Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

To assess the efficacy of simple aspiration as a treatment for pneumothorax, 40 consecutive pneumothoraces (28 spontaneous, 12 iatrogenic, all estimated at greater than or equal to 20% collapse on visual inspection of the chest X-ray) in 38 symptomatic patients were treated initially by small-lumen catheter (SLC) aspiration. SLC aspiration avoided the need for large-lumen intercostal catheter (LIC) underwater drainage in 28 cases (70%)--20 of 28 spontaneous and eight of 12 iatrogenic pneumothoraces. Outcome was not predicted by clinical variables or pneumothorax size, whereas an initial aspirate volume of less than or equal to 4 L (n = 33) was predictable of success in 28 cases (85%). Minor local subcutaneous emphysema and vasovagal reactions were encountered infrequently but with similar frequency to LIC drainage. No episodes of re-expansion pulmonary oedema occurred. The results confirm previous reports of the efficacy of simple aspiration as a treatment for spontaneous or iatrogenic pneumothorax. Initial treatment by SLC aspiration is recommended for all but life-threatening presentations of pneumothorax. Although not encountered in this study, the potential risk of re-expansion pulmonary oedema suggests that patients should be observed closely for four hours after aspiration.
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PMID:Pneumothorax: treatment by small-lumen catheter aspiration. 229 26

A 22 year-old man was brought to our hospital about twenty-three minutes following a high-speed motorbicycle accident in which he had blunt chest trauma. He was in severe respiratory distress with marked dyspnea and restless with extensive subcutaneous emphysema involving anterior chest wall, cervical and bilateral inguinal regions. A chest X-ray revealed bilateral pneumothorax involving mediastinal emphysema and also fracture of right submandibular and clavicula. In spite of orotracheal intubation and insertion of bilateral chest tube, continuous air leak and pneumothorax did not improve. Bronchoscopy revealed the disruption of mucosa of the right main bronchus at the bifurcation. Emergency right thoracotomy was performed and there was the complete disruption of the right main bronchus. Anastomosis of the right main bronchus with circumferential resection was undertaken on May 30, 1987 about two hours after trauma. About three months after reconstruction, bronchoscopic examination revealed stomal stenosis with deformation of tracheobronchial cartilage and granulation. The stenosis showed severe irregularity by deformed cartilage and thickened scar, so widening by Nd-YAG laser vaporization was inadequate in effect. Seven months after first reconstruction, we performed re-reconstructive operation, right upper sleeve lobectomy with partial resection of carcina and right wall of trachea for scar with severe deformation of cartilage. Following the operation, the patient suffered from sepsis with pneumonitis accompanied by lung edema. This complication was treated successfully. We considered that acute pneumonitis was caused by reventilation with increase of perfusion after tracheobronchial reconstruction. Consequently, we thought it important to treat such patients with long term IPPB postoperatively with adequate medication for respiratory system.
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PMID:[Successful re-reconstruction for complete disruption of the right main bronchus by blunt chest trauma]. 232 99

A flood source containing 25 mCi of technetium-99m (99Tcm) was used to measure thoracic tissue thickness (Tt) in 20 healthy subjects, 14 patients with cardiogenic pulmonary oedema, 8 patients with biopsy proven cryptogenic fibrosing alveolitis (CFA) and 10 subjects with radiographic evidence of severe, widespread emphysema. Unattenuated counts from the flood source were acquired first, and then with the subject seated between the flood source and the gamma camera, a second scan of transmitted counts was acquired. Assuming a constant linear attenuation coefficient of 0.135 cm-1, we calculated Tt per pixel of the gamma camera image, thus creating a profile of Tt throughout the length of the thorax. In normal subjects mean (S.D.) Tt at the base of the right lung was 10.8 (2.4) cm. In patients with pulmonary oedema, CFA and emphysema, mean (S.D.) values for Tt, in cm, were 12.9 (2.7) p less than 0.05, 14.4 (1.9) p less than 0.001 and 6.0 (1.1) p less than 0.0001 respectively. This simple, quick and inexpensive technique could be used to give regional measurements of Tt.
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PMID:Thoracic tissue thickness measured by transmission scintigraphy with 99Tcm. 235 68

Between February 1988 and December 1989, 15 combined heart-lung, 2 double lung and 5 single lung transplants were performed at our institution for end stage lung disease. The indication for heart-lung transplantation was primary lung disease with associated secondary heart failure in 11 cases, diffuse pulmonary disease with extensive adenopathy of the hilum in 2 cases and profuse and antibiotic-resistant tracheobronchial infection due to Pseudomonas in 2 cases. A double lung transplant was performed in 2 patients with hypertensive emphysema. The indication for a single lung transplantation was emphysema in 2 cases and pulmonary fibrosis in 3 cases; in this last indication, transplantation should be performed on the right side with a slight lengthening of the main bronchus to avoid the side-effects of mediastinal shift. There were 2 early deaths, 7 secondary deaths (from the 2nd to the 5th month) due to viral or bacterial infectious complications, and 1 late death in the 7th month (infection due to a syncitial virus). All 12 surviving patients have an excellent functional result; the size of the tracheal or bronchial anastomosis ranges from 85% to 100% of normal. From this experience, we conclude that specificity and severity of lung hazards are mainly related to bronchial infection, dependence on steroids and pleural adhesions. Moreover, posttransplant pulmonary oedema, mucociliary dysfunction and the differential diagnosis between rejection and infection require careful endobronchial suction and periodical sampling.
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PMID:Lung and heart-lung transplantation for end-stage lung disease. The Bordeaux Lung and Heart-Lung Transplant Group. 236 Oct 20

