Rounded atelectasis. Clinical experience with 74 patients

Rounded atelectasis is an atelectasis of a peripheral part of the lung due to pleural adhesions and fibrosis causing deformation of the lung and bending of some small bronchi. From 1970 to 1986, some 74 patients with rounded atelectasis have been seen at the Lung Department. Sixty-four of these patients had been exposed to asbestos. The lesion was secondary to a benign asbestos pleurisy in nine patients and resulted from a slowly increasing pleural fibrosis in 13 patients; in the remaining 39 patients with exposure to asbestos, rounded atelectasis was a sudden finding, with earlier roentgenograms showing only plaques or being normal. Three patients had bilateral lesions, and one had no fewer than three small rounded atelectases. All of the asbestos-exposed patients were men. Ten patients (four women and six men) had not been exposed to asbestos. Two of these cases occurred after trauma and four after a pleural exudate. One of the latter was the only one which disappeared spontaneously. The lingula was affected in 33 cases, the middle lobe in 16, the right lower lobe in 12, the left lower lobe in 11, the right upper lobe in six, and the left upper lobe (except the lingula) in one. Nine patients underwent surgery. Operation should be avoided; the typical roentgenologic and CT findings combined with negative results of bronchoscopy (and, in some cases, fine-needle biopsy) will suffice to exclude malignancy.     

Clinical study of 8 patients with round atelectasis associated with asbestos exposure]

Matsubase town (where our hospital is located) has a history of environmental exposure to asbestos. We reviewed the clinical and radiological features of 8 patients with round atelectasis associated with asbestos exposure who had been examined at our hospital between 1988 and 1997. The subjects were followed up over a period ranging from 6 months to 10 years (mean: 54 months). Round tumors were detected in 6 of the patients by chest CT scans but not by chest X-ray films. Five of those patients underwent transbronchial lung biopsies, and 1 was examined by bronchography. Two patients had a history of pleural effusion. Seven of the patients exhibited round atelectasis in their lower lung fields. The clinical course of round atelectasis was unchanged in all patients. Although round atelectasis is sometimes suspected of being bronchial carcinoma, it can be diagnosed without thoracotomy, on the basis of the patient's medical history and a careful examination of radiological findings.     

Rounded atelectasis and respiratory compromise secondary to pergolide use

Rounded atelectasis is an unusual form of peripheral atelectasis that develops as a consequence of pleural disease. It is usually thought to be a benign process after malignancy and infection have been excluded. Pergolide is an ergot-derived dopamine agonist that has been associated with pleuropulmonary fibrosis and fibrotic cardiac valve disease. Pergolide-associated rounded atelectasis has occurred in patients with known asbestos exposure. We report a patient with no known asbestos exposure who developed rounded atelectasis and subsequent symptomatic diffuse restrictive pleural disease. Physicians should consider drugs early on in their work-up of rounded atelectasis as discontinuation of the agent may reverse the process.     

Rounded atelectasis complicated by obstructive pneumonia and pulmonary arterial thrombosis

A patient with a history of asbestos exposure developed rounded atelectasis. The mass was associated with local bronchial obstruction, obstructive pneumonia and arterial thrombosis. Autopsy demonstrated marked pleural thickening and radiographically inapparent asbestosis. This is the first reported case in which seemingly benign rounded atelectasis not only increased morbidity, but also contributed to mortality through airway obstruction and local arterial thrombosis.     

Asbestbedingte benigne Pleura- und Lungenerkrankungen

Asbestos particles are able to provoke fibrinogenic effects of the lung parenchyma in the sense of an asbestosis, mostly in the form of hyalines and calcified pleural plaques. Further benign reactions are pleural effusion (asbestos pleurisy), diffuse pleural fibrosis and rounded atelectasis. Plaques are the commonest pleural manifestation and are considered to be markers of exposure to asbestos. Indications of an asbestos genesis of lung parenchymal disease are a high intensity of exposure and the combination of pulmonary fibrosis and pleural plaques. The proven carcinogenic potency of asbestos particles represents a life-threatening factor. Asbestos-associated tumors are lung cancer, laryngeal carcinoma and mesothelioma. For benign pleural and pulmonary diseases estimation of the reduction in the capacity to work is oriented towards the data on pulmonary function and the results of X-ray examinations. For the recognition of lung cancer as an occupational disease, an asbestosis, an asbestos-associated pleural disease or a cumulative asbestos fibre fine particle dose at the workplace of at least 25 fibre years must be present. Alternatively, the histologic diagnosis of a minimal asbestosis is necessary.     

