracheobronchitis 30 cases). Lethality of the group with pulmonary complications was 97% as compared to 16% in the group without pulmonary complications. Pathogenesis of pulmonary complications is not completely clear; different mechanisms are being discussed like central mechanisms, vascular lesions caused by metabolic or toxic factors, cardiac failure, and increased susceptibility to infection. In 9 out of 59 cases (15.3%) with respiratory failure no morphological changes could be observed in the lungs; in these cases intrapulmonary shunts might have been the cause for the pulmonary complications. The incidence of pulmonary complications increased by a factor of 2.4 during intensive care unit treatment of the patients; this increase shows, that intensive care unit treatment still has to be improved.
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PMID:[Pulmonary complications in hepatic coma]. 682 Jun 75

In their review article the authors overview the primary and secondary pulmonary complications of rheumatoid arthritis with the help of bibliographic data. They emphasize the pulmonological complications of disease modifying antirheumatic drugs used for the pharmaceutical therapy of rheumatoid arthritis, of which they discuss the methotrexate induced pulmonary diseases. Methotrexate participates nearly in all of additive double and triple--O'Dell-scheme--combined disease modifying antirheumatic drugs therapy. Because of that, the early detection of drug-induced pulmonological complications is important. For rheumatologists the treatment of methotrexate resistant rheumatoid arthritis is always getting a higher and higher challenge. Biological therapeutical drugs act as cytokine antagonists, by blocking TNF-alpha and, compared to disease modifying antirheumatic drugs, they can more effectively inhibit the progression of the disease. These are the biological response modifiers. Their main representatives are infliximab, adalimumab, and etanercept. At the end, the authors discuss secondary pulmonary complications caused by biological response modifiers, e.g. the biological response modifiers associated pulmonary tuberculosis, bacterial tracheobronchitis, bacterial pneumonia, bronchiectasia, pulmonary oedema, rapid fibrosing alveolitis, and coccidioidomycosis. At 3% of patients with rheumatoid arthritis, treated with biological response modifiers, who live in Arizona, California, Nevada, pulmonary and systemic mycosis--coccidioidomycosis can appear with a 15% of mortality. As a consequence of frequent earthquakes, the spores getting into the air from the ground infect immunosuppressed patients treated with biological response modifiers. The authors draw attention to the fact that patients who receive biological therapy and travel to the above-mentioned endemic or earthquake-active regions, have a potential high risk, so it is indispensable that they are informed by the doctor. Testing and use of newer and newer groups of biological response modifiers are expected in the near future in the therapy of rheumatoid arthritis. Nowadays--in patients, who are non-reactive for TNF-alpha inhibitor treatment--the use of B-lymphocyte inhibitor rituximab, characteristic in non-Hodgkin lymphoma therapy is possible. The pulmonary complications of rheumatoid arthritis therapy of that cytokine are not known yet. Today, antirheumatic therapy results in a significant improvement of patients' life-quality, whilst the more and more modern therapeutical methods cause more complications.
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PMID:[The pulmonological manifestations of rheumatoid arthritis]. 1861 67

Oxygen administration is uniformly used in emergency and intensive care medicine and has life-saving potential in critical conditions. However, excessive oxygenation also has deleterious properties in various pathophysiological processes and consequently both clinical and translational studies investigating hyperoxia during critical illness have gained increasing interest. Reactive oxygen species are notorious by-products of hyperoxia and play a pivotal role in cell signaling pathways. The effects are diverse, but when the homeostatic balance is disturbed, reactive oxygen species typically conserve a vicious cycle of tissue injury, characterized by cell damage, cell death, and inflammation. The most prominent symptoms in the abundantly exposed lungs include tracheobronchitis, pulmonary edema, and respiratory failure. In addition, absorptive atelectasis results as a physiological phenomenon with increasing levels of inspiratory oxygen. Hyperoxia-induced vasoconstriction can be beneficial during vasodilatory shock, but hemodynamic changes may also impose risk when organ perfusion is impaired. In this context, oxygen may be recognized as a multifaceted agent, a modifiable risk factor, and a feasible target for intervention. Although most clinical outcomes are still under extensive investigation, careful titration of oxygen supply is warranted in order to secure adequate tissue oxygenation while preventing hyperoxic harm.
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PMID:Bench-to-bedside review: the effects of hyperoxia during critical illness. 2627 83

Introduction: Intubation is required to maintain the airways in comatose patients and enhance oxygenation in hypoxemic or ventilation in hypercapnic subjects. Recently, the Centers of Disease Control (CDC) created new surveillance definitions designed to identify complications associated with poor outcomes. Areas covered: The new framework proposed by CDC, Ventilator-Associated Events (VAE), has a range of definitions encompassing Ventilator-Associated Conditions (VAC), Infection-related Ventilator-Associated Complications (IVAC), or Possible Ventilator-Associated Pneumonia - suggesting replacing the traditional definitions of Ventilator-Associated Tracheobronchitis (VAT) and Ventilator-Associated Pneumonia (VAP). They focused more on oxygenation variations than on Chest-X rays or inflammatory biomarkers. This article will review the spectrum of infectious (VAP & VAT) complications, as well as the main non-infectious complications, namely pulmonary edema, acute respiratory distress syndrome (ARDS) and atelectasis. Strategies to limit these complications and improve outcomes will be presented. Expert commentary: Improving outcomes should be the objective of implementing bundles of prevention, based on risk factors amenable of intervention. Promotion of measures that reduce the exposition or duration of intubation should be a priority.
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PMID:Limiting ventilator-associated complications in ICU intubated subjects: strategies to prevent ventilator-associated events and improve outcomes. 3046 Aug 68


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