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PubMed1990

Recurrent pneumothoraces and mediastinal emphysema in systemic lupus erythematosus.

Neither pneumothorax or mediastinal emphysema are well recognized pulmonary manifestations of systemic lupus erythematosus (SLE). We describe a 41-year-old woman with severe lupus pneumonitis complicated by recurrent pneumothoraces and mediastinal emphysema. Other features of SLE were minimal. She died of progressive respiratory failure. Autopsy revealed innumerable blebs in both lungs responsible for the pneumothoraces and mediastinal emphysema. Both pneumothoraces and mediastinal emphysema occurred during a course of corticosteroid therapy. The course of her illness was unaffected by treatments that included high dose corticosteroids, immunosuppressives and plasmapheresis. Better medical treatment for these lupus complications should be sought in addition to surgery.

Adrenal Cortex Hormones↗
PubMed1990

[Significance of expiratory bronchiolar collapse symptoms in the diagnosis of emphysema].

A club-shaped resistance curve as recorded using wholebody plethysmography, as an expression of expiratory bronchial collapse is often interpreted as a sign of pulmonary emphysema. Within the framework of a prospective study involving 32 consecutive patients, a quantification of the resistance loops was carried out. The results obtained indicate that dynamic airway collapse is not specific to emphysema. Rather, there is a highly significant correlation between the degree of bronchial collapse and the elevation of total lung capacity irrespective of whether the latter is due to a reversible hyperinflation associated with bronchospasm or to emphysema of the lungs. It can, however, be seen that, in patients with reversible hyperinflation, intensive anti-obstructive treatment also leads to a decrease in, or the disappearance of, the signs of bronchiole collapse with simultaneous decrease in TLC. We conclude from this that a repeat wholebody plethysmographic examination following a lengthy period of treatment is suitable for distinguishing between bronchiole collapse in reversible hyperinflation and emphysema.

Aged↗
PubMed1990

Alpha 1-protease inhibitor moderates human neutrophil elastase-induced emphysema and secretory cell metaplasia in hamsters.

A study was undertaken to determine whether emphysema and airway secretory cell metaplasia, induced in hamsters by intratracheal treatment with human neutrophil elastase (HNE), could be moderated by pretreatment with human alpha 1-protease inhibitor (API). API (4.9 mg) was given intratracheally to hamsters 1 h before 0.3 mg HNE. Eight weeks later, lung volumes and pressure-volume relationships were measured in the anaesthetized animals. Mean linear intercepts and secretory cell indices were measured in lung sections. API given 1 h before HNE moderated the development of bronchial secretory cell metaplasia. The severity of emphysema was reduced by 75%. Clearance studies indicated that 80% of the functional activity of instilled API could be lavaged from the lungs after 1 h, indicating a 4 h half-life in the lavageable compartment of the lungs. We calculate that for 50% protection from emphysema the molar ratio of lavageable API to HNE at the time of HNE instillation was 4.8 as compared with 0.78 for 50% inhibition of elastolytic activity in vitro, indicating that API is only 16% as efficient in vivo as compared with its in vitro HNE inhibitory effectiveness. Nevertheless, we conclude that human API given intratracheally is efficacious against HNE-induced emphysema and secretory cell metaplasia.

Animals↗
PubMed1989

[The role of human neutrophil elastase in the development of human emphysema].

It has been proposed that the development of human emphysema is related to an imbalance between elastase and its inhibitors in the lung. This report describes the immunolocalization of human neutrophil elastase (HNE) in the alveolar interstitium of 6 patients with emphysema by using immunohistochemical, ultrastructure technique. The results showed that HNE is localized in the azurophil granules of neutrophils, and extracellularly on the elastic fibers of alveolar interstitium and basement membranes of epithelium and endothelium in four emphysematous lungs with chronic bronchitis. The damage of elastic fibers and basement membranes can also be observed. The HNE level of the alveolar interstitium is obviously elevated and closely related to the severity of emphysematous lesions by measuring mean linear intercept (MLI), with the correlation coefficient r = 0.84. This suggests HNE can bind to elastic fibers and basement membranes in the emphysematous lung, and damage these tissues, which might play an important role in the development of human emphysema. These findings support the elastase-antielastase imbalance hypothesis concerning the pathogenesis of human emphysema.