Cadmium is a highly toxic element that is cumulative and has a long biological half-life in mammals. The severe toxicity of cadmium in man has been known for more than 100 years. Despite the knowledge that cadmium is toxic, only 20 human cases of poisoning via ingestion were recorded prior to 1941, whereas in the ensuing five-year period more than 680 cases of cadmium poisonings from accidental oral ingestion of this metal were documented. Some of the recorded effects of exposure to cadmium in laboratory animals include renal tubular damage, placental and testicular necrosis, structural and functional liver damage, osteomalacia, testicular tumors, teratogenic malformations, anemia, hypertension, pulmonary edema, chronic pulmonary emphysema, and induced deficiencies of iron, copper, and zinc. Some of these effects have also been observed in human after accidental exposures to cadmium oxide fumes and are characteristic of the syndrome described in Japan as Itai Itai disease in which ingestion of cadmium is the inciting chemical.
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PMID:Cadmium inhalation and male reproductive toxicity. 240 89

Two characteristics, volatility and biotransformation, make mercury somewhat unique as environmental toxicant, and make mercury poisoning as one of occupational diseases in the industry. Acute mercury vapor poisoning is a rare event. It often occurs during industrial accident or ignorant experiment. We report a case, a 28-year-old male waterworks technician, who developed dyspnea, cough, chest pain, metallic taste and ache in the whole body three hours after heating approximately 30 ml of liquid mercury during an experiment. Diarrhea with tarry stool occurred the next day. Chest roentgenogram revealed diffuse pulmonary infiltrates similar to pulmonary edema in both lungs, and was complicated by pneumomediastinum and subcutaneous emphysema later. The concentration of mercury in the plasma was over the toxic level. The urinary excretion of mercury greatly exceeded normal value. During hospitalization, the patient's liver and renal function tests were both normal. He was treated with penicillamine, 300 mg every six hours orally for 10 days in addition to a support treatment and oxygen therapy. He was discharged on the 15th hospital day with partial resolution of pulmonary infiltrates and was free of symptom.
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PMID:[Acute pneumonitis caused by inhalation of mercury vapor--report of a case]. 276 70

This study describes an experimental model of smoke inhalation injury in sheep in which the same pathophysiologic alterations occur as with clinical inhalation injury in man. Diffuse pulmonary mucosal sloughing with atelectasis and emphysema with concomitant development of pulmonary edema results in a decrease in arterial oxygen and progressive pulmonary deterioration which results in a substantial mortality. Increased pulmonary edema fluid is shown to be caused by an increased microvascular permeability to protein with pulmonary lymph and tracheobronchial fluid, a filtrate of plasma. Concomitant with this increase in microvascular permeability is an influx of neutrophils, release of proteolytic enzymes and an identified presence of the metabolite of the prostanoid thromboxane A2 which are postulated as contributors to the progressive pulmonary dysfunction post inhalation injury.
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PMID:Etiology of the pulmonary pathophysiology associated with inhalation injury. 302 79

Heart and lung transplantation has only provided long-term survival for patients with end-stage cardiopulmonary disease. Many more patients of potential recipients cannot receive the transplantation because of a pause of satisfactory donors. One of its reason is difficulty in prolonged heart-lung preservation and this has imposed a significant barrier to donor procurement. Using Autoperfusion of heart and lung, six hours preservation was successfully achieved in six mongrel dogs and an adequate condition for preservation was evaluated. 1. Glucose metabolism, 2. Electrolytes, 3. Acid-base balance, 4. Pulmonary blood flow, 5. Temperature, 6. Ventilation were considered important factors for long hours preservation. Heart and lung preserved for six hours were transplanted in thirteen dogs in heterotopic and orthotopic models and their functions were evaluated two hours after transplantation. The cardiac function was well preserved and pathological changes in cardiac muscle were minimum. But lung preservation was not so stable. Levels of PaO2 were variable and pathological changes of the donor lungs such as pulmonary edema, emphysema, etc were observed. Further studies were needed for lung preservation.
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PMID:[An experimental study on the heart and lung preservation and transplantation. Autoperfusion method and cardiac and pulmonary functions after transplantation]. 314 58

Continuous measurement of arterial oxygen saturation (SaO2) using pulse oximetry has become a common monitoring and management technique in critically ill hospitalized patients. To determine the impact of SaO2 monitoring on emergency patient management, we conducted a prospective uncontrolled clinical trial on 40 adult patients presenting to the emergency department with acute respiratory illness, such as emphysema, asthma, or pulmonary edema. Recorded data included hemograms, arterial blood gases, subsequent therapy, and response to treatment. Additionally, the "early warning" capability of SaO2 monitoring was analyzed by recording the severity and outcome of hypoxemic events during treatment. Mean duration of usage for the 40 oximeters in the ED was 1.8 hours; all probes functioned reliably over a wide range of systolic pressures (80 to 206 mm Hg), heart rates (40 to 180 beats per minute), and hematocrits (20% to 58%). There was good correlation between simultaneous pulse oximeter values and both directly measured SaO2 (r = 0.95) and saturations derived from measured arterial PaO2 (r = 0.94). The device detected several otherwise unrecognized drops in arterial saturation that were confirmed by laboratory analysis. Other clinical situations in which the pulse oximeter was found useful in the ED are reviewed. We conclude that continuous measurement of SaO2 can improve the monitoring of ED patients, increase the precision of therapy, detect hypoxemia during intubation, suctioning, and other treatments, and detect clinically unsuspected changes in arterial oxygenation.
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PMID:Continuous emergency department monitoring of arterial saturation in adult patients with respiratory distress. 336 26


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