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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the authors observed an excess of dyspnea complaints in coalminers without bronchitis, massive fibrosis or emphysema in different epidemiological surveys. An abnormally high prevalence of dyspnea complaints in coalminers has also been reported by other investigators in different countries. It seems therefore necessary to study whether the type of complaints observed in our country can be validated by appropriate functional investigations. A research on this problem is in progress in our laboratory. In this preliminary publication a review of the literature concerning the mechanisms of dyspnea is presented. Such a study was necessary in order to make an adequate choice of the functional measurements usable for our validation study.
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PMID:[Dyspnea symptoms in coalminers]. 12 19

Peripheric circulatory disturbances and acrocyanosis in Moselle vinedressers injured by arsenic. During the years 1972--1975 a total number of 100 vine-dressers came for medical treatment because of late injures caused by arsenic intoxication. That is an average of 400 examinations per year 1600 control examinations within four years. These patients belonged to the age-classes 1890--1923, and the average time of exposure to arsenic was 20 years. After years of being exposed to arsenic, and even years after the exposure to it has stopped, there are those so-called late injures caused by arsenic. There are typical arsenic melanisms on the forehad-temple-rim where the hair begins to grow, on the nape of the neck, on the shoulders, chest, arms, and on the back of the hands which pass into precanceroses and carcinomas. The average time until the first late injuries caused by arsenic occur is 26 years. However, there have been latence periods of up to 50 years. This depends mainly on the amount of arsenic absorbed during the time. There are skin alterations which resemble very much an acrodermatitis chronica atrophicans Herxheimer. Histological examinations rather showed the symptoms of an endangiitis obliterans with atrophy of the cutis. These symptoms were found in 60--70% of the 50--60 years old patients, in 80--90% of the 60--70 years old patients, and in 90--95% of the 70--80 years old patients. Simultaneously there are distinct peripheric circulatory disturbances, cyanosis of the lips, dyspnoea, and an emphysema together with typical cardiac insufficiency. Foot and finger pulse are distinctly slower, and the temperature of the skin is remarkably lower. While people grow older the cyanosis gets worse. With a control group of patients who hadn't been exposed to arsenic these symptoms had only been found on 1--2%.
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PMID:[Peripheral circulatory disorders and acrocyanosis in arsenic exposed Moselle wine-growers]. 13 69

Spontaneous pneumomediastinum is a relatively rare disease, the clinical signs of which may be misleading, and the physiopathology is still unknown. The authors report 7 cases collected over a period of 3 years and note the etiology, the clinical findings and the X-ray findings. The disease often affectsyoung sybjects, without any sex predominance. The initial symptom is thoracic pain and is often accompanied by dispnea. Subcutaneous emphysema only appears secondarily and may be mild. The association with pneumothorax is not rare. Among the etiological circumstances, pneumomediastinum often occurs after an effort or a respiratory infection with dyspnea. The diagnosis depends on the discovery of subcutaneous emphysema and on radiological signs in A.P. and lateral chest views. Treatment should be as conservative as possible in the usual benign forms. It should be limited to bed rest, analgesics and sedatives. In severe cases, supra-sternal drainage permits decompression of the mediastinum. The physiopathological mechanisms are discussed, but the usually accepted theory is rupture of an alveolus into the pulmonary interstitial tissue. The pressure gradient necessary for this rupture may be due to variations in alveolar or vascular pressure.
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PMID:[Spontaneous pneumomediastinum]. 17 Jun 84

In four outbreaks of indoor calf pneumonia, dyspnoea was a prominent clinical finding. At necropsy it was associated with pneumonia involving the cranial lobes of the lung and severe pulmonary emphysema. Histological examination of lung tissue revealed bronchiolitis and alveolitis with alveolar epithelial cell hyperplasia and multinucleate syncytium formation. Intraalveolar haemorrhage, intra-alveolar oedema and hyaline membrane formation were also noted. In all cases parainfluenza type 3 (PI3) virus was isolated from the lungs. In each of the four outbreaks there was evidence of PI3 virus and respiratory syncitial virus (RSV) infection.
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PMID:Observations on outbreaks of respiratory disease in calves associated with parainfluenza type 3 virus and respiratory syncytial virus infection. 21 84

Two sisters were found to homozygous for alpha-1-antitrypsin deficiency. One was disabled by breathlessness and had advanced clinical and radiological emphysema which was confirmed on lung function testing. The other, of similar age and smoking history, was symptom-free with a normal chest radiograph. She had a slightly increased airways resistance, a reduced gas transfer, a bilaterally reduced apex--base perfusion gradient and a small but generalized increase in physiological dead space in all zones. The minor pulmonary and vascular abnormalities present in the younger sibling suggest that we are witnessing early changes in the evolution of the panacinar emphysema characteristic of alpha-1-antitrypsin deficiency. The reason for the different rates of progress of the disease in these two sisters is not understood.
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PMID:Lung function in alpha-1-antitrypsin deficient sisters. 30 59