Adult↗
PubMed1989

Alpha 1-PI for emphysema due to alpha 1-antitrypsin deficiency.

Alpha 1-antitrypsin deficiency is a genetic disorder that may result in premature pulmonary emphysema. Affected persons are deficient in the protective protein, alpha 1-proteinase inhibitor (alpha 1-PI). The diagnosis should be considered in patients with signs of emphysema by age 40 (especially nonsmokers), those with predominantly lower lobe disease and those with a family history of premature emphysema. Recently, human alpha 1-PI has been purified and is available to prevent the development of disabling emphysema in affected individuals. Weekly infusion of the concentrate is effective in raising serum levels and is very safe, with only rare minor adverse effects.

Blood Proteins↗
PubMed1989

[Differential diagnosis of pulmonary emphysema using the CT index: LL%w].

We measured the computed tomography (CT) index, LL%w, in 81 patients of chronic obstructive pulmonary disease (COPD) and asthma. In this study we defined LL%w as the mean value of the proportion of the low density area under -950 Hounsfield units in the six lung fields: upper, middle and lower lung fields bilaterally, at deep expiration. In order to examine the usefulness of LL%w in differentiating pulmonary emphysema (PE) from bronchial asthma (BA) and chronic bronchitis (CB), we excluded the overlapped cases of each diseases. Mean value (+/- standard deviation) of LL%w in PE was 24.6 +/- 20.2% (n = 40), whereas it was 0.5 +/- 0.8% (n = 27) in BA and 0.2 +/- 0.3% (n = 14) in CB respectively. There were clear statistically differences in the values of LL%w between clinically diagnosed emphysema and others. In this quantitative study we considered that the value of LL%w within 1% would be observed nonspecifically, because the frequent existence of low density areas originated in bronchial tangents and/or motion artifacts mainly in the left lower lung field. Thus we judged that cases with over 1% of LL%w had abnormal CT findings. The relationship between clinically diagnosed emphysema and CT abnormality (LL%w greater than 1%) was significant in the analysis of the four-fold table; The CT sensitivity for diagnosing PE was 100%, the CT specificity was 87.8%, and CT accuracy was 93.8%. When cases of LL%w greater than 1% were shown in BA or CB, it would be better to consider the existence of complicated emphysema or the presence of air trapping or air spaces of any origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[The effect of bronchodilators in aerosol form on pulmonary function in patients with pulmonary emphysema].

The effects of inhaling 400 micrograms of fenoterol were investigated in patients with clinical and radiological evidence of pulmonary emphysema. Pulmonary function tests were consistent with emphysema in all patients. There was a small rise in the forced expiratory volume in one second (FEV1), but there was a much greater increase in forced vital capacity (FVC). There was not consistent change in the FEV1/FVC ratio after fenoterol administration and this ratio is misleading as an indicator of bronchodilator responsiveness in patients with emphysema. Symptomatic improvement after fenoterol is thus a valuable addition to treatment in patients with pulmonary emphysema and the response to treatment is best judged by measuring the improvement in FVC.

Adult↗
PubMedDate not supplied

Cournand lecture. Expiratory partial pressure curves in the diagnosis of emphysema.