Environmental asbestos exposure and malignant pleural mesothelioma.

Asbestos-related benign and malignant pleural diseases are endemic in some rural parts of central Turkey because of environmental exposure to asbestos fibres. We report here epidemiological data on 113 patients with diffuse malignant pleural mesothelioma (DMPM) diagnosed in our clinic in Eski?ehir, located in central Turkey. Of the 113 patients, 59 were men and 54 women (male:female ratio = 1). Ninety-seven patients (86%) had non-occupational asbestos exposure; all were living in villages. Their mean age was 56 years. As the patients had been exposed to asbestos from birth, the latency period was equivalent to the age of the patients. Twenty-eight patients (29%) had lived in villages their entire lives. The other 69 (71%) had been born in a village but migrated to the city or had given up white-soil usage for various reasons. The mean exposure time was 55 years for those with a long exposure period and 25 years for those with a short exposure period, but there was no significant difference between the age of the disease appearance for both groups (55 and 56 years, respectively). Thus, the latency time of mesothelioma due to environmental exposure to asbestos was longer than that due to occupational exposure, but independent of the length of exposure. Soil samples from 67 villages were analysed, comprising a population of 10,120 villagers. Tremolite and some other types of asbestos were found. In conclusion, DMPM in our region is due to mainly to environmental exposure to asbestos. The risk is substantial as a large proportion of the villagers are exposed. After smoking, asbestos exposure is one of the most serious health hazards in our rural population.     

Pleural and parenchymal fibrosis mainly affecting the upper lung lobes in persons exposed to asbestos

From the County of Uppsala, Sweden, more than 1600 persons with pleural plaques and/or asbestos-related pleural thickening have been seen at the Uppsala University Hospital during a period of about 15 years. During the observation time, 40 patients developed lesions mainly affecting the upper lobes of the lung. They were all men, 41 to 78-years-old, and all had been occupationally exposed to asbestos. The mean latency time from the first exposure was 34 years. The mean width of the apical pleural thickening was 21 mm. In 21 patients the lesions were on the right side, in 15 they were bilateral, and in only four patients was the left side alone affected. Biopsies from the pleura were available in twelve patients and from the lung parenchyma in eight. The biopsies of the lungs all showed varying degrees of asbestosis and of the pleura nonspecific pleuritis. The lesions tended to progress and in all cases except one they were part of a diffuse pleural and parenchymal fibrosis involving the rest of the lung. Consequently, the pulmonary function was impaired, with the vital capacity reduced to an average of 62% and total lung capacity to 68% of the predicted value. In many patients there was contraction of the upper lobe and deviation of the trachea towards the same side. Upper lobe changes are a relatively rare complication of exposure to asbestos but are important to recognise. Other possible causes of upper lobe changes such as tuberculosis must always be excluded before the diagnosis is made.     

Hypoxemia in acute pulmonary embolism

Most patients with severe, acute pulmonary embolism (PE) have arterial hypoxemia. To further define the respective roles of ventilation to perfusion (VA/Q) mismatch and intrapulmonary shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean PaO2, 67 +/- 11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVA/QT 16.6 +/- 5.1 percent) was present in all patients. The relative contributions of VA/Q mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study. Although all patients had some degree of VA/Q mismatch, the two patients studied early (ie, less than 48 hours following acute PE) had normal chest x-ray film findings and no significant shunt; VA/Q mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 +/- 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute PE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.     