Clinical data from 246 adult Swedish individuals with severe alpha1-antitrypsin deficiency, Pi Z, diagnosed in 1963--77, were analyzed. Primary emphysema was present in 109 cases. Of 75 Pi Z patients with other types of chronic obstructive pulmonary disease (COPD), all but 7 showed signs of emphysema. Median age at onset of dyspnoea in Pi Z smokers was 40 years, compared to 53 in non-smokers (p less than 0.001). Of the Pi Z individuals over the age of 50, 19% had a diagnosis of liver cirrhosis and 15% signs of glomerular renal damage. Of 91 deceased patients, 56 died from COPD and 12 from liver disease. A greatly reduced survival was demonstrated in Pi Z individuals, regardless of sex. Smoking Pi Z individuals had a significantly lower life expectancy than Pi Z non-smokers (p less than 0.01).
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PMID:Natural history and life expectancy in severe alpha1-antitrypsin deficiency, Pi Z. 30 8

The disease course is described in 21 patients with low serum concentrations of alpha1-antitrypsin of the phenotype Z (genotype pi ZZ). 13 of these patients have long-standing disease characterized by bronchitis or dyspnea beginning before the age of 40 and progressing to emphysema (11 patients) and to corpulmonale (7 patients). The remaining 8 patients are children with hepatopathy characterized by prolonged jaundice at birth, persistent hepatomegaly and persistently elevated liver enzymes. In 2 children, the evolution to cirrhosis was ascertained by biopsy.
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PMID:[Severe alpha 1-antitrypsin deficiency: clinical observations of 21 patients]. 31 May 77

A study of the pathogenesis of bovine ephemeral fever confirmed that the major clinical signs were fever lasting no more than 2 days, with increased respiratory rate, dyspnoea and some degree of lameness. Haematological observations revealed a neutrophilia with a left shift and a lymphopaenia at the time of peak clinical reaction. The net result was a slight leucopaenia on the day after this reaction. The most prominent pathological changes involved the lungs and synovial joints. Pulmonary emphysema and alveolar collapse with bronchiolitis, degenerative changes in synovial membranes and increased synovial fluid were observed. Specific fluorescence indicating the presence of BEF viral antigen could be detected at the time of peak clinical response in individual cells in the lungs, spleen and lymph nodes as well as neutrophils. Before and after the peak fever some fluorescence was seen in cells which appeared to be reticular cells in the lymph nodes. Viral isolation in mice could be made from blood, lungs, spleen and lymph nodes over a period of no more than 3 days. It is postulated that viral growth takes place mainly in the reticuloendothelial cells in the lungs, spleen and lymph nodes and not in vascular endothelium or lymphoid cells.
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PMID:Studies on the pathogenesis of bovine ephemeral fever. 33 60

Clinical symptoms such as mediastinal and tissue emphysema, impaired inflow with cyanosis and extreme dyspnoea, signs of tension pneumothorax suggest rupture of a bronchus; nonstop loss of air via intercostal drainage is an almost certain sign and bronchoscopy provides the final proof. Injury to smaller bronchi may remain asymptomatic. 1,600 persons were treated for chest injury during the past 17 years, 7 of them on account of a ruptured bronchus. The right and left main bronchus were involved in 4 cases and one case respectively. The bronchus of the right upper lobe and the trachea were ruptured in one case each. Once the injury has been diagnosed surgical repair should follow quickly, although the results of anastomoses performed at a later stage were also satisfactory. Closure was by chromcut knotted sutures. Partial pneumonectomy is indicated only if damage to the lungs is extensive. The postoperative respiratory function of the injured lung was satisfactory in all cases.
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PMID:[Diagnosis and treatment of injuries to the tracheo-bronchial system (author's transl)]. 37 50

In experimental models pulmonary emphysema may be produced in hours to days; however, in human subjects emphysema commonly develops over a period of many years. In this report we document a case of severe emphysema which developed in less than six months in association with an unexplained illness characterized by dyspnea, hypoxemia and bilateral lung parenchymal disease. There was no hereditary predisposition. The diffuse alveolar injury syndrome must be considered as a potential cause of alveolar disruption.
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PMID:Rapid onset of emphysema associated with diffuse parenchymal disease. 46 38


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