The deformation of expiratory partial pressure curves of respiratory and inert gases (O2, CO2, He, Ar, SF6), as measured by means of mass spectrometry, was analysed in healthy subjects and in patients with asthma, chronic bronchitis and/or pulmonary emphysema. Patients with emphysema could best be distinguished from the other groups when the comparison was based on the shape of expirogram phase II. Phase II was characterized by the volume V25-50 which was expired between 25% and 50% of the inspiratory/end-tidal partial pressure difference. Comparative measurements of V25-50 of O2, CO2, He and SF6 in 10 healthy subjects (mean age: 30.8 yr) and in 10 patients with advanced emphysema (mean age: 60.8 yr) showed a linear increase of V25-50 with increasing inspired volume (VI) being 3-5 times higher in the patients than in normals. V25-50 increased with the sequence He less than SF6 approximately equal to CO2 less than O2 in both groups. The separation between phase II volumes of He and SF6 was more pronounced in the patients with emphysema than in the healthy subjects. Variations of the breathing pattern in eight healthy subjects revealed a linear increase of V25-50 with increasing VI and, to a lower extent, with increasing respiratory frequency, while a decrease of V25-50 with increasing breath-holding time and only very small changes with variations of inspiratory as well as expiratory duration were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

[Pulmonary emphysema induced by elastase: influence of the dose and effect of added collagenase].

The endotracheal deposition of pancreatic porcine elastase (EPP) at 40 u X kg-1 body weight provokes a typical pulmonary emphysema (alveoli disruption) in rats. This emphysema is significant (p less than 0.001) when quantitatively compared to a placebo (100% increase of the mean linear intercept, ILM). The EPP-treated lungs are very heterogeneous and the size of the alveoli vary as much as 30% versus 19% in controls. The emphysema is more effective at a 80 u X kg-1 dose and the individual disparities are reduced (dose effect). When bacterial collagenase (200 u X kg-1 body weight) is added to EPP, the pulmonary abnormalities (disruptions, ILM) are in no way increased (no enzymatic synergy, repair by collagenesis?). In contrast, alveolar dilation is slightly reduced 8 weeks after enzyme administration (p less than 0.05): EPP is not altered in vitro by collagenase and despite several hypothesis, the moderating effect of collagenase in vivo still remains unexplained. This result suggests that the joint presence of several proteases is not necessarily an aggravating factor in the etiopathogenesis of emphysema.

Animals↗
PubMed1988

Intrapleural injection of elastase: a model for inducing subpleural emphysema?

Subpleural emphysema induction was attempted by injecting elastase intrapleurally into rats and cats. Microscopic evaluation of emphysema (alveolar dilation and septal rupture) was compared with a quantification of alveolar dilation (Fawell-Newman method). The emphysema found in animals treated with an intrapleural injection of porcine pancreatic elastase did not appear to be specifically located in a subpleural zone, and was identical to the focal emphysema induced by an enzyme instillation into the airways. It should be noted that a placebo instillation into the feline airways sometimes induced alveolar dilation without septal disruption presumably by causing bacterial contamination. Cats were seen to be very sensitive to pleural stress since this enzyme injection produced an alveolar dilation (increased mean intercept) as significant as that in cats treated by an intrabronchial instillation of elastase (P less than 0.001).

Administration, Inhalation↗
PubMed1987

High-frequency ventilation in the treatment of infants weighing less than 1,500 grams with pulmonary interstitial emphysema: a pilot study.

Pulmonary interstitial emphysema is one of the most serious complications of the respiratory distress syndrome. Its presence significantly increases morbidity and mortality. Preliminary reports have demonstrated the success of high-frequency ventilation in the treatment of pulmonary interstitial emphysema. In a previous investigation, we were able to develop a formula for predicting death in infants weighing less than 1,500 g with pulmonary interstitial emphysema. Using this subgroup of severely affected infants, we studied the efficacy of high-frequency ventilation in nine infants. Using the Volumetric Diffusive Respirator, we observed improvement in all respiratory values measured (pH, PCO2, and PO2), a significantly decreased mean airway pressure (MAP), and improvement in neonatal mortality. Complications of severe bleeding diatheses, hypotension, bronchopulmonary dysplasia, and necrotizing tracheobronchitis were observed. Our investigation was the first to systematically choose infants who might benefit from high-frequency ventilation and to compare them with similar infants with known outcomes. We realize that the study was rescue in nature using historical controls, but we felt compelled to assure the safety of the device before randomizing less sick infants. High-frequency ventilation appears to be effective in the acute management of low birth weight infants with pulmonary interstitial emphysema.

Humans↗
PubMed1986

Ranking the severity of emphysema on whole lung slices. Concordance of upper lobe, lower lobe, and entire lung ranks.

This study describes a modification of a standard method for grading emphysema that was originally described by Thurlbeck for postmortem lungs. The study was based on pneumonectomy specimens that were fixed in inflation and sliced sagittally. The midsagittal slice was impregnated with barium sulphate and examined under water by 2 observers on 2 separate occasions. It was then re-examined on 2 additional occasions with either the upper or the lower lobe covered and the grade assigned using the uncovered lobe. In each case, the grade was assigned by comparing the specimen with the panel of pictures of paper sections of lung provided by Thurlbeck and coworkers. The data showed good agreement between grades assigned on separate observations of the same lobe. They also showed that the order of cases from no emphysema to severe emphysema was changed little when the grade was assigned by observing either the upper or the lower lobe. We conclude that this modification of the previous technique described by Thurlbeck and coworkers provides a simple reliable method of ranking surgical lung specimens as to the severity of emphysema present.

Emphysema↗
PubMed1979

Differential lung blood flows in experimental unilateral emphysema: nonvalidity of perfusion scans.

As part of an evaluation of the effects of left lung transplantation in dogs with papain emphysema of the right lung, differential lung blood flows were estimated by in vivo scintiscan of 99Mc-macroaggregated albumin (99mTc-MAA) and, after sacrifice, by direct counting of isotopically labeled carbonized microspheres. In six dogs, percentage flow to the right lung was calculated at the following four times: before and after induction of papain emphysema and 2 and 6 weeks after left lung autotransplantation. After the induction of right lung emphysema, the right lung in four of six animals continued to receive more than 50 percent of the total pulmonary blood flow. No correlation could be established between right lung blood flow determined by carbonized microsphere distribution (true right lung blood flow) and the flow determined by anterior and posterior scintiscans (apparent right lung blood flow). This discrepancy was caused by gross distortion of the right, emphysematous lungs, which had herniated into the left hemithoraces. This herniation was demonstrated by coronal slices taken through the thoraces of two additional dogs with right lung emphysema that were given radiolabeled carbonized microspheres and 99Tc-MAA and frozen after sacrifice. These results indicate that external scintiscans for which the particulate distribution technique are used are invalid in circumstances of altered lung geometry.

Albumins↗
PubMed1985

Diagnostic morphometry in emphysema and chronic bronchitis.

A morphometric technique of point counting was developed for macroscopic use in emphysematous lungs and microscopic use in bronchi to obtain actual areas and volumes, as opposed to ratios or percentages, of emphysema and submucosal glands. The results in emphysematous lungs showed that the volume of emphysema seen in one slice of one lung cannot be used to predict the volume in other slices, nor the volume of emphysema in one lung to predict the volume of emphysema in the other. The results in the airways showed that, if the volume of bronchial glands in each generation along an airway is expressed per unit of luminal surface area, a distinctive profile of gland distribution along the airway is obtained, as well as the mean volume per gland. These results are discussed in relation to the application of morphometry in individual cases for diagnostic purposes, revealing a need for a central repository of validated methods, so that each method is not repeatedly revalidated, and normal baseline data for the diagnostic morphometrist to use in deciding whether the findings in his or her individual patients are of diagnostic significance.

Bronchitis↗
PubMedDate not supplied

The role of fibrosis in the small airways in centrilobular emphysema.

Small non-respiratory bronchi of lungs of patients suffering from slight and severe centrilobular emphysema of city dwellers and from focal dust emphysema, has been studied, by means of serial sections assessing the importance of the connective tissue proliferation in relation to the cross-sectional morphology of the bronchus, its diameter and longitudinal profile. Camera lucida drawings of parietal muscle and reconstructions of the bronchial wall and lumen were done. A positive relationship between the amount of the connective tissue proliferation, the severity of emphysema and the changes in the parameters indicated was found. The repercussion of fibrosis in the small airways disease of centrilobular emphysema, can be summarized as follows: the production of areas of localized stenosis, the contribution to the development of bronchiolar deformities, the obliteration of some airways and the alteration of bronchial muscle. It can be concluded, therefore, that the fibrosis, as second main cause of small airways obstruction, has a more wide repercussion on the bronchiolar structure than that of alveolar loss, and that it can probably affects not only the "static" characteristics of the bronchial wall, but also their "dynamic" behaviour by means of disorganization of the muscle.