Mesothelioma and asbestos-related pleural diseases

At present, the use of asbestos is not regulated at a worldwide scale. Moreover, there is a latency period between asbestos exposure and the manifestations of asbestos-related diseases. Consequently, pulmonologists are still dealing with consequences of asbestos exposure, which mainly occur at the pleural surface. The aim of this review is to provide an overview of asbestos-related pleural diseases. We summarized the most relevant data for the diagnosis and the management of benign asbestos pleural effusions, pleural plaques, diffuse pleural thickening and rounded atelectasis. Special attention is dedicated to malignant pleural mesothelioma, given the challenging issues of this disease, the recent advances in its management and the dynamism of research in this area.     

Distribution of pulmonary blood flow in relation to atelectasis in premature ventilated lambs

To investigate the ability of the preterm, ventilated lung to redirect blood flow away from atelectatic regions, we studied lambs with respiratory distress syndrome and spontaneous atelectasis or atelectasis caused by bronchial obstruction with a balloon catheter. Pulmonary blood flow distributions were measured by quantifying 15-mu, microsphere-associated radioactivity within multiple pieces of lung. Lambs with well aerated or very atelectatic lungs had relatively uniform blood flow/gram lung in all pieces of lung. Blood flow was much less uniform in lungs with both aerated and atelectatic regions. In 9 lambs with spontaneous atelectasis that included 25 +/- 5% (mean +/- SE) of the lungs by weight, blood flow was 29 +/- 4% less to atelectatic than to aerated lung volumes (p less than 0.01). In 5 lambs with well-aerated lungs, 18 +/- 3% of the lung by weight was made atelectatic by balloon occlusion of a major lower lobe bronchus. There was a 44 +/- 11% decrease in blood flow to the atelectatic lung segments. These studies document the ability of the lung of the premature, ventilated lamb to shunt pulmonary blood flow away from atelectatic lung volumes.     

Rounded atelectasis associated with pulmonary lymphangioleiomyomatosis

Rounded atelectasis is an unusual form of lung collapse that develops as a consequence of pleural diseases. Among a variety of conditions, asbestos inhalation has been attributed in most cases, but many other causes have also been implicated. Here, we describe the first case of rounded atelectasis and pneumothorax associated with pulmonary lymphagioleiomyomatosis.     

Association between neutrophil concentration in bronchoalveolar lavage fluid and recent losses in diffusing capacity in men formerly exposed to asbestos.

It has been observed widely that some individuals exposed to asbestos will experience continued losses of lung function after asbestos exposure ceases. Unfortunately, there are few data on factors that determine clinical course, limiting the clinician's ability to determine prognosis in an individual case and restricting the possibility for testing or targeting any potential intervention to alter the course among the millions at risk. In an attempt to address this question, we studied a volunteer population of 50 such men from among a stable, heterogeneous population of asbestos-exposed workers who had been continuously followed in our occupational medicine clinics for up to 12 years (mean, 6.3 years); most had some clinical or roentgenographic sign of asbestos effect, pleural or parenchymal. Each subject was reexamined clinically, functionally, and roentgenographically. Asbestos and tobacco exposure histories were carefully reviewed with the subjects and quantified based on these reports and available data regarding the various work environments from which they came. Subsequently, each underwent a bronchoalveolar lavage to assess cellularity and levels of various proteins. The levels of risk factors, clinical findings, and biologic parameters from lavage were examined for their relationship to serial changes in lung function during the period over which they had been previously followed. Results of the study demonstrate that serial changes in lung function were not closely related to level or length of prior exposure, smoking behavior, chest roentgenographic findings, or lung volumes. Progressive loss of diffusing capacity for carbon monoxide (Dco) was significantly associated with two factors: level of neutrophil concentration in lavage fluid (0.043 +/- 0.016 ml/min/mm Hg/yr drop for each 0.1 x 10(4) neutrophils per milliliter, p = 0.02) and the level of Dco itself (0.17 +/- 0.07 ml/min/mm Hg/yr drop for each 10 percent decrease in percent Dco predicted, p = 0.01). The relationship with neutrophil concentration was statistically independent of the association with Dco itself and stronger; it persisted when loss of Dco was adjusted for baseline value. Lung volume changes were not associated with any predictor variables, alone or in combination. We conclude that the presence of neutrophils in bronchoalveolar lavage fluid is associated with recent disease progression that may have implications in studies of the mechanisms of asbestos-associated disease and in clinical treatment of patients at risk.     

Resection of the right middle lobe and lingula in children for middle lobe/lingula syndrome

STUDY OBJECTIVE: To review our experience with specific characteristics, indications, and results of pulmonary resection in children with middle lobe/lingula syndrome. DESIGN: Retrospective cohort study. SETTING: Thoracic Surgery Department, Chest Diseases Hospital, Kuwait. Patients and intervention: Thirteen children with middle lobe, lingula, or both syndromes were treated with pulmonary resection from January 1995 to December 1999. RESULTS: The mean age was 7.5 years (range, 5 to 10 years). Eight patients were girls, and five were boys. All patients underwent high-resolution CT and bronchoscopy. Bronchiectasis and atelectasis of right middle lobe, lingula, or both was noted in nine patients. Bronchial stenosis and inflammation of the bronchus was found endoscopically in four patients. The indications for surgery were recurrent respiratory tract infection with persistent atelectasis and bronchiectasis in nine patients, and recurrent respiratory tract infection with bronchiectasis in four patients. A right middle lobectomy was done on seven patients and a lingulectomy on four patients. Two patients underwent staged thoracotomies (right middle lobectomy and lingulectomy). There were no operative deaths. Only two patients had postoperative complications: atelectasis (n = 1), and pneumothorax (n = 1). Mean follow-up was 3.5 years (range, 3 to 5 years) for all patients. Nine patients were asymptomatic, and four patients had improved. CONCLUSION: Right middle lobe or lingula syndrome with the presence of bronchiectasis, bronchial stenosis, or failure of lung to re-expand are indications for early pulmonary resection.     

Bronchoalveolar lavage cell and lymphocyte phenotype profiles in healthy asbestos-exposed shipyard workers

The cellular and lymphocyte phenotypic composition of bronchoalveolar lavage (BAL) fluid and peripheral blood (PB) from 15 healthy, nonsmoking, asbestos-exposed shipyard workers (AEW) and 10 nonsmoking, age-matched unexposed workers (UEW) were compared. None of the AEW had clinical, radiographic, or physiologic evidence of asbestosis, but six had radiographic evidence of pleural plaques and/or thickening. The mean duration of asbestos exposure was 16.3 +/- 2.3 yr, and the mean period since exposure was 10.8 +/- 0.5 yr. All but three of the AEW and none of the UEW had asbestos bodies detected in the first 20 ml of BAL fluid recovered (0.1 to 35 asbestos bodies/ml). The AEW had a significantly higher mean percentage (19.1 +/- 2.8% versus 9.7 +/- 1.6%) and concentration (31.6 +/- 5.2 x 10(3) cells/ml versus 14.7 +/- 2.5 x 10(3) cells/ml) of BAL lymphocytes compared with that in the UEW, with an increased mean concentration of each phenotype measured. In PB, the mean lymphocyte concentration was also higher in the AEW than in the UEW (2.0 +/- 0.3 x 10(3) cells/ml versus 1.5 +/- 0.3 x 10(3) cells/ml), but the difference was not statistically significant, and there was no increase of any phenotype measured. BAL lymphocytosis did not correlate with exposure history or BAL asbestos body count, but was greater in AEW with pleural abnormality (30.1 +/- 2.9% versus 11.8 +/- 1.6%). BAL concentrations of CD-20, CD-3, and CD-4, but not of CD-8 cells were significantly increased compared with those in the AEW without pleural abnormality. Further longitudinal studies are needed to determine the prognostic significance of these findings.     

Impaired cardiac autonomic functions in patients with environmental asbestos exposure: a study of time domain heart rate variability

Environmental asbestos exposure is related to diffuse pleural disease (thickening and calcification) and restrictive pulmonary disease. To assess cardiac autonomic system, we investigated the time domain heart rate variability (HRV) by Holter monitoring and their correlation with pulmonary function tests in patients with pleural disease caused by environmental asbestos exposure. We studied 45 patients (26 men, 19 women, aged 62.67 +/- 10.1 years) and 35 healthy patients who had similar sex and age profile to the patients (24 men, 11 women, aged 59.31 +/- 8.4 years). The asbestosis group was divided into 3 subgroups according to the severity of forced vital capacity (FVC) severe (group 1) (n = 12): FVC less than 50% of expected, moderate (group 2) (n = 16): FVC 64%-51% of expected and mild (group 3) (n = 17): FVC 65%-80% of expected. HRV parameters were significantly different among all groups (P<.0001). Comparing the 4 groups (subgroups and control group), group 1 had the lowest mean HRV values and controls had the highest mean HRV values (P<.0001). Severity of autonomic dysfunction was correlated with the severity of FVC and arterial oxygen pressure. Right ventricular end-diastolic internal diameter (RVEDID) and right ventricular end-systolic internal diameter (RVESID) values were significantly increased in patients (P <.0001, P < 0.0001, respectively). Pulmonary acceleration time (AcT) values were shorter in all patient groups than control group (P <.0001). It was shortest in group 1. Group 2 and 3 had shorter AcT values than control group. HRV parameters were correlated positively with AcT values and negatively with RVEDID and RVESID values. In conclusion, patients with restrictive pulmonary disease due to environmental asbestos exposure had autonomic dysfunction, which was correlated with the severity of restriction. This was thought to be the result of chronic hypoxia, pulmonary hypertension, and right ventricular enlargement.     

Epidemiology of pleural mesothelioma in a population with non-occupational asbestos exposure

Background and objective:   This study describes the epidemiology of malignant pleural mesothelioma (MPM) in a rural population with environmental asbestos exposure.
Methods:   Patients with diagnosed MPM were recruited and their relevant demographic and exposure data were analysed.
Results:   A total of 131 patients with MPM (59 men, 72 women) were studied. The patients' mean age was 57.8 years and the mean exposure duration was 28.9 years. The cumulative fibre count of the villagers ranged from 0.19 to 14.61 fibre/mL-years. Of the 131 patients, 85 had epithelial cell type, 20 had mixed, and eight had sarcomatous pleural mesothelioma. No significant relationship was found between asbestos fibre type and age, exposure period, or cellular type of MPM; similarly, no significant relationship could be found between the cellular type and age or exposure period. Patients with sarcomatous mesotheliomas were considerably older. Only five of 131 (3.8%) patients had a family history of mesothelioma.
Conclusions:   Environmental exposure to asbestos begins at birth and this may be important in the age of disease onset, if a threshold model for cancer initiation is operative. Both men and women had an excess risk of mesothelioma. Given that a family history of MPM was not common in this relatively homogenous patient group, a genetic predisposition to mesothelioma appears unlikely.     

Assessment of 18F-fluorodeoxyglucose dual-head gamma camera in asbestos lung diseases.

The purpose of this study was to evaluate the performance of 18F-fluorodeoxyglucose (18FDG) imaging via coincidence detection emission tomography (CDET) in identifying malignant lesions in subjects exposed to asbestos. A total of 30 patients exposed to asbestos underwent 18FDG-CDET between January 2000 and June 2003. A CDET scan of the thorax and abdomen was performed 60 min after injection of 18FDG in fasting patients, and results were obtained in slices in three axes. The CDET results were compared to those from computed tomography (CT), and pleural or surgical biopsy in patients with positive 18FDG-CDET results. All primary malignant mesotheliomas accumulated 18FDG (n=6), and, in two patients, CDET findings were superior to those of CT, allowing early detection. In two cases, lung carcinomas with malignant pleural effusion were also detected. There were five false positive CDET results: three unilateral pleural thickening, one rounded atelectasis, and one benign lung nodule. All patients with pleural plaques showed no significant 18FDG uptake. Malignant diseases were detected by 18FDG-CDET imaging with a sensitivity of 89% and specificity of 71%. Coincidence detection emission tomography can identify malignant mesothelioma in selected subjects exposed to asbestos. Coincidence detection emission tomography appears to be a useful noninvasive method for the follow-up of subjects with exposure risk of asbestosis.     

Macroscopic subtypes of asbestosis in relation to the amount of asbestos in 63 Japanese autopsy cases]

Atelectatic induration (AI) and honeycombing (HNCB) are two distinct macroscopic features of asbestosis. The current study was undertaken to clarify whether or not there might be a relation between the macroscopic type of asbestosis and burden of asbestos fibers in the lung. The material (N = 63) derived from 58 autopsies and 5 surgically removed lungs with lung cancers, which comprised 22 cases of AI (mean age: 67 years: 20 males and 2 females) and 41 cases of HNCB (mean age: 66 years: 38 men and 3 women) types of asbestosis, respectively. The quantification of asbestos bodies (AB) and fibers (AF) was carried out using Kohyama's method. The AI type showed 260,000 +/- 460,000 AB per 1g of wet lung and 920,000 +/- 1,360,000 AF per 1g of dry lung, whereas HNCB showed 44,000 +/- 93,000 AB and 200,000 +/- 490,000 AF, respectively. These differences were statistically significant between the types of asbestosis (p < 0.01). Diffuse pleural thickening and upper lobe involvement were more advanced in the AI type and the differences were statistically significant between subtypes (p < 0.05). In conclusion, asbestos load is considered to be a factor related to the macroscopic subtype of asbestosis.     

A case of triple malignancies (gastric cancer, lung cancer and malignant pleural mesothelioma) after asbestos exposure]

This case study centers on a seventy-eight-year-old man with triple malignancies, namely, gastric cancer, lung cancer and malignant pleural mesothelioma, all of which developed at different times. The histological types were adenocarcinoma of the stomach, squamous cell carcinoma of the lung and sarcomatous malignant pleural mesothelioma. Gastric cancer was treated by endoscopic mucosal resection 2 years ago. The patient presented with a chief complaint of dyspnea, and right pleural effusion was found on chest radiography. The right-side effusion disappeared spontaneously, but a small mass on the left side was diagnosed as lung cancer, and so left inferior lobe resection was performed. Malignant pleural mesothelioma appeared after one year of pleural effusion and the patient died of mesothelioma one year after diagnosis. At autopsy, the gastric cancer and lung cancer had not relapsed and malignant pleural mesothelioma had metastasized to the lung, liver, adrenal gland and small intestine. He was a sailor by profession and it was obvious that he had been exposed to asbestos, because 538 asbestos bodies per 5 g of wet lung tissue were detected. His advanced age was one of the risk factors for the multiple malignancies, and the asbestos exposure was considered to have compounded these hazards to cause the triple malignancies. It is well known that lung cancer and malignant mesothelioma are induced by asbestos exposure, but multiple cancers including lung cancer and malignant mesothelioma are extremely rare.     

Round atelectasis in sarcoidosis

ABSTRACT: Round atelectasis is a benign inflammatory condition most frequently observed in patients with asbestos exposure but it can also result from a variety of chronic pleural diseases like infection. It has not previously been described in sarcoidosis. We report the occurrence of round atelectasis in four previously diagnosed sarcoidosis patients who were under follow up at our outpatient clinic. Three patients had symptoms consisting of thoracic pain, dry cough and sensation of fullness at the posterior thorax, respectively. Chest roentgenogram showed subpleural or pleural based opacity with diameters ranging from 2 to 3 cm in each of the patients. Chest computerized tomography (CT) revealed features of round atelectasis. Fiberoptic bronchoscopy with transbronchial lung biopsy was performed. Diagnosis was confirmed by the histopathologic examination of the biopsy samples. The mechanical influence of a prior pleural effusion due to sarcoidosis may be the predominant mechanism underlying the onset of round atelectasis in these patients. Clinicians should bear in mind the possibility of sarcoidosis as an etiologic factor for round atelectasis.