Airway Obstruction↗
PubMed1978

[Lung function tests in emphysema].

Several lung function tests are capable of detecting typical functional abnormalities in pulmonary emphysema, such as reduced elastic recoil of lung tissue, elevation of intrathoracic gas volumes, expiratory bronchial collapse or uneven patterns of ventilation. The measurement of elastic recoil by means of an esophageal catheter also seems to be a reliable technique for detecting early stages of emphysema, but its use for routine clinical investigations remains impracticable. The elevation of intrathoracic gas volumes determined by body plethysmography or helium dilution technique may sometimes be influenced by reversible bronchial obstructions or additional restrictive ventilatory defects. Expiratory collapse of the intrathoracic airways, however, proves to be a regular finding in advanced pulmonary emphysema. It results from decreased stability of the peripheral and central bronchial wall as well as from a shifting of bronchial and transmural pressure gradients to the peripheral airways. The occurrence of a pressure dependent expiratory stenosis can easily be demonstrated by the spirometric flow-volume curve during forced expiration, thus differentiating patients with asthma from those with chronic bronchitis and emphysema. The minimal program for detection and evaluation of emphysematous alterations of the lung by functional tests should consist in the measurement of intrathoracic gas volumes, recording of the forced expiratory volume and the analysis of the flow-volume curve.

Emphysema↗
PubMed1984

Two decades of research in the pathogenesis of emphysema.

Alpha 1 antiprotease is the major antiprotease (or antielastase) in the lungs. Neutrophils are the major source of elastase. Elastases damage interstitial elastic fibers giving rise to elastase-antielastase imbalance and to emphysema. Lung volume and volume-pressure (VP) curve is shifted up and to the left in elastase treated hamsters compared to the controls; quasi-static compliance increases from 0.52 ml/cm to 0.92 ml/cm in the elastase treated animals. The histologic, stereologic and physiologic data of hamster's emphysema are all similar to the changes observed in human emphysema. Cigarette smoke is rich in oxidants inactivating alpha 1 antiproteases. There is also a decrease in the level of alpha 1 antiproteases in lavage fluid of smokers. An intensive search is now underway for synthetic antielastases which might be safely given to persons who are at risk of developing emphysema.

Amino Acid Chloromethyl Ketones↗
PubMed1980

[Physiopathology of diffuse and bullous emphysema (author's transl)].

In emphysema, structural modifications (alveolar distension with destruction of the walls and of the pulmonary capillary bed) contribute to the understanding of pathophysiological disorders, such as increase of the static pulmonary volumes, loss of elastic recoil, impairment in gas transfer. In panlobular emphysema, the simultaneous destruction of ventilatory and circulatory structures explains the absence of shunt effect. The loss of elastic recoil is the main cause of maximal expiratory flow limitation and of bronchial obstruction which is qualified as "extrinsic". For a same degree of bronchial expiratory obstruction, the disorders of gas exchange and pulmonary haemodynamics are less pronounced in emphysema (panlobular) than in chronic bronchitis. The effects of voluminous bullae associated with diffuse emphysema are difficult to study and to demonstrate. The bullae accentuate the altered elastic properties of the emphysematous lung and contribute therefore to the expiratory flow limitation. The bullae are usually neither ventilated nor perfused; a dead-space effect is thus rare, but should be investigated. The effects of compression by the bullae of the adjacent parenchyma (excepting the haemodynamic effects) can be evaluated only by relatively sophisticated regional exploration methods, while taking into account morphological data (X-ray, angiography).

Humans